Critical care management of traumatic brain injuryYoumans Chapter 334Claudia RobertsonLeonardo Rangel-Castilla

Outline

• Traumatic brain injury• Neurological intensive care monitoring• Neurological intensive care management

Traumatic brain injury

Traumatic brain injury

• The primary injury : occurs before arrival at the hospital• The secondary injury : prevent secondary ischemic insult• Factor

– Age– Preinjury health– Genetic factors : ε4 allele of the apolipoprotein E gene

worst outcome

Primary brain injury• Concussion : loss of consciousness < 6 hr with amnesia• DAI : traumatic coma than 6 hr

– Mild DAI : coma 6 – 24 hr– Moderate DAI : longer than 24 hr with decerebrate posturing– Severe DAI : : longer than 24 hr with decerebrate posturing or

flaccidity

Neurological intensive care monitoring

• Monitor neurological status• Monitor for secondary injury processes

– Intracranial hypertension– Cerebral ischemia

• Monitoring for secondary ischemic insult– Cerebral cause– Systemic cause

Monitoring of Neurological status

• Mental status• Cranial nerve• Pupillary• Motor function• 24 hr for one sheet

Monitor for secondary injury processes

• Intracranial hypertension• Cerebral ischemia

Intracranial hypertension• Ventriculostomy catheter is standard

– Tip at frontal horn of lateral ventricle– Can be reset to zero– Intermittent drainage CSF

• Microsensor transducer, fibreoptic transducer– Subdural space or into brain tissue– No lumen to become obstruct– Cannot reset to zero

• Insert at end of the surgical procedure or after CT scan• Continue as long as treatment of intracranial

hypertension required (3-10 days)

Intracranial hypertension

Intracranial hypertension• Complication

– Ventriculitis• Risk factor : IVH,SAH,cranial fracture with CSF

leakage,craniotomy, systemic infection• Increasing risk for first 10 day• Systemic prophylactic antibiotics and routine catheter

exchange are not recommended in the current TBI guidelines

• Reducing infection : ATB-impreanated, minimize duration– Hemorrhage

• 1-2%• Coagulopathy(INR > 1.6)

Intracranial hypertension• Normal intracranial pressure values

– Resting < 10 mmHg– Sustain > 20 mmHg abnormal, management in TBI– Moderate Intracranial hypertension : 20-40 mmHg– Severe : > 40 mmHg

• Indications for intracranial pressure monitoring– severe TBI : defined as a GCS score of 3 to 8 after resuscitation

and abnormal findings on CT (level II recommendation)– severe TBI and normal CT findings if two or more of the

following features are present at admission: age older than 40 years, unilateral or bilateral motor posturing, or systolic BP lower than 90 mm Hg (level III recommendation)

Cerebral ischemia• Monitor cerebral perfusion

– Cerebral perfusion pressure• CPP = MAP – ICP• Normal lower regulation : 50 mmHg• Limit to ischemia from decrease BP or increase ICP

– Transcranial Doppler flow Velocity• Flow volume = cross sectional area x Flow velocity

– Cerebral blood flow• Classic Kety-Schmidt technique with nitrous oxide• Stable xenon-CT or perfusion CT• Thermal diffusion method• Laser Doppler method

Cerebral ischemia• Monitor cerebral perfusion

– Cerebral blood flow Adequacy• Jugular venous Oxygenation Saturation(SjVO2)• Brain tissue Po2• Adequacy of CBF relative to cerebral metabolic requirement• When CBF is low (25 to 30 mL/100 g per minute)

– appropriate cerebral metabolic requirements : SjVo2 normal

– brain is hypoperfused oxygen extraction increase Sjvo2 decrease

Cerebral ischemia• Monitor cerebral perfusion

– Cerebral blood flow Adequacy• Jugular venous Oxygenation Saturation(SjVO2)

• Mortality was higher in pt with one episode(37%) or multiple episode of desaturation(69 %) than in those no episode(21%)

• Normal 55%-77%• High SjVO2(> 75%) : hyperemia or after infarction• Sjvo2 < 50 % TBI guidline recommend treat• Complication : carotid artery rupture, injury to nerves in

the neck, pneumothorax, infection, increase ICP, venous thrombosis

Cerebral ischemia• Monitor cerebral perfusion

– Cerebral blood flow Adequacy• Brain tissue Po2

– Sjvo2 can’t identified regional ischemia– Normal 20-40 mmHg– < 15 mmHg : TBI guidline recommend treat

Monitoring for secondary ischemic insult

• Monitor for cerebral causes of secondary ischemic insult– Intracranial hypertension

• Most common cause of jugular venous desaturation– Seizures

• CMRO2 increase 150%-250%• CBF is marginal or uncoupled cerebral ischemia• Pt are often sedated, seizure may be subclinical monitor

EEG

Monitoring for secondary ischemic insult

• Monitor for systemic causes of secondary insult– Hypotension

• Ability to main normal CBF (wide range mean BP 50 – 150 mmHg) TBI lose of autoregulation

• Increase mortality rate by 150%• Arterial catheter : goal MAP greater than 80-90 mmHg

CPP remain at least 60 mmHg• Most common cause of Sjvo2 desaturation

Monitoring for secondary ischemic insult

• Monitor for systemic causes of secondary insult– Hypoxia

• Decrease in arterial Po2 increase in CBF vasodilatation increase ICP

• Pulmonary complicatiom hypoxia• Pulse oximetry : >95% arterial oxygen saturation

Monitoring for secondary ischemic insult

• Monitor for systemic causes of secondary insult– Hypocapnia

• Hyperventilation vasoconstrict reduce global CBF and cerebral volume

• Hyperventilation rapidly lower ICP• End-tidal Co2 in pt without pulmonary disease• ABG in pulmonary pt• Secondary cause of Sjvo2 desaturation

Monitoring for secondary ischemic insult

• Monitor for systemic causes of secondary insult– Anemia

• Decrease CaO2 increase in CBF• TBI, cerebral vasculature can’t dilate drop in CaO2

ischemia• Hemoglobin should be measure at least daily

– Fever• Increase metabolic rate 10-13 % per 1 C• Tempearatue at lateral ventricle, epidural space, tympanic

membrane, rectum

Neurological intensive care management

• General measure to minimize intracranial hypertension/Improve cerebral perfusion

• Other general measures• Timing of surgery for other injuries• Treatment of secondary injury processes : intracranial

hypertension• Treatment of secondary ischemic insult

General measure to minimize intracranial hypertension/Improve cerebral perfusion

• Minimize venous outflow resistance – head elevation 30 , head neutral position

• Sedation/Analgesia– Avoid drug hypotensive side effect– Propofal : short half-life, decrease BP > decrease ICP reduce

CPP– Propofal infusion syndrome : hyperkalemia, hepatomegaly,

lipemia, metabolic acidosis, myocardial failure, rhabdomyolysis, and renal failure (5 mg/kg per hour)

General measure to minimize intracranial hypertension/Improve cerebral perfusion

• Treatment of systemic hypertension– SBP > 160 mmHg, autoregulation is impaired after TBI – Increase ICP cerebral edema– Nicardipine : short acting,reverse and prevent vasospasm in pt with

moderate to sever TBI

• Airway protection/controlled ventilation– Coma pt can’t protect airway intubated– Hypoxia,hypercapnia

General measure to minimize intracranial hypertension/Improve cerebral perfusion

• Treatment of fever– Potent cerebral vasodilator and increase ICP– Increase cerebral metabolic requirement

• Prevention of seizure– Risk factor : subdural hematoma, skull fracture, loss of

consciousness or amnesia > 1 day, > 65 years old– Phenyltoin : reduce incidence during in the first week then

tapered and discontinue– Levetiracetam :not require serum monitoring

Other general measures• Prevention of ventilator-associated pneumonia 40%

– Association with aspiration– Prophylaxis : cefuroxime 1500 mg IV for 2 dose or

Unasyn(ampicillin - sulbactam) 3 gm iv q 6 hr x 3 days– Oral intubation, continue aspiration of subglottic secretion, ET

cuff at least 20 cmH2O, semirecumbent position

• Prophylaxis for thromboembolism 58%– Risk factor : spinal cord injury, pelvic, femoral or tibial fracture ,

surgery , blood transfusion and old age– Venous compression device preferred low dose heparin

Other general measures• Prophylaxis for gastric ulcers

– Early erosion can progress to clinical significant hemorrhage– Risk factor : severity of brain lesion, burn > 25 of BSA,

respiratory failure, hypotension, sepsis, jaundice, peritonitis, coagulopathy, and hepatic failure

– H2blocker : increase risk for nosocomial pneumonia– Proton pump inhibitor or sucralfate for prophylaxis

• Prophylaxis ATB to prevent meningitis– Associate with otorrhea and rhinorrhea– ATB recommend only when symptom or sign of meningitis

develop

Other general measures• Nutritional support

– Sever head injury : hypermetabolic and catabolic stage– TBI : 140% normal resting energy expenditure(REE)– Enteral feeding as soon as possible– Gradually increase feeding to full caloric in 1 wk

Management of Fluid/Electrolyte• Hyponatremia syndrome• Hypernatremia : Diabetes insipidus• Hyperglycemia• Hypopituitarism

Hyponatremia syndrome• SIADH and cerebral salt wasting• SIADH : secretion of ADH

– hyponatremia (serum sodium <135 mEq/L)– hypo-osmolarity (serum osmolarity <280 mOsm/L)– urine osmolarity greater than serum osmolarity– inappropriately high urine sodium concentration (>40 mEq/L)– Rx : limitation fluid intake 800-1000 ml/day– Severe hyponatremia with symptoms hypertonic NSS

• CSW : circulating natriuretic factor– Hypovolemic,high urine serum sodium(>40 mEq/L)– Rx : replacement with NSS– Sodium loss in urine : salt tablet

Hyponatremia syndrome

Hypernatremia : Diabetes insipidus

• inadequate circulating quantities of ADH, which results in an inability to concentrate urine

• hypovolemic hypernatremia• disruption of the hypothalamic-hypophysial axis : severe

brain injury is usually a grave prognostic sig• Mild to moderate DI : water replacement, may

exacerbate intracranial hypertension• intravenous administration of aqueous desmopressin

acetate (DDAVP), 2 to 4 µg, will decrease free water clearance for 8 to 12 hours

• Correct slowly over a period of 48 hours

Hypoglycemia• 80-110 mg/dL• Reduction in infection, acute renal failure

Hypopituitarism• Pathologic : hemorrhage of hypothalamus, hemorrhage of posterior

lobe, infarction of the anterior pituitary• Adrenal insufficiency : hypotension, hypoglecemia, hyponatremia• Risk factor

• common in younger patients• severely injured patients• patients with preceding ischemic events (hypoxia, hypotension,

severe anemia)• patients who received etomidate• use of barbiturate coma

• Rx : indication hypotension, hyponatemia• Hydrocortisone 50-100 mg q 8 hr or continuous infusion 0.18 mg/kg/hr

Timing of surgery for other injuries

• Systemic injury life-threatening : go to surgery• Non-emergency : postpone until intracranial

hypertension resolve

Treatment of secondary injury processes : intracranial hypertension

• Pharmacologic paralysis– analgesia/sedation : morphine or lorazepam– muscle relaxant : cisatracurium or vecuronium

• Hyperventilation : Paco2 of 20 to 25 mm Hg– not recommended in the current TBI guidelines– Hyperventilation should be withdrawn over a period of several

days to avoid this increase in ICP

• Drainage of cerebrospinal fluid– removal of 1 mL of CSF : not changeICP < 1 - 2 mm Hg– brain becomes more swollen, the ventricles collapse

Treatment of secondary injury processes : intracranial hypertension

• Osmotherapy– Mannitol, peak effect 20-60 min, duiration 1.5 – 6 hrs– 0.25 to 1 g/kg BW– side effects : hypovolemia, hyperosmolarity(keep less than 320

mOsm), and renal failure

• Barbiturate coma– loading dose is 10 mg/kg given over a 30-minute period,

followed by 5 mg/kg each hour for three doses, maintenance dose is 1 to 2 mg/kg per hour

Treatment of secondary injury processes : intracranial hypertension

• Hypothermia– Reduce : cerebral metabolic rate, increased ICP, cerebral

edema formation, frequency of epileptic discharges, and opening of the BBB

– 32°C and 33°C , rewarming period lasting less than 24 hours, continue at least 24 hr

– Complication : thrombocytopenia, cardiovascular and pulmonary complications, infections

• Decompresive craniectomy

Treatment of secondary ischemic insult

• cerebral ischemia– goal of therapy is to optimize oxygen delivery to the brain– Hb : 10 g/dl

• Treatment of Hypotension– CVP monitor– Cystalloid solution for hypovolemia– Other condition : cardiac contusion or tamponade, and tension

pneumothorax

• Treatment of Hypoxia– PEEP ; increase ICP by increasing intrathoracic pressure, central

venous pressure, and cerebral venous pressure, decreasing venous return to the heart, BP can be reduced. reduction in CPP

Treatment of Secondary Ischemic Insults

• Treatment of Anemia– hematocrit of greater than 25% to 30% may be required for

maximal oxygen delivery to the brain.

• Treatment of Seizures– Diazepam, 5 to 10 mg intravenously, or lorazepam, 2 to 3 mg

intravenously– Phenyltoin loading dose of 15 to 20 mg/kg

Maintenance doses of phenytoin, 300 to 400 mg/day

• Treatment of Cerebral Vasospasm– treated similar to vasospasm after SAH– Nimodipine – Hypervolemic hemodilution, hypertension