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University of Santo Tomas

THE GRADUATE SCHOOL


ADVANCED MEDICAL-SURGICAL NURSING I
CASE SCENARIO
THE CLIENT WITH NEUROLOGIC ALTERATIONS
Prepared by: John Henry O. Valencia, RN, RM
Master of Arts in Nursing tudent
55y/o male office worker has a history of HTN which had been treated with hydrochlorothiazide,
when he suffered a stroke during an altercation with a neighbor. He is also a known diabetic, Type 1
and is on NH insulin co!erage e!ery morning. "n admission to the #$ of a nearby hospital, he was
comatose. %ollowing a brain scan, which showed a large hemisphere lesion, and a spinal puncture,
which re!ealed increased intracranial pressure and bloody spinal fluid, the client was diagnosed as
ha!ing suffered an intracerebral hemorrhage. %ollowing administration of &'( ml )annitol solution *+, he
slowly regained consciousness and was found to ha!e right hemiplegia and e,pressi!e aphasia.
INSTRUCTIONS
1. *dentify the !earnin" iss#es -at least ./ related to pathophysiology -%ocus on Neuro/ that you
can draw out from this case.
'. repare to discuss these learning issues with the class on Tuesday, 0eptember 1(, '(1& after
the 2+ case scenario discussion.
1. %rom your 3ournal readings, what can you draw out as an identified pathophysiologic
contro!ersial issue related to neurological care4 ro!ide a short discussion based on your
3ournal resources.
&. 5our written answer to 6 1 7 1 will be submitted ne,t Tuesday8s class. Typed in 9& size, arial
narrow, font 11.
DIA$ETES MELLITUS T%&E '
:eta 2ell ;estruction
<ack of *nsulin release
$educe Tissue uptake of =lucose
age ( of )
*ntracellular Hypoglycemia
#,tracellular Hyperglycemia
*ncrease =lucogenesis and
=luconeogenesis
:reakdown of %ats
;ecrease rotein
0ynthesis
2ache,ia, <ethargy and
olyphagia
;ecrease >
globulins
*mpaired wound
healing
Hyperosmotic lasma
;ehydration of cells
;ecrease arterial fle,ibility
*ncreased 9rterial 0tiffiness
:lood =lucose ? $enal threshold
=lycosuria
*ncreased @rine 0pecific
=ra!ity
"smotic ;iuresis
$990 9cti!ation
*ncreased :lood
+olume
H%&ERTENSION
*ncreased =lycoprotein cell
wall deposits
9ccelerated
9therosclerosis
%ormation of laAue
deposits
Thrombosis
"cclusion of )a3or :lood
+essel
*% )9N9=#;B
ossibleB
D* cranial 2T scan, ;oppler, #T
scan, )$*, cerebral angiography,
lumbar puncture, ##=/#2=, skull
,Cray, carotid ultrasonography
T* aspirin, thrombolytics, carotid
stenting, hypothermia,
anticoagulants, surgical
decompression -hemicraniectomy/,
carotid endartectomy
=@9$;#; $"=N"0*0
*% N"T )9N9=#;B
<ysed or )o!ed Thrombus
from the !essel
+ascular wall becomes
weakened and fragile
<eaking of blood from the
fragile !essel
INTRACERE$RAL
HEMORRHAGE
age + of )
*% )9N9=#;B
Dx: !" scan, MR#, cerebral angiography,
arteriography, lu$bar puncture, s%ull &'ray
Tx: chronic hypertensi(es, surgical
deco$pression, e(acuation and aspiration,
ad$inistration of fresh fro)en plas$a *ith
fibrinogen or cryoprecipitate
Hematoma e!acuation
%ormation of ca!ity surrounded by
dense gliosis
D 1( ml
hemorrhage
1(CE( ml
hemorrhage
? E( ml
hemorrhage
oor prognosis *ntermediate
prognosis
=ood prognosis
Decreased
ICP
*% N"T )9N9=#;B
0,B, headache,
unconsciousness,
nausea+(o$iting,
(isual disturbances
)ass of blood forms and grows
:lood seeps into the !entricles
"bstruction of 20%
passageway
9ccumulation of 20% in the
!entricles
+entricles dilate behind the
point of obstruction
INCREASED IC&
*% )9N9=#;B
Ventriculosto$y, VP shunt, #!P
Monitoring
9lternati!e route for
return of 20% in the
circulation
2ompression of brain
tissues will not occur
=uarded rognosis
*% N"T )9N9=#;
@nrelie!ed obstruction
%ormation of small and large
hematomas
<odges onto other
cerebral arteries
+asospasms of tissue and arteries
CERE$RAL H%&O&ER,USION
*mpaired distribution of o,ygen
and glucose
Tissue hypo,ia and
cellular star!ation
2erebral *schemia
*nitiation of ischemic
cascade
)ismatch of cerebral bloodflow and
metabolic demands -"' F =lucose/
#lectric %ailure
*onic pump failure
otassium efflu, -from neurons/
0odium *nflu, -into neurons/
2alcium influ,
9naerobic metabolism by
mitochondria
=enerates large amounts of
lactic acid
<actic 9cidosis
%ailure production of
adenosine triphosphatase
%ailure of energy dependent
process
-ion pumping/
age - of )
hospholipase 9'
9cti!ation
9rachidonic 9cid 9cti!ation -and other free
fatty acids/
2ycloCo,ygenase
<ipoCo,ygenase
Hydropero,ides
<eukotrienes
rostagladin
#ndopero,ides
Thrombo,ane 9'
-potent !asoconstrictor and platelet
aggreagnt/
roduction of o,ygen free radicals
and other reacti!e o,ygen species
$elease of e,citatory
neurotransmitter glutamate
*nflu, of calcium
9cti!ates enzymes that digest cell
proteins, lipids and nuclear
material
%ailure of mitochondria
TRANSIENT ISCHEMIC ATTAC.
%urther energy
depletion
;amage to the blood !essel
endothelium
*% )9N9=#;B
Ct'PA ,uro%inase, strepto%inase-
'calciu$ channel bloc%ers
*% N"T )9N9=#;B
=uarded rognosis
:rain sustains an irre!ersible cerebral
damage
9lters cerebral metabolism
;ecreased 2erebral perfusion
;amage of hemisphere of brain
2ascade of biochemical processes
2ompression of tissue
*schemic cascade threaten cell
)embrane depolarization of cell wall
*nflu, of sodium
age / of )
edema
+ascular 2ongestion
*ncreased intracranial pressure
*mpaired cerebral perfusion and function
)iddle 2erebral 9rtery 9nterior cerebral artery
osterior 2erebra*
9rtery
*nternal 2arotid 9rtery
+ertebrobasilar 0ystem 9nteroinferior
2erebellar
osteroinferior cerebellr
<ateral hemisphere,
frontal, parietal and
temporal lobes, basal
ganglia
.rontal /obe
Occipital lobe0 anterior
and $edial portion of
te$poral lobe
1ranches into
ophthal$ic, P!A,
anterior choroidal,
A!A, M!A
!erebellu$ and brain
ste$
!erebellu$
!erebellu$
S*
2ontralateral hemiparesis or
hemiplegia, unilateral
neglect, altered
consciousness,
homonymous hemianopsia,
inability to turn eyes toward
affected side, !ision
changes, dysle,ia,
dysgraphia, aphasia,
agnosia, memory deficits,
!omiting
S*
2ontralateral hemiparesis,
foot and leg deficits
greater than the arm, foot
drop, gait disturbances,
contralateral hemisensory
alterations, de!iation of
eyes toward affected side,
e,pressi!e aphasia,
confusion, amnesia, flat
affect, apathy, shortened
attention span, loss of
mental acuity, apra,ia,
incontinence
S*
)ild contralateral hemiparesis,
intention tremor, diffuse
sensory loss, pupillary
dysfunction, loss of con3ugate
gaze, nystagmus, loss of depth
perception, cortical blindness,
homonymous hemianopsia,
perse!eration, dysle,ia,
memory deficits, !isual
hallucinations
S*
contralateral
hemiparesis with facial
asymmetry, contralateral
sensory alterations,
homonymous
hemianopsia, ipsilateral
periods of blindness,
aphasia if dominant
hemisphere is in!ol!ed,
)ild Horner8s syndrome,
carotid bruits
S*
9lternating motor
weaknesses, ata,ic gait,
dysmetria, contralateral
hemisensory impairments,
double !ision,
homonymous hemianopsia,
nystagmus, con3ugate
gaze, paralysis, dysarthria,
memory loss,
disorientation, drop attacks,
tinnitus, hearing loss,
!ertigo, dysphagia, coma
S*
*psilateral ata,ia,
facial paralysis,
ipsilateral loss of
sensation in face,
sensation changes
on trunk and limbs,
nystagmus, Horner8s
syndrome, tinnitus,
hearing loss
0,B
9ta,ia, paralysis of
the laryn, and soft
palate, ipsilateral
loss of sensation
in face,
contralateral on
body, nystagmus,
dysarthria,
Horner8s
syndrome, hiccups
and coughing,
!ertigo, nausea
and !omiting
age 0 of )
*% )9N9=#;B
alliati!e careC
%reAuent !ital sign and
neuro!ital signs, intubation,
mechanical !entilation,
!asodilators, osmotic
diuretics, !entriculostomy,
*2 monitoring
*% N"T )9N9=#;B
2ontinued insufficiency of blood flow
%urther compression of tissues
2omatose
2erebral ;eath
<oss of neural feedback mechanisms
2essation of physiologic functions
=ood cerebral perfusion
=ood impro!ement
=ood rognosis
2ardio!ascular 0ystem
"ther systems
<oss of cardiac muscle
function
0ystemic %ailure
DEATH
$ela,ation of !enous
!al!es
0,B
bradycardia
0,B
hypotension
;ecreased cardiac
output
ulmonary 0ystem
%ailure of accessory muscles
for breathing
<oss of lung
mo!ement
0,B apnea
2ardiopulmonary arrest
=astrointestinal Tract
$ela,ation of intestines and
sphincters
<oss of bowel
control
=enito@rinary 0ystem
Neurogenic
bladder
<oss of sphincter
control
0,B restlessness,
abnor$al
ther$oregulation, $ental
confusion, increased
secretions, decreased
urinary output.
"ther 0ystems
LEARNING ISSUES
A1 ISCHEMIC CASCADE as a res#!t of !a23 of $!oo4 S#55!y to t6e 7rain 4#e to 6aemorr6a"e
#MPOR"AN" "2P O. "H2 #!HA2M#! !A!A32:
'1 Githout adeAuate blood supply and thus lack of o,ygen, brain cells lose their ability to produce
energy C particularly adenosine triphosphate -9T/.
(1 2ells in the affected area switch to anaerobic metabolism, which leads to a lesser production of
9T but releases a byCproduct called lactic acid.
+1 <actic acid is an irritant, which has the potential to destroy cells by disruption of the normal
acidCbase balance in the brain.
-1 9TCreliant ion transport pumps fail, causing the cell membrane to become depolarizedH
leading to a large influ, of ions, including calcium -2aII/, and an efflu, of potassium.
/1 *ntracellular calcium le!els become too high and trigger the release of the e,citatory amino
acid neurotransmitter glutamate.
01 =lutamate stimulates 9)9 receptors and 2aIICpermeable N);9 receptors, which leads to
e!en more calcium influ, into cells.
81 #,cess calcium entry o!ere,cites cells and acti!ates proteases -enzymes which digest cell
proteins/, lipases -enzymes which digest cell membranes/ and free radicals formed as a result
of the ischaemic cascade in a process called e,citoto,icity.
age 8 of )
)1 9s the cellJs membrane is broken down by phospholipases, it becomes more permeable, and
more ions and harmful chemicals enter the cell.
91 )itochondria break down, releasing to,ins and apoptotic factors into the cell.
':1 2ells e,perience apoptosis.
''1 *f the cell dies through necrosis, it releases glutamate and to,ic chemicals into the en!ironment
around it. To,ins poison nearby neurons, and glutamate can o!ere,cite them.
'(1 The loss of !ascular structural integrity results in a breakdown of the protecti!e blood brain
barrier and contributes to cerebral oedema, which can cause secondary progression of the
brain in3ury.
:.
age ) of )

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