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7/30/2019 Non-Neurologic Complications of Brain Injury2
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Non-Neurologic Complications of
Brain Injury
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Non-Neurologic Complications of Brain
Injury
Medical complications recognized as
significant contributors to patient outcome
s/p severe neuro injury
Etiology of complications poorly understood
Initial studies focused on SAH; now clear that
other neuro insults (TBI) are also susceptible
to these complications
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Non-Neurologic Complications of TBI
209 patients with severe TBI
89% developed non-neurological organ systemdysfunction
35% developed overt organ failure 23% respiratory dysfunction
Independently associated with mortality and
Glasgow Outcome Score Mortality rose sharply with each sequential organ
failure
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Respiratory System
Most common medical complication in brain-
injured patient
Responsible for up to 50% of deaths after TBI
Structural parenchymal abnormailties
Ventilation-Perfusion mismatch
Neurogenic Pulmonary Edema
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Etiology of Respiratory Dysfunction
Structural parenchymal abnormalities
Hypoventilation & hyperventilation common after TBI
Combined with poor cough & retention of secretions
leads to atelectasis & consolidation Ptx or rib fxs directly lead to respy failure
Release of brain & systemic inflammatory mediatorscontribute to peripheral organ dysfunction
Aspiration causes systemic inflammatory response Invasive ventilation causes barotrauma & volutrauma,
triggering release of pulmonary cytokines
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Etiology of Respiratory Dysfunction
Brain injury causes intense sympathetichyperactivity + high circulating catecholamines
HTN & tachycardia
Increases in alveolar capillary barrier permeability &pulmonary lymph flow
Increased risk for VAP
Early (1st 4 days) S. aureus, Hemophilus influenzae, S.
Pneumoniae Late (Pseudomonas aeruginosa, Enterobacteriaceae,
Acinetobacter)
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Risk Factors for VAP in TBI
Altered GCS
Aspiration
Emergency intubation
IPPV >> 3 days
Re-intubation
Age > 60 years
Supine position Co-existing disease
Prior antibiotic use
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Ventilation-Perfusion mismatch
Hypoxemia without radiographic evidence of
interstitial or alveolar edema
Ventilation-perfusion mismatch
Redistribution of pulmonary blood flow
mediated by hypothalamus
Pulmonary micro-embolism causing increaseddead space
Depletion of surfactant
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Neurogenic Pulmonary Edema
Onset within 4 hours of initial cerebral insult; mayoccur 14 days after insult
Not associated with aggressive fluid loading or
pre-existing cardio-respiratory disease 90% diffuse bilateral infiltrates on CXR
Mortality up to 10%
Survivors recover quickly In SAH, NPE associated with increased age and
bleed
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Neurogenic Pulmonary Edema -
Etiology
Requires a normal circulating volume to occur
Blood is shunted from systemic circulation to
increase pulmonary vascular volume
Likely due to massive catecholamine surge
with alpha- & beta-adrenoceptor activation &
cardiac injury
Increased transpulmonary pressures &
pulmonary edema
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Neurogenic Pulmonary Edema
Typical CV profile: nl BP, reduced CO & LVSWI,
variable PCWP
Bilateral diffuse infiltrates
Hypoxemia
Markedly elevated PVR
Clinical dx + exclusion of other possibilities(ALI, aspiration at time of injury)
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Neurogenic Pulmonary Edema
Supportive Rx
PPV
Careful volume resuscitation with colloid boluses
High levels of oxygen & PEEP often required
Inotropes (dobutamine or milrinone), epi insevere cases
Pressors (norepi or phenylephrine) to maintainBP
Good outcomes
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Ventilating TBI Patient
Prevent collapse & consolidation
Prevent lung infections
Accelerate weaning from IPPV ASAP Resp Rx balanced against need to optimize
cerebral hemodynamics by maintaining
normocapnia, minimizing intrathoracic
pressure
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Ventilating TBI Patient
Prevention of collapse & consloidation
Moderate levels of PEEP, recruitment maneuvers
Careful fluid balance using ICP-targeted protocols
Prevention of lung infection Prophylactic Abx, selective decontamination: NO
30o head of bed
Regular oropharyngeal suction to removesubglottic secretions
Early use enteral nutrition
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Accelerated weaning
Aggressive chest physiotherapy (caution with
high ICP levels)
Positioning & regular turning
Early tracheostomy
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Cardiovascular Complications
EKG changes due to increase in sympatheticactivity following posterior hypothalamicstress
Massive surge in catechols directly damagesheart by a toxic effect or increasing afterload
Little consistency between EKG changes and
cardiac enzymes or mechanical hypokinesis onECHO
Minor changes should not delay definitive Rx
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Cardiovascular Complications
HTN is common after brain injury
Should not be treat> 180 on usual
antihypertensives, treat
Labetalol has little effect on CBF or ICP
Hydralazine & nipride may increase both CBF
& ICP
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Cardiovascular Complications:
Ventricular Dysfunction
Wide spectrum of pathophysiological events,constantly changing
Hypokinesia, reduced ejection fraction, & perfusionabnormalities
Milrinone may be helpful if systolic function isdepressed by BP & SVR preserved
Severe myocardial stunning may respond to milrinone_ vasopressin
NPE: carefully administered fluid boluses (vs. diuretics)
Despite moribund appearance, aggressive Rx
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Water & Electrolyte Disturbances
Hyponatremia
Stress causes increased ADH & aldosterone -
increased water reabsorption
SIADH: hyponatremia, plasma hypotonicity, U Na >
20, extracellular volume expansion
Fluid restriction 1 1.5 l/day
ADH antagonist: demeclocycline Hypertonic saline if severe, symptomatic (Na rise 0.5
mmol/hr)
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Water & Electrolyte Disturbances
Hyponatremia: Cerebral Salt Wasting Syndrome
Release of brain natruiretic peptide (response tomassive sympathetic outflow? ) which antagonizesadrenergic effects on systemic & pulmonarycirculation)
Failure of Na transport at renal tubules
Decreased intravascular volume stimulates ADH -hyponatremia
Protects against NPE & cardiac stunning at risk ofhyponatremia, volume contraction, risk of cerebralinfarction
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Water & Electrolyte Disturbances
Diagnosis CSWS
Severe salt wasting, hyponatremia, serum hypo-
osmolality, high urine osmolality, EXTRACELLULAR
VOLUME CONTRACTION
Orthostatic changes in pulse & BP, dry mucous
membranes, negative fluid balance
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Calculation of Na replacement
80 kg pt, Na 125, Urine Na 40, urine output 6000
ml/day. AIM: increase Na from 125 to 135 over
24 hours
0.6 x wt x ([Na} goal
{Na} actual = 0.6 x 80 .(135-125) = 480 mmol
Calculate on-going Na losses: UO 6 L/day with 40
mmol Na/L : 240 mmol Na lost in urine /day Normal daily Na requirements 100 mmol (0.7
1.4 mmol/kg/day)
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Calculation of Na replacement
Replacement over 24 h: 480 + 240 +100 = 820
mmol Na 2733 ml hypertonic 1.8% NaCl
113 ml/hr (1000 ml 1.8% NaCl contains 300
mmol Na)
As renal Na loss may change over time,
plasma & rine Na must be reugarly measured
& adjusted
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Hypernatremia
Osmotic & loop diuretics
High caloric enteral feeds
Phenytoin: ADH inhibition Inadequate IVF due to increased ICP
Mild elevations often left untreated to
minimize vasogenic edema Aggressive reduction of Na may lead to
cerebral edema
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Hypernatremia
Diabetes insipidus: lack of ADH with loss of
dilute urine
Hypernatremia, hypovolemia, plasma
hyperosmolality
Rx arginine vasopressin (DDAVP 0.5-1.0 mcg IV
boluses prn) & hypotonic fluids (0.455 NaCl)
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Hypokalemia
Iatrogenic hyperventilation
Osmotic & loop diuretics
Therapeutic hypothermia with increasedlevels of aldosterone
Hyperkalemia is rare, nearly always associated
with renal failure
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Anemia
Repeated iatrogenic sampling
Hemodilution
Associated injuries
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Coagulation Disorders
Hypercoagulable state followed by enhanced
fibrinolytic activity
41% have mild coagulopathy
5% have DIC
Fibrinolytic activity shortly after injury
correlated with severity of brain injury & may
be prognostic
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Coagulation Disorders
Secondary thrombocytosis (>750,000)
common after TBI, esp with extensive bony
trauma
Low dose aspirine (75 mg QD) _ routine
LMWH
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GI System
Most with TBI have some gastric erosion
Splanchnic ischemia may result in stress
ulceration
H2 recepter blockers, proton pump inhibitors,
or sucralfate should be given as prophylaxis
until full enteral feeding is tolerated
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Summary
Non-neurological organ dysfunction is
common after TBI
Associated with significatn morbidity &
mortality
Understanding of relevant pathophysiology _
vigilant monitoring & aggressive treatment is
required