Non accidental head injury - how to improve outcome

Non Accidental Injury – How to Improve outcomes

Alex Khoo Peng Chuan

[email protected]

EssenDals

•  Non Accidental Head Injury is not only another type of traumaDc head injury but THE most severe form of traumaDc head injury

Disclosure

OUTCOME

1/3 die 1/3 no sequelae 1/3 permanent neurological damage Poorer than accidental impact injury (translational forces)

Haviland et al Arch Dis Child 1997;77:504-507

The pyramid and iceberg of disease

1 Diseased, diagnosed & controlled

2 Diagnosed, uncontrolled

3 Undiagnosed or wrongly diagnosed disease

4 Risk factors for disease

5 Free of risk factors

Diagnosed disease

Undiagnosed or wrongly diagnosed disease

Causes begin to exert their influence here

Disease and first manifestation can be diagnosed here, eg.

Time

Infancy childhood adolescence adulthood old age

Full health

Death

Recurrence and death

NATURAL HISTORY AND OUTCOMES

SUBDURAL HEMATOMA

EPIDURAL HEMATOMA

SUBDURAL vs EPIDURAL HEMATOMA

•  EPIDURAL – Requires linear

force – Associated with

skull fracture and torn artery. Brain often uninjured

–  “Lucid” interval common

– Common in accidental trauma

•  SUBDURAL –  Requires significant

rotational forces –  Associated with brain

injury and torn bridging veins

–  Neurologic symptoms from the start

–  Common in infants with abusive head trauma

COUP -‐ CONTRA COUP INJURY

Cerebral Contusion Most common Focal brain Injury

Sites Impact site/ under skull #

Anteroinferior frontal

Anterior Temporal Occipital Regions

Petechial hemorrahges coalesce Intracerebral Hematomas later on.

We are not alone •  1783 Monro & Kellie

define closed box concept •  1866 Lyden measures ICP

via trephine •  1866 Knoll produces

graphic CSF pressure trace

•  1870s Duret observes deleterious effects of injecDng fluid in to dogs skulls

• 1891 Quinke introduces LP allowing CSF sampling & measurement

• 1900 Cushing describes the classic Triad seen with

severely elevated ICP •  systolic hypertension with widened pulse pressure

•  bradycardia •  respiratory irregulariDes

• 1960 Lundberg introduced long term conDnuous ICP

monitoring via an indwelling intraventricular

catheter.

PLAN A , PLAN B , PLAN C

50% are unconscious immediately. Focal deficits common

Hemiparesis – 50%

Pupillary abnormality-‐ 28-‐78%

Seizures – 6-‐22%

Rx-‐ larger-‐ urgent removal

Small -‐

Small with mass effect/ significant change in conscious/ focal deficits

Removed

Small with significant brain injuries + mass effect out of proporDon to size of clot

Non operaDve approach

DAI

Hallmark of severe traumaDc Brain Injury

DifferenDal Movement of Adjacent regions of Brain during acceleraDon and DeceleraDon.

DAI is major cause of prolonged COMA ader TBI, probably due to disrupDon of Ascending ReDcular connecDons to Cortex.

Angular forces > Oblique/ Sagital Forces

The shorn Axons retract and are evident histologically as RETRACTION BALLS.

Located predominantly in

1. CORPUS CALLOSUM 2. PERIVENTRICULAR WHITE MATTER 3. BASAL GANGLIA 4. BRAIN STEM

Pathophysiology of Brain Injury

Brain Injury

Primary Secondary

1.Delayed cell death 2.Intracranial hypertension and mass effect

3.Ischemia systemic hypoxia,hypercarbia and

hypotension

Primary Brain Injury

Primary

Focal @SITE

Contra-‐coup

Diffuse DAI

PredicDng outcomes

OXYGENATION

•  Early episodes of hypoxemia greatly increases mortality and morbidity.

•  Hypoxia is apnoea or cyanosis in the field or an oxygen saturaOon (SaO2) < 90%.

•  IntubaOon of unconscious and unresponsive child improves outcome.

•  General rule : intubate if apnea / cyanosis GCS 8 , airway compromise and signs of herniaOon

Cerebral Perfusion

Haemoglobin

Deep tendon and superficial reflexes

•  DTR’s exaggerated ader trauma is due to corDcal disinhibiDon

•  Decreased / absent ader Spinal cord injury •  Asymmetric DTR’s unilateral brain/spine injury •  Superficial lost/decreased in corDcospinal dysfuncDon and helpful in localizing lesions

•  Plantar response

Normal reflex Intact descending corOcospinal inhibiOon

PosiDve Babinski Interrupted inhibiDon pathways

Intracranial Hypertension

•  Pathophysiology –  ICP monitoring and control are the cornerstones of TBI management

– Normal ICP •  Adults <10mmhg •  Children 3-‐7mmhg •  Infants 1.5-‐ 6mmhg

– When to treat? •  Adults > 20 •  Children >15 •  Infants >10 { Arbitrary numbers most commonly used, pending outcome studies}

Device / method Risk / benefit

1. Intraventricular catheter Adv-‐ drainage of CSF to reduce ICP DisAdv-‐ infecDon/ ventricular compression leads to inaccuracy

2. subdural/ subarachnoid bolts ( Philadelphia, Leeds, Richmond bolts)

Occlusion of port in device leads to inaccuracy

3. FiberopDc cath ( Camino labs) Improved fidelity & longevity Can be placed Intraparenchymal/ intraventricular/ subdural Used to drain CSF Accuracy maintained even with fully collapsed ventricles Single cath can be used as long as needed

POST TRAUMATIC SEIZURES •  Complicate 10% pediatric head injuries 1.  Impact seizures follow minor injury ,

occur on impact 2.  Early posvraumaDc seizures within min

to hours of injury.

1.  No radiological intracranial injury noted in many cases

2.  Do not portend later epilepsy

3.  Most do not need Rx

4.  Outcome good.

•  Late seizure >24 hrs ader injury

–  Visible intracranial injury.

–  PenetraDng injuries/ depressed #/ SDH/ Lower GCS score

–  Long term risk of epilespy high-‐ need Rx for 6-‐12 mo.

•  Seizure prophylaxis Only during first week Or Dll

intracranial hypertension phase is passed.

Prolonged usage has cogniDve deficits on long term follow ups.

Phenytoin commonly used

TAKE HOME MESSAGE Have a plan , a back-‐up plan and and anDcipate the curve ahead

Karak Highway

Acknowledgments

Doctors and Nurses of HRPB IPOH

Non accidental head injury - how to improve outcome

Health & Medicine

Transcript of Non accidental head injury - how to improve outcome