Case 1: Diagnosis and Management of Head Trauma

Case 1: Diagnosis and Management of Head Trauma

Lee Chuy, KatherineLee, Sidney Albert

Demographic Data

• GT• 22 year old• Male• Side swept by 10 wheeler truck while walking

along Forbes St. and taken by bystanders to USTH

PE

• Vital Signs– BP: 110/70– PR: 95/min– RR: 20/min

PE

• Skin– 5 cm laceration on left temporal area– Multiple abrasions and lacerations over the face

and extremities

PE

• Neurologic – Confused– Spontaneous eye opening– Localizes upon pain stimuli– Pupils 2mm, ERTL

Imaging

• X-ray– Linear fracture over left temporal area

After X-ray

• Less responsive• Left extremity withdraws to pain• Right in extension• Eye opening on painful stimuli• No verbal output• Pupils: 3mm, RTL, right; 5mm, non-reactive,

left

Head Injury

Head Injury

• A head injury is any trauma that leads to injury of the scalp, skull, or brain

• The injuries can range from a minor bump on the skull to serious brain injury.

http://www.nlm.nih.gov/medlineplus/ency/article/000028.htm

– Closed head injury• hard blow to the head by striking object, but object did not

break the skull

– Open or Penetrating head injury• hit with an object that broke the skull and entered the brain • which the dura mater, the outer layer of the meninges, is

breached

– Compressive head injuries• The Skull is compressed between two forces. Massive injury that

usually results in instantaneous death

http://web.archive.org/web/20030821142023/http://cats.med.uvm.edu/cats_teachingmod/pathology/path302/np/home/neuroindex.html

Classification of Head Injury

• Primary injury is induced by mechanical force and occurs at the moment of injury.

• Secondary injury is not mechanically induced. It may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury

Primary injury• 2 main mechanisms that cause primary injury

– contact (eg, an object striking the head or the brain striking the inside of the skull) , may result in injury to the scalp, fracture to the skull, and surface contusions

– acceleration-deceleration, results from unrestricted movement of the head and leads to shear, tensile, and compressive strains. These forces can cause intracranial hematoma, diffuse vascular injury, and injury to cranial nerves and the pituitary stalk.

• Contusions are distinct areas of swollen brain tissue. They are typically found on the poles of the frontal lobes, the inferior aspects of the frontal lobes, the cortex above and below the operculum of the sylvian fissures, and the lateral and inferior aspects of the temporal lobes.

Secondary injury• Secondary injury may occur hours or even days after the inciting traumatic

event. • Injury may result from impairment or local declines in cerebral blood flow (CBF)

after a TBI. • Decreases in CBF are the result of local edema, hemorrhage, or increased

intracranial pressure (ICP). As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium and sodium. Resultant calcium and sodium overload may contribute to cellular destruction.

• Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of the ion pumps.

• As the cascade continues, cells die, causing free radical formation, proteolysis, and lipid peroxidation.

• These factors can ultimately cause neuronal death.

• The exact role of the inflammatory response in secondary injury is not known. However, it is believed to contribute to cell damage.9

• Clinical conditions associated with the risk of a decreased CBF are arterial hypotension, hypoxemia, intracranial hemorrhage and malignant brain edema, and hyperthermia.

• Focal or Diffuse• These 2 forms of injury are commonly found together.– Focal injuries include scalp injury, skull fracture, and

surface contusions and are generally be caused by contact.

– Diffuse injuries include DAI, hypoxic-ischemic damage, meningitis, and vascular injury and are usually caused by acceleration-deceleration forces.

• http://emedicine.medscape.com/article/326643-overview

• Classification and Complications of Traumatic Brain Injury

• Author: Percival H Pangilinan Jr, MD• April 2, 2008

http://emedicine.medscape.com/article/326643-overview

http://emedicine.medscape.com/article/326643-overview

2. Differentiate primary brain injury from secondary brain injury.

Primary Brain Injury

• physiological and anatomic damage to the brain, occurring at the superficial layers of the brain and extending inward as mechanical force increases.

• Results from the initial trauma to the brain

Primary Brain Injury

• Intracerebral hemorrhage• Subdural hemorrhage• Subarachnoid hemorrhage• Epidural hemorrhage• Cerebral contusion• Cerebral laceration• Axonal stretch injury

Primary Brain Injury• classified as penetrating or closed, depending on the mechanism of

injury:

1. Penetrating injuries are characterized by the velocity of the missile at impact and the location of the missile impact:

– The higher the velocity of the missile, the more severe the injury.

– The most severe injuries are caused by high-velocity bullets– The lower the missile tract, such as in the brainstem, basal

ganglia, or large artery, the more severe the injury.

Primary Brain Injury2. Closed injuries are classified as mild, moderate, or severe, depending

on the neurological status of the patient soon after the injury .

-Moderate or Severe Closed Injuries are characterized by the velocity and vector of forces applied to the head, such as motor vehicle accidents, assaults, or falls.

- There are two types of closed injuries. a. "Coup" injuries, caused by the impact of the head with an obstacle

b. "Contrecoup" injuries, caused by the brain rebounding within the skull from the initial "coup" injury.

Secondary Brain Injury• Subsequent neuronal damage due to the sequelae of

trauma

Mechanisms of secondary injury• hypoxia• hypotension• hydrocephalus• intracranial hypertension• intracranial hematoma

Schwartz’s Principles of Surgery, 9th ed

• The focus of basic research into brain trauma, critical care medicine, and neurosurgical intervention is to decrease the effects of secondary injury


ABCDs of resuscitation

• Airway• Breathing Assessed and stabilized• Circulation

• Hypoxia and hypotension worsen outcome in traumatic brain injury due to secondary injury making cardiopulmonary stabilization critical

• Disability (GCS score)


• Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.

• GCS was initially used to assess level of consciousness after head injury, and the scale is now used by first aid, EMS, and doctors as being applicable to all acute medical and trauma patients. In hospitals it is also used in monitoring chronic patients in intensive care.GCS is used as part of several ICU scoring systems, including APACHE II, SAPS II, and SOFA, to assess the status of the central nervous system.

1 2 3 4 5 6

Eyes Does not open eyes

Opens eyes in response to

painful stimuli

Opens eyes in response to

voiceOpens eyes

spontaneously N/A N/A

Verbal Makes no sounds

Incomprehensible sounds

Utters inappropriate

wordsConfused,

disorientedOriented, converses normally

N/A

Motor Makes no movements

Extension to painful stimuli (decerebrate

response)

Abnormal flexion to

painful stimuli (decorticate response)

Flexion / Withdrawal to painful stimuli

Localizes painful stimuli

Obeys commands

• Generally, brain injury is classified as:• Severe, with GCS ≤ 8• Moderate, GCS 9 - 12• Minor, GCS ≥ 13.

Patients score

• EYE– Spontaneous eye opening– Score of 4

• VERBAL– Noted to be confused– Score of 4

• MOTOR– Localizes on painful

stimuli– Score of 5

• GCS total of 13– BRAIN INJURY

On the way back…

• EYE– Eye opening on painful

stimuli– Score of 2

• VERBAL– No verbal output– Score of 1

• MOTOR– Withdraws to pain– Score of 4

• GCS total of 7– SEVERE BRAIN INJURY

Brain herniation syndromes

Lim, John HaroldLim, Mary

Brain Herniation

• Brain tissue, cerebrospinal fluid, and blood vessels are moved or pressed away from their usual position in the head.

• Occurs when something inside the skull produces pressure that moves brain tissues.

• Most often the result of brain swelling from a head injury.

General symptoms indicating brain herniation

• Cardiorespiratory distress• Coma • Irregular breathing• Irregular pulse• Loss of all brainstem reflexes (blinking,

gagging, pupils reacting to light)• Progressive loss of consciousness

5 main types of brain herniation syndromes

• TRANSTENTORIAL HERNIATION• ALAR OR SPHENOID HERNIATION • SUBFALCINE HERNIATION • FORAMEN MAGNUM HERNIATION• EXTRACRANIAL (Calvarial) HERNIATION

Herniation

1. &2. Descending transtentorial herniation

3. Subfalcine Herniation4. Extracranial (calvarial)

herniation5. Ascending transtentorial

(upward) herniation6. Foramen magnum (tonsillar)

herniation

Herniation• Alar (Sphenoid)

herniation

Descending transtentorial herniation

• Caused by mass effect in the cerebrum which pushes the supratentorial brain through the incisura to the posterior fossa

• Clinical presentation includes occulomotor (CN III) paresis, Mydriasis (ipsilateral dilated pupil), abnormal EOM's, contralateral hemiparesis, and at times ipsilateral hemiparesis


• Imaging findings of descending transtentorial herniations include ipsilateral ambient cistern widening and ipsilateral prepontine cistern widening. A contralateral temporal horn is also widened.


• ipsilateral ambient cistern widening


• ipsilateral prepontine cistern widening


• Widened contralateral temporal horn

Ascending transtentorial herniation

• Less common then descending transtentorial herniation.

• Usually caused by a slowly growing cerebellar or brainstem process, such as a diffusely infiltrating astrocytoma.

• Clinical presentation includes nausea and vomiting followed by obtundation

Ascending transtentorial herniation

• “Spinning top” appearance of the midbrain– Due to compression

bilaterally on the posterolateral aspects of the midbrain as the posterior fossa squeezes through the incisura from below.

Ascending transtentorial herniation• Subsequent narrowing of

the bilateral ambient cisterns as the cerebellar tissue extends through the ambient cisterns.

• Finally, there is filling of the quadrigeminal plate cistern as the cerebellum again persistently extends upward through the incisura.

Alar or Sphenoid herniation• Clinical symptoms are generally minimal.• Associated with other herniations such as subfalcine or

transtentorial herniations which are more clinically apparent.

• Divided into posterior and anterior herniations.– Frontal lobe masses will cause a posterior alar herniation

as the frontal lobe extends posterior and inferiorly over the sphenoid ridge.

– Temporal lobe lesions or lesions of the insula can cause anterior alar herniations. This occurs as the temporal lobe extends superiorly and anteriorly over the sphenoid bone.

Alar or Sphenoid herniation• Imaging findings of alar

herniation are best demonstrated utilizing the middle cerebral artery.– anterior or posterior

displacement of the middle cerebral artery

• CT: Anterior left alar herniation– Cerebellum filling the

quadrigeminal plate cistern and ambient cisterns from an ascending transtentorial herniation

Subfalcine herniation

• Occur as the brain extends under the falx in the supratentorial cerebrum.

• Occur in conjunction with transtentorial herniation or in isolation.

• Can present clinically as headache. Later on as the herniation progresses, contralateral leg weakness can occur.

Subfalcine herniation

• Amputation of the ipsilateral anterior aspect to the frontal horn.– occurs as the mass effect

truncates the anterior aspect of the frontal horn and widens the contralateral frontal horn

Foramen Magnum herniation

• Clinical symptomatology maybe subtle until the patient becomes obtunded.

• Patients with a Chiari malformation may have little or no clinical symptomatology or may demonstrate Lhermitte’s phenomenon.– changed or dysesthesia in the arms or legs with

forward bending of the head.– occur as the anterior spinal tracts within the ventral

spinal cord, become compressed against the bone of the posterior vertebral bodies.

Foramen Magnum herniation

• Imaging findings include on the axial images, cerebellar tonsils at the level of the dens.

Extracranial (Calvarial) herniation• Shift of the brain through an

extracranial defect• Generally post traumatic or

post surgical• The brain can become

ischemic and infarct.• Post trauma patients or

patients with significant intracranial mass effect may undergo craniectomy to remove the ipsilateral, overlying bone. This will allow the brain to decompress through the defect.

Guide Question 5

Differentiate cerebral concussion, contusion, and diffuse axonal injury.

• trauma-induced change in mental status, with confusion and amnesia, and with or without a brief loss of consciousness

• occurs when the head hits or is hit by an object, or when the brain is jarred against the skull, with sufficient force to cause temporary loss of function in the higher centers of the brain

• mostly caused by motor vehicle accidents and sports injuries

1.Evans, R. Neurology and Trauma. W. B. Saunders Co., 1996.2.American Academy of Neurology. 1080 Montreal Ave., St. Paul, MN 55116. (612) 695-1940.

Cerebral Concussion

Symptoms of concussion include:– headache– disorientation as to time, date, or place– confusion– dizziness– vacant stare or confused expression– incoherent or incomprehensible speech– loss of coordination or weakness– amnesia for the events immediately preceding the blow– nausea or vomiting– double vision– ringing in the ears

• last from several minutes to several hours• more severe or longer-lasting symptoms may indicate more severe

brain injury

1.Evans, R. Neurology and Trauma. W. B. Saunders Co., 1996.2.American Academy of Neurology. 1080 Montreal Ave., St. Paul, MN 55116. (612) 695-1940.

Contusion• bruising of the brain tissue• often caused by a blow to the head in coup or contre-coup

injuries– coup injuries (brain is injured directly under the area of impact)– contre-coup injuries (brain is injured on the side opposite the

impact)• occur primarily in the cortical tissue, especially under the site

of impact or in areas of the brain located near sharp ridges on the inside of the skull– contused when it collides with bony protuberances on the inside

surface of the skull• can present with weakness, lack of motor coordination,

numbness, aphasia, and memory and cognitive problems

Diffuse Axonal Injury

• result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in auto accidents, falls, and assaults

• In the brain,parts of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter

• one of the major causes of unconsciousness and persistent vegetative state after head trauma

Acute Epidural Hematoma

• Accumulation of blood in the potential space between the dura and the bone

• Maybe intracranial or spinal• Results from a linear contact force to the

calvaria that separates periosteal dura from bone

• Symptoms of epidural hematoma include the following: – Headache– Nausea/vomiting– Seizures– Focal neurologic deficits (eg, visual field cuts,

aphasia, weakness, numbness)

• Spinal epidural hematoma typically causes severe localized back pain with delayed radicular radiation that may mimic disk herniation. Associated symptoms may include the following: – Weakness– Numbness– Urinary incontinence– Fecal incontinence

CT scanning performed before and after surgical evacuation of an intracranial epidural hematoma

Causes• Trauma• Anticoagulation• Thrombolysis• Lumbar puncture• Epidural anesthesia• Coagulopathy or bleeding diathesis• Hepatic disease with portal hypertension• Cancer• Vascular malformation• Disk herniation• Paget disease of bone• Valsalva maneuver• Hypertension• Chiropractic manipulation2

MANAGEMENT OF INCREASED INTRACRANIAL PRESSURE

Patient Positioning

• Moderate head elevation of 15 to 30 degrees (CPP is maintained at >70 mmHg) is adequate.

• Avoid sharp head angulations. • Tight bandages around the neck should be

avoided as they can impede cerebral venous return and thereby rise in ICP.

Increased Intracranial PressureAshwani Kumar Chaudhary, Anurag TewariJ Anaesth Clin Pharmacol 2005; 21(3) :

247-256

Care of Endotracheal Tube• Regularly check the patency of the tube. • Avoid aggressive endotracheal suctioning as it

causes brief elevations in ICP. • Pretreatment with:– aerosolized (1% to 4%) or IV (1-2 mg/kg) lidocaine or– IV thiopental (1-2 mg/kg) prior to suctioning• may be used to prevent elevations of ICP.


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Temperature Management

• Fever should be aggressively treated :– high temperature increases cerebral metabolic rate

of oxygenation which increases blood flow and thereby ICP, leading to hypoxic-ischemic injury.

• Hydrotherapy, antipyretics, acetaminophen and cooling blankets should be used.

• Indomethacin can also be used if necessary, and may actually have a direct effect in reducing ICP


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Emergency Measures for ICP reduction

Primary goal of ICP management:– to maintain ICP <20 mm Hg and CPP >70 mmHg

The following emergency measures should be instituted only when ICP is >20mmHg for a period of 10 or more minutes:

1. Elevate head of bed 15-30 degrees2. Normal saline (0.9%) at 80-100 cc/hr 3. Intubate and ventilate (target pCO2 30-35 mmHg)4. Mannitol 20% 1-2 g/kg via rapid IV infusion5. Urinary catheter6. CT scan / MRI7. Neurosurgical consultation Increased Intracranial Pressure

Ashwani Kumar Chaudhary, Anurag TewariJ Anaesth Clin Pharmacol 2005; 21(3) :

247-256

Stepwise treatment protocol for elevated ICP (>20 mmHg for > 10 minutes)

1. Repeat CT scanning and/or surgical removal of anintracranial mass lesion and/or ventricular drainage

2. Intravenous sedation3. Reduction of blood pressure if CPP remains >120 mmHg, or

pressure infusion if CPP <70 mmHg4. Mannitol 1-2 g/kg IV

-(repeat every 2-6 hours as needed)5. Hyperventilation to pCO2 1evels of 30-35 mm Hg6. Pentobarbital therapy7. Hypothermia Increased Intracranial Pressure


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Removal of Intracranial Mass Lesions orCerebrospinal Fluid

• If a ventricular catheter is in place, the system should be opened to drainage and 5-10 ml of CSF removed

• Consider craniotomy or ventriculostomy


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CRANIOTOMY• Craniotomy is any bony opening

that is cut into the skull.

• a section of skull, called a blone flap, is removed to access the brain underneath

• If the bone flap is not replaced, the procedure is called a craniectomy.

VENTRICULOSTOMY• It is done by surgically placing a

tube through the skull such that it terminates in the ventricle of the brain.

• Ventriculostomy is done primarily to monitor the intracranial pressure as well as to drain CSF (primarily) or blood to relieve pressure from the CNS.

Sedation• Since parenteral sedatives can cause both apnea and

hypotension:– patients receiving them must be intubated and have arterial

pressure monitors

• Propofol (ideal sedative for patients with neurological disease because of short half-life)

• Other short acting IV sedatives for ICP management:– Morphine sulphate– Fentanyl– Midazolam Increased Intracranial Pressure


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During neuroanaesthesia or Critical Care:

• If brain tissue is considered to be ‘at risk’– use of nitrous oxide should be avoided because it

causes• increase in cerebral bloodflow• increase in cerebral metabolism• increase in intracranial pressure

• The increase in cerebral blood flow may be particularly detrimental if autoregulation is impaired.

Blood pressure Management• If both MAP and ICP remain elevated after sedation:

– lowering the systemic blood pressure may lead to a reduction of ICP– If CPP is > 120 mm Hg and ICP is > 20 mm Hg

• a short-acting antihypertensive agent should be administered until CPP reaches approximately 100 mm Hg

• The favored agents in patients with increased ICP:- Labetolol (alpha-1 and Beta-1 blocker, dose 2-3 mg/min) - Nicardipine (calcium channel blocker, dose 5-15 mg/hr)

• Nitroprusside should be avoided if possible because it has been shown to induce cerebral vasodilatation and may further raise ICP

Mannitol• Osmotic diuretic and excreted by the kidney • MOA: – To increase the osmotic gradient across the distal

tubule, thereby drawing free water with it– Main effect:• Rapid dehydration of brain tissue since it does not

cross the blood brain barrier on first pass• This effect causes prompt reduction in brain

volume caused by either cytotoxic or vasogenic edema, and thereby lowers ICP.

Mannitol (MOA)

• reduces ICP through a prolonged dehydrating effect on the brain, caused by secondary hyperosmolality.

• may be related to its ability to reduce blood viscosity, which may transiently increase CBF, resulting in reflex vasoconstriction and a decrease in CBV


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Hyperventilation

• Hyperventilation sufficient to lower pCO2 to levels of 30 mmHg can lower ICP within minutes.

• Alkalosis causes cerebral vasoconstriction whichleads:- to decreased CBV and thereby- decreased ICP.

• The peak effect of hyperventilation is achieved within 30 minutes with ventilatory rate of 16 to 20cycles per second.


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Hyperventilation

• As compensatory acid-base buffering mechanisms correct the CSF alkalosis– the effect diminishes over the next 1 to 3 hours

• Once ICP is stabilized:– hyperventilation should be tapered slowly over 6

to 12 hours because abrupt cessation can lead to vasodilation and rebound ICP increase.


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Hyperventilation

• Profound hyperventilation must be avoided because of its potential to cause cerebral ischemia through excess vasoconstriction

• Prolonged hyperventilation may occasionally be necessary in cases where increased ICP is due to severe cerebral hyperemia.


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High dose pentobarbital

• Barbiturates decreases CBF and brain metabolism– in high doses can lower CBV and ICP.

• In patients treated with pentobarbital for ICP control:– vasopressor support to maintain CPP > 70 is

mandatory


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Hypothermia

• Induced hypothermia has been shown to decrease cerebral and may thereby reduce CBF, CBV, and thus ICP.

• Various studies have shown that lowering the room temperature also results in favorable outcome in critically ill patients.


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• Initial Open Head Injury Treatment– determine extent of skull and brain damage with

MRI, ICP or CT scans. – determine whether a patient needs surgery

and/or rehabilitation for traumatic brain injury.

Management for Open Skull fracture

http://emedicine.medscape.com/

• Requires repair of the scalp & operative debridement

Indications for craniotomy:- depression greater than the cranial thickness- intracranial hematoma- frontal sinus involvement

Schwartz’s Principles of Surgery 9th ed

Open Head Injury Surgery

Open Head Injury Surgery

• remove bone fragments to minimize brain swelling and/or implant synthetic skull pieces to protect fragile brain tissue from further injury.

• Postoperatively monitor for secondary complications:– intracranial pressure– brain swelling.


Open Head Injury Rehabilitation

• to regain important neurological functions, including cognitive thinking skills– Physiatrists– Neuropsychologists– Physical therapists

* aim not only to treat brain injury victims but also to help their families cope with the tragedy.


Closed Skull Fractures

Principles of Management

Principles of Management – Closed Skull Fracture

• Require no specific treatment • Patient with skull fracture - ↑ risk of epidural

hematoma• Treatment similar to severe concussion, unless Sx of

↑ ICP develop• Traditionally – surgery to elevate depressed fragments• Patients with this injury should be treated as for those

patients with severe concussion, unless symptoms of elevated intracranial pressure develop

Management of Cerebral Concussion

Workups: • Complete history and PE, w/ neurological exam• Cervical spine x-rays and other radiographs as

indicated• Blood alcohol level and urine drug screen CT

scan of the head in all patients except those who are completely asymptomatic and neurologically normal

Management of Cerebral Concussion

• Tylenol or Narcotic pain medication for headache• Non-phenothiazine antiemetic medication for

nausea and vomiting (frequently present after mild or severe concussion)

• Discharge when- Patient is neurologically normal- Nausea and vomiting has ceased- Headache has ceased / is controlled

CSF Leak Management.

• When cranial CSF leak is suspected, due to discharge of fluid from the nose or ear that is potentially CSF, fluid can be collected and then tested with a beta-2 transferrin assay.– This test can positively identify if the fluid is

cerebrospinal fluid.

• Many CSF leaks will heal with elevation of the head of the bed for several days.

• A lumbar drain can augment this. – a catheter is placed in the lumbar CSF cistern to

decompress the cranial vault and allow the defect to heal by eliminating normal hydrostatic pressure.

• epidural blood patches– has a 90% success rate in treating dural holes, higher than – the conservative treatment of bed rest and hydration.– Through the injection of a person's own blood into the area of the hole in the

dura, an epidural blood patch uses blood's clotting factors to clot the sites of holes.

– blood patches alone do not succeed in closing the dural tears, fibrin glue can be added and mixed into the autologous blood patch during a repeat treatment. • This has been demonstrated to raise the level of effectiveness of forming a

clot and arresting CSF leakage.• In extreme cases of intractable CSF leak:

surgical lumbar drain• decrease spinal CSF volume while increasing intracranial CSF pressure and

volume.• restores normal intracranial CSF volume and pressure while promoting the

healing of dural tears by lowering the pressure and volume in the dura.• has led to positive results leading to relief of symptoms for up to one year.

http://en.wikipedia.org/wiki/File:Epidural_blood_patch.svg

http://en.wikipedia.org/wiki/File:Epidural_blood_patch.svg

Case 1: Diagnosis and Management of Head Trauma

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