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Moderate to Severe TBI: Classic Complications, Treatment and Prognosis Peter Esselman, MD MPT Professor and Chair Department of Rehabilitation Medicine University of Washington

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Page 1: and Prognosis Classic Complications, Treatment … · Classic Complications, Treatment and Prognosis Peter Esselman, ... –Hyponatremia –Euvolemic ... L. S. et al. CMAJ 2003;169:681-693

Moderate to Severe TBI:Classic Complications, Treatment

and Prognosis

Peter Esselman, MD MPTProfessor and Chair

Department of Rehabilitation MedicineUniversity of Washington

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Prognosis: Glasgow Outcome Scale• 1 = DEAD• 2 = VEGETATIVE STATE 

Unable to interact with environment; unresponsive• 3 = SEVERE DISABILITY

Able to follow commands/ unable to live independently• 4 = MODERATE DISABILITY

Able to live independently; unable to return to work or school

• 5 = GOOD RECOVERY Able to return to work or school

http://www.tbims.org/combi/gos/index.html 2017 2

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Prognosis• Predictors of poor prognosis (death, GOS 1-3)

– Older age (association present after age 40)– Low GCS– Absent pupil reactivity– Presence of major extracranial injury– Obliteration of third ventricle or basal cisterns on

CT scan• Influenced by Low/middle income or High

income country

2017 3

CRASH Trial, BMJ 2008 336:425-9.

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TBI Prognosis Calculator

2017 4Iorio-Morin C Clinical Neurology and Neurosurgery 142 (2016) 48-53.

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Functional Prognosis• Severe disability (according to GOS) unlikely

when– Time to following commands is < 2 weeks– Duration of PTA is < 2 months

• Good recovery (according to GOS) is unlikely when– Time to following commands is > 1 month– Duration of PTA is > 3 months– Age older than 65 years– MRI indicates bilateral brainstem injury

2017 5Zasler, Katz & Zafonte, Brain Injury Medicine: principles and practice, Demos Medical Publishing: New York. 2013

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Acute Management• Primary injury – physical damage caused by

the trauma• Secondary injury – caused by those processes

that follow the injury– Hypoxia– Hypotension– Cerebral edema– Metabolic abnormalities

For review see Chesnut RM, Crit Care Clin 20:25-55, 2004.

2017 6

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Edema and Increased ICP

Hutchinson PJ Curr Opin Crit Care 2004;10:101-104

2017 7

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Elevated ICP Treatment• ICP treatment may be initiated at an upper

threshold of 20 - 25 mmHg• Treatment goal is to maintain adequate

Cerebral Perfusion Pressure (CPP)CPP = Mean arterial pressure (MAP) – ICP

• CPP guideline > 60 mm Hg, but can be individualized.

2017 8

For review see Chesnut RM, Crit Care Clin 20:25-55, 2004.

Recent update: Chesnut R Annals NY Academy of Sciences 1345: (2015) 99-107 and 1345: (2015) 74-82.

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Conceptual approach to managing severe traumatic brain injury“The goal is to determine if there is a risk of ischemia at a lower CPP”

Annals of the New York Academy of SciencesVolume 1345, Issue 1, pages 99-107, 16 JUL 2014 DOI: 10.1111/nyas.12483http://onlinelibrary.wiley.com/doi/10.1111/nyas.12483/full#nyas12483-fig-0001 2017 9

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Decompressive Craniectomy

2017 10

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Treatment to Improve Outcome

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Amantadine• 184 subjects

– minimally conscious or vegetative• 4 -16 weeks after TBI• Amantadine or placebo for 4 weeks

– Followed for another 2 weeks• Results

– Amantadine accelerated the pace of functional recovery during active treatment as measured by the disability rating scale

2017 13Giacino JT N Engl J Med. 2012 Mar 1;366(9):819-26

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142017 14

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Hydrocephalus• Obstructive (Non-communicating)

• Blockage of the normal flow of CSF• Communicating (Most common in TBI)

• Impaired CSF absorption at arachnoid villa• Normal-pressure hydrocephalus is a form of

communicating hydrocephalus• Hydrocephalus ex vacuo

• Ventriculomegaly caused by atrophy

2017 15

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Risk Factors for Hydrocephalus• Subarachnoid hemorrhage• Severe TBI• Skull fractures (depressed)• Infectious processes

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Diagnosing Hydrocephalus

• CT findings:• Enlarged lateral

ventricles• Normal or absent

sulci• Periventricular

lucency

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Diagnosis of Hydrocephalus

• Lumbar puncture (CSF Tap Test)• Assess patient for clinical improvement after

removal of 50 ml of CSF• CSF Drainage trial

• Prolonged CSF drainage with spinal catheter over 3-5 days

• Clinical improvement - increased predictive value of shunt success

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Shunting for Hydrocephalus

• Ventriculoperitoneal Shunt• Drains to peritoneum• Adjustable flow control valve that can be

adjusted non-invasively

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Shunt Complications• Shunt Failure

• Headache, irritability, confusion, lethargy• Proximal or distal obstruction

• Infection• Low grade fever, malaise, erythema over shunt• Staphylococcus epidermidis – most common

• Over drainage • Orthostatic headache, dizziness, diplopia, nausea

• Chronic subdural hematoma and hygroma2017 20

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Post-traumatic Seizures

• Immediate seizures– Occur within 24 hours

• Early seizures– Occur after 1 day and ≤7 days post-injury

• Late seizures– >7 days post-injury

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Seizure prophylaxis

• All patients with moderate to severe TBI should receive prophylaxis with Phenytoin for one week.

Temkin et al N Eng J Med 323:497, 1990

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Risk factors for Late Seizure• Risk factors for late seizures

– Biparietal contusions– Dural penetration with metal fragments– Multiple intracranial operations– Subdural hematoma with evacuation– Midline shift >5mm– Multiple or bilateral cortical contusions– Early seizure

Englander et al Arch PM&R 2003;84:365-73 2017 23

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Incidence of Post-traumatic Seizures• When does initial late seizure occur?

– 50-66% within the first year– 75-80% within 2 years

• Patients with moderate/severe TBI continue to have some increased long-term risk of late seizure

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252017 25

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CSF Leak• Rhinorrhea

– Fracture ethmoid air cells or frontal sinus– Diagnosis

• Glucose strips – unreliable• Beta-2 transferrin assay – sensitive and specific

– High resolution CT scan – used to localize – Increased risk of meningitis

2017 26

Oakley GM, Int Forum Allergy Rhinol. 2016;6:8–16.

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CSF Leak• Otorrhea

– Temporal bone fracture, dural tear and tympanic membrane tear

– Usually resolves spontaneously

2017 27

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Pituitary Injury• Mechanism of Injury

– Infarction– Hemorrhage

• Risk factors– Fracture of middle cranial fossa– Severity of injury

2017 28

By Patrick J. Lynch, medical illustrator - Image:Skull and brain sagittal.svg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=2893765

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Anterior Hypopituitarism• Anterior Pituitary

– Adrenocorticotropic hormone (ACTH)– Thyroid stimulating hormone (TSH)– Luteinizing hormone (LH)– Follicle stimulating hormone (FSH)– Prolactin– Growth hormone

JAMA 2007 298(12):1429-14382017 29

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Anterior Hypopituitarism• Prevalence after TBI 27.5%• Hormone replacement recommended in acute

phase of injury for– Adrenal insufficiency– Thyroid insufficiency

• No clear evidence for replacement of sex steroids in acute phase.

JAMA 2007 298(12):1429-1438Chigo E et. al. Brain Injury 19(9):711-724

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Posterior Hypopituitarism• Posterior Pituitary

– Storage organ for hypothalamic hormones oxytocin and antidiuretic hormone (vasopression)

• Posterior hypopituitarism– Central diabetes insipidus (with hypernatremia,

polyuria, polydipsia)• Unable to resorb free water• Treatment - Desmopressin (DDAVP)• Prevalence after TBI – 26% in acute phase and 7% in

long-term survivorsJAMA 2007 298(12):1429-1438Chigo E et. al. Brain Injury 19(9):711-724 2017 31

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SIADH• Syndrome of Inappropriate Antidiuretic

Hormone (SIADH)– Hyponatremia– Euvolemic– Hypotonic serum– Elevated urine osmolality and sodium– Treatment

• Fluid restriction• Do not correct quickly - risk of central pontine

myelinolysis

2017 32

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Cerebral salt wasting• Hypovolemic hyponatremia

– Lethargy, nausea, seizures– Results from renal losses of water and sodium

• Treatment– Volume repletion– Salt tabs or other sodium correction

• Fluid restriction contraindicated

2017 33

John C Critical Care Nurse 32:2, April 2012Kirkman MA Neurocrit Care (2013) 18:406-416

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SIADH Cerebral Salt Wasting

Diabetes Insipidus

Volume Status * Euvolemic * Hypovolemic Euvolemic

Serum Sodium HyponatremiaUrine Hyper osmoSerum Hypo osmo

HyponatremiaUrine hyper osmo Serum Hypo osmo

HypernatremiaUrine hypo osmoSerum hyper osmo

Labs Serum osmo < 275Urine Na > 25U osmolality > 100

Serum osmo < 275UNa > 25 mEq/LU osmolality > 100

Uosm < 200Serum osmo >295

Underlying Driver Excess ADH -Increased renal reabsorption of water

Renal - decreased reabsorption of Na in volume contracted state

Decreased secretion of ADH leading to polyuria

Treatment -Free water restrict-Increase sodium intake

-Replete water volume and sodium-Restriction of fluids contraindicated

-Free water access-DDAVP 2017 34

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Cranial Nerve Abnormalities• Olfactory Nerve

– Incidence• 7% of all individuals with TBI• Moderate TBI - 19% • Severe - 25%

– Injury results in decreased smell and altered taste of food

– Can occur with mild TBI

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Cranial Nerve Abnormalities• Optic Nerve

– Occurs in up to 5% of individuals with TBI– Primary lesion

• Hemorrhage or tear of nerve– Ischemic neuropathy

• Circulation impairment

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Oculomotor Nerve (CN III)• Oculomotor nerve palsy

– Eye abducted with inability to adduct– Eyelid ptosis– Dilated and fixed pupil in complete palsy

• A blown pupil (fixed, dilated pupil) is sign of herniation

• Treatment– Patching/block visual input to eliminate diplopia– Surgery delayed 6-9 months

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2017 39

From Wilson-Pauwels, Akesson and Stewart Cranial Nerves: Anatomy and Clinical Comments 1988.

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2017 40

From Wilson-Pauwels, Akesson and Stewart Cranial Nerves: Anatomy and Clinical Comments 1988.

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Trochlear Nerve (CN IV)

• Superior Oblique muscle– Intorsion– Downward gaze

• Compensate by tilting head away from affected side

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LateralMedial

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From Wilson-Pauwels, Akesson and Stewart Cranial Nerves: Anatomy and Clinical Comments 1988.

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2017 43

From Wilson-Pauwels, Akesson and Stewart Cranial Nerves: Anatomy and Clinical Comments 1988.

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Abducens (CN VI)

• Lateral Rectus Muscle– Eye Abduction

2017 44

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below)Bartleby.com: Gray's Anatomy, Plate 785, Public Domain, https://commons.wikimedia.org/w/index.php?curid=541631

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Transverse

Longitudinal2017 45

• Temporal bone fractures• Transverse - unilateral loss

of vestibular function in > 50% patients

• Longitudinal - concussive injury to the membranous labyrinth

Vestibular Dysfunction

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Balance and Dizziness

• Benign Paroxysmal Positional Vertigo (BPPV)– Displacement of

otoliths– Dix-Hallpike Test– Epley maneuver– Vestibular

Rehabilitation

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Fig. 6: Dix-Hallpike manoeuvre (right ear)

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Fig. 6: Dix-Hallpike manoeuvre (right ear)

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Dix-Hallpike• Nystagmus

– Onset has a brief latency (1-5 seconds)– Limited duration (typically less than 30 seconds)

• Head to right – tests right posterior canal• Head to left – tests left posterior canal

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Fig. 8: Particle repositioning manoeuvre (right ear)

Eply Maneuver

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Carotid Cavernous Sinus Fistula• What structures go through the cavernous

sinus?

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Carotid Cavernous Sinus Fistula• Symptoms

– Visual impairment– Supraorbital bruit– Exopthalmous– Orbital congestion– Oculomotor palsies– Trigeminal nerve involvement

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