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HEAD INJURY AN OVERVIEW Dr.B.Selvaraj MS;Mch;FICS; Professor of Surgery Melaka Manipal Medical College Melaka 75150 Malaysia
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HEAD INJURY- AN OVERVIEW

Apr 12, 2017

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Page 1: HEAD INJURY- AN OVERVIEW

HEAD INJURY

AN OVERVIEW

Dr.B.Selvaraj MS;Mch;FICS;Professor of Surgery

Melaka Manipal Medical CollegeMelaka 75150 Malaysia

Page 2: HEAD INJURY- AN OVERVIEW

Normal cerebral blood flow is 55mL/100 gm/min If this rate drops below 20 mL/100 gm/min infarction will resultThe flow rate is related to cerebral perfusion pressure (CPP)CPP (75–105 mmHg) = MAP (90–110 mmHg) − ICP (5–15 mmHg).Monro-Kellie Hypothesis:Skull is a confined rigid space contains the brain, CSF and bloodThe sum of the Intracranial volumes of blood, brain, CSF is

constant, and that an increase in any one of these must be compensated by an equal decrease in another, otherwise pressure will rise.

Once ICP rises, it results decreased CBF and eventually brain herniation

Patho Physiology Of Head Injury

Page 3: HEAD INJURY- AN OVERVIEW

The uncus of the temporal lobe may herniate over the tentorium resulting in pupil abnormalities usually occurring first on the side of any expanding hematoma.

Cerebellar tonsillar herniation through the foramen magnum compresses medullary vasomotor and respiratory centres, producing Cushing’s triad of hypertension, bradycardia and irregular respiration

Patho Physiology Of Head Injury

Page 4: HEAD INJURY- AN OVERVIEW

First ensure that the ABCs have been adequately assessed and patient is stabilised.

Thorough neurological examination including GCS in secondary survey, pupil size and reaction to light, an extremity assessment including thorough motor/sensory examination.

Once the patient is hemodynamically stable, a head CT should be performed.

Patients alert and fully oriented brain injury less likely. Head and facial trauma combined with agitation possible brain injury.

Combination of the patient’s neurological examination and the head CT help the neurosurgeon determine the best course of action, be it close neurological monitoring in the ICU, ventriculostomy, or an emergency surgical intervention.

CLINICAL APPROACH

Page 5: HEAD INJURY- AN OVERVIEW

What was the mechanism of injury? Was it a gunshot wound, an assault, a motor vehicle accident or a fall?

Was there loss of consciousness? How long?What medications or drugs has the patient received or taken

that might affect mental status?Does the patient have a previous neurological disorder or

baseline impairment?AMPLE (Allergies; Medications; Past medical hx; Last meal;

Events leading to presentation)

HISTORY/SYMPTOMS

Page 6: HEAD INJURY- AN OVERVIEW

Is the patient too lethargic to maintain an adequate airway? GCS<8 Is the respiratory rate regular and not too fast or too slow?Do the vital signs point to a missed source of bleeding, or is the

patient herniating? Is the patient’s neurological examination deteriorating? Are skull or

facial fractures evident? Is there a large scalp laceration that requires washout and closure?Cushing’s triad of hypertension, bradycardia and irregular

respiration indicate impending brain herniation

PHYSICAL EXAMINATION/SIGNS

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PHYSICAL EXAMINATION/SIGNSMild- 14 to 15Moderate- 9 to 13 Severe-5

to 8Critical- 3 to 4

Page 8: HEAD INJURY- AN OVERVIEW

CBC with automated differential: Looking for adequate platelet count should neurosurgical intervention be necessary

PT/PTT/INR: Looking for coagulation abnormalities that would require correction to stop bleeding and allow for neurosurgical intervention

Urine toxicology screen: Looking for evidence of substances that might impair the neurological examination

Serum alcohol level: Looking for an intoxicated patient who could be belligerent for reasons not directly related to neurological injury

Head CT without contrast: Looking for haemorrhage and skull fractures, and the effect on the brain parenchyma

INVESTIGATIONS

Page 9: HEAD INJURY- AN OVERVIEW

INVESTIGATIONS

Page 10: HEAD INJURY- AN OVERVIEW

A. Prevention of secondary injury:Avoid hypotension keep MAP > 80 to

90 mm Hg to maintain adequate CPP.Avoid hypoxia early intubation to

ensure adequate PaO2 and optimal brain oxygenation

Treatment of increased ICP before ICP monitoring by -Elevating the head after R/O spinal injury

-Temporary hyperventilation to maintain PaO2 around 35 mms of Hg

Initial Management of Head Injury

Page 11: HEAD INJURY- AN OVERVIEW

- Mannitol treats increased ICP by causing cellular dehydration and increasing serum osmolarity. High-dose mannitol (1.2 to 1.4 g/kg) can be used as a temporizing measure prior to neurosurgical procedure. - Hypertonic saline Maintenance of serum sodium = 145 to 155 mmol/L via bolus dosing or continuous infusion of 3% normal saline Seizure prophylaxis: 20 % to 25% will have at least one post-

traumatic seizure. The frequency of early post-traumatic seizures is significantly reduced by administration of antiepileptic drugs (AEDs) like phenytoin and Levetiracetam

Treatment of coagulopathy: Serial coagulation profiles should be sent during the first 24 to 48 hours post-injury with aggressive correction of abnormal values via fresh-frozen plasma, prothrombin complex concentrate, or vitamin K.

Initial Management of Head Injury

Page 12: HEAD INJURY- AN OVERVIEW

- B. ICP Monitoring: ICP monitor be placed in patients with a

GCS 3 to 8 and either one of the following: Abnormal CT scan or normal CT scan with 2 of the following at admission – age > 50, systolic BP < 90 mms of Hg or unilateral or bilateral motor posturing

ICP monitoring requires bedside placement of ventricular catheter as it provides a way to treat increased ICP via drainage of cerebrospinal fluid (CSF).

Initial Management of Head Injury

Page 13: HEAD INJURY- AN OVERVIEW

Skull fracturesEpidural HematomaSubdural HematomaCerebral ContusionSubarachnoid HemorrhageDiffuse axonal injury

Different Varieties of Head Injury

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SKULL FRACTURES Etiopathogenesis

Clinical Features

Diagnosis Treatment

-A skull fracture is a break in the bones of the skull-Skull fractures indicate head injury of significant force.- MVA, assault or fall

- Skull fractures are usually associated with moderate to severe traumatic brain injury, although some patients may be awake andoriented.

- Clinical evidence of basilar skull fractures includes raccoon’s eyes, Battle’s sign and cerebrospinal fluid (CSF) leaks through the nose (CSF rhinorrhea) or ears (CSF otorrhea).- Head CT is usually the best test

-Closed skull fractures-no surgical tx unless there is significant bony depression> thickness of skull -CSF rhinorrhea or otorrhea-treat conservatively, but persistent leaks require lumbar drainage or an epidural blood patch.-Open skull fractures- wash out to prevent infection in patients who survive their injury.

Page 15: HEAD INJURY- AN OVERVIEW

SKULL FRACTURES

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BASILAR SKULL FRACTURES

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EPIDURAL HEMATOMA- EDH Etiopathogenesis

Clinical Features

Diagnosis Treatment

-An epidural hematoma is a collection of blood between theinner table of the skull and the dura mater-usually caused by meningeal artery avulsions or tears, the most common being the middle meningeal artery.

-Patients present with Lucid Interval from the time of the injury until they suddenly deteriorate due to enlarging hematoma and impending brain herniation.

-Epidural hematomas are associated with a skull fracture in the temporal bone near the middle meningeal artery- They usually have a lenticular appearance on CT and do not cross suture lines (coronal or lambdoid sutures).

- Epidural hematomas usually require emergent neurosurgicalevacuation, but small stable hemorrhages in an intact patientmay be observed closely.

Page 18: HEAD INJURY- AN OVERVIEW

EPIDURAL HEMATOMA- EDH

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SUBDURAL HEMATOMA- SDH Etiopathogenesis

Clinical Features

Diagnosis Treatment

- Hematoma that occurs in the spacebeneath the dura.-Caused by rupture of the bridging veins that pass from the surface of the brain to the dura, or by acerebral contusion that has bled into the subdural space.

-Subdurals are common in moderate and severe head injury-can also be brought about by relatively minor trauma in the aging patient whose brain is atrophied and separated from theoverlying skull and dural membranes.

-Acute and chronic subdural hematomas are easily detected onhead CT scans.-The hematoma iscrescent-shaped on head CT and will cross suture lines.-Commonly associated with significant underlying brain injury.

-Large, symptomatic subdurals are evacuated in the OR.-Smallerhemorrhages must be followed as they tend to become chronic and may enlarge over time.

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SUBDURAL HEMATOMA- SDH

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EDH/SDH

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CEREBRAL CONTUSION Etiopathogenesis

Clinical Features

Diagnosis Treatment

-Bruising of brain parenchyma occurs over bony prominences as a result of suddendeceleration of the head -Coup-Countrecoup injury describes contusions directly beneath the point of impact as well as directly opposite the point of impact .

-Contusions are often associated with other head injuries.-Small contusions can be seen with relatively minor trauma, but largecontusions typically imply a significant injury.

- By CT scans.- Appear on the surface of the brain, where the cerebrum has impacted the inner table of the skull-Small contusions difficult todetect on CT scan

-Most contusions can be followed with serial head CTs.-Large, symptomatic contusions may require more aggressiveintervention by a neurosurgeon.

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CEREBRAL CONTUSION

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SUBARACHNOID HEMORRHAGE-SAH

Etiopathogenesis

Clinical Features

Diagnosis Treatment

-Trauma is the most common cause-Ruptured cerebral aneurysm is an another cause and this possibility should beconsidered, based on the location of the blood.

-SAH is most often associated with other brain injuries, such as skull fractures/contusions-It is usuallyseen near the convexity and in the sulci.

-The hemorrhage is visualized on head CT.-A lumbar puncture is not indicated in the setting of head trauma.

-The management of traumatic SAH isexpectant.-Serial neurologic examinations and follow-up head CTscans are usually sufficient to exclude and/or watch forassociated injuries.

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SUBARACHNOID HEMORRHAGE-SAH

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DIFFUSE AXONAL INJURY- DAI Etiopathogenesis

Clinical Features

Diagnosis Treatment

- DAI is a primary lesion of rotational acceleration/deceleration of the head producing a shearing injury of deep white matter tracts.(particularly in the corpus callosum and rostral brain stem).

-The forces required to produce this type of injury result in severe traumatic brain injury.-Patients present in coma or with severely depressed mental status but without a significant brain mass that would explain their condition.

-The dx is largely clinical, with corroborating radiographicevidence.-Small, punctate hemorrhages at the gray-white junctionare sometimes seen

-Depending on the patient’s other neurological injuries a ventriculostomy may be required to monitor theICP, which is often normal-Supportive care as required by the patient’s condition.

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DIFFUSE AXONAL INJURY

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Treatment Algorithm- Head Injury

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