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CASE PRESENTATION

CASE PRESENTATION. R MAHARAJ. CASE STUDY. 11 year old LM...involved in a pedestrian –vehicle accident on Koeberg Road. Taken to nearby fire station by motorist – attended to by paramedic. Initial assessment – BP 80/55, P 121, sats 82%, B/S 5 GCS –E 1, V 2, M 5

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CASE PRESENTATION

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  1. CASE PRESENTATION R MAHARAJ

  2. CASE STUDY • 11 year old LM...involved in a pedestrian –vehicle accident on Koeberg Road. • Taken to nearby fire station by motorist – attended to by paramedic. • Initial assessment – BP 80/55, P 121, sats 82%, B/S 5 GCS –E 1, V 2, M 5 • Injuries – haematoma L temporal area, swollen L elbow, deformed L lower leg (clinically fractured) no vascular deficit, Abrasion L Hip • On scene management: • A- intubated – after sedation with midazolam, morphine, C collar • B-ventilated • C- IV access before intubation, given 200ml R/L bolus • Packaged and airlifted to Red Cross Hospital

  3. AT RED CROSS TRAUMA: • PRIMARY ASSESSMENT: • A – size 6 ETT in situ, C-collar in situ • B- ventilated – sats 87% on FiO2 100% • C – no obvious bleeding, BP 109/57 P110 • D- GCS – E 1, M 4, V T …PEARL No focal signs blood sugar 5.7 • SECONDARY SURVEY: • Injuries as noted • Lodox – C spine –no fractures • Chest – R midzone infiltrate, no visible hemo or pneumothoraces • Pelvis no fractures • Fracture L proximal ulna, L tib-fib

  4. Urine dipstix – 1+ blood • CT Brain – small subdural L parietal area, brain swelling, no midline shift • CT abdomen – no evidence of solid organ injury, no free fluid • HB, U/E – normal • ABG – Ph 7.35, PCO2 6.49, PO2 6.46, HCO3 25.2, BE 1.6, Sats 85% • Patient taken to theatre for insertion of intracranial pressure monitor(Licox device) • Fractures put in casts • Transferred to ICU for neuro-intensive care & monitoring

  5. DISCUSSION POINTS • Aims in mxn of paediatric head injury. • Secondary insult to brain – what are they, how can they be prevented/addressed early in the Pre-hospital/ ED phase. • What is Neuro-intensive care and current evidence.

  6. AIMS IN THE MANAGEMENT OF HEAD INJURY • Prevention of secondary insult • Maintain adequate Cerebral perfusion pressure • Prevent rise in intracranial pressure • Early neuro-surgical intervention

  7. WHAT ARE SECONDARY INSULTS TO BRAIN • HYPOXIA – give supplemental oxygen, intubate/ventilation early • HYPOVOLAEMIA – look for other injuries that may cause hypovolaemia, early control of bleeding and fluid resuscitation • HYPO/HYPERGLYCAEMIA • HYPERCARBIA • HYPERTHERMIA

  8. ANATOMICAL CONSIDERATIONS ADULT vs CHILD • OPEN SUTURES –more prone to injury, allow for greater amount of intracranial expansion, delayed onset of herniation • Brain tissue LESS MYELINATED cf to adult – predisposed to greater shearing forces • SECONDARY INSULTS – result in more profound secondary brain injury – worse outcomes cf adults

  9. PATHOPHYSIOLOGY OF SECONDARY BRAIN INJURY

  10. PRE-ICU CONSIDERATIONS • AIRWAY MXN • Intubation if GCS </= 8, or hypoxia • RSI • WHAT DRUGS TO USE: “ IDEAL AGENT – KEEPS PATIENT HAEMODYNAMICALLY STABLE” • Thiopentone, Propofol, Midazolam – use with caution -> can cause hypotension, and decreased CPP • Ketamine – not usually used – Increases ICP and cerebral oxygen consumption. • Recent studies downplay these adverse effects -> Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of sedation with ketamine in severe head injury patients: comparison with sufentanil. Crit Care Med 2003;31:711–7. • Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viiand X, Martin C. Effects of sufentanil or ketamine administered in targetcontrolled infusion on the cerebral hemodynamics of severely brain-inured patients. Crit Care Med 2005;33:1109–13. • Himmelesher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005;101:524–34. • Etomidate – safe agent – minimal changes in BP, also thought to have neuroprotective effects • Premedication with Lignocaine – no conclusive evidence

  11. PARALYTIC AGENT: • Scoline – agent of choice • May transiently increase ICP – no clinical evidence that that this increases mortality/morbidity. Brown MM, Parr MJ, Manara AR. The effect of suxamethonium on intracranial pressure and cerebral perfusion in patients with severe head injuries following blunt trauma. Eur J Anaesth 1996;13:474–77. • Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity, or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994;78:469–73. • Other agents: Rocuronium, Atracurium(RXH ICU) • Cochrane review – scoline superior d/t shorter duration of action. Perry JJ, Lee JS, Sillberg VAH, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev 2007;(3):CD002788.

  12. VENTILATION: • Current recommendation: EUCAPNIA • HYPERVENTILATION – reserved solely for patients with impending cerebral herniation • CIRCULATION: • hypotension increases short term mortality the most. • Mortality increased when SBP < 75th centile Vavilala MS, Bowen A, Lam AM, et al. Blood pressure and outcome after severe pediatric traumatic brain injury. J Trauma 2003;55:1039–44. • Look for sources of blood loss • Fluid resus with normal saline

  13. NEURO-INTENSIVE CARE • INTRACRANIAL PRESSURE DIRECTED vs CEREBRAL PERFUSION PRESSURE DIRECTED • Indications for ICP monitoring: • Severe TBI with GCS<8, and abnormal CT Brain changes … ( Haemotoma, cerebral contusion, cerebral oedema, compressed basal cisterns) Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 5 Indications for intracranial pressure monitoring in pediatric patients with severe traumatic brain injury. Pediatr Crit Care Med 2003;4(3Suppl):S19–24. • Aim to keep ICP<20cm H20

  14. CONTROL OF ICP: • MEDICAL: • FLUID THERAPY – Head Injury Fluid (5% dextrose saline, K suppl) for maintainence • Hyperosmolar fluid therapy: Hypertonic saline vs Mannitol • Mannitol: IV bolus 1g/kg – lowers ICP in 1-5 min, peak effect 20-60 min Action – osmotic effects - rheologic effects - free radical scavenger • Disadvantage – osmotic diuresis  hypovolaemia • Hypertonic saline – some studies – hypertonic saline more effective in reducing ICP, dose 3 -5ml/kg • Advantages over mannitol – no osmotic diuresis, augments I/V volume • Disadvantages- bleeding diathesis, hypernatraemia ( RXH – keep Na 145-150)

  15. STEROIDS – not recommended – CRASH TRIAL • HYPOTHERMIA – decreases inflm response, excitotoxicity and metabolic demands suggested temp 32 – 34 degrees C. RXH – aim for normothermia. Treat hyperthermia aggressively. • EARLY SEIZURE PROPHYLAXIS – some studies recommend anticonvulsants. No superior agent identified. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children and adolescents. Chapter 19. The role of antiseizure prophylaxis following severe pediatric traumatic brain injury. Pediatr Crit Care Med 2003;4(3 Suppl):S72–5.

  16. ADEQUATE SEDATION/ANALGESIA • NO one sedative regimen is superior. • Benzodiazapines – decr CMRO2 and CBF, no change in ICP • Narcotics nil effect on above • Watch for hypotension • SURGICAL: • Cerebral spinal fluid drainage • Decompressive craniectomy • OTHER MEASURES: • avoid cerebral venous blood flow restriction – • Keep head in midline, avoid compressive dressings around neck, head elevation to 30 degrees

  17. PATIENT PROGRESS • ICP stabilised with neuro-intensive measures • Hypoxia corrected with ventilation – weaned by day 3 and extubated day 4 • GCS 14/15 • Transferred to trauma ward: • 2 days post d/c from ICU – GCS deteriorated 8/15, developed seizures • Needed reintubation, given phenobarbitone 20mg/kg for seizures • CAUSES FOR DETERIORATION…

  18. REBOUND INCREASE IN ICP- reflex brain oedema, rebleed • INFECTION – meningitis vs systemic infection • ELECTROLYTE ABN. • HYPOGLYCAEMIA • THROMBO-EMBOLIC • HYPOXIA • DIRECT COMPLICATION OF HEAD INJURY-  SIADH vs CEREBRAL SALT WASTING vs DIABETES INSIPIDUS

  19. INVESTIGATION • ELECS – Na 117, K 4.7, Ur 2.3, Cr 60 • FBC – normal • CRP – NO increase • Rpt CT brain – no new bleeds, resolving brain oedema. No midline shift • Readmitted to ICU – • Ventilated • Hyponatraemia corrected slowly with hypertonic sline • Phenytoin • Investigated for SIADH, cerebral salt wasting • Extubated 24 hrs later

  20. SIADH – Hyponatraemia -dilutional -intravascular volume normal/mildly incrd - urine osmolality > serum osmolality - urine sodium normal • CEREBRAL SALT WASTING- Hyponatraemia (imprd renal tubular function –unable to conserve salt) - intravascular volume depletion – incr urea, serum protein. - incr urine sodium • DIABETES INSIPIDUS – post. pituitary lesion(ADH def) - polyuria - low urine sodium

  21. REFERENCES • Neurointensive Care for Traumatic Brain Injury in Children, Felice Su, MD, FAAP, Instructor of Pediatrics, Division of Critical Care Medicine, Stanford University; Attending Physician, Department of Pediatrics, Division of Critical Care Medicine, Lucile Packard Children's Hospital • Evaluation and Management of Moderate to Severe Pediatric Head Trauma • Anand Swaminathan, MD, MPH; Phil Levy, MD; Eric Legome, MD • EMERGENCY MEDICINE ONLINE • Published: 08/31/2009

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