Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.



Published on


Dear viewers,
Greetings from “Surgical Educator”
Today I have uploaded a video on Head injury- an important topic in trauma because 50% of trauma deaths are due to head injuries. I haven’t talked elaborately but have included the essential minimum an undergraduate medical student should know. I have talked about pathophysiology, clinical approach, symptoms, signs, investigations, different individual types of head injuries and management of all the varieties of head injuries. My aim is after watching this video all of you should be able to arrive at a correct working diagnosis of the type of head injury and should also be able to institute immediate lifesaving treatment to the patients if there is a need. You can watch the video in the following links:
Thank you for watching the video.

Published in: Health & Medicine


  1. 1. HEAD INJURY AN OVERVIEW Dr.B.Selvaraj MS;Mch;FICS; Professor of Surgery Melaka Manipal Medical College Melaka 75150 Malaysia
  2. 2.  Normal cerebral blood flow is 55mL/100 gm/min  If this rate drops below 20 mL/100 gm/min infarction will result  The 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 blood  The 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
  3. 3.  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
  4. 4.  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
  5. 5.  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
  6. 6.  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
  7. 7. PHYSICAL EXAMINATION/SIGNSMild- 14 to 15 Moderate- 9 to 13 Severe-5 to 8 Critical- 3 to 4
  8. 8.  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
  10. 10.  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
  11. 11. - 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
  12. 12. - 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
  13. 13.  Skull fractures  Epidural Hematoma  Subdural Hematoma  Cerebral Contusion  Subarachnoid Hemorrhage  Diffuse axonal injury Different Varieties of Head Injury
  14. 14. 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 and oriented. - 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.
  17. 17. EPIDURAL HEMATOMA- EDH Etiopathogenesis Clinical Features Diagnosis Treatment -An epidural hematoma is a collection of blood between the inner 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 neurosurgical evacuation, but small stable hemorrhages in an intact patient may be observed closely.
  19. 19. SUBDURAL HEMATOMA- SDH Etiopathogenesis Clinical Features Diagnosis Treatment - Hematoma that occurs in the space beneath the dura. -Caused by rupture of the bridging veins that pass from the surface of the brain to the dura, or by a cerebral 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 the overlying skull and dural membranes. -Acute and chronic subdural hematomas are easily detected on head CT scans. -The hematoma is crescent-shaped on head CT and will cross suture lines. -Commonly associated with significant underlying brain injury. -Large, symptomatic subdurals are evacuated in the OR. -Smaller hemorrhages must be followed as they tend to become chronic and may enlarge over time.
  21. 21. EDH/SDH
  22. 22. CEREBRAL CONTUSION Etiopathogenesis Clinical Features Diagnosis Treatment -Bruising of brain parenchyma occurs over bony prominences as a result of sudden deceleration 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 large contusions 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 to detect on CT scan -Most contusions can be followed with serial head CTs. -Large, symptomatic contusions may require more aggressive intervention by a neurosurgeon.
  24. 24. 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 be considered, based on the location of the blood. -SAH is most often associated with other brain injuries, such as skull fractures/contusions -It is usually seen 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 is expectant. -Serial neurologic examinations and follow-up head CT scans are usually sufficient to exclude and/or watch for associated injuries.
  26. 26. DIFFUSE AXONAL INJURY- DAI Etiopathogenesis Clinical Features Diagnosis Treatment - DAI is a primary lesion of rotational acceleration/deceler ation 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 radiographic evidence. -Small, punctate hemorrhages at the gray-white junction are sometimes seen -Depending on the patient’s other neurological injuries a ventriculostomy may be required to monitor the ICP, which is often normal -Supportive care as required by the patient’s condition.
  28. 28. Treatment Algorithm- Head Injury