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Neurologic Emergencies in Pediatrics

this ppt will give you brief explanation about brain anatomy and circulation, Intracranial pressure and brain herniation, Traumatic Brain injury, and Approach to coma in Children including causes, neurological evaluation, assessment of brainstem function and Coma care.<br>

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Neurologic Emergencies in Pediatrics

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  1. Neurologic Emergencies andStabilization Abdureshidkedir(PCHR3) 19/02/2013 E.C Moderator- Dr.AyalewMoges(Pediatrician and Pediatric Neurologist,Consultant))

  2. Case scenario • Case - A 4 years old male child came to EOPD with a complaint of loss of consciousness of 2 hour’s duration after he fall down from height of 6 meter to floor …. What do you look for and how you do proceed in managing this child??

  3. Outlines • brain anatomy and Circulation • Intracranial pressure and brain herniation • Traumatic Brain injury • Approach to coma in Children • Causes • Neurological Evaluation • Assessment of brainstem function • Coma care • References

  4. The Coverings of the Brain

  5. BRAIN METABOLISM AND CEREBRAL BLOOD FLOW • The brain has high metabolic demands • Total brain volume doubles in the 1st yr of life and increases by an additional 15% over the 2nd yr. • Total brain volume at age 1 mo is ≈36% of adult volume but by age 1 yr is ≈ 72% (83% by 2 yr) • Brain oxygen consumption is about 3.5 ml /100 g/1min • The brain utilizes about 25 % of the body's total oxygen consumption • The brain relies on glucose for about 90% of its energy requirements • Normal cerebral blood flow is approximately • 55 ml /100 g/1min • 15 % of the CO

  6. ICP • Common neurological complication in critically ill children. • Pressure on the brain tissue by blood and cerebrospinal fluid (CSF). • The cause may be either an increase in • Brain volume • Cerebral blood flow • Cerebrospinal fluid (CSF) volume Monro-Kellie doctrine • Volume of the cranial vault cannot change • Increased volume of one component displaces the other.

  7. Clarification

  8. Raised ICP… • Closed system(compensation for ICP ) • Displacement of blood and CSF • ICP remains normal • Limits of compensation reached • Increase in ICP (decompensatedphase) • In infants with open cranial sutures • The system is considered as “open” • Initial compensation -bulging at the anterior fontanel • Change in volume of head • Splaying of the cranial sutures

  9. Raised ICP…

  10. Raised ICP… • The Davsonequation • ICP = Pss + (Iformation x RCSF) • Normal values : • Sagittal sinus pressure (Pss) – 5-8 mmHg • CSF formation rate (Iformation) – 0.3-0.4mL/min • Resistance to CSF outflow (RCSF) – 6-10mmHg/mL/min

  11. Cerebral perfusion pressure • CPP = MAP – ICP • Normal ICP <20 mmHg • Normal MAP >60 to 80 mmHg • MAP = 1.5 x Age + 55 mmHg • Normal CPP in children:40 to 60 mmHg.

  12. Cerebral blood flow • Ohm's law: • CBF = (CAP - JVP) ÷ CVR • CAP is carotid arterial pressure • JVP is jugular venous pressure • CVR is cerebrovascularresistance • Factors impact CBF: • PaO2 • PaCO2 • Hypercapniacauses cerebral vasodilatation and increased CBF • Hypocapnia reduces CBF

  13. Autoregulation • Maintenance of CBF over wide range of perfusion pressures. • 4 mechanisms • Myogenic-change with transmural pressure • Neurogenic-nerve supply to cerebral vessels • Metabolic • Endothelial-nitric oxide(vasodilator)

  14. Potential Problems Exacerbating Raised ICP • Calibration of ICP transducers and monitors • Neck vein obstruction • Airway obstruction • Inappropriate PEEP,secretions, bronchospasm etc. • Inadequate muscle relaxant • Breathing against ventilation • Muscle spasms • Hypoxia/hypercapnia • Incomplete analgesia,incomplete sedation and anaesthesia • Seizures, Pyrexia, Hyponatremia, Hypovolaemia

  15. Pathophysiology of Cerebral edema • Increase in brain water • Three major categories • Vasogenic edema • Increased permeability of the endothelial cells of brain capillaries • Cytotoxic edema • Influx of water into cells • Interstitial edema • CSF diffuses into the periventricular white matter • seen with hydrocephalus

  16. Brain Herniation Syndromes • Cranial cavity is divided into compartments by semirigid, densely fibrous folds of dura mater • The tentorium is an extension of the duramater that separates the cerebellum from the cerebrum • Falxcerebri • Tentoriumcerebelli • There are two major classes of herniation: • Supratentorial • Infratentorial

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  20. Traumatic brain injury (TBI) • External force cause damage to the brain • Mechanical,thermal, chemical ,electrical and radiation • occurs following a blow to the head, a fall, a bullet, a high-speed crash, or explosion injuries • could be an open (penetrating) or closed type • Globally, TBI is projected to be the third leading cause of death and injury by the World Health Organization in 2020 . • Pediatric TBI is reported to be the most common cause of injury-related death, and it commonly follows road traffic accidents and falls

  21. Traumatic Brain Injury • Mechanisms of TBI include motor vehicle crashes, falls, assaults, abusive head trauma, child abuse. • Most TBIs in children are from closed-head injuries. • TBI results in primary and secondary injury. • Primary injury from the impact produces irreversible tissue disruption • Epidural, subdural, and parenchymal intracranial hemorrhages can result. • Injury to gray or white matter is also commonly seen and includes focal cerebral contusions, diffuse cerebral swelling, axonal injury, and injury to the cerebellum or brainstem. • Patients with severe TBI often have multiple findings; diffuse and potentially delayed cerebral swelling is common

  22. Classification of TBI • Based on severity • Minor head injury: GCS 15 with no LOC • Mild head injury: GCS 14 or 15 with LOC • Moderate head injury: GCS 9–13 • Severe head injury: GCS 3–8 • Critical : GCS 4 & 5

  23. Types of brain injuries Based on Pathological features

  24. TBI ….. • Head injury is more Broad term • Scalp injury • Skull fracture and Types • Linear • Comminuted • Depressed • Basal

  25. TBI… • Traumatic brain injury can lead to several pathologic injuries, most of which can be identified on neuroimaging : • Skull fracture • Epidural hematoma • Subdural hematoma • Subarachnoid hemorrhage • Intraparenchymalhemorrhage • Cerebral contusion • Intraventricularhemorrhage • Focal and diffuse patterns of axonal injury with cerebral edema

  26. Primary brain injury • occurs at the time of trauma. • Common mechanisms • direct impact • rapid acceleration/deceleration • penetrating injury, and • blast waves. • The damage that results includes a combination of • focal contusions and hematomas, • shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling.

  27. Primary and secondary Head Injury • Primary • LOC occur immediately on impact • No LOC once consciousness regained • Secondary • LOC occur hours to days after the injury • Lucid interval • Patterns of primary head injury • Concussion • Contusion • Diffuse axonal injury • Hematomas • -Epidural • -Subdural • -SAH • -Intraparenchymal • - Intraventricular • Penetrating brain injury

  28. Concussion • Mildest form of diffuse injury • are commonly seen in the basal frontal and temporal areas, which are particularly susceptible due to direct impact on basal skull surfaces in the setting of acceleration/deceleration injuries. • Brief LOC,Headeache ,Nausia/vomiting

  29. Clinical features And grading • Confusion • Amnesia • Loss of consciousness • Others …… headache , dizziness , vertigo, nausea and vomiting • Vacant state, delayed verbal expression, inability concentrating, disorientation.. • Head CT is usually normal • Colorado grading system • grade 1…. Only confusion • grade 2 …. With amnesia/ LOC < 5 min • grade 3…. LOC > 5 min.

  30. Second impact syndrome • Complication of concussion • After a concussion the cerebral vascular auto- regulation become disrupted • Even trivial injury after this can cause vascular congestion and sever cerebral edema

  31. Contusion • It’s a bruise of the brain due to break of small vessels and extravasation of blood into the brain • The contused area appears bright on CT scan • Frontal , occipital and temporal • Coup and counter-coup • May cause hematoma • change in loc,CNSdysfunction,seizure,focaldamage

  32. Coup and counter-coup

  33. Diffuse axonal injury • It’s a damage to axons of the brain due to rotational acceleration then deceleration • Axons may be completely disrupted and retract forming axon ball • Hemorrhage on corpus callosum and dorsolateral midbrain

  34. Penetrating brain injury • When the impact passes through or penetrate and stay in the brain • Complex injury and highly fatal • Classified as • Missile • Non missile

  35. Cont. • Skull X-ray, CT and cerebral angiography • Operative exploration is necessary • Debridement ,irrigation , hemostasis and definitive closure • Small objects inside the brain substance are often left in place • Antibiotics

  36. Secondary brain injury -Secondary brain injury occurs after the moment of impact and is often preventable. -The principle causes of secondary brain injury are; • Hypoxia: PO2 < 8 kPa • Hypotension: systolic blood pressure (SBP) < 90 mmHg • Raised intracranial pressure (ICP): ICP > 20 mmHg • Intracranial hematoma • Brain swelling • Seizures • Infection -Both the initial treatment and later definitive care are primarily intended to prevent these secondary injuries

  37. Hypotension and hypoxemia • The most significant factors leading to a poor neurologic outcome or death. • Hypotension appears to be more deleterious than hypoxemia . • Adequate oxygenation and ventilation are essential to the management of these patients. • Elevated Paco2 may lead to cerebral vasodilation and increased cerebral blood volume.

  38. Intracranial hematomas • These are the most common cause of deterioration and death • The commonest hematomas in TBI are:- • Extradural hematomas(epidural) • subdural hematomas Acute Subacute Chronic • Subarachnoid hemorrhage

  39. Extradural hematomas(Epidural hematoma) • The skull fracture is associated with tearing of a meningeal artery • It occurs in the space between bone and dura • The most common site is temporal. • may also occur in other regions such asfrontal as well as in the posterior fossa. • They are not always arterial: disruption of a major Dural venous sinus can result in an EDH.

  40. Cont. lucid interval -The classical presentation of an EDH -The patient complains of a headache but is fully alert and orientated with no focal deficit -Contralateral hemiparesis, -Reduced conscious level and - Ipsilateral pupillary dilatation -Occurring in less than one-third of cases • A patient with an EDH may also sustain a primary brain injury and have a reduced conscious level from the time of injury

  41. Similarly, a subgaleal hematoma may result from decompression of an EDH through an associated skull fracture. • Other signs include : • Irritability • Anemia • Cephalohematoma • Vomiting • A bulging anterior fontanelle • Lethargy • Coma • Seizures

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