Neurosurgery Head Injury

• Monro-Kellie hypothesis is a pressure-volume relationship that aims to keep a dynamic equilibrium among the essential non-compressible components inside the rigid compartment of the skull.
• The average intracranial volume in the adult is around 1700 mL, composed of brain tissue (~1400 mL), CSF (~150 mL), and blood (~150 mL). 
• The volume of these three components remains nearly constant in a state of dynamic equilibrium. 
• Thus, a decrease in one component should be compensated by the increase in other and vice-a-versa

1. absence of brainstem reflexes

• A. fixed pupils {no response to light)
• B. absent corneal reflexes
• C. absent oculovestibular reflex {calories)
• D. absent oculocephalic reflex {doll's eyes)
• E. absent gag & cough reflex

2. Apnea test - apnea with arterial pC02 > 60 mm Hg - starting from normocapnea, the average time to reach PaC02 = 60 mm Hg is 6 minutes

3. no response to deep central pain

4. vital signs & general criteria

• A. core temp > 32.2• C {90• F)
• B. SBP >90 mm Hg
• C. no drugs that could simulate brain death

Cerebral angiography - absence of intracranial flow at the level of the carotid bifurcation or circle of Willis

EEG - no electrical activity

Cerebral radionuclide angiogram (CRAG)- No uptake in brain parenchyma - "hollow skull phenomenon"

Transcranial doppler

• Mild - 13-15
• Moderate - 9-12
• Severe - ≤ 8

Definition of Severe traumatic brain injury (TBI) - head trauma associated with a Glasgow Coma Scale (GCS) score of 3 to 8.

In general, TBI is divided into two discrete periods: primary and secondary brain injury.

Primary brain injury - physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue.

• Secondary brain injury - result of a complex process, following and complicating the primary brain injury in the ensuing hours and days. It includes 
• - cerebral edema,
• - hematomas,
• - hydrocephalus,
• - intracranial hypertension,
• - vasospasm,
• - metabolic derangement,
• - excitotoxicity,
• - calcium ions toxicity,
• - infection, and
• - seizures.

The fundamental goals of resuscitation of the head-injured patient are the restoration of circulating volume, blood pressure, oxygenation, and ventilation as per ATLS guidelines.

• A) Intracranial mass lesions
• - Hemorrhage (Epidural, Subdural, intraparenchymal)
• - Brain tumor
• - Cerebral abscess

• B) Increased brain volume (cytotoxic edema and/or osmotic edema)
• - Ischemic stroke
• - Global hypoxia
• - Reye's syndrome
• - Acute hyponatremia
• - Hepatic encephalopathy
• - Idiopathic (pseudotomor cerebri)
• - Toxins and medications (lead, tetracycline, doxycycline, rofecoxib, retinoic acid)

• C) Increased CSF volume
• - Hydrocephalus (Communicating, Non-communicating)
• - Choroid plexus papilloma
• - Decreased CSF absorption (ie, venous sinus thrombosis)
• - CSF outflow obstruction from leptomeningeal metastasis

• D) Increased blood volume (vasogenic edema, breakdown of tight endothelial junctions which make up the blood-brain barrier (BBB))
• - Impaired auto-regulation (ie, endarterectomy)
• - Traumatic brain injury
• - Tumoral associated vasogenic edema
• - Meningitis
• - Encephalitis
• - Vasculitis
• - Hypertensive encephalopathy
• - Eclampsia
• - Subarachnoid hemorrhage
• - Dural sinus thrombosis
• - Altitude-related cerebral edema (HACE)
• - Hypoxia
• - Hypercarbia
• - Hyperpyrexia
• - Seizure
• - Jugular venous obstruction
• - Mechanical ventilation (when peak and expiratory pressure > baseline intracranial pressure)

• Symptoms:
• Headache
• Vomiting
• Disorientation
• Lethargy

• Signs:
• Depressed level of consciousness (lethargy, stupor, coma)
• Hypertension, with or without bradycardia
• Papilledema
• Sixth cranial nerve palsy
• Cushing's triad (hypertension, bradycardia, and irregular respiration)
• Spontaneous periorbital bruising

Invasive monitoring of ICP may be indicated in patients who meet all three of the following criteria:

• 1. The patient is suspected to be at risk for elevated ICP.
• 2. The patient is comatose (Glasgow coma scale score ≤ 8).
• 3. The prognosis is such that aggressive ICU treatment is indicated

• Suspicion of elevated ICP generally is based on clinical findings, CT scan and the patient’s medical history.
• CT scans may show significant intracranial mass effect with midline shift or effacement of the basal cisterns, patients with initial normal CT scans may have elevated ICP.

• Invasive ICP Monitoring Devices
• Intraventricular Catheters
• Intraparenchymal Pressure Transducers
• Subarachnoid Bolts
• Epidural Transducers
• ICP Waveforms

• Noninvasive ICP Monitoring
• Transcranial Doppler (TCD) Ultrasonography
• Optic Nerve Sheath Diameter
• Monitoring Of Midline Shift By Transcranial Duplex Sonography
• Electroencephalography And Somatosensory Evoked Potentials Monitoring

• 1. Elevate HOB to 30-45' - decrease ICP by enhancing venous outflow, but also reduces mean carotid pressure.
• 2. Keep neck straight, avoid tight trach tape - constriction of jugular venous outflow causes increased ICP
• 3. Avoid hypotension (SBP < 90 mm Hg) - Normalize intravascular volume and use pressors if needed
• 4. Control hypertension if present - nitroprusside if not tachycardic, beta-blocker if tachycardic (labetalol, esmolol . . ), avoid overtreatment
• 5. Avoid hypoxia (Pa02 < 60 mm Hg or 02 sat < 90%) - hypoxia may cause further ischemic brain injury
• 6. Ventilate to nonnocarbia (PaC02 = 35-40 mm Hg) - avoid prophylactic hyperventilation
• 7. Light sedation: e.g. codeine 30-60 mg IM q 4 hrs/SOS PRN
• 8. Controversial: prophylactic hypothermia. If used, hold at target temp > 48 hrs
• 9. NCCT scan for raised ICP problems to rule out surgical condition

• 1. Hyperosmolar therapy - 
• Osmotic agents reduce brain tissue volume by drawing free water out of brain tissue and into the systemic circulation, where it is then excreted by the kidneys. The beneficial effect of hyperosmolar therapy requires that the blood–brain barrier (BBB) be intact. Both mannitol and hypertonic saline can be given as a bolus if signs of acute neurologic deterioration or cerebral herniation are present.

• 2. Hyperventilation -
• Hyperventilation should be used only acutely to achieve PaCO2 to 26 to 30 mmHg; it rapidly reduces ICP through vasoconstriction and decreasing the intracranial blood volume. If used, hyperventilation should be tapered slowly over 4-6 hours to avoid vasodilatation and rebound increases in ICP. Therefore, hyperventilation is used most effectively as a temporizing measure until more definitive treatments for increase intracranial pressure are instituted.

• 3. Barbiturates - 
• - induce electroencephalographic burst suppression
• - not indicated for prophylactic administration.
• - reduce brain metabolism and cerebral blood flow, thus lowering ICP and exerting a neuroprotective effect.

• 4. Therapeutic hypothermia -
• - decreases cerebral metabolism and may reduce CBF and ICP.
• - initiated early, continued for an appropriate duration of time (2–5 days), and followed by a gradual rewarming.

• 5. CSF Drainage
• If the CSF compartment is contributing to the elevated ICP, as in the case of obstructive or communicating hydrocephalus from SAH or intraventricular hemorrhage; the treatment strategy of choice is CSF diversion.  

• 6. Decompressive craniectomy - 
• - if the patient is deteriorating rapidly or if the ICP continues to rise despite ongoing medical management.
• - Indications - a) diffuse swelling is evident on CT imaging, b) the injury is less than 48 hours old, c) there are no sustained episodes of elevated ICP before surgery, d) GCS has been greater than 3 on at least one prior assessment, e) there is evidence of an evolving cerebral herniation syndrome.

• Mannitol - 0.25 to 1 g/kg of 20% mannitol given over 10 to 20 minutes. Diuresis-induced hypovolemia should be corrected by rapid administration of normal saline boluses.
• Hypertonic saline - 5 to 10 mL/kg of 3% hypertonic saline solution given over 5 to 10 minutes. The goal of serum sodium concentration of 145-155 mmol/L to be reached within 6 hours.

Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate, is not recommended for preventing late posttraumatic seizures.

• Anticonvulsants may be used to prevent early PTS in patients at risk which are :
• - GCS <10;
• - Hematoma - subdural, epidural, intracerabral 
• - cortical contusion;
• - penetrating head injury;
• - seizure within 24hrs

• Immediate - Seizures that occur within 24 hours after brain injury  
• Early PTS - occur within 1 week after injury 
• Late PTS - occur more than 1 week after injury

Immediate and early seizures are thought to be a direct reaction to the injury, while late seizures are believed to result from damage to the cerebral cortex. 

• Antiepileptic drugs are widely recommended for a short time after head trauma to prevent immediate and early, but not late, seizures.
• No treatment is widely accepted to prevent the development of epilepsy. However, medications may be given to repress more seizures if late seizures do occur.

Replace 140% of resting metabolism expenditure in non-paralyzed patients and 100% in paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.

1. Acute epidural or subdural hematoma - Significant hematomas should be evacuated immediately upon detection.

2. Contusions 

• 3. Skull Fractures - Operations definitely indicated only if it is a compound (open) fracture (not over sagittal sinus) or if the fracture is so extensive that it causes mass effect.
• Closed depressed skull fractures are usually treated conservatively, but operation may be appropriate in selected cases to reduce mass effect or correct disfigurement.

• For small hemorrhagic contusions or other small intracerebral lesion a conservative approach is generally adopted.
• But operation should be considered urgent for large intracerebral lesions with high or mixed density on CT scan. 

• Specific indications for operations include:
• a) Clinical deterioration
• b) Size > 1cm thick
• c) Volume > 25 – 30 ml in intracerebral hematomas
• d) Midline shift > 5 mm.
• d) Enlargement of contralateral ventricle (temporal horn).
• e) Obliteration of basal cisterns or third ventricle.
• f) Raised or increasing ICP

An epidural hematoma (EDH) occurs when blood accumulates between the skull and the dura mater, the thick membrane covering the brain. They typically occur when a skull fracture tears an underlying blood vessel. EDHs are about half as common as a subdural hematoma and usually occur in young adults. They occur four times as often among males compared with females and rarely before age 2 or after age 60.

Source of bleeding: 85% are arterial bleeding (the middle meningeal artery is the most common source of middle fossa EDHs). Many of the remainder of cases are due to bleeding from middle meningeal vein or dural sinus.

• • Classic symptoms of EDH involve brief loss of consciousness followed by a period of awareness that may last several hours before brain function deteriorates, sometimes leaving the patient in a coma.
• • Lucid interval may be followed by obtundation, contralateral hemiparesis, ipsilateral pupillary dilatation
• • If untreated, the condition can cause increased blood pressure, difficulty breathing, damage to brain function and death.
• • Other symptoms include headache, vomiting and seizure.
• • Shift of the brain stem away from the mass may produce compression of the opposite cerebral peduncle on tentorial notch which can produce ipsilateral hemiparesis (so called Kernahan's phenomenon or Kernohan'snotch phenomenon)"', a false localizing sign.

"Classic" CT appearance occurs in 84% of cases: high density biconvex (lenticular) shape adjacent to the skull.

1. EDH volume > 30 cm³ should be evacuated regardless of GCS

2. EDH with the all of the following characteristics can be managed nonsurgically with serial CT scans and close neurological observation in a neurosurgical center:

• A. Volume <30 cm3
• B. Thickness < 15 mm
• C. Midline shift (MLS) < 5 mm
• D. GCS > 8
• E. No focal neurologic deficit

It is strongly recommended that patients with an acute EDH and GCS < 9 and anisocoria undergo surgical evacuation ASAP

A burr hole is a hole that is surgically placed in the skull, or cranium. 

• Indications
• • To relieve pressure on the brain by draining chonic blood
• • To begin a larger incision, such as a craniotomy
• • To place a monitor that reads the pressure inside the skull or device to study electrical activity of the brain
• • To remove a tumor for biopsy
• • To remove a foreign object and drain abscess
• • To place a medical device, such as a shunt or chemotherapy wafers

• o GCS < 8
• o Epidural or Subdural bleed with midline shift on CT*, and (*CT not necessary in crashing patient with high suspicion.)
• o Unequal pupils
• o Timely Neurosurgical service NOT available

• 1. Keen's Point : Parietal Burr hole - 3 cm above and 3 cm behind the external auditory meatus.
• Direction of canula - Perpendicular to the cortex and slightly cephalic.
• Length of insertion about 4 to 5 cm. [@ Keep point is कान point] 

• 2. Kocher's Point : Frontal Burr hole - 2 to 3 cm lateral to mid line and 1 cm anterior to coronal suture in the mid pupilaary line.
• Direction of canula - Coronal plane towards ipsilaterl inner canthus and AP plane towards EAM.
• Length of insertion about 5 to 6 cm.

• 3. Dandy's point : Occipital burrhole - 2 cm lateral to the midline and 3 cm above the inoin. In infants this usually corresponds with the lambdoid suture in the mid pupillary line.
• Direction of canula - Perpendicular to the cortex and slightly cephalic.
• Length of insertion about 4 to 5 cm.

• 4. Frazier's point : 3 to 4 cm lateral to the midline and 6 cm above the inion.
• Direction of canula - Perpendicular to the cortex.
• Length of insertion about 4 to 5 cm.

• • Seizure
• • Bleeding
• • Stroke
• • Infection of the incision or brain
• • Bleeding of the brain
• • Brain damage, including changes in the senses, memory problems, coordination difficulties and speech impairments
• • Swelling of the brain
• • Coma
• • Problems with anesthesia
• • No relief from symptoms and need for a surgery such as a craniotomy

• Patients to be shifted to neurosurgery facility
• Care of incision site
• Patients to be kept flat for 24- 48 hrs
• Antibiotics to be given to prevent infections

• Diffuse axonal injury is the shearing (tearing) of the brain's long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull.
• A lesion of rotational  acceleration/deceleration head injury
• DAI usually causes coma and injury to many different parts of the brain.
• The changes in the brain are often microscopic and may not be evident on computed tomography (CT scan) or magnetic resonance imaging (MRI) scans.

• Lack of consciousness, which can last up to six hours or more.
• A person with a mild or moderate diffuse axonal injury who is conscious may also show other signs of brain damage, depending upon which area of the brain is most affected

• Grade I: 
• - involves grey-white matter interfaces, 
• - most commonly: parasagittal regions of frontal lobes, periventricular temporal lobes

• Grade II: 
• - involves corpus callosum in addition to stage I locations, 
• - most commonly: posterior body and splenium but does advance anteriorly with increasing severity of injury

• Grade III: 
• - involves brainstem in addition to stage I and II locations, 
• - most commonly: rostral midbrain, superior cerebellar peduncles, medial lemnisci and corticospinal tracts

1. CT head - Head CT frequently does not identify pathology associated with DAI. Only 10% of patients with DAI demonstrate hemorrhagic punctate lesions of the corpus callosum and gray–white matter junctions of the cerebrum and pontine–mesencephalic junction near the cerebellar peduncles. Weeks after injury, atrophic changes may occur in the white matter, dependent on the degree and topography of injury

2. MRI - MRI is more sensitive for the diffuse and physically small pathology found in DAI as opposed to head CT. Shearing forces associated with DAI transect small blood vessels running in parallel with axons, resulting in detectable microscopic hemorrhages forming in these areas.

3. Electrophysiologic methods identifying altered evoked potentials in DAI patients may also provide insight into patterns of disrupted cerebral connectivity following injury.

• DAI currently lacks a specific treatment
• Stabilization of the patient
• Limit increases in intracranial pressure (ICP).

• Rehabilitation - The rehabilitation phase may include:
• • Speech therapy
• • Physical therapy
• • Occupational therapy
• • Recreational therapy
• • Adaptive equipment training
• • Counseling

• Acute -  1 to 3 days -  hyperdense
• Subacute - 4 days to 2 or 3 wks - isodense
• Chronic - usually > 3 wks and < 3-4 months -   hypodense (approaching density  of CSF)

• Chronic subdural haematoma (CSDH) is an encapsulated collection of old blood, mostly or totally liquefied and located between the dura mater and arachnoid.
• CSDHs often occur in the elderly after a trivial injury without any damage to the underlying brain and usually there is a period of weeks to months before it becomes clinically evident.
• It has a peak incidence in the sixth and seventh decade of life.

• • Advancing age.
• • Fall.
• • Head injury.
• • Anticoagulants/antiplatelet drugs.
• • Bleeding diatheses.
• • Alcohol.
• • Epilepsy.
• • Low intracranial pressure.
• • Haemodialysis.

• Many CSDHs probably start out as acute SDH. Blood within the subdural space evokes an inflammatory response. A day after the haemorrhage, the outer surface of the haematoma is covered by a thin layer of fibrin and fibroblasts. Within days, fibroblast invade the clot and form neomembranes on the inner (cotical) and outer (dural) surface. This is followed by ingrowth of neocapillaries, enzymatic fibrinolysis and liquefaction of blood clot. Fibrin degradation products are incorporated into new clots and inhibit hemostasis.
• Rebleeding, exudates from the outer membrane, osmotic theory, and rapid enlargement due to CSF entrapment are considered as possible causes of expansion of hematomas.

• Common presentations
• • Altered mental state.
• • Focal neurological deficit.
• • Headache.
• • Falls.
• • Seizures.
• • Transient neurological deficits.

• Atypical presentations
• • Isolated neurological deficits.
• • Extrapyramidal syndromes.
• • Rare neurological syndromes.
• • Ease of falling.

• CSDH is usually diagnosed by CT scan. Hematomas are usually hypodense, but isodense or mixed density lesions are also observed. Although these are usually concavo-convex, rarely they may mimic acute epidural hematomas.
• MRI is more sensitive than CT in determining the size and internal structures of CSDH, such as multiple loculations and intrahematoma membranes. Fresh bleeding, hemolysis, and hemoglobin changes can also be observed by MRI.

1. Small hematomas are managed conservatively like stopping the offending drugs (antiplatelets drug); correction of coagulopathy

2. Seizure prophylaxis: anti-epileptic drug (AED) prophylaxis could be given in higher-risk patients.

3. Corticosteroids might be beneficial in the treatment of CSDH.

4. Appropriate hydration in subarachnoid hemorrhage is well recognized. Intravenous fluid administration of at least 2000 ml for 3 days postoperatively has been found to be associated with better clinical outcome and reduced recurrence in CSDH

5. Surgery

• a. Indications
• i. Symptomatic lesions including focal deficit, mental status changes
• ii. Subdurals with maximum thickness greater than 1 cm

b. Options - twist drill, burr hole craniostomy or craniotomy

c. Complications - Recurrence, Seizure, Tension pneumocephaluis

• Kerrison punch - 

Weitlaner Retractor - 

• Classically CSDHs contains dark "motor oil" fluid which does not clot. 
• When the subdural fluid is clear (CSF), the collection is termed a subdural hygroma

• ASDH with thickness > 10 mm or midline shift (MLS) > 5 mm (on CT) should be evacuated regardless of GCS
• ASDH with thickness < 10 mm* and MLS < 5 mm should undergo surgical evacuation if:
• A. GCS drops by , 2 points from injury to admission
• B . and I or the pupils are asymmetric or fixed and dilated
• C. and / or ICP is > 20 mm Hg

Monitor ICP in all patients with ASDH and GCS < 9

• GCS score
• 3-4: 2 points
• 5-12: 1 point
• 13-15: 0 points

• ICH volume
• ≥30 cm 3: 1 point
• < 30 cm 3: 0 points

• IVH
• Yes: 1 point
• No: 0 points

• Infratentorial origin of ICH
• Yes: 1 point
• No: 0 points

• Age
• Age 80 years or older: 1 point
• Younger than 80 years: 0 points.  

[@ GIA TV - GCS, Intraventricular, Age, Tentorium, Volume] ] 

• Mortality rate based on ICH Score - ICH scores with corresponding mortality risk are as follows:
• 0 points: 0%
• 1 point: 13%
• 2 points: 26%
• 3 points: 72%
• 4 points: 97%
• 5 points: 100%
• 6 points: 100% (estimated)

• Size of nidus
• - small (<3cm) = 1
• - medium (3-6cm) = 2
• - large (> 6cm) = 3

• Eloquence of adjacent brain
• - non-eloquent = 0
• - eloquent = 1

• Venous drainage
• - superficial only = 0
• - deep = 1

A grade between 1 and 5. Grade 6 is used to describe inoperable lesions. The score correlates with operative outcome.