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8th Annual NKY TBI Conference 3/28/2014
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Medical
Complications
of Traumatic Brain InjurySarah Wagers, MDUniversity of Louisville Department of Neurosurgery
Frazier Rehab Institute
Robley Rex VA Medical Center
Early Complications� While still in ICU
� CSF leak
� Hydrocephalus
� Seizures
� Pneumonia
� Urinary tract infection
� DVT
� Soft tissue infection
� Renal failure
� Sepsis
Goals
� Acute Rehab Setting
� Management of the medical complications
� Organ systems can be affected from the
injury or from immobilization
� The more severe the injury the more
complications to watch for.
� Consider interplay of behavioral, cognitive,
psychosocial, and physical issues.
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Discomfort and Pain� Common causes
� Neuropathic pain� Occult fracture� Complex Regional Pain Syndrome
� Soft tissue injury� Urinary tract infection
� Vaginal yeast infection� Constipation
� Spasticity� Skin lesions� Headache
� Visual disturbance
Discomfort and Pain
� Sometimes hard to recognize because of decreased communication
� Can manifest as agitation or aggression
� Consider treating pain prior to restraining patient either physically or chemically.
� Can affect ability to focus and participate
� Balance between sedation and pain control.
Respiratory
� Aspiration
� Atelectasis
� Pneumonia
� Pulmonary embolus
� Tracheostomy complications
� Swallowing therapy, facial exercises, tongue exercises, positioning all improve pulmonary hygiene
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Cardiovascular� Signs and symptoms of deconditioning
include� Tachycardia, hypotension, hypertension, lower
extremity edema, deep venous thrombosis.
� Hypotension� Compression stockings, abdominal binder, fluid
status, nutrition, anemia, certain medications
� DVT-� Evaluate with a venous doppler
� If positive treat with Low molecular weight heparin and coumadin, or newer agents
Sleep
� Very common to have sleep disturbances after TBI.
� Obstructive sleep apnea
� Hypersomnia
� Narcolepsy
� Periodic limb movements
� Excessive daytime sleepiness
� Sleep-wake cycle disruption
Sleep
� Adequate sleep affects alertness, cognition, cooperation.
� Identify premorbid sleep patterns
� For example shift work
� ID difficulty falling asleep vs. difficulty staying asleep.
� Sleep medications may cause hangover effect.
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Sleep
� Minimize night time interruptions.
� Keep busy during the day.
� May eventually need a sleep study.
Dysautonomia
� Paroxysmal sympathetic hyperactivity/Central storming
� Seen in acute severe TBI.
� Posturing, hyperthermia, hypertension, tachycardia, fever, diaphoresis.
� Exacerbated by infection, pain, hydrocephalus. Look for a noxious stimuli, treat pain.
Spasticity/Upper Motor Neuron
Syndrome
� Spasticity-velocity dependent increased resistance to stretch
� Clonus- sometimes can be confused as seizures.
� Oral medications can be sedating.
� Starting to use botulinum toxin injections and intrathecal baclofen therapy earlier.
� Positioning to prevent contractures.
� Splints, serial casting
� Avoid skin breakdown
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Spasticity
� Nerve blocks
� Can use lidocaine for just a temporary
diagnostic block.
� Techniques may need to be combined
Gastrointestinal
� Dysphagia
� 33% of patients with TBI, 60% of severe TBI
� Risk for aspiration
� Therapy to teach therapeutic and compensatory strategies
� Gtubes early
� Bedside and VFSS
� Adjustment in diet consistency
� Monitor dehydration- Frazier Water Protocol
GI
� Injury to frontal lobes can lead to bowel incontinence or constipation
� Constipation present from immobility/medication side effects/poor hydration/diet.
� Bowel management program
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GI
� Oral thrush
� Poor oral hygiene, changes in pH,
decreased saliva transit
� Can affect appetite
� Treat with nystatin swish or oral.
� Maximize good oral hygiene
GI� Recurrent vomiting
� Acute inflammatory process� Incresed ICP
� Metabolic abnormalities
� Side effects of medications� Gastritis/esophagitis/dysmotility
� Changes in taste/smell
� Dizziness/vertigo� Infections
� Constipation
� Treatment will be based on the cause
GI
� Diarrhea
� C diff-can be spread to others
� Antibiotic exposure, low immune response,
proton pump inhibitor, prolonged length of stay in a health care setting, GI surgery.
� Treat with antibiotics, probiotics, contact
precautions, immunotherapy
� G tubes, intolerance to tube feeding
� Impaction
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Genitourinary
� Incontinence
� Hyperactive bladder function-urinating
small amounts of urine frequently
� Overflow in urinary retention
� Foley catheters only if skin
breakdown,injuries to GU tract, or IV
fluids/monitoring I/Os.
� Bladder retraining, timed voids
� Medications for overactive bladder/spasms
GU
� Polyuria
� Infection
� Endocrine dysfunction-Diabetes Insipidus
� UTI
� Can present with vomiting, bowel issues,
behavioral issues, increased spasticity,
dysautonomia, or cognitive changes
Heterotopic
Ossification/Myositis Ossificans
� HO-formation of bone inside soft tissues
� Incidence ranges from 11-73%.
� More common in women with severe TBI
� Less common in children and elderly
� Hip, shoulder, elbow, knee
� MO- bone formation in muscle
� More common adolescents and young adults
� Thigh, anterior compartments of the arm
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HO/MO
� Risk factors
� Tissue hypoxia, sympathetic changes,
immobilization, remobilization, spasticity.
� Prolonged coma, mechanical ventilation,
surgically treated bone fractures,
autonomic dysregulation.
HO/MO� Present with
� Local heat, palpable mass, and/or contracture
� Elevated ESR, Alkaline phosphatase
� Can look like a DVT, accelerated bone healing, metastasis
� Complications
� Contractures, nerve entrapment, vascular entrapment, joint ankylosis, Complex Regional Pain Syndrome, osteoporosis, infection, pressure ulcers.
HO/MO
� Diagnosis
� Triple phase bone scan can detect within 2-
4 weeks of development
� High sensitivity, low specificity
� Xray/CT scan after a month
� MRI is also sensitive but not specific and is
expensive
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HO/MO� Management
� Resting the affected joints in functional position during the inflammatory stage
� Passive ROM and mobilization� Indomethacin and radiation therapy for prophylaxis and
early treatment.
� Radiation with/without excision associated with elevated risk of sarcoma.
� Bisphosphonates prophylactic if used early, but effects only last as long as taking it.
� If lesions progress- surgery is indicated.
� May delay 12-18 months to mature, but recurrence may be more common in late resection so can consider earlier resection to prevent functional limitations.
Hemiplegic Shoulder
� Function, pain, immobility
� Can cause behavioral issues and limit progress
� Positioning is important.
� Look for peripheral nerve injuries.
� General weakness leading to subluxation.
� Spasticity may develop.
Complex Regional Pain
Syndrome
� Previously known as Reflex Sympathetic Dystrophy
� May be triggered by
� CNS trauma, peripheral trauma, inflammation, hypoxia, sympathetic
dysregulation
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CRPS
� Localized autonomic changes in the affected area
� Vasomotor changes
� Temperature changes
� Edema
� Color difference
� Sweating
� Atrophy
CRPS� Diagnosis usually made clinically
� Can use Triple phase bone scan but not that accurate
� Management
� Therapy, steroids, beta blockers, anticonvulsants.
� Sympathetic blocks-stellate ganglion block-diagnostic and therapeutic.
� Radiofrequency denervation after postivediagnostic block.
Missed Fractures
� Occasionally missed because of other significant trauma.
� Once patient more alert and can localize pain- may be found.
� May find a palpable bony prominence at the site- from healing.
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Neurosurgical
� Hydrocephalus
� Risks-Thick SAH, IVH, infection, bifrontaldecompression
� Incontinence, ataxia, change in mental status
� Many TBI patients in acute setting have these issues anyway
� Monitor for declining function
� Eval with CT scan and possible a lumbar puncture.
Hydrocephalus
� Diagnosis is radiographic and clinical.
� Eval the clinical response to draining the CSF from a LP.
� Determination of treatment made in conjunction with neurosurgeons.
� Possible V-P shunt placement.
Subdural hygromas
� Accumulation of serous fluid or CSF in the subdural space.
� At higher risk for lower GCS scores, midline shift< 5 mm, SAH, delayed hydrocephalus, tearing of the arachnoid membrane.
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Dizziness
� Vestibular deficits
� Orthostatic hypotension
� Visual deficits
� Patients may not be able to describe
� May present with hearing or balance deficits
� Increased agitation
� Vomiting
Dizziness
� Visual input from enclosure beds and fluorescent lights may be overstimulating
� Medication side effects
� Medications used to treat may cause other side effects.
� Headache may coexist.
Seizures
� PTS will be observed in approximately 35%–65% of patients with Penetrating TBI
� PTS - single or recurrent seizures occurring after TBI and are commonly classified into early (< 1 week after TBI) and late (> 1 week after TBI).
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Seizures
� Post-traumatic epilepsy (PTE) -disorder characterized by recurrent late seizure episodes not attributable to another obvious cause in patients with TBI .
Seizures� Medications that possibly lower the seizure
threshold
� Buproprion
� Tricylics
� Data that SSRI’s could possible lead to increase, but have been determined to be the safest treatment for depression in TBI.
� Clozapine
� Antibiotics – quinolones and imipenem
lessen risk by ensuring appropriate dosing in ill patients with reduced renal clearance.
Seizures-continued� Dopamine agonists- amantadine and
bromocriptants -only anecdotal evidence.
� Cocaine
� High dose caffeine
� Rarely amphetamine related drugs at appropriate doses- methylphenidate and dextroamphetamine do not increase risk of seizures
� Tramadol especially mixed with antidepressants
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Seizures
� The presence of focal motor, sensory, or language deficit of new onset should alert the clinician to the possibility of a recent unwitnessed PTS
Endocrine
� Symptoms of hypopituitarism
� Fatigue, neuropsychiatric and cognitive
deficits, are attributed to postconcussive
disorder but may be from hormone deficiencies.
� Increased risk
� Severity of injury, basilar skull fractures, local
edema or hemorrhage, systemic inflammation, severe hypotension
Endocrine
� Manifestations
� Hypoglycemia
� Hyponatremia
� Hypotension
� Deficiencies
� Testosterone/gonadotropins, growth
hormone, corticotropin, vasopressin
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Endocrine
� Manifestations
� SIADH
� Low sodium, increase in urine output,
decrease in urine osmolality.
� Treat with fluid restriction
� Cerebral salt wasting
� Treat with hypertonic saline, oral NACL
replacement.
Endocrine� Manifestations
� Diabetes Insipidus
� Polyuria, polydipsia
� Patient cannot concentrate urine
� If no response to medications for depression-look for hyopthyroidism.
� 21-25% of post TBI patients will have at least one deficiency.
� Increased disability, poor quality of life, greater likelihood of depression.
Study� Gulhane Military Medical Academy,
Department of Physical Medicine and Rehabilitation, Turkish Armed Forces Rehabilitation Center, Ankara, Turkey.
� Study that followed patients from 2000-2006 recorded medical complications.
� 116 patients were followed
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Results� This study detected aphasia in 19.0%, dysarthria in 30.2%, dysphagia in 17.2%,
pressure ulcers in 6.9% and DVT in 2.6% the our patients with TBI.
� Urinary and fecal incontinence on admission were 32.7% and 26.7%, respectively. Patients with incontinence had poorer cognitive function than those with normal continence.
� HO rate was 18.1% and the ambulation levels of patients with HO were worse than those without HO.
�
PTS was seen in 13.8% of the patients on admission and this ratio increased to 21.6% during the follow-up. In these patients, the etiological risk factors for PTS were gunshot and fall injuries.
References� Bontke, Catherine F. MD, et al. Medical complications and associated injuries of persons treated in the traumatic brain injury model systems programs. Journal of Head Trauma Rehabilitation: June 1993
� Zasler, Nathan MD, et al. Brain Injury Medicine. Second Edition. Demos Medical Publishing. 2013
� Safaz, Ismael, et al. Medical complications, physical function and communication skills in patients with traumatic brain injury: A single centre 5-year experience. Brain In 2008, Vol. 22, No. 10 , Pages 733-739.