Hemorrhage Flashcards
extravasation of blood into subarachnoid space, particulary of basal cisterns and into cerebral spinal fluid pathways
subarachnoid hemorrhage
most subarachnoid hemorrhages due to what? can also be from what?
head trauma
spontaneous (intracranial saccular aneurysms)
what commonly appears in SAH?
AV malformations
some RFs of SAH?
intracranial aneurysms associated with coarctation of aorta
AV malformaition
polycystic dx of kidneys
fibromuscular dysplasia do renal arteries
HTN
s/s of SAH?
abrupt HA “worst HA of life”
maybe LOC
maybe hemiparesis or dilated pupil
drug for SAH?
Nimodipine (pevents cerebral vasospasm)
surgery for SAH is done to what?
eliminate source of hemorrhage, obliterate aneurysm, fluid, HTN therapy, shunting for hydrpcephalus, AV malformation obliteration, radiosurgery for deep AV malfor
pts with SAH die from what?
aneurysm (2ndary to cerebral vasospasm)
90% of these are caused by head trauma with a skull fracture that crosses a portion of the middle meningeal artery or vein?
epidural hemorrhage
the middle meningeal artery is torn how often in epidural hemorrhage?
60% of the time
classic problem with epidural hemorrhage?
pt falls and hits head, LOC, pts wakes up (EDH is expanding and increasing intracranial pressure), pts LOC again and dies from herniation
Cushings Triad?
systemic HTN
bradycardia
Respiratory depression
(this occurs when cerebral perfusion is compromised by increased intracranial pressure)
tx of epidural hemorrhage?
stabilization
evacuation and control of hemorrhage
embolization and observation
this can lead to stroke, more likely to result in death than ischemic stroke or subarachnoid hemorrhage, when accompanied with edema it may disrupt or compress adjacent brain tissue leading to neurological dysfunction
ICH (intracerebral hemorrhage)
causes of ICH:
HTN autoregulatroy dysfunction with excessive cerebral blood flow aneurysm or AVM arteriopathy altered hemostasis hemorrhagic necrosis venous outflow obstruction nonpenetrating/penetrating cranial trauma
ICH s/s?
alteration in level of consciousness
N/V, HA, seizures, focal neurological deficits
Labs for ICH?
CBC/platelets
PT/PTT
CMP
Toxicology/serum alcohol
tx of ICH:
slowly lower BP to MAP less than 130mmHg
stabilize vital signs and get emergent CT
use normotonic fluids
avoid hyperthermia
correct coagulopahty with FFP, vit K, protamine, platelet transfusions
fosphenytoin for seizures or lovar hemorrhage
intubate and hyperventiliate if ICP increased (mannitol)
ICH prognosis:
good or bad?
larger hematomas
lobar hemmorhage
significant volume of intraventricular blood
hydrocephalus
bad
better than deep hemorrhage
bad
bad
labetalol:
lowers what?
BP
nicardipine:
CCB
mannitol:
reduces what?
reduces cerebral edema with help of osmotic forces, resulting in reflex vasoconstrictio and lowering of ICP
Fosphenytoin:
stabilizes neuronal membranes and decreases seizure activity
Phytonadione/vit K:
promotes hepatic synthesis of clotting factors that inhibit warfarin effects
protamine:
forms a salt with heparin and neutralizes its effects
Famotidine:
H2 blocker (reduces gastric acid)
rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane (subacute and chronic phases)
subdural hematoma
acute SDH:
what kind of pressure venous bleeding?
cerebral injury results from what?
low
direct pressure, increased ICP, intraparenchymal insults
SDH:
in the subacute phase, the clotted blood does what?
liquefies
SDH:
in the chronic phase, cellular elements have disintegrated and what remains in the subdural space?
collection of serous fluid
SDH frequency is related to what?
incidence of blunt trauma
SDH more common in who and why?
elderly, more predisposed to cerebral atrophy, less resilient bridging veins that can be damaged more easily
bilateral SDH are more common in who?
intrhemispheric SDHs are associated with what?
infants (lack of adhesions)
child abuse
simple SDH means there is no what?
complicated means there is what?
parenchymal injury (20% mortality)
parenchymal injury (50% mortality)
hx of SDH:
acute:
chronic:
blunt head trauma
1/2 cases have no head trauma, progressive s/s
any what should heighten suspicion of SDH:
coagulopathy
also hemophiliacs, alcoholics
on PE SDH:
focal neurological signs following blunt trauma, signs of external trauma, abnormal mental status
what is seen in acute/subacute SDH, what is needed for atleast 1 year?
sig neurological disability/impairment of function, seizure prophylaxis
Chronic SDH:
mortaility is decreased, most pts resume functional status, what can reoccur?
hematoma, infx, seizures
defects of circulatory system that are generally believed to arise during embryonic/fetal development or soon after birth, snarled tangles of arteries/veins
AV malformations
s/s of AVM:
HA with no pattern, seizures, weakness, paresthesias, paralysis, focal finding, bruit
tests for AVM:
CTA, MRA, Arteriogram
tx for AVM:
conventional surgery, endvascualr embolization, radiosurgery
saccular (berry) aneurysm:
rounded/pouch like sac of blood attahced by a neck or stem to an artery or branch of blood vessel
lateral aneurysm:
bulge on one wall of blood vessel
fusiform aneurysm:
formed by the widening along all walls of the vessel
aneurysms are usually what? tx options?
asymptomatic, same as AVM
