By the end of this we shall be able to know the following definition.of intracranial hemorriage Classification of intracranial hemorriage Types of intracranial hemorriage. Causes of intracranial hemorriage. Signs and symptoms of intracranial hemorriage Investigations specific management. Complication. Ongoing nursing care.

1. INTRACRANIAL
HAEMORRHAGE
A PRESENTATION
BY
DR. NAMPOGO KYOZIRA A
BSN MBCHB MPH (MUK)

2. Order of Presentation
1. Objectives of presentation
2. Definition & epidemiology
3. Etiology & risk factors
4. Etiology, Classification & Pathophysiology
5. Intracerebral hemorrhage
6. Clinical manifestations
7. Subarachnoid hemorrhage
8. Manifestations.
9. Epidural hematoma
10. Subdural hematoma
11. General manifestaions
12. Complications
13. Investigations/ diagnosis
14. Medical management
15. Surgical management
16. Nursing diagnoses
17. Nursing interventions

3. Objectives of this session
By the end of this session, the class members
should be able to;
 Understand what intracranial hemorrhage is
 Identify the commonest presentations of ICH
 Identify the most important nursing
diagnoses of ICH
 Manage ICH patients following the nursing
diagnoses, also patient with pending ICH

4. Definition& epidemiology
 Hemorrhagic bleeding into the brain tissue, the
ventricles or the subarachnoid space
 Mortality rate of almost 48%, 30 days after the
bleed
 Account for 15- 20% of cerebrovascular disorders

5. Etiology & risk factors
 Atherosclerosis leading to aneurysms
 Congenital defects e.g. arteriovenous
malformation especially in young girls
 Hypertensive vascular disease; seen in kids with
pheochromocytoma, nephritic syndrome etc.
 Blacks
 Increased age

6. Etiology, classification&
pathophysiology
 Hemorrhage into the brain may be;
 Traumatic
 Non-traumatic
 Spontaneous; there are two main types of spontaneous
intracranial hemorrhage:
o Intracerebral hemorrhage- which is usually of hypertensive
origin.
o Subarachnoid hemorrhage, which is commonly aneurysmal in
origin.
o Other causes of spontaneous intracranial hemorrhage include;
o vascular malformations which produce mixed intracerebral
and subarachnoid hemorrhage.
o Hemorrhagic diathesis
o Hemorrhage into tumors.

7. Intracerebral Hemorrhage
 Spontaneous intracerebral hemorrhage occurs
mostly in patients of hypertension. Children with
systemic diseases that manifest with HTN are at risk
because they have micro aneurysms in very small
cerebral arteries in the brain tissue.
 Rupture of one of the numerous micro aneurysms is
believed to be the cause of intracerebral
hemorrhage
 Not common to have recurrent intracerebral
hemorrhages like is the case of subarachnoid
hemorrhages
 The common sites of hypertensive intracerebral
hemorhage are the region of the basal ganglia
(particularly the putamen and the internal capsule),
pons and the cerebellar cortex

8. Clinical features
 usually sudden with headache
 loss of consciousness.
 Depending upon the location of the lesion,
hemispheric, brainstem or cerebellar signs will be
present.
 About 40% of patients die during the first 3-4
days of hemorrhage, mostly from hemorrhage
into the ventricles.
 The survivors tend to have hematoma that
separates the tissue planes which is followed by
resolution and development of an apoplectic cyst
accompanied by loss of function.

9. Subarachnoid Hemorrhage
 Hemorrhage into the subarachnoid space is most
common
 caused by;
 rupture of an aneurysm,
 and rarely, rupture of a vascular malformation.
 Of the three types of aneurysms affecting the
larger intracranial arteries—berry, mycotic and
fusiform,
 berry aneurysms are most important and most
common.

10. Subarachnoid hemorrhage
 Berry aneurysms are saccular in appearance with rounded
or lobulated bulge arising at the bifurcation of intracranial
arteries and varying in size from 2 mm to 2 cm or more.
 They account for 95% of aneurysms which are liable to
rupture.
 Berry aneurysms are rare in childhood but increase in
frequency in young adults and middle life.
 They are, therefore, not congenital anomalies but develop
over the years from developmental defect of the media of
the arterial wall at the bifurcation of arteries forming thin-
walled saccular bulges.
 Although most berry aneurysms are sporadic in
occurrence, there is an increased incidence of their
presence in association with congenital polycystic kidney
disease and coarctation of the aorta.

11. Subarachnoid hemorrhage
 In more than 85% cases of subarachnoid
hemorrhage, the cause is massive and sudden
bleeding from a berry aneurysm on or near the
circle of Willis.
 The four most common sites are;
1. In relation to anterior communicating artery.
2. At the origin of the posterior communicating artery
from the stem of the internal carotid artery.
3. At the first major bifurcation of the middle cerebral
artery.
4. At the bifurcation of the internal carotid into the
middle and anterior cerebral arteries

12. Circle of Willis

13. Subarachnoid hemorrhage.,
 The remaining 15% cases of subarachnoid
hemorrhage are the result of rupture;
o In the posterior circulation
o Vascular malformations
o Of mycotic aneurysms that occurs in the setting
of bacterial endocarditis.
o In all types of aneurysms, the rupture of thin-
walled dilatation occurs in association with
sudden rise in intravascular pressure

14. Manifestations
 Clinically, berry aneurysms remain asymptomatic
prior to rupture.
 On rupture, they produce;
 Severe generalized headache of sudden onset
 Frequently followed by unconsciousness and
neurologic defects.
 Initial mortality from first rupture is about 20-
25%.
 Survivors recover completely but frequently suffer
from recurrent episodes of fresh bleeding

15. Epidural Hematoma
 Epidural hematoma is accumulation of blood
between the Dura and the skull following fracture
of the skull
 Most commonly from rupture of middle
meningeal artery.
 The hematoma expands rapidly since
accumulating blood is arterial in origin and
causes compression of the Dura and flattening of
underlying gyri
 The patient develops progressive loss of
consciousness if hematoma is not drained early.

16. Epidural hematoma

17. Subdural hematoma
 Subdural hematoma is accumulation of blood
between the Dura and subarachnoid.
 Develops most often from rupture of veins which
cross the surface convexities of the cerebral
hemispheres.
 Subdural hematoma may be acute or chronic.
• Acute subdural hematoma; develops following
trauma and consists of clotted blood, often in the
front parietal region.
o There is no significant compression of gyri
o Since the accumulated blood is of venous origin,
symptoms appear slowly and may become chronic
with passage of time if not fatal.

18. Subdural hematoma
 Chronic subdural haematoma; occurs often with
brain atrophy
 less commonly following trauma.
 Chronic subdural haematoma is composed of
liquid blood.
 Separating the haematoma from underlying brain
is a membrane composed of granulation tissue.

19. Subdural hematoma

20. General manifestations
 Severe headache
 Vomiting due to increased ICP
 Changes in LOC
 Focal seizures after brain stem involvement
 Nuchal rigidity
 Visual disturbances

21. Complications.
 Hypovolemic shock
 Acute hydrocephalus
 Focal seizures/ seizure disorders

22. Investigations.
 CT scan
 MRI
 Cerebral angiography; dx of intracranial
aneurysm
 Lumbar puncture; only if no evidence of increased
ICP, negative CT and if subarachnoid bleed must
be confirmed

23. Medical management.
 Bed rest with sedation
 Fresh frozen plasma and vitamin K
 Anti-seizure agents, given prophylactically for a
while
 Analgesia
 Sequential compression devices or anti-
embolism stockings to prevent DVT

24. Surgical management
 Craniotomy; to evacuate blood
 Endovascular treatment; to occlude paretnt artery
 Aneurysm coiling; obstruct aneurysm site with
coil

25. Nursing diagnosis
 Ineffective tissue perfusion related to bleeding
 Disturbed sensory perception related to medically
imposed restrictions
 Anxiety related to illness/ medically imposed
restrictions etc.

26. Interventions.,
 Monitor closely for neurological deterioration,
maintain neurological flow record
 Check BP,PR, LOC, RR, Temps and Pupillary
responses to light, report changes ASAP
 Implement aneurysm precautions; absolute bed
rest, quiet, non-stressful setting, restrict visitors
except for family
 Elevate head of bed 15-30 degrees or a ordered
 Apply anti-embolism stockings or sequential
decompression devices
 Observe legs for signs of DVT

27. Interventions.,
 Avoid activities that suddenly increase BP e.g.
Valsalva maneuver., straining by;
o Instruct patient to exhale during voiding/
defecation
o Eliminate caffeine
o Minimize external stimuli
o Administer all personal care
 Administer drugs as prescribed including; fluid
volume expanders, anti- seizure medications,
analgesics
 Report sudden severe headache, vomiting
decreased LOC etc

28. Thank you!
‘’HE WHO SAYS IT CANNOT BE DONE SHOULD NOT
INTERRUPT THE PERSON DOING IT.’’