Traumatic Brain Injury 23.09.2020

First-line   therapy   consists   of   repetitive   fluid   boluses   with   crystalloids.

Pure   α-adrenergic   sympathomimetics   are   the   vasopressor   drugs   of   choice.

Tachycardia   and   hypotension   are   pathognomonic   signs   of   neurogenic   shock.

The   absence   of   a   cervical   collar   can   be   used   to   rule   out   neurogenic   shock.

Dopamine   is   the   preferred   vasopressor   agent.

Hemicraniectomy   is   first-line   therapy   for   elevated   ICP.

Hypertonic   saline   is   superior   to   mannitol   for   osmotherapy

Prolonged   hyperventilation   is   a   benign   method   for   lowering   elevated   ICP.

Maintenance   of   elevated   cerebral   perfusion   pressure   (CPP)   may   be   more   important   in   improved   neurologic   outcome   at   the   expense   of   high   ICP.

Persistent   hyperventilation   is   a   terrific   method   to   sustain   alkalization   and   combat   acidosis   in   the   brain   for   long   periods.

Hypotension   is   often   the   direct   result   of   intracranial   trauma.

Decerebrate   posturing   is   a   common   response   to   diffuse   cortical   injury.

A   score   of   5   on   the   GCS   is   associated   with   a   poor   prognosis.

The   syndrome   of   inappropriate   antidiuretic   hormone   secretion   (SIADH)   should   be   suspected   when   the   serum   sodium   level   exceeds   150 mEq/L.

Brain   injury   takes   predominance   over   any   other   injury,   and   therefore   initial   evaluation   and   management   should   focus   only   on   the   neurologic   examination.

CT   should   be   performed   to   exclude   the   diagnosis   of   intracranial   hemorrhage   or   a   mass   lesion   before   starting   therapy

Cerebral   edema   caused   by   head   injury   is   vasogenic   and   not   cytotoxic   in   origin.

Steroids   are   useful   for   the   treatment   of   head   trauma.

Hypercapnia   induces   cerebral   vasoconstriction   and   is   useful   for   decreasing   intracerebral   blood   volume.

Within   a   few   hours   (1   to   3   hours)   after   injury,   maximal   cerebral   edema   has   already   formed,   so   further   monitoring   is   unnecessary   if   the   patient   is   clinically   stable.

Most   are   caused   by   basilar   skull   fractures   and   close   spontaneously.

The   risk   for   infection   is   greater   with   rhinorrhea   than   with   otorrhea.

They   often   do   not   require   immediate   surgical   repair   to   avert   infection.

They   may   be   observed   for   up   to   14   days   if   there   is   no   evidence   of   infection.

The   presence   of   a   traumatic   CSF   leak   mandates   the   use   of   prophylactic   broad-spectrum   antibiotic   coverage.