Non-Neurologic Complications of Brain Injury2

7/30/2019 Non-Neurologic Complications of Brain Injury2

1/31

Non-Neurologic Complications of

Brain Injury


2/31

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


3/31

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


4/31

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


5/31

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


6/31

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)


7/31

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


8/31

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


9/31


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


10/31

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


11/31


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)


12/31


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


13/31

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


14/31

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


15/31

Accelerated weaning

Aggressive chest physiotherapy (caution with

high ICP levels)

Positioning & regular turning

Early tracheostomy


16/31

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


17/31

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


18/31

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


19/31

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)


20/31


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


21/31


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


22/31

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)


23/31

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


24/31

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


25/31

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)


26/31

Hypokalemia

Iatrogenic hyperventilation

Osmotic & loop diuretics

Therapeutic hypothermia with increasedlevels of aldosterone

Hyperkalemia is rare, nearly always associated

with renal failure


27/31

Anemia

Repeated iatrogenic sampling

Hemodilution

Associated injuries


28/31

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


29/31

Coagulation Disorders

Secondary thrombocytosis (>750,000)

common after TBI, esp with extensive bony

trauma

Low dose aspirine (75 mg QD) _ routine

LMWH


30/31

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


31/31

Summary

Non-neurological organ dysfunction is

common after TBI

Associated with significatn morbidity &

mortality

Understanding of relevant pathophysiology _

vigilant monitoring & aggressive treatment is

required

Non-Neurologic Complications of Brain Injury2

Documents

Transcript of Non-Neurologic Complications of Brain Injury2