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Intracranial Hemorrhage

 

Richard Schmidt, M.D.

 

 

Objectives:

 

1.  Understand the different anatomic types of intracranial hemorrhage, their common causes, and their radiographic appearance on CT.

 

2.  Describe the general neurologic signs and symptoms indicative of elevated intracranial pressure, and of subarachnoid and intracerebral hemorrhage.

 

3.  Describe the diagnostic workup of a patient with suspected or proven subarachnoid hemorrhage, and the main treatment options for a ruptured cerebral aneurysm.

 

4.  Understand the differentiating features of hypertensive intracerebral hemorrhage from hemorrhage due to a vascular malformation.  Describe the workup of hemorrhage due to a suspected arteriovenous malformation.

 


 

I.  Classification of Intracranial Hemorrhage:

A.        Anatomic Classification

 

Epidural

Subdural

            acute

            chronic

Subarachnoid

Intracerebral

Intraventricular

 

B.         Etiologic Classification

 

Most Common:

Trauma

Arteriovenous malformation

Aneurysm

Hypertensive

Coagulopathy

 

Less Common:

Neoplastic (hemorrhage into malignant tumor)

Vasculitis

Infectious (bacterial or mycotic aneurysm)

Amyloid angiopathy

Venous thrombosis

Hemorrhage into infarct

 

II.    Intracranial hemorrhage produces signs and symptoms by two general mechanisms

            -focal deficits related to injury of a specific brain area

                        eg. Hemiparesis, dysphasia, visual field cut

 

            -global deficits related to elevation of intracranial pressure (ICP), including:

                        Headache, nausea/vomiting

                        Decreased level of consciousness

Lethargy-stupor-obtundation-coma

                        Cushing's reflex (hypertension with bradycardia)

                        Changes in respiratory pattern

                        Rostro-caudal motor deterioration (see Glascow Coma Scale)             

                        Cerebral herniation, pupillary dilation

 

Glascow Coma Scale: Used universally for grading level of consciousness on a scale of 15 (normal) to 3 (deep coma)

            

 

Score Motor Verbal Eye Opening
6 Obeys commands
5 Localizes Oriented
4 Withdraws Confused Spontaneou s
3 Decorticate Inappropriate words To speech
2 Decerebrate Incomprehensible To pain
1 Nil Nil Nil 


III.  Assessment and treatment of patients with suspected intracranial hemorrhage

           

A.    History - Suspect intracranial hemorrhage in any patient with sudden severe headache, especially if associated with nausea and vomiting, decreased level of consciousness, or focal neurological deficit.

 

B.    Examination - Rapid neurological assessment is essential (1-3 minute exam)

            Respiration and blood pressure

GCS exam: motor function, verbal response and eye opening

            Pupil size and reactivity (CN 2, 3 and midbrain)

            Doll's eyes (CN 8, 3, 6, medulla, pons and midbrain)

            Corneal reflex (CN 5, 7, pons)

            Gag (CN 9,10, medulla)

                                   

C.    Management of Elevated ICP

            Intubate, modest hyperventilation to pCO2 of 30

            Mannitol, 0.5-1.0 gm/kg iv push

            Furosemide 5-20 mg iv

            Elevate head 20-30 degrees, avoid any neck vein compression

            Sedate and paralyze if necessary with morphine and vecuronium (struggling,       coughing etc will elevate intracranial pressure)

            Avoid using antihypertensives to lower blood pressure

 

            D.  Diagnostic workup of patient with suspected intracranial hemorrhage:

            STAT CT scan (essential in every patient)

Cerebral angiogram if hemorrhage is confirmed (not necessary in case of classic hypertensive hemorrhage).

MRI scan (not the initial study of choice, it may be helpful in select cases and in surgical planning for vascular malformations)

 

 

IV.  Subarachnoid hemorrhage

 

A.    Radiologic appearance:  Acute hemorrhage within CSF-containing cisterns, especially around vessels of Circle of Willis.

B.    Etiology:  Usually due to ruptured cerebral aneurysm

 

C.    Presenting symptoms:  Explosive or thunderclap headache, “worst headache of my life”, frequently with nausea and vomiting, decreased level of consciousness or coma.  Signs of meningeal irritation (nuchal rigidity, photophobia) may develop after several hours.

              

40% of major SAHs are preceded by a sentinel hemorrhage which is less severe in intensity.  Maintain a high index of suspicion for SAH in a patient presenting with an uncharacteristic headache.

 

D.   Incidence, prevalence and significance:

30,000-35,000 cases of aneurysmal SAH/year in US

1-2% of adults have cerebral aneurysms

Risk of hemorrhage from unruptured aneurysm is 1-3% per year

Death or permanent disability occurs in 25-50% of patients with aneurysmal subarachnoid hemorrhage.

Unless promptly treated, risk of rehemorrhage after aneurysm rupture is 20% over next 2-3 weeks, and 50% over next 6 months.  Rebleeds are nearly always fatal.

The main goal of treatment is to prevent rebleed.

 

E.   Work-up of suspected SAH:

Head CT scan in all patients

Perform lumbar puncture if SAH is suspected and CT scan is negative

Cerebral angiogram if SAH is detected

                       

F.  Management of patients with aneurysmal SAH:

              Prompt referral to cerebrovascular neurosurgeon

              Goal is to permanently seal off aneurysm within 24-48 hours of hemorrhage

                          - direct surgical clipping is treatment of choice in most patients

- Angiographic insertion of GDC coils in poor surgical risk patients

 

 

V.  Intracerebral hemorrhage:

 

          A.  Radiologic appearance:  Blood within the substance of the brain causing mass effect

         

          B.  Etiology:       

                        Hypertensive vasculopathy- most common, 70-90% of all spontaneous ICH

                        Ruptured arteriovenous malformation, 10-20% of ICH

                        Many misc. causes

 

          C.  Clinical presentation:  Rapidly progressive severe headache, building over several minutes, often accompanied by focal neurological deficits, nausea and vomiting, decreased level of consciousness.

 

          The neurological deficit depends upon the site of hemorrhage:

                        basal ganglia/internal capsule -               hemiparesis, dysphasia

                        cerebellum -                                          ataxia, vertigo

                        pons -                                                   cranial nerve deficits, coma

cerebral cortex -                                    hemiparesis, hemisensory loss, hemianopsia, dysphasia (depending upon site within cortex)

          D.  Hypertensive intracerebral hemorrhage

                        1.  Classical features:

                                    Most patients are > 45 years old

                                    Patients have history of HTN (treatment may not be preventative)

                                    Hemorrhage occurs in a few characteristic areas

                                                basal ganglia/internal capsule -   60%

                                                deep cerebellar nuclei-                          10-15%

                                                pons -                                                  10%

                                                thalamus -                                             10%

                       

                        2.  Workup:

                                    Head CT scan in all patients with suspected hemorrhage

Angiography not necessary if all features of classical hypertensive hemorrhage are present

                        3.  Treatment:

                                    Symptomatic management of elevated intracranial pressure

                                    Surgery to reduce mass effect in selected cases

                                    Risk of rebleed at same site is very low

 

          E.  Hemorrhage from ruptured vascular malformation

1.  Arteriovenous malformations are congenital developmental defects in the cerebral vasculature consisting of tangles of arteries feeding directly into tangles of veins without intervening capillary network.

 

     AVMs may occur anywhere in the brain, with an incidence of 0.5% of population.  Hemorrhages usually occur in patients between age of 20-40, but may occur at any age.

 

     Always suspect an AVM as cause of hemorrhage if classic features of hypertensive hemorrhage are not present

 

2.  Workup:

           Head CT scan in all patients with suspected intracranial hemorrhage

Cerebral angiography is essential in any patient suspected of having an  AVM

           MRI scan may provide additional anatomic details

    

3.  Treatment:

           Symptomatic treatment of elevated intracranial pressure

Since rebleed rate is 10% in first year, ultimate treatment goal is to eliminate the AVM

            Angiographic embolization - adjunct to surgery, not curative      

            Surgical resection - Stereotactic radiosurgery in selected cases

 

 

 

 

 

 

 

 

 

 

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                                              Last updated:  10/05/2002                                                          © 2000-2002 John Rose, MD  University of Utah School of Medicine