8th Annual NKY TBI Conference 3/28/2014bridgesnky.org/public/GS-Wagers-web Medical... · 8th Annual...

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.

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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.

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