Subarachnoid Hemorrhage (SAH)
Causes –
1. Head trauma (Commonest cause)
2. Rupture of a Berry aneurysm
3. Bleeding from vascular anomaly
4. Extension from primary intra cerebral hemorrhage.
Pathology
1. Saccular (Berry) aneurysms occur at the bifurcations of the large to medium-sized intracranial arteries; rupture is into the subarachnoid space in the basal cisterns and often into the parenchyma of the adjacent brain.
2. Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis.
3. As an aneurysm develops, it typically forms a neck with a dome. The length of the neck and the size of the dome vary greatly and are factors that are important in planning neurosurgical obliteration or endovascular embolization.
4. The arterial internal elastic lamina disappears at the base of the neck.
5. The media thins, and connective tissue replaces smooth-muscle cells. At the site of rupture (most often the dome) the wall thins, and the tear that allows bleeding is often ï‚£0.5 mm long.
6. Aneurysm size and site are important in predicting risk of rupture.
7. Those >7 mm in diameter and those at the top of the basilar artery and at the origin of the posterior communicating artery are at greater risk of rupture.
Clinical features
1. Sudden Severe onset headache, never experienced before, in the absence of focal neurological deficit, is the hallmark of SAH.
2. Transient loss of consciousness.
3. Neck rigidity may be present mimicking meningitis. Neck stiffness & vomiting: are common associations
4. Focal neurological deficit: uncommon.
5. Associated prodromal symptoms (suggest location of progressively enlarging unruptured aneurysm)
a. Third cranial nerve palsy : aneurysm at junction of PCA & ICA (NEET 2017)
b. Sixth nerve palsy: aneurysm in cavernous sinus
c. Occipital and posterior cervical pain: inferior cerebellar artery aneurysm (Ant. or Post.)
d. Pain behind the eye: MCA aneurysm
6. Aneurysms may undergo small ruptures or leaks, so called sentinel bleeds.
Extra Edge
1. Most common site of berry aneurysm is junction of ACA with anterior communicating artery.
2. Vertebral A is the least common site of berry aneurysm.
3. Most common nerve involved in berry aneurysm is IIIrd nerve. (NEET 2018)
Complication of SAH –
1. Rerupture → Occur in 1st month (30%) with the peak in the 1st 7 days. It is associated with 60% mortality rate and
poor outcome.
2. Hydrocephalus –
a. Acute→ causes stupor, coma.
b. Subacute→develop over a few days or weeks and causes slowed mentation with urinary incontinence.
c. Chronic → develop weeks to months after SAH and manifest as gait difficulty, incontinence, or impaired
mentation
3. Vasospasm →Most frequently at 3 – 7 days, major cause of delayed morbidity and death.
4. Hyponatremia → it can develop quickly in the first 2 weeks following SAH. There is both natriuresis and volume depletion with SAH, so that patients become both hyponatremic and hypovolemic. Both ANP and BNP have a role in producing CSWS. It clears over 1-2 weeks.
5. Severe cerebral edema → In patients with infarction from vasospasm may increase the ICP enough to decrease
cerebral perfusion pressure. Treatment with mannitol, hyper ventilation and hemicraniectomy.
Most common cause of late CNS deterioration in SAH is Vasospasm. (AIIMS May 2018)
Investigations of SAH
1. NCCT head (Non contrast CT scan) (Best Initial test) Sensitivity is 90% Investigation of choice (LP is not indicated prior to an imaging procedure). Blood is seen in the sylvian fissure. Do not use contrast when looking for blood.
2. CSF examination: (Most accurate test)
a. Hallmark is blood in CSF (Normal ratio= I WBC for every 500 to 1000 RBC.
b. Xanthochromic CSF – lysis of RBCS and Subsequent conversion of Hb to bilirubin stains the spinal fluid yellow
within 6 – 12 hours. Peak 48 hours & lasts for 1 – 4 weeks.
3. MR angiography – For unruptured aneurysm.
Treatment –
1. Medical support
a. Airway protection
b. BP management
c. Prevent vasospasm – Nimodipine, volume expansion.
Extra Edge; -Nicardipine has also been approved to prevent vasospasm
2. Triple H method of Rx → Hypertension, hemodilution & hypervolemia
3. Phenytoin given as prophylactic therapy. To prevent seizure
4. Surgery – Clipping of aneurysm.
5. Recent Advances= Endovascular coiling (Embolization) uses a catheter to clog up the site of bleeding. It is superior to surgical clipping
Extra Edge
1. Vasospasm remains the leading cause of morbidity and mortality following aneurysmal SAH.
2. Treatment with the calcium channel antagonist nimodipine improves outcome, by preventing ischemic injury rather than reducing the risk of vasospasm.
3. Symptomatic cerebral vasospasm can also be treated by increasing the cerebral perfusion pressure by raising mean arterial pressure through plasma volume expansion and the judicious use of IV vasopressor agents, usually
phenylephrine or norepinephrine.
4. Raised perfusion pressure is associated with clinical improvement in many patients, but high arterial pressure may promote rebleeding in unprotected aneurysms.
5. Treatment with induced hypertension and hypervolemia generally requires monitoring of arterial and central venous pressures; it is best to infuse pressors through a central venous line as well.
6. Volume expansion helps prevent hypotension, augments cardiac output, and reduces blood viscosity by reducing the hematocrit.
7. This method is called “triple-H” (hypertension, hemodilution, and hypervolemic) therapy.
B. Subdural Hematoma
Pathogenesis
1. Most commonly caused by rupture of superior cerebral veins (Bridging veins that connect the cerebral cortex to superior sagittal sinus)
2. Repeated cycles of recurrent bleeding into subdural space and resorption of the resultant hematoma.
Etiology
1. Head Trauma (Usually trivial and unnoticed in upto 25% of cases) so It is very common in alcoholic patient.
2. Patients with bleeding problems
a. Anticoagulation b. Thrombocytopenia c. Liver failure. d. Alcoholism
3. Dural lesions
a. Sarcoma’s AV malformations b. Metastatic cancer
4. Low CSF volume
a. CSF shunts b. Renal dialysis c. Excess diuretics
Acute subdural hematoma
1. A unilateral headache and slightly enlarged pupil on the side of the hematoma are frequently, present.
2. Stupor or coma, hemiparesis, and unilateral pupillary enlargement are signs of larger hematomas.
Chronic Subdural Hematoma
1. The presence of progressive hemiparesis and aphasias together with signs of raised ICT (papilledema) in an elderly patient, developing weeks after sustaining a mild head injury is characteristic of chronic subdural hematoma.
2. Gradual accumulation of blood in subdural space and classically presenting 3 weeks after the initial bleed.
Clinical Features
Gradual onset of signs and symptoms over several weeks (characteristically >3 weeks for chronic subdural hematomas)
1. Headache: Constant and relatively mild & usually lateralized to the side of lesion
2. Deterioration of mental status with confusion lethargy and memory disturbance
3. Progressive contralateral hemiparesis and Aphasias (speech disturbance)
4. Papilledema
5. Others: a. Cranial Nerve abnormalities b. Hemianopsia
6. Diagnosis = CT scan
7. Treatment: Burr hole surgery
C. Extradural Hematoma
1. Most common cause – Trauma to temporal bone
(Temporal bone fracture)
2. Blood vessel involved are – Rupture of middle
meningeal artery & vein.
3. The clinical presentation:
a. Sudden onset of altered sensorium
b. After some time patient regain consciousness for a short period (Lucid interval)
c. Patient again become unconscious.
4. Diagnosis: CT scan
5. Treatment: Urgent Burr hole surgery.
Extra Edge
1. Coma with a dilated pupil after a lucid interval following a head injury must be assumed to represent an epidural hematoma.
2. Emergency evacuation of the clot without time-consuming studies is vital to restore cerebral function. With a patient in less critical condition, a CT scan is the appropriate diagnostic study.
