Intracranial bleeding encompasses all bleeds that may occur within the cranial cavity including Epidural, Subdural, Sub arachnoid, intraparenchymal and Intraventricular haemorrhages. all are discussed in these slides and relevant references are provided for detailed information. It is important to note that medicine is not learnt online but through series of organised events under specialised supervision in recognised institutions of learning.

1. INTRACRANIAL BLEEDING
Authors
1. Nelson Ssewante MBChB V
2. Ronald Mujuni MBChB V
Tutor
Mr. Muhindo A.
Department of Surgery, Makerere University.

2. Outline
1. Introduction with relevant anatomy
2. Neurologic assessment
3. Epidural hemorrhage
4. Subdural hemorrhage
5. Subarachnoid hemorrhage
6. Intracerebral hemorrhage
7. Intraventricular hemorrhage

3. Introduction
• Intracranial bleeding is the pathological accumulation of blood
within the cranial vault.
• This can be with in the meningeal spaces or the brain parenchyma
• It can be classified as intra-axial (parenchymal or intraventricular)
or extra-axial hemorrhage(Epidural or subdural or subarachnoid)

4. Relevant anatomy
• The brain parenchyma is protected by the bony shield called the cranium.
• The brain is divided into;
i. Cerebral hemispheres
ii. The midbrain
iii. The brain stem(pons and medulla)
iv. The cerebellum
• It is covered by 3 protective membranes, from inside out; the pia matter,
arachnoid and dura matter.

5. Blood supply
• Arterial supply • Venous drainage

6. Ventricular system Coverings of the brain

7. Neurologic Assessment
• History
• Examination Findings
• Mental status examination(GCS)
• Cranial nerve examination
• Motor examination
• Deep tendon reflexes
• Sensation
• Cerebellar function

9. Epidural Hemorrhage
• EDH is collection of blood in the extradural space between the dura and
skull
• It commonly results from rupture of Middle meningeal artery(85%)
• Other vessels may include; middle meningeal vein, Dural sinus or
diploic veins

10. Epidemiology of EDH
• EDH is one of the most serious complications of head injury, requiring
immediate diagnosis and surgical intervention.
• Occurs in ~2% of all patients with head injuries and 5−15% of patients with
fatal head injuries
• EDH may be acute (58%), subacute (31%) or chronic (11%).
• It is more common in young adults. Rare in children <2 years and after 60
years

11. Pathophysiology
Direct blow on the head(due to RTA, Falls Coup, Counter-coup
injuries)
Fracture of the scalp(Commonly the temporal
bone)
Disruption of the integrity between the dura and
the bone
Tearing of the vessels(Commonly middle meningeal
artery)
Bleeding with resultant hematoma
formation
Gradual stripping of the dura from the skull & collection
of blood
Hematoma
expansion

12. Clinical presentation
• Classic sequence (seen in <30%):
 Post-traumatic reduced LOC, a lucid interval of several hours, then obtundation, hemiparesis, ipsilateral
pupillary dilatation, and coma.
• Signs and symptoms depend on severity;
 Headache
 Nausea & Vomiting
 Amnesia
 Altered LOC
 Aphasia
 Seizures, HTN, and respiratory distress may also occur
• Deterioration can take hours to days

13. Diagnosis
• Laboratory
 CBC, grouping and crossmatch
 Prothrombin time(PT)/activated partial thromboplastin time (aPTT)
 Serum chemistries, including electrolytes, blood urea nitrogen (BUN), creatinine, and glucose
 Toxicology screen and serum alcohol level
• The diagnosis of EDH must be considered when the plain skull X-rays show a
fracture
• CT scan is modality of choice
 a hyperdense, biconvex (lenticular) mass adjacent to the skull

14. Big Arrow: Fracture Small arrows: Epidural
hematoma

15. Management
• Candidates for non-surgical management include;
I. Small EDH (≤1 cm maximal thickness)
II. Subacute or chronic EDH
III. Minimal midline shift(<5mm)
IV. No focal deficit
• These should be admitted and close neurological observation with serial CT done.

16. Continued…
Indication for surgery
 Any symptomatic EDH.
 An acute asymptomatic EDH >1 cm
 EDH in pediatric patients
 Failure of non-surgical (conservative) management.
Objectives of surgery;
 To remove the clot (to reduce ICP & eliminate focal deficit)
 Achieve absolute hemostasis.
 Prevent reaccumulation by placing dural hitch sutures (tack-up sutures).

17. Continued…
Surgery
• Craniotomy and hematoma evacuation is the mainstay surgical treatment
• This involves identification and ligation of the bleeding vessels
• Appropriate antibiotics should be initiated preoperatively
• Appropriate analgesia
• Mannitol pre-operatively if elevated ICP or signs of brain herniation

18. Prognosis
• Good with prompt management,
• Worse prognosis if bilateral Babinski or
decerebration pre-operative
• Death is usually due to respiratory arrest from
uncal herniation (injury to the midbrain)

19. Subdural hemorrhage
• Collection of blood between the dura and the arachnoid membranes
• It is due to injury to the cortical veins and/or laceration of cortex of
brain
• It can be acute or chronic

20. Epidemiology
• Acute SDH complicates approximately 11% of mild to severe head
injuries and 20% of severe traumatic brain injuries.
• The elderly and chronic alcoholics are at a high risk due to brain
atrophy.

22. Pathophysiology
• SDH usually results from tearing of a bridging veins running from the
cerebral cortex to the dural sinuses.
• Arterial rupture can also result in SDH in 20-30% of cases.
• This commonly follows acceleration injuries.
• Brain atrophy can create traction on arachnoid leading to tearing of veins
since the dura is firmly adherent to the skull
• Intracranial hypotension(Low CSF pressure) is another mechanism that can
result in SDH. This is due to a reduction in brain buoyancy with resultant
traction on vessels.

23. Continued…
Chronic SDH
• It occurs approximately 2 weeks after acute SDH.
• There's increased collagen synthesis and deposition of fibroblasts on the outer
surface of the dura
• This creates a thin inner membrane that completely encapsulates the clot.
• Chronic SDH may liquefy to form a hygroma, and the membranes may calcify.
• In some cases, hematoma expansion can occur as a result of recurrent bleeding
(Acute on Chronic) or osmotic draw of water.

24. Clinical presentation
• Common presentation include;
 Altered level of consciousness
 Headache
 Focal deficits
 Features of raised intracranial pressure (such as blurred vision, N/V, worsening headache)
 Seizure activity
• Clinical features of an acute SDH occur quickly, whilst those of a chronic SDH have a
latent period of weeks (or even months) before symptoms appear.
• In children, it is important to survey for other injuries with suspected SDH as there
might be signs of non-accidental injury.

25. Diagnosis
• Patients should have initial routine bloods, including FBC, CRP, U&Es, LFTs, and a
clotting, which will also aid in assessing for differential diagnosis.
• Non-contrast CT scan is the gold standard
 a crescent-shaped hematoma over one hemisphere, with or without associated midline shift
• Others include; MRI, Angiography

26. Acute on chronic SDH. Acute component is denser than
chronic. Arrow heads are defining the outline of the
hematoma.
A: Chronic SDH B: Acute SDH

27. Management
The decision between surgical or medical management of SDH is
based upon;
• Glasgow Coma Scale score
• CT findings; mainly SDH clot thickness, degree of midline shift, and
presence of associated brain lesion
• Neurologic examination, including pupillary signs
• Clinical stability or deterioration over time
• Acuity of SDH
• Presence and severity of comorbidities and associated trauma
• Age

28. Continued…
Medical SDH care focuses on;
(a) Management of intracranial hypertension (ICP < 22 mmHg)
(b) Maintenance of adequate cerebral perfusion (CPP > 60 mmHg)
(c) Seizure prevention and treatment,
(d) Maintenance of normothermia, eucarbia, euglycemia, and euvolemia,
(e) Early initiation of enteral feeding, mobilization, and physical therapy

29. Continued…
Surgery
• Craniotomy is the recommended surgical technique for patients with
acute SDH and coma
• Decompressive craniectomy
• Burr hole trepanation/trephination

31. Subarachnoid Hemorrhage
• The extravasation of blood into the subarachnoid space
between the pial and arachnoid membrane.
• It occurs in various clinical contexts, the most common being
head trauma.
• Nontraumatic (or spontaneous) cases occurs in the setting of a
ruptured cerebral aneurysm or arteriovenous malformation
(AVM).

32. Etiology
Risk factors
• HTN
• Pregnancy/parturition in patients with
pre-existing AVMs, eclampsia
• Oral contraceptive pill
• Substance abuse (cigarette smoking,
cocaine, alcohol)
• Conditions associated with high
incidence of aneurysms

33. Clinical features
• Sudden onset of severe headache with vomiting.
• Features of raised intracranial pressure.
• Photophobia.
• Neck stiffness.
• Focal neurological deficits: hemiplegia, dysphasia.
• Eye changes: ptosis, dilated pupil, changes in the eyeball movements.
• Sudden loss of consciousness.
• Features of brain oedema and cerebral ischemia.
• In 40% of recovered patients, rebleeding occurs in 6–8 weeks which is commonly fatal.

34. Grade Hunt & Hess system Fischer system WFNS system
1 Asymptomatic or minimal headache and slight
neck stiffness
70% survival
No subarachnoid blood seen
on CT scan
GCS 15, no motor deficit.
2 Severe headache and neck stiffness, No
neurologic deficit except cranial nerve palsy
60% survival
Diffuse or vertical layers of
SAH less than 1 mm thick
GCS 13-14 without deficit
3 Drowsy; minimal neurologic deficit
50% survival
Diffuse clot and/or vertical
layer greater than 1 mm
thick
GCS 13-14 with focal
neurological deficit
4 Stuporous; moderate to severe hemiparesis;
possibly early decerebrate rigidity and
vegetative disturbances
20% survival
Intracerebral or
intraventricular clot
with diffuse or no
subarachnoid blood
GCS 7-12, with or without
deficit.
5 Deep coma; decerebrate rigidity; moribund
10% survival
N/A GCS <7 , with or without
deficit
Grading systems for SAH

35. Diagnostic evaluation
• Routine Labs
• Lumbar puncture.
 In subarachnoid hemorrhage, blood stained CSF is collected.
• CT scan.
• Carotid and vertebral angiogram.

36. Treatment
• Clipping, or wrapping the aneurysm.
• Craniotomy and proceed.
• Ligation of common carotid artery-there is risk of hemiplegia.
• Therapeutic embolization.
• Excision of vascular malformations.
• Coiling of aneurysm with instruments.

38. Intracerebral hemorrhage
• Bleeding within brain parenchyma. It is the second most common
cause of stroke.
• Common sites of involvement
 Basal Ganglia/Internal Capsule (50%)
 Thalamus (15%)
 Cerebral White Matter (15%)
 Cerebellum/Brainstem – usually pons (15%)
 Other (5%)

40. Etiology
• Traumatic
• Hypertensive vasculopathy
 Commonly occur at the branching points between small penetrating arteries and their
parental vessels- area of maximal pressure
 usually causes bleeds at putamen, thalamus, pons, and cerebellum
• Cerebral amyloid angiopathy(CAA)
 Usually asymptomatic, CAA is an important cause of primary lobar ICH in older adults
 Due to deposition of amyloid in small- to medium-sized blood vessels of the brain and
leptomeninges.

41. Etiology continued…
Others
• Hemorrhagic transformation (reperfusion post stroke, surgery, strenuous exercise)
• Vascular anomalies
 Aneurysms, AVMs, and venous sinus thrombosis
• Tumors (1%): often malignant (e.g. GBM, lymphoma, metastases)
• Drugs (amphetamines, cocaine, alcohol, anticoagulants)
• Coagulopathy (iatrogenic, leukemia, TTP, aplastic anemia)
• CNS infections (fungal, granulomas, herpes simplex encephalitis)

42. Risk factors
• Increasing age (mainly >55 years)
• Male gender
• HTN
• Black/Asian > Caucasian
• Previous CVA of any type (23x risk)
• Both acute and chronic heavy alcohol use; cocaine, amphetamines
• Liver disease
• Anticoagulants

43. Clinical features
• TIA-like symptoms often precede ICH, can localize to site of impending
hemorrhage
• Gradual onset of symptoms over minutes-hours, usually during activity
• Headache, Nausea and Vomiting, and decreased LOC are common
• Focal deficits depending on location of ICH

44. Continued…
• Putaminal hemorrhage
 Hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy, stupor, and coma.
• Internal capsule hemorrhage
 Mild dysarthria, contralateral hemiparesis and sensory deficit
• Thalamic hemorrhage
 Hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia.
• Lobar hemorrhage
 Vary in their neurologic signs depending upon location(common in Parietal or occipital)
 These bleeds are associated with a higher incidence of seizures
• Pontine hemorrhage
 Characterized by deep coma, total paralysis, pinpointed pupil that is reactive to light or ocular
bobbing, facial palsy, deafness, and dysarthria when the patient is awake

45. Investigations
Labs
• CBC, PT, aPTT, electrolytes, blood urea nitrogen, creatinine, and glucose
Neuroimaging
• CT or MRI is mandatory to confirm the diagnosis
• CT Angiography
 spot sign (contrast in the hematoma) demonstrate high likelihood of clot growth

46. A small focus of enhancement is seen peripherally
on CTA source images, consistent with the spot
sign (arrow)

47. Medical management
• Initial Resuscitation
• ICH is managed as an emergence.
• Control raised ICP
 Avoid corticosteroid use
• Seizure prophylaxis (phenytoin or levetiracetam)
• Correct any electrolyte abnormalities
• Assess for coagulation disorders and correct if any

48. Cyrus K Dastur, and Wengui Yu Stroke Vasc Neurol 2017;2:21-29

49. Surgical management
Indications of craniotomy
• Symptoms of raised ICP or mass effect
• Rapid deterioration (especially if signs of brainstem compression)
• Favourable location (e.g. cerebellar, non-dominant hemisphere)
• Young patient (<50 yr)

50. Interventricular Hemorrhage
• Also known as intraventricular bleeding, is a bleeding into the brain's ventricular
system
• The ventricular system is contains freely flowing CSF.
• These include paired lateral ventricles, the 3rd ventricle, and 4th ventricle.

52. Etiology
• Primary IVH(30% of cases)
 HTN
 Intraventricular trauma
 Aneurysm
 Vascular malformations
 Tumors
• Secondary(70% of cases)
 These results as an expansion of existing parenchymal or subarachnoid
hemorrhage

53. Clinical presentation
• Sudden onset of headache
• Nausea and vomiting.
• Alteration of the mental state and/or level of
• consciousness.
• Focal neurological signs are either minimal or absent.
• Focal and/or generalized seizures may occur

54. Investigations
• CT is the test of choice
• MRI
• Angiogram
• Carotid duplex
Lab studies
 Electrolyte studies
 Coagulation profile(Platelet counts, PT, aPTT)
 CBC

56. Management
General measures focuses on;
 Cessation of bleeding
 relieving hydrocephalus
 Controlling intracranial pressure.
• Patients who have a moderate to severe IVH should be followed up in ICU
• Patient positioning should be at 300 to reduce risk of aspiration
• Fluid resuscitation using isotonic crystalloid solutions
• any elevations in body temperature should be treated aggressively
• Prophylaxis against deep venous thrombosis
• Seizures prophylaxis

57. Continued…
Specific management is tailored according to the cause
• Blood pressure management
 The optimum blood pressure management in patients with IVH remains undefined. It is
recommended to lower BP gradually.
• External ventricular drain(EVD)
 a small catheter inserted through the skull usually into the lateral ventricle to drain excess
CSF.
 Indicated for patients with IVH with hydrocephalus and neurologic decline
• Intraventricular thrombolysis

58. References
1. F. Charles Brunicardi, Ashwin G. Ramayya, Saurabh Sinha, M. Sean Grady. Schwartz’s
Principles of Surgery; 11th edition volume 1 (2019). Chapter 42 pages 1849-1853
2. Prakash Narain Tandon, Ravi Ramamurthi and Pradeep Kumar Jain N. Ramamurthi &
Tandon’s manual of Neurosurgery 1st edition (2014); chapters 33-36, pages 270-287
3. David S Liebeskind, Helmi L Lutsep, Edward L Hogan. Epidural Hematoma;
https://emedicine.medscape.com/article/1137065-overview Medscape 2018.
4. David S Liebeskind, Francisco Talavera, Howard S Kirshner, Jeffrey L Saver. Intracranial
Hemorrhage; https://emedicine.medscape.com/article/1163977-overview Medscape
2018.
5. Sriram Bhat M; SRB’s Manual of Surgery 5th Edition. Chapter 27 Pages 1090-1098

59. The End!