The curious case of Kevin, A cat and SDH

Lisa Housel NAR Jake Sareerak NAR Samuel Merritt Universit Anatom and !h siolo"

,ase Stud
#$ o Male %resentin" to %h sician &ith c'o HA ( ) &eek Hit head on %orch &hile searchin" for his cat S m%toms+
Headache *e"an at this time or shortl after HA continue to occur after ar"uments &ith &ife ,ontinuous HA, all over head and e(tend to %osterior neck muscles Ti"ht neck muscles -ision and hearin" are .NL Denies nausea Hasn/t *een slee%in" &ell No relief &ith A!A! and i*u%rofen

!h sical 4(amination
A01(2 -S are .NL Neck is su%%le and 3R1M T m%anic mem*rane, o%tic refle(es and retinae are intact Stead "ait and DTR intact Dia"nosed &ith muscle tension headache and treated &ith sedative, muscle rela(ant and %ain medication
,all MD if HA does not im%rove over the &eekend

3ollo&@u%
Returns to %h sician on Monda mornin" due to no im%rovement in HA A%%earance and manners are chan"ed from 3rida Una*le to drive Dro&s 5ncreased %ain6 thro**in" &hen su%ine or fle(es neck -ision intact Diminished a%%etite6 denies emesis 7!8)9:';: <3rida 8)=:'>:? 3R1M in neck6 fle(ion increases HA ,ranial nerve, o%tic, and "ait'*alance tests are .NL and s mmetrical Skull8tender to touch

Dia"nostic Tests
7lood tests <,7,, .7,, Differential? .NL ,T scan of the head reveals a lar"e, *ilateral su*dural hematoma of uncertain a"e
A*sence of skull f(

Treatment
Referred to neurosur"eon
!erforms craniotom &ith evacuation of hematoma !er sur"eon, &hen skull %ierced, *lood is initiall released at a hi"h %ressure

HA minimal after sur"er 6 "ood s%irits &ith famil at *edside

Primary Traumatic Brain Injury:

Result of immediate mechanical disruption of brain tissue.
Shear injury Contusion Intraparenchymal hematoma Subarachnoid hemorrhage Subdural hematoma Epidural hematoma S ull fracture !iffuse brain s"elling #ascular injuries Cer$ical spine injury

%ir"ay &anagement:
A Intubation: Indications for TBI patients:
BRespiratory distress. B&otor posturing'absence of response to pain. B(ypo)ia'hypercapnia. B*CS + ,. BSei-ures. BIncreased ICP. B.eed for analgesics'sedati$es. BSignificant associated injuries.

Secondary Brain Injury:

Pathophysiological response to primary neuronal injury (ours to days after primary insult. Progressi$e. (ypo)ia'hypotension are main causes for /nd injury. (igh ICP. (yperthermia. Brain edema. (emorrhage . The primary focus of neurocritical care for TBI is the prevention, identification, and treatment of secondary brain injury.

Subdural (ematoma
Tearing of bridging $eins: ASecondary to acceleration'deceleration. ACresent shaped hematoma. AHematoma much slower to develop (venous origin) into a mass large enough to produce sx !amage due to impact: A(igher impact than that of E!(. A&ore brain injury and edema. Treatment: ASymptomatic 0 1 cm thic at its biggest point ASmaller subdurals may be obser$ed. &ortality: ARange is 234536. (igh mortality rate if: A!elay of surgery is 0 7 hrs.

Type cute Su'actue %hronic

T %es of SDH Occurrence after Progression of Treatment Injury Symptoms !"#"$ Hr after Immediate %raniotomy&
severe deterioration evacuation and "$ hr#!trauma w( after Initial )vacuation and decompression sever trauma *ee(s& months& unconsiousness& .onspecific& )vacuation and gradual usually + !, nonlocali/ing decompression& improvement& days after progressionmem'ranectomy deterioration injury- often progressive over hours& injury seemed alteration in dilation trivial or 0O% of pupils& ptosis forgotted 'y patient

Classification of Head (Brain) Injury

Minimal
no loss of consciousness or amnesia GCS 15

Clas"o& ,oma Scale

Mild
amnesia or brief (< 5 min) L C! or im"aired alertness! memory GCS 1#$15 %ost$concussi&e syndrome

Moderate
L C ' 5 min! or focal neurolo(ic deficit GCS )$1*

Se&ere
GCS < +

7est Motor Res%onse+ 1*e s # LocaliDes %ain $ 3le(ion &ithdra&al 9 3le(ion a*normal <decorticate? 2 4(tension <decere*rate? = No res%onse ) 7est -er*al Res%onse+ 1riented and converses $ Disoriented and converses 9 5na%%ro%riate &ords 2 5ncom%rehensi*le sounds = No res%onse

SDH in 4lderl
The %eak incidence of SDH is in the #th and Eth decades of life &hen a lar"er SD s%ace is availa*le as a result of *rain atro%h The enlar"ed s%ace accounts for the %resentin" com%laint of focal s m%toms rather than those associated &ith increased 5,! S m%toms ma mimic other health %ro*lems+ somnolence, confusion, lethar" , and memor lossF

!ossi*le ,auses of Headache

Headache results from *lood accumulation *et&een the dura mater and arachnoid la er causin" an increase in 5,! Headache also results from *rain com%ression6 SDH slo&l enlar"es due to re%eated *leedin" until a mass effect occurs Headache is usuall severe or moderatel severe, and in the first fe& da s after the inGur , the headache is a%t to *e constantF 5t/s usuall "eneraliDed, ho&ever sometimes it could *e localiDed to the as%ect of the hematomaF

Si"nificance of S m%toms

,urrent headache is continuous

,ommon s m%tom due to the mass effect of hematoma causin" increase 5,! and cere*ral edema SDH &as *ilateral in ori"in, therefore, no lateraliDation occurred Stiffness of the neck and neck %ain could additionall *e %resent &hen *lood has *een e(travasated into the su*@arachnoid s%ace

Headache is all over his head, and e(tends into his %osterior neck muscles, &hich are ti"ht

-ision and hearin" are normal and he has no nausea

-isual and hearin" deficits &ould *e noted &ith an 5,H SDH is located *et&een the dura and arachnoid s%ace &hich causes %ressure6 venous in nature and usuall slo& *leedF

T lenol and 5*u%rofen A!A! and 5*u%rofen did not relieve headache .HHIII
HA related to *lood in su*dural s%ace increasin" 5,! Skull is ri"id, inelastic container that houses the *rain, *lood volume and ,S3
Since inelastic container, onl small increases in volume &ithin the com%artment can *e tolerated *efore %ressure increases dramaticall <conce%t is defined * Monro@ Kellie Doctrine? 5ntracranial volume is fi(ed6 if %ressure in com%artment rises, com%ensator action occurs *ut is limited

A!A! and 5*u%rofen are NSA5Ds that inhi*it ,1J) and ,1J= &hich leads to the inhi*ition of %rosta"landin s nthesis and decreased formation of %recursors
Anal"esia is %ro*a*l %roduced via %eri%heral

Results of !h sical 4(am .hat is the si"nificance of each of the follo&in"

findin"s+ Kevin &as alert 0 oriented, and his vital si"ns &ere normal6 his neck &as su%%le and had normal ran"e of motion6 his skull &as normal on %al%ation6 there &ere no si"ns of a*normal cranial nerve function6 his t m%anic mem*ranes &ere normal, as &ere his o%tic refle(es and retinae6 his "ait and dee% tendon refle(es &ere also normalI .hat %ossi*le %ro*lems &ere ruled out in the course of this e(aminationI His s m%toms did not correlate &ith neurolo"ical deficits that &ould result from a dramatic increase in 5,! or herniation His s m%tom reflect the a*ilit for the intracranial com%artment to com%ensate for the e(tra *lood * decreasin" ,S3 %roduction to attem%t to maintain homeostasis in relation to %ressure

Si"nificance of s m%tomsI

5na*ilit to drive Dro&s .orsenin" of headache 5ncreased thro**in" %ain &hen l in" do&n Lack of a%%etite

!atho%h siolo"
7lood collected in the su*dural s%ace dra&s &ater due to osmosis 3urther com%ressin" *rain tissue ,ausin" ne& *leeds * tearin" other *lood vessels

5,!

So much room &ithin the skull Ri"id *o( >:K occu%ied * *rain tissues ):K 7lood su%%l ):K * ,S3

5ncreased thro**in" %ain &hen l in" do&nI

.h IIIIII H17 )$ to 9$ de"ree L 5,! H17 M 9$ de"ree L ,!! H17 flat M 5,! 8 More headache and %ain !ositionin"@@H17 elevated &ith head midline to avoid im%edin" venous return

,linical !resentations

De%ends on the siDe of the hematoma and the de"ree of an associated %arench mal *rain inGur headache, nausea, confusion, %ersonalit chan"e, decreased level of consciousness, s%eech difficulties, other chan"e in mental status, im%aired vision or dou*le vision, and &eakness A dilated or nonreactive %u%il i%silateral to the hematoma <or earlier+ a %u%il &ith a more limited ran"e of reaction? Hemi%aresis contralateral to the hematomaF

S mmetr vs As mmetr I

,ranial Nerve 1%tic Cait'*alance As mmetr 8 involvement at the center of the *rain
Si"ns and s m%toms de%end on the severit and location

 7ilateral fi(ed and dilated %u%ils are secondar to inadeNuate cere*ral %erfusion
,ere*ral h %o(ia and severe increased 5,!

!u%ils that are fi(ed and dilated

5rreversi*le inGur

A unilateral fi(ed <unres%onsive? and dilated %u%il

5nvolvement of o%tic nerve

A unilateral dilated %u%il that does not res%ond to either direct or consensual stimulation
transtentorial herniation

A core o%tic %u%il is a %u%il that a%%ears irre"ular in sha%e

mid*rain inGuries

7alance and Cait

A findin" of si"nificant as mmetr durin" the motor e(amination ma *e indicative of a hemis%heric inGur and raises the %ossi*ilit of a mass lesionF
Mid*rain controls ocular motion !ons coordination of e e and facial movement Hearin" and *alance

Signs of Cerebral (erniation

8nconscious'unresponsi$e Patient
%symmetric pupils. !ilated or fi)ed pupil9s:: unilaterally or bilaterally. 8nresponsi$e to painful stimuli. Patient displays posturing.
;irst abnormal fle)ion: decorticate. Then abnormal e)tension: deceberate.

Cushing<s Triad may be present:

Bradycardia= apnea and hypertension.

7lood test
Si"nificance of normal vs a*normal *lood test
A*normal ,7,, 4lectrol tesOFF !T'!TT and !lts+ defective coa"ulation H'H ma *e lo& .7, normal to sli"htl elevated To(icolo" %anel for altered %atient to r'o su*stances a*used A*normal la*orator values ma need to *e correctedOieF 5ncreased 5NR due to coumadin and !lts d sfunction

Hi"h 1%enin" !ressure

.hat does this indicatesI
Hi"h 5,!