4. management of head injury 6th aug 14

Management of Head Injury

by:Pawan KB Agrawal

MDGP Resident, Year II.6th August, 2014, Wednesday.

Outline►Introduction►Assessment►Treatment►Other complications of head injury►Additional care

Introduction►Head injury is a frequent cause of

emergency department attendance, accounting for approximately 3.4% of all presentations1.

►It is the most common cause of death in young adults (age 15–24 years) and is more common in males than females.

Introduction►Road traffic accidents (RTAs) are the

most common cause of head injury , followed by falls and assaults1.

►Although the majority of injuries are mild, around 10.9% are classified as moderate or severe and many patients are left with significant disability2.

Assessment ►Assessment should be done under

these three headings1. Mechanism of injury:

►Blunt Vs Penetrating Glassgow Coma Scale:

►minor head injury: GCS 15 with no loss of consciousness (LOC);

►mild head injury: GCS 14 or 15 with LOC;►moderate head injury: GCS 9–13;►severe head injury: GCS 3–8.

Assessment Morphology:

►Scalp: laceration, hematomas►Skull: Vault (linear, depressed or

communited) or basilar fractures►Intracranial: hematomas (epi/subdural,

subarachnoid or parenchymal) , contusions and diffuse axonal injury.

Investigations►CT Scan:

Recent guidelines suggest CT in all head injury with GCS ≤14.

NICE guidelines for computerised tomography in head injury►Glasgow Coma Score (GCS) <13 at any point►GCS 13 or 14 at 2 hours►Focal neurological deficit►Suspected open, depressed or basal skull

fracture►Seizure►Vomiting > one episode

Investigations CT Scan should also be considered if

►Age > 65►Coagulopathy (e.g. on warfarin)►Dangerous mechanism of injury (CT within 8

hours)►Antegrade amnesia > 30 min (CT within 8

hours)►Electrolytes: Na/K►Random blood sugar►X-ray C-spine:

Investigations As per NEXUS (National Emergency X-

radiography Utilisation Group) criteria, C-spine injury can be clinically ruled out if:►Normal level of alertness i.e. GCS 15►No evidence of intoxication.►No C-spine tenderness.►No focal neurological deficits.►No distracting injuries (esp long bone

fractures)

Treatment►Minor/mild head injury1:

Examination and a period of observation of 24 hours especially if CT is not available.

The following criteria must be met before discharge: the patient must have a GCS of 15/15 with no focal neurological deficit; the patient must be accompanied by a responsible adult and should not be under the influence of alcohol or other drugs.

Treatment►Advice must be given to return to the

emergency department if persistent or worsening headache despite analgesia, persistent vomiting, drowsiness, visual disturbance such as double or blurred vision, and development of weakness or numbness in the limbs.

Treatment►Moderate/severe head injury:►ABCDE as per primary trauma care.►Cervical immobilization is required

until clearance obtained.►Severe head injury also requires

intubation and is best managed in neuro-intensive care settings even if neurosurgical intervention is not performed1.

Treatment►Treatment should aim to avoid

hypoxia and hypotension2. Maintain SaO2 >97, Maintain a PaCO2 value

of 4.5–5.0 kPa. Maintain MAP >80 (BTF)-90 (AAGBI) mm Hg3-5.

Replace intravascular volume, avoid hypotonic and glucose-containing solutions.

►Glucose management : Hyperglycemia is associated with worsened outcome in a variety of neurologic conditions including severe TBI.6-8

Treatment►Temperature

management — Fever worsens outcome after stroke and probably severe head injury, presumably by aggravating secondary brain injury 10.Hence, current approaches emphasize maintaining normothermia.

Treatment Medical management of raised

intracranial pressure > 20-25 mm Hg 10 :►Position head up 30º►Avoid obstruction of venous drainage

from head keeping head in midline and cervical immobilisation collar should not obstruct venous return from the head.

►Sedation +/– muscle relaxant

Treatment►Normocapnia 4.5–5.0 kPa►Diuretics like furosemide, mannitol (0.5-1

g/kg bd- tds) to reduce cerebral swelling. ►Seizure control: Seizures increase the

brain metabolic rate and should be controlled. Prophylactic use of anticonvulsants reduce seizures in the first week is recommended11-12.

►Normothermia

Treatment►For intracranial hypertension

refractory to medical therapy, ventriculostomy or decompressive craniectomy can be employed1.

Treatment►Sodium balance: Severely brain-injured

patients are susceptible to disturbances of sodium haemostasis such as diabetes insipidus and syndrome of inappropriate antidiuretic hormone (SIADH).

►Barbiturates►Steroids in severe head injury are

associated with increased mortality and should not be used13.

► Further steps are aimed at specific morphological injuries.

Treatment Scalp:►Scalp laceration: debridement

and primary closure if possible.►Scalp hematoma: Observation

with analgesics.

Treatment Skull:►Open fractures should be considered for

debridement and subsequent closure if possible.

►But operative intervention is considered if 3,14

skull fractures depressed greater than the thickness of the cranium

dural penetration Associated with significant intracranial

hematoma frontal sinus involvement wound infection or contamination pneumocephalus

Treatment►Depressed fractures — Patients with

depressed skull fractures are at increased risk of infection and seizures, and prophylactic measures are recommended 15: tetanus prophylaxis given as appropriate. prophylactic antibiotics be given for five

to seven days to prevent the risk of subsequent CNS infection.

anticonvulsants are often given to reduce the risk of seizures.

Treatment Cerebrospinal fluid leaks: ►The majority of CSF leaks resolve

spontaneously within one week of injury and without CNS complications 16,17.

►The incidence of bacterial meningitis rises substantially if the leak persists past seven days prophylactic antibiotics should be given in such cases 18.

Treatment When to intervene??19

►Persistent for 7-10 days.►Ceased leak that recurs after 7-10 days.►Clinical evidence of large defect like

herniation of brain tissue through nostrils.►Meningitis or brain abscess.

Treatment Intracranial hematomas:►Consider in cases of depressed skull

fractures, focal neurological deficits including cranial nerve palsies, ipsilateral pupillary dilatation and contralateral paralysis, ataxia (esp in elderlies).

►Epidural hematoma —Surgical guidelines recommend evacuation of an epidural hematoma (EDH) if20: larger than 30 mL coma (GCS score ≤8) who have

pupillary abnormalities (anisocoria).

Treatment Subdural hematoma — Surgical

evacuation if21:► acute SDH >10 mm in thickness►midline shift >5 mm on CT ►GCS ≤8 ►Decrease in GCS by ≥2 points from the

time of injury to hospital admission►asymmetric or fixed and dilated pupils► intracranial pressure measurements are

consistently >20 mmHg.

Treatment Subarachnoid haemorrhage: ►Trauma is the most common cause

of SAH followed by rupture of aneurysm. Treated with: Triple H therapy: Hypervolemia,

hemodilution & hypertension. Nimodipine Statins 22.

Treatment►Intracerebral

hemorrhage — Surgical evacuation of a traumatic intracerebral hemorrhage (ICH) in the posterior fossa is recommended if: significant mass effect (distortion,

dislocation, obliteration of the fourth ventricle, compression of the basal cisterns, or obstructive hydrocephalus) 23.

Treatment►For traumatic ICH involving the

cerebral hemispheres, consensus surgical guidelines recommend craniotomy with evacuation if24: the hemorrhage exceeds 50 cm3 in

volume GCS score <8 with a frontal or temporal

hemorrhage greater than 20 cm3 with midline shift of at least 5 mm and/or cisternal compression on CT scan.

Other complications in head injury

►Cranial nerve injuries: Occurs in 1/3rd of patients with moderate

to severe head injury. Recovery is more likely with injury of CN III, IV & VI and less with CN VII & VIII19.


►Post traumatic seizures: About one-half of early post-traumatic

seizures occur during the first 24 hours, and one-quarter occur within the first hour 25.

Early seizures occurring within one week are acute symptomatic events and are more common with intracranial hematoma, depressed skull fracture, severe injury, and in young children.


In patients who have not had but appear to be at risk for early seizures, AED treatment reduces the incidence of early seizures and may be used because of similar concerns for secondary complications 26,27.

Between 17 to 33 percent of patients with early seizures will develop epilepsy.


Recurrence of seizures without treatment is likely, as high as 86 percent in the first two years 28.As a result, long-term anticonvulsant treatment is recommended for patients after an initial late seizure.


►Coagulopathy: Approximately one-third of patients with

severe head injury develop a coagulopathy, which is associated with an increased risk of hemorrhage enlargement, poor neurologic outcomes and death 29-33.

Severe head injury produce a coagulopathy through the systemic release of tissue factor and brain phospholipids into the circulation leading to inappropriate intravascular coagulation and a consumptive coagulopathy 34.


►Coagulation parameters should be measured in the emergency department in all patients with severe head injury and efforts to correct any identified coagulopathy should begin immediately.


►SIADH: Fluid restriction, salt administration, and

vasopressin receptor antagonists. Fluid restriction is a mainstay of therapy

in most patients with SIADH, with a suggested goal intake of less than 800 mL/day 35.

Use of hypertonic saline:►An effective initial regimen is 100 mL of 3

percent saline given as an intravenous bolus, which should raise the serum sodium concentration by


►approximately 1.5 meq/L in men and 2.0 meq/L in women, thereby reducing the degree of cerebral edema. If neurologic symptoms persist or worsen, a 100 mL bolus of 3 percent saline can be repeated one or two more times at ten minute intervals.


►Cerebral Salt wasting characterized by hyponatremia and

extracellular fluid depletion due to inappropriate sodium wasting in the urine.

Volume repletion with isotonic saline is the recommended therapy in CSW.

Additional Care►Peptic ulcer prophylaxis►Trophic sore prophylaxis►Physiotherapy►Bowel and bladder care.

References1. Hamilton Bailey ; Macneil Love. (2008). Short Practice of

Surgery. London NW1 3BH: Edward Arnold (Publishers) Ltd.2. Dinsmore, J. (2013). Traumatic brain injury: an evidence-

based review of management. Continuing Education in Anaesthesia, Critical Care & Pain j .

3. Brain Trauma Foundation. Management and prognosis of severe traumatic brain injury. J Neurotrauma 2007; 24: S1–106

4. Mass AI, Dearden M, Teasdale GM et al. EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium. Acta Neurochir (Wein) 1997; 139: 286–94

5. The Association of Anaesthetists of Great Britain and Ireland. Recommendations for the Safe Transfer of Patients with Brain Injury. London: The Association of Anaesthetists of Great Britain and Ireland, 2006

References6. Rovlias A, Kotsou

S. The influence of hyperglycemia on neurological outcome in patients with severe head injury. Neurosurgery 2000; 46:335.

7. Jeremitsky E, Omert LA, Dunham CM, et al. The impact of hyperglycemia on patients with severe brain injury. J Trauma 2005; 58:47.

8. Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 1991; 75:545.

9. Andrews PJ, Sleeman DH, Statham PF, et al. Predicting recovery in patients suffering from traumatic brain injury by using admission variables and physiological data: a comparison between decision tree analysis and logistic regression. J Neurosurg 2002; 97:326.

10. Brain Trauma Foundation. Management and prognosis of severe traumatic brain injury. J Neurotrauma 2007; 24: S1–106

References11. Chang BS, Lowenstein DH, Quality Standards Subcommittee

of the American Academy of Neurology. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003; 60:10.

12. Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2001; :CD000173.

13. Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet 2004; 364:1321.

14. Qureshi NH, Harsh GR. Skull fractures. eMEDICINE, 2001. file://emedicine.medscape.com/article/248108-overview (Accessed on June 24, 2009).

15. Al-Haddad SA, Kirollos R. A 5-year study of the outcome of surgically treated depressed skull fractures. Ann R Coll Surg Engl 2002; 84:196.

References16. Ratilal BO, Costa J, Sampaio C, Pappamikail

L. Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures. Cochrane Database Syst Rev 2011; :CD004884.

17. Santos SF, Rodrigues F, Dias A, et al. [Post-traumatic meningitis in children: eleven years' analysis]. Acta Med Port 2011; 24:391.

18. Brodie HA, Thompson TC. Management of complications from 820 temporal bone fractures. Am J Otol 1997; 18:188.

19. Oxford Textbook of Surgery. (2000). Oxford Press.20. Bullock MR, Chesnut R, Ghajar

J, et al. Surgical management of acute epidural hematomas. Neurosurgery 2006; 58:S7

References21. Bullock MR, Chesnut R, Ghajar

J, et al. Surgical management of acute subdural hematomas. Neurosurgery 2006; 58:S16.

22. Sillberg VA, Wells GA, Perry JJ. Do statins improve outcomes and reduce the incidence of vasospasm after aneurysmal subarachnoid hemorrhage: a meta-analysis. Stroke 2008; 39:2622.

23. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of posterior fossa mass lesions. Neurosurgery 2006; 58:S47.

24. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of traumatic parenchymal lesions. Neurosurgery 2006; 58:S25.

25. Pagni CA. Posttraumatic epilepsy. Incidence and prophylaxis. Acta Neurochir Suppl (Wien) 1990; 50:38.

References26. Chang BS, Lowenstein DH, Quality Standards Subcommittee

of the American Academy of Neurology. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003; 60:10.

27. Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2001; :CD000173.

28. Haltiner AM, Temkin NR, Dikmen SS. Risk of seizure recurrence after the first late posttraumatic seizure. Arch Phys Med Rehabil 1997; 78:835.

29. Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic brain injury. Acta Neurochir (Wien) 2008; 150:165.

30. Allard CB, Scarpelini S, Rhind SG, et al. Abnormal coagulation tests are associated with progression of traumatic intracranial hemorrhage. J Trauma 2009; 67:959.

References31. Wafaisade A, Lefering R, Tjardes

T, et al. Acute coagulopathy in isolated blunt traumatic brain injury. Neurocrit Care 2010; 12:211.

32. Stein SC, Young GS, Talucci RC, et al. Delayed brain injury after head trauma: significance of coagulopathy. Neurosurgery 1992; 30:160.

33. Murray GD, Butcher I, McHugh GS, et al. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma 2007; 24:329.

34. Zehtabchi S, Soghoian S, Liu Y, et al. The association of coagulopathy and traumatic brain injury in patients with isolated head injury. Resuscitation 2008; 76:52.

35. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581.

►Thank You…

4. management of head injury 6th aug 14

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