Head trauma

HEAD TRAUMADr. Isa Basuki

Department of Surgery, AWS General Hospital

Faculty of Medicine, Mulawarman University

INTRODUCTION

Head trauma or Traumatic brain injury (TBI) is a disruption or alteration of brain function due to external forces

The external forces creating the injury may be the result of: acceleration or deceleration, direct compression, penetrating objects, combined effects, complex mechanisms

INTRODUCTION

It may produce: fractures, contusion, subarachnoid hemorrhage (SAH), subdural hemorrhage (SDH), epidural hemorrhage (EDH), Intraparenchymal hemorrhage (IPH), diffuse axonal injury (DAI).

All injuries and symptoms should be taken seriously

EPIDEMIOLOGY

Approximately 1.4 million people per year suffer TBI

1.1 million are treated and released, 240,000 are hospitalized, and 50,000 die

Common causes: Falls (28%), Motor vehicle accidents (20%), Pedestrian impact (19%), Assault (11%)

Age distribution with the greatest risk in 0–4 and 15- to 19-year-olds.

Males have 1.5 times the risk of females

PATHOPHYSIOLOGY

Primary injuries disruption of scalp (lacerations), bone (cranial vault, skull base,

facial bones), vasculature

(SDH/EDH/IPH/intraventricular hemorrhage [IVH], traumatic aneurysm),

brain parenchyma (contusion, DAI)

Secondary injuries hypoxemia, ischemia, initial hyperemia, cerebral edema, expansion of hemorrhages

increased intracranial pressure (ICP),

seizures, metabolic abnormalities systemic insults

GENERAL PRINCIPLES

SYSTEMIC EVALUATION AND RESUSCITATION

Assessment and treatment often begins in the prehospital setting

The basic principles of trauma resuscitation rapid assessment and maintenance of an airway, breathing, and circulation

medical and surgical history should be obtained including: the events preceding a trauma, a description of the accident scene, accurate description of the patient’s neurological baseline, any subsequent changes to the neurological status

SYSTEMIC EVALUATION AND RESUSCITATION

In the newborn or premature infant cephalohematoma may allow enough displacement of blood to produce hemodynamic instability

Raccoon’s eyes (periorbital ecchymosis),

Battle’s sign (postauricular ecchymosis), suggest a basilar skull fracture

otorrhea/rhinorrhea

Puncture wounds penetrating injury to the brain, spinal cord, sympathetic plexus, or vasculature

Bruits of the carotid artery carotid dissection or carotidcavernous fistula

NEUROLOGICAL EXAMINATION

Accurate neurological examination is essential

The exam may be limited due to: patient’s age level of education native language presence of sedative or paralytic medication

• Illicit drugs • hypotension • hypoxia • hypothermia• hypoglycemia

PUPILLARY RESPONSE

parasympathetic, pupilloconstrictor, and light reflex (pupillary reflex) can be easily and rapidly assessed in the unconscious patient

Damage to the Edinger–Westphal nucleus or uncal compression of CN III at the tentorial notch pupillary dilatation (≥4 mm)

Direct orbital trauma can also result in pupillary dilation/fixation in the absence of temporal lobe herniation or intracranial hypertension (ICHTN).

GLASGOW COMA SCALE

standard for objective measurement of TBI severity

three parameters: best eye opening [E] best verbalization [V], best motor function [M]

GCS = 13 – 15 mild TBI

GCS = 9 – 12 moderate TBI

GCS = 3 – 8 severe TBI

If the patient is intubated 1 for the verbal component and the overall scored is annotated with a “T.” Examples: M4/VT/E2 = 4 + 1 + 2 = 7T

GLASGOW COMA SCALE (RECOMMENDED FOR AGE ≥4)

GLASGOW COMA SCALE FOR CHILDREN (RECOMMENDED FOR AGE <4)

RADIOGRAPHIC EVALUATION

PLAIN X-RAYS

For evaluating and clearing the cervical spine.

The spine is imaged from the occiput to T1 and a C-collar

AP, lateral and odontoid views are the most useful

T- and L-spine films are obtained based on: mechanism of injury, degree of neurological deficits, pain

CT SCAN

CT scan findings after trauma: SDH, EDH, SAH, IPH, IVH contusions hydrocephalus cerebral edema or anoxia skull fractures ischemic infarction (if >12 hours

old) mass effect midline shift

Indications for an initial post-traumatic CT scan: GCS ≤ 14 unresponsiveness, focal deficit, amnesia for the injury, altered mental status, signs of basilar skull fracture

MRI

better parenchymal resolution

can evaluate infarction, ischemia, edema, and DAI

helpful to determine ligamentous injury of the spine or traumatic cord injury

generally performed after the initial trauma evaluation and resuscitation have been completed

Disadvantages: limited availability slower image acquisition time increased cost

CLASSIFICATION AND SURGICAL MANAGEMENT OF SPECIFIC

INJURIES

SKULL FRACTURES

can be described by: The state of the overlying scalp (closed or open), The number of bone fragments (simple or compound), The relationship of bone fragments to each other (depressed or nondepressed), Whethert the fracture enters or widens an existing cranial suture (diastatic,

more common in children), and whether it involves the cranial vault or skull base

lower force impacts (falls from standing) more linear, closed, and without dural laceration

Higher force impacts (MVA, falls from heights, penetrating trauma) compound, open fractures with underlying dural or cerebral injury

“Ping-pong” fractures are greenstick-type fractures usually seen in newborns

CT bone windows showing ping-pong skull fracture.

The multiple nondisplaced linear lucencies are normal sutures.

SKULL FRACTURES

Associated clinical signs of: calvarial skull fractures gross deformity and palpable skull fracture in

patients with open scalp lacerations Basilar skull fractures postauricular or periorbital ecchymosis,

hemotympanum or laceration of the external auditory canal, and CSF rhinorrhea or otorrhea

Cranial nerve injuries: fractures of the cribriform plate (CN I, anosmia) optic canal (CN II, visual deficit) temporal bone (CN VII, facial weakness; or CN VIII, hearing loss)

Severe basilar skull fractures pituitary gland injury endocrinopathies

SKULL FRACTURES

Direct injury to vasculature that penetrates the skull base Arterial dissection, Traumatic aneurysm formation, Traumatic carotid-cavernous sinus fistula with symptoms:

cranial neuropathies chemosis bruits Strokes

SKULL FRACTURESRADIOGRAPHIC DIAGNOSIS

Differential Diagnosis of Fractures on Skull X-Rays

SKULL FRACTURESRADIOGRAPHIC DIAGNOSIS

Most skull fractures are discovered by CT scan

Plain films may be superior to CT scan in discovering linear calvarial fractures parallel to the skull base

CT angiograms/venograms to assess fractures involving skull base foramen containing vasculature (e.g.,

carotid canal, foramen magnum) fractures that cross major venous sinuses (superior sagittal or transverse

sinuses, jugular foramen).

Closed, nondisplaced fractures do not require immediate intervention

Open skull fractures should be debrided and carefully inspected and all should receive antibiotics

SKULL FRACTURES

Relative indications for surgical elevation of a depressed skull fracture: depression of more than 8–10 mm or more than the thickness of the

skull Focal neurological deficit clearly attributable to compressed underlying

brain, Significant intraparenchymal bone fragments (implying dural

laceration), Persistent deformity after all swelling has subsided

Current recommendations: surgical repair open fractures depressed greater than the thickness of

the cranium nonoperative management open depressed cranial fractures if there

is no evidence of dural penetration

CT bone windows showing a depressed skull fracture that

required surgical elevation and dural repair.

The patient also had an underlying brain contusion and presented with

a receptive aphasia

SKULL FRACTURES

Indications for surgery: significant intracranial hematoma, depression >1 cm, frontal sinus involvement, Gross cosmetic deformity, wound infection, pneumocephalus, gross wound contamination

FOCAL CEREBRAL INJURIESCEREBRAL CONTUSION

Injuries to the superficial gray matter of the brain

External forces acceleration of the intact skull or fractured skull fragments toward the

brain surface or the brain continues to move toward the rapidly decelerating skull and

dural folds of the falx or tentorium

“Coup” lesions ipsilateral to the impact site adjacent calvarial fractures

“Contrecoup” lesions opposite the coup lesion rebounding brain striking the inner table of the skull

CT scans patchy, hyperdense lesions with a hypodense background

FOCAL CEREBRAL INJURIESINTRAPARENCHYMAL HEMORRHAGE

8.2% of all TBI and up to 35% of severe TBI cases

Delayed traumatic intracerebral hemorrhage (DTICH) approximately 20% of cases and most occur within 72 hours of the initial trauma

Indications for surgical decompression: neurological decline referable to the TICH lesion TICH > 50 cm3

GCS = 6 – 8 with frontal or temporal contusions >20 cm3 with midline shift ≥5 mm and/or cisternal compression on CT scan

Surgical procedures range Localized frontal or temporal craniotomy with resection of underlying focal

clot Extensive craniectomies with duraplasty, evacuation of severely contused

brain, or temporal lobectomy

FOCAL CEREBRAL INJURIESEPIDURAL HEMORRHAGE

blood collects in the potential space between the dura and inner table of the skull

1% of all head trauma admissions and in 5–15% of patients with fatal head injuries

more common in males (M:F = 4:1)

usually occurs in young adults

90% of EDHs are due to arterial bleeding fracture at the middle meningeal artery groove

10% are due to venous bleeding violation of a venous sinus by an occipital, parietal, or sphenoid wing fracture


Location of EDH: lateral convexity of a cerebral hemisphere (70%), frontal (5–10%), parieto-occipital (5–10%), posterior fossa locations (5–10%)

CT scan hyperdense, biconvex (lenticular) mass adjacent to the inner table of

the skull (84%) medial edge being straight (11%) crescentic resembling an SDH (5%)

Additional associated findings SDHs and cerebral contusion

CT showing epidural hemorrhage. Note the biconvex- or lenticular-shaped hemorrhage.

On the bone windows this was adjacent to a diastatic left lambdoid suture.


Clinical presentation: Brief post-traumatic loss of consciousness

(LOC) 40% Lucid interval (80%) Obtundation Contralateral hemiparesis, Ipsilateral (85%) pupillary dilatation (60%)

Kernohan’s phenomenon (a false localizing sign) local hemispheric mass effect compression of the contralateral brainstem

against the tentorial notch ipsilateral hemiparesis

Mortality unilateral EDH (5–12%) Bilateral EDH (15–20%) no lucid interval (20%) posterior fossa location (25%)

concurrent acute SDH (25–90%)


Rapid diagnosis and intervention when indicated optimize the outcome

Guidelines: Surgical EDH of >30 cm3 should be evacuated regardless of GCS score Conservative EDH of <30 cm3 and <15 mm of thickness and >5 mm

midline shift (frequent neurological examinations and serial CT scan)

Relative indications EDHs that are neurologically symptomatic or have a maximal thickness >1 cm.

Absolute indication acute EDH in coma (GCS ≤ 8) and anisocoria

Craniotomy complete clot evacuation with meticulous hemostasis and use of tackup sutures to decrease the potential epidural space

FOCAL CEREBRAL INJURIESSUBDURAL HEMORRHAGE

blood collects between the arachnoid and inner dural layer

Type/variants: hyperacute (<6 hours), acute (6 hours to 3 days), subacute (3 days to 3 weeks), chronic (3 weeks to 3 months)

Etiologies: traumatic stretching and tearing of cortical bridging veins coagulopathy, subdural dissection of ICH, rupture of a vascular anomaly (AVM, aneurysm, cavernoma, dural AV

fistula) into the subdural space

CT showing an acute subdural hemorrhage. Note that crescentic hemorrhage crosses under the right coronal suture.

APPEARANCE OF SDH ON CT AND MRI

FOCAL CEREBRAL INJURIESSUBDURAL HEMORRHAGE

Guidelines suggestion for SDH evacuation: acute SDH with thickness >1 cm or a midline shift >5 mm regardless GCS

score acute SDH <1 cm thick and midline shift <5 mm and in coma (GCS ≤8) if:

GCS decreases by 2 points. pupils that are asymmetric or fixed/dilated. the ICP ≥20 mm Hg.

Craniotomy ASAP, may require craniectomy and duraplasty for ICP control

Mortality 50% to 90% (related more to the underlying injury, increased in the elderly and in patients on anticoagulants)

Outcome mortality improvements from 66–90% down to 30–59% if the patient was operated on in less 4 hours

FOCAL CEREBRAL INJURIESSUBARACHNOID HEMORRHAGE

blood located between the pial and arachnoid membranes

results from venous tears in the subarachnoid space

33% of patients with moderate head injury and is found in nearly 100% of trauma patients at autopsy.

CT scan sulcal hyperdensity

MRI FLAIR hyperintensity

Clinical presentation headache, emesis, and lethargy

Treatment supportive using IV fluids, anticonvulsants, and nimodipine (to prevent vasospasm)

CT with arrow pointing to a small traumatic subarachnoid hemorrhage in left central sulcus

CT AND ANGIOGRAM OF ICH

DIFFUSE CEREBRAL INJURIESCONCUSSION

an alteration of consciousness resulting from nonpenetrating injury to the brain

Classic symptoms: headache confusion amnesia LOC

Additional symptoms: Deficits of motor function (incoordination, stumbling), Speech (slowed, slurred, incoherent), Memory or processing (amnesia, short-term memory loss, difficulty concentrating or

focusing, inattention, perseveration, easy distractibility), Orientation (vacant stare, “glassy eyed,” unable to orient to time/date), Irritability

CONCUSSION GRADING

DIFFUSE CEREBRAL INJURIESCONCUSSION

Physiological responses transient increase in cerebral blood volume due to loss of vascular autoregulation

mild cases mild cerebral swelling, or hyperemia

more severe cases malignant cerebral edema elevated ICPs refractory to nearly all measures and 50–100% mortality “second impact syndrome”

CT scan subtle or nonexistent and include mild diffuse swelling secondary to hyperemia

Treatment recognition of injury

DIFFUSE CEREBRAL INJURIESDIFFUSE AXONAL INJURY

traumatic axonal stretch injury caused by overlying cerebral cortex and underlying deep brain structures moving at different relative speeds

Mild axonal stretching + transient neuronal dysfunction

Severe axonal shearing + permanent neuronal damage

80% microscopic and nonhemorrhagic with impaired axonal transport and delayed axonal swelling

CT scans normal (50–80%) or hyperdense petechial hemorrhage (20–50%)

MRI multifocal hyperintense T2 at frontal lobes (67%), corpus callosum (20%), and brainstem (10%)

Prognosis generally related to the patient’s age, presenting neurological status, and trajectory of neurological improvement.

MANAGEMENT OF TRAUMATIC BRAIN INJURY

MEDICAL MANAGEMENT

Basic measures: ICU setting with frequent monitoring of:

vital signs, fluid intake and output neurological examinations (as permitted)

Multiple invasive lines for: blood pressure (arterial line), volume assessment (Swan–Ganz), administration of fluids, medication, or nutrition (central venous catheter), urine output or temperature (Foley catheter), ICP, cerebral tissue oxygenation, or cerebral blood flow (CBF)

MEDICAL MANAGEMENT

kept normothermic and euvolemic with isotonic fluids

GI prophylaxis against Cushing’s (stress) ulcer

head of bed should be elevated to 30–45°

neck should be kept midline

cervical collar and endotracheal tube stabilizer prevent compression of the jugular veins promote venous outflow from the head

BLOOD PRESSURE AND OXYGENATION

single episode of hypoxemia (apnea, cyanosis or O2 saturation <90% in the field, or PaO2 < 60 mmHg) or hypotension (SBP < 90 mmHg) predictor of worse outcome

Oxygen saturation and blood pressure monitoring started in the field and continued at hospital setting

Goal identifying, avoiding, and rapidly correcting hypoxemia or hypotension

Oxygen administration start as early as possible (may require endotracheal intubation)

isotonic or hypotonic saline, plasma, colloid, blood, or intravenous pressors to avoid hypotension

INTRACRANIAL PRESSURE ASSESSMENT

modified Monro–Kellie hypothesis Assuming that the skull is completely inelastic, the ventricular space is

confluent pressures are equally and readily transmitted throughout the intracranial space

balance between the brain, blood volume, and CSF in the intracranial space Increases in the volume or addition of new components compensatory

decreases in other constituents to maintain the same ICP

Mildly increased, localized pressure in the brain neurological dysfunction of the immediate area

severe pressure increases local tissue compression, shift of intracranial structures, subfalcine and transtentorial herniation

most severe compression at the level of the brainstem, occlusion of brainstem vasculature, infarction, and death.

ICP MONITORING

Normal ICPs: <10–15 mm Hg in adults 3–7 mm Hg in children 1.5–6 mm Hg in infants

ICP monitoring is recommended for: patients with severe TBI (GCS= 3 – 8) abnormal CT scan or with severe TBI considered in patients without an accurate neurological examination

due to sedatives, paralytics, or general anesthesia required

Higher mortality ICP persistently above 20 mm Hg.

ANALGESICS AND SEDATIVES

Pain and agitation can cause increased sympathetic tone, increased temperature, and hypertension increased venous and ICP, increased metabolic demand, resistance to controlled ventilation

may require sedatives or psychotropic medication to prevent self-injurious behavior and dislodgement of airway, vascular lines, or monitoring equipment

If on ventilators, may require sedatives or paralytics to allow appropriate lung excursion or timing of breath patterns.

side effects hypotension, alteration or obliteration of the neurological examination, and rebound ICP elevation

ANALGESICS AND SEDATIVES

AGENTS ADVANTAGESHaloperidol relatively nonsedating quality useful for

agitation

fentanyl and its related derivatives (remifentanil, sufentanil)

short acting, reversible, and conducive to administration by continuous infusion for acute and longer-term analgesia

Midazolam short-acting benzodiazepine effective for sedation of the ventilated TBI patient.

Propofol hypnotic anesthetic with rapid onset and a very short half-life facilitates rapid neurological assessment, reduces cerebral metabolism and oxygen consumption and exerts a neuroprotective effect

HYPEROSMOLAR THERAPY

Mechanism of Mannitol: first few minutes produces immediate plasma expansion with reduced

hematocrit and blood viscosity improved rheology, and increased CBF and O2 delivery reduces ICP

Over the next 15–30 minutes produces an osmotic effect with increased serum tonicity and withdrawal of edema fluid from the cerebral parenchyma.

Bolus ICP reduction is evident at 1–5 minutes and peaks at 20–60 minutes

Initial bolus of mannitol 1 g/kg

Subsequent administration at smaller doses and longer intervals (i.e., 0.25–0.5 g/kg Q 6 hours)

Furosemide may also be used synergistically with mannitol

HYPEROSMOLAR THERAPY

Serum osmolality should be monitored (>320 mOsm/L use of mannitol should be restricted)

Larger dose (1,4 g/kg) improved outcome of the comatose patients with: operative subdural hematomas operative intraparenchymal temporal lobe hemorrhages abnormal pupillary dilatation

HYPERTONIC SALINE

lower ICP through two mechanisms:1. oncotic pressure gradient, across the BBB, results in mobilization of water from brain

tissue and hypernatremia2. rapid plasma dilution and volume expansion, endothelial cell and erythrocyte dehydration,

and increased erythrocyte deformability improvements in rheology, CBF, and oxygen delivery

Administration: continuous infusion of 25–50 mL/h of 3% saline bolus infusions of 10–30 mL of 7.2%, 10%, or 23.4% saline solution

Onset minutes and may last for hours

Serum sodium and osmolality levels should be aggressively followed central pontine myelinolysis (most often in patients with preexisting, chronic hyponatremia)

may also induce or exacerbate pulmonary edema in patients with underlying cardiac or pulmonary deficits

HYPERVENTILATION

lowers PCO2 with subsequent vasoconstriction, reduction of cerebral volume, and reduction in ICP

Time of onset 30 seconds to 1 hour,

Peak effect 8 minutes and may last up to 15–20 minutes

should be avoided during the first 24 hours postinjury CBF is most reduced

after the first 24 hours short-term, mild HPV (PCO2 = 30 – 35) ICP control

moderate HPV should be avoided

Prophylactic HPV (PCO2 ≤ 25) is contraindicated increased ischemia and worse outcomes

DECOMPRESSIVE CRANIECTOMY

The bone is removed, the lesion is resected, and the dura and bone are replaced

Severe cases diffuse cerebral edema, contusions of large size in eloquent areas, or multiple, coalesced contusions leave the bone flap off.

Most common unilateral hemispheric

Bifrontal and bilateral hemispheric craniectomies based on the location and severity of the underlying lesion(s)

The dura is opened widely and areas of noneloquent contused and devitalized brain can be removed if required

hemispheric technique at least 12-cm cranial flap is removed

CT of a bilateral hemispheric decompressive craniectomy performed in a patient with severe edema from a likely second impact syndrome.

BARBITURATES

Benefit: decreasing metabolic demand for oxygen (CMRO2) decreasing free radicals and intracellular calcium lowering ICPs

Side effects: immunosuppression hypotension (reduced sympathetic tone and mild cardiodepression)

Patients exclusion: hemodynamic instability, sepsis, respiratory infection, cardiac risk factors

BARBITURATES

loading dose 10 mg/kg over 30 minutes followed by a 5 mg/(kg h) infusion for 3 hours

maintenance dose 1 mg/(kg h)

Serum barbiturate levels 3–4 mg%

HYPOTHERMIA

Improve outcome in patients with severe TBI through reduction of: cerebral metabolism, ICP, inflammation, lipid peroxidation, excitotoxicity, cell death, Seizures

Side effects: Decreased cardiac function thrombocytopenia elevated creatinine clearance pancreatitis shivering

HYPOTHERMIA

patients who were hypothermic on admission had improved outcomes when hypothermia was maintained

target temperature 32–33°C (maintained for greater than 48 hours)

patients should be closely monitored for electrolyte abnormalities, hypocoagulability, and cardiac rhythm alterations

Rewarming very slow (not exceeding more than 1° per 24 hours)

STEROIDS

Glucocorticoids are not recommended

Side effects of steroid: coagulopathies, hyperglycemia, increased infection

SPECIFIC SYSTEM CONSIDERATIONS

NUTRITION

All injured patients show an increase in basal energy expenditure (BEE)

Patients who are sedated and paralyzed 120–130% of baseline

Comatose patients (GCS ≤8) with isolated head injury 140% (range 120–250%)

at least 15% of calories should be supplied as protein

nutritional replacement should start by 72 hours postinjury

Enteral feeding is preferred over parenteral nutrition enhanced immunocompetence and a reduced risk profile

Total parenteral nutrition if enteral feeding is not possible if higher nitrogen intake is required

INFECTION

Source of infection: gross wound contamination immunosuppression, iatrogenically from open surgical procedures, intubation for mechanical ventilation, invasive monitoring equipment

Antibiotic coverage should be targeted toward specific organisms

Perioperative antibiotics only recommended for the first 24 hours

COAGULOPATHY PROPHYLAXIS

Coagulopathies should be rapidly and aggressively treated normal coagulation profile.

Effects of warfarin anticoagulation may be reversed by: vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrate

Effects of heparin may be reversed with protamine sulfate

Thrombocytopenia or platelet deactivation may be treated with donor platelet transfusion

DVT PROPHYLAXIS

Neurological risk factors for DVT and PE: stroke spinal cord injury, prolonged surgery prolonged bed rest

incidence of DVTs in neurosurgical patients 19% to 50%.

Prophylactic measures passive range of motion, early ambulation, rotating beds, electrical stimulation of calf

muscles

Pharmacologic anticoagulation increase the effectiveness of DVT prophylaxis

Low-molecular-weight heparins can be added to pneumatic compression boots (PCBs) without significantly increased risk of hemorrhage

ALGORITHM FOR MANAGEMENT OF MINOR BRAIN INJURY

ALGORITHM FOR MANAGEMENT OF MODERATE BRAIN INJURY

ALGORITHM FOR INITIAL MANAGEMENT OF SEVERE BRAIN INJURY

OUTCOMEGLASGOW OUTCOME SCORE

PROGNOSIS

Worse prognosis when: bilaterally dilated (> 4 mm) absent pupillary light reflexes, absent oculocephalic or

oculovestibular reflexes, increased injury severity scale

(> 40), extreme age (> 60 and possibly

< 2),

hypotension (SBP < 90 mmHg , worse with concomitant hypoxemia),

abnormal CT scan (extensive tSAH, compression or obliteration of basal cisterns),

persistent ICP > 20 mm Hg, elevated ICP during the first 24

hours lower GCS subscores (motor ≤3,

eye opening ≤2, verbal response ≤2)

BRAIN DEATH DETERMINATION AND ORGAN DONATION

Brain death the absence of any observable neurological activity in the brain and the irreversibility of cessation of the cardiopulmonary system or the entire brain.

Requirements No complicating conditions: Hypothermia <32.2°C, Hypotension [SBP<90] Exogenous sedatives, Paralytics drug/alcohol Hepatic encephalopathy, Hyperosmolar coma, Atropine Recent CPR/shock/anoxia

BRAIN DEATH DETERMINATION AND ORGAN DONATION

Patient’s condition: fixed, dilated pupils no observable corneal, oculocephalic, oculovestibular, gag, or cough

reflexes no movement to deep central or peripheral pain no spontaneous breathing is seen on disconnection from the ventilator

with PaCO2 >60 mm Hg (i.e., apnea test).

Head-injured patients who progress to brain death may be candidates for organ donation

Organ donation can provide family members with a slightly more positive conclusion to a series of unfortunate events.

REFERENCES

1. Mattox K, Moore E, Feliciano D. Trauma, Seventh Edition. McGraw Hill Professional; 2012.

2. Jr HRJ Jr, Srinivasan J, Allam GJ, Baker RA. Netter’s Neurology. Elsevier Health Sciences; 2011.

3. American College of Surgeons, Committee on Trauma. ATLS, advanced trauma life support for doctors: student course manual. 8th ed. Chicago, IL: American College of Surgeons; 2008.

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Health & Medicine

Head trauma