Icu care after acute head injury

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Icu care after acute head injury

  1. 1. INTENSIVE CARE AFTER ACUTE HEAD INJURY Moderator : Dr Anand Kulkarni Presenter : Dr Nikhil M.P
  2. 2. <ul><li>Introduction </li></ul><ul><li>One third of all trauma deaths </li></ul><ul><li>15-45 years of age </li></ul><ul><li>49%-road traffic accidents,28%-falls,23%-gun shot injuries and other causes </li></ul><ul><li>Inpatient case fatality rates </li></ul><ul><li>all head injuries- 2.6%to6.5% </li></ul><ul><li>severe injuries - 15 to 50% </li></ul><ul><li>Good outcome-Glasgow outcome scale of 1or 2 </li></ul>
  3. 3. <ul><li>Glasgow outcome scale </li></ul><ul><li>1= good recovery. </li></ul><ul><li>2= moderate disability. </li></ul><ul><li>3= severe disability. </li></ul><ul><li>4= vegetative state. </li></ul><ul><li>5= dead. </li></ul>
  4. 4. <ul><li>Determinants of outcome in acute head injury </li></ul><ul><li>Primary vs. secondary insults </li></ul><ul><li>Little can be done about the primary </li></ul><ul><li>injury to brain </li></ul><ul><li>Presence and severity of secondary neuronal injury </li></ul><ul><li>Physiological insults are additive in their effects on outcome </li></ul><ul><li>Opportunity on avoiding, identifying & treating-physiological derangements </li></ul>
  5. 5. No yes Cerebral perfusion pressure( CPP<5OmmH g) No yes Intracranial hypertension> 30mm Hg No yes Pyrexia>38deg Celsius No yes Hypoxia (spO 2 <90%) No yes Duration of hypotension (SBP< 90mm Hg) Significant relation to grades within GOS Mortality Insult
  6. 6. <ul><li>Monitoring </li></ul><ul><li>A rational approach to select monitoring modalities </li></ul><ul><li>maintaining cerebral blood flow and oxygenation </li></ul><ul><li>Ischemia a consistent finding in head injury </li></ul>
  7. 7. <ul><li>Monitoring systemic physiology </li></ul><ul><li>ABP with measurement of ICP </li></ul><ul><li>Placement of right atrial or pulmonary artery catheter </li></ul><ul><li>Pulse oximetry </li></ul><ul><li>ABG </li></ul><ul><li>Core temperature </li></ul><ul><li>Blood sugar </li></ul>
  8. 8. Intracranial pressure monitoring <ul><li>Normal resting ICP is 0 to 15 mm Hg </li></ul><ul><li>Transient elevation (straining, coughing and trendelenburg position) </li></ul><ul><li>>20 mm Hg  moderate </li></ul><ul><li>>40 mm Hg  severe </li></ul><ul><li>Intracranial HTN develops in 50% of patients in coma caused by severe head injury. </li></ul>
  9. 9. <ul><li>50-75% after evacuation of an intracranial haematoma </li></ul><ul><li>postoperative haematoma </li></ul><ul><li>progressive swelling of focal </li></ul><ul><li>contusions </li></ul><ul><li>diffuse brain swelling </li></ul>
  10. 10. <ul><li>Severe intracranial HTN can result in </li></ul><ul><li>secondary injury to the brain, due to </li></ul><ul><li>ischemia produced by reducing CPP and it can also distort and compress the brainstem. </li></ul>
  11. 11. Measurement of intracranial pressure in ICU <ul><li>To treat intracranial HTN effectively. </li></ul><ul><li>No reliable clinical indicators in patients with head injury. </li></ul><ul><li>Symptoms of raised ICP are impossible to elicit in a comatose patients. </li></ul><ul><li>Papilledema is uncommon after head injury even in patients with intracranial HTN. </li></ul>
  12. 12. INDICATIONS OF ICP MONITORING <ul><li>GCS<8 and abnormal CT scan </li></ul><ul><li>or </li></ul><ul><li>GCS<8 and normal CT scan but with adverse features </li></ul><ul><li>age>40yrs </li></ul><ul><li>hypotension </li></ul><ul><li>decerebrate </li></ul><ul><li>Inability to monitor serial neurological examinations </li></ul><ul><li>Treatment that increase ICP (PEEP) </li></ul>
  13. 13. Modalities <ul><li>Ventriculostomy catheters </li></ul><ul><li>remains the preferred choice. </li></ul><ul><li>allows treatment of elevated ICP by intermittent drainage of CSF. </li></ul><ul><li>Microsensor transducer </li></ul><ul><li>Fiberoptic transducer </li></ul>
  14. 15. <ul><li>How long ? </li></ul><ul><li>As long as ICP remains elevated </li></ul><ul><li>Active management of ICP </li></ul><ul><li>For 3 days in the absence of significant </li></ul><ul><li>ICP elevation </li></ul>
  15. 16. Complications <ul><li>Ventriculitis </li></ul><ul><li>Intracerebral hemorrhages </li></ul><ul><li>contraindications </li></ul><ul><li>severe coagulopathies </li></ul>
  16. 17. Cerebral perfusion monitoring <ul><li>Normal cerebral blood flow is 54+12 ml/100 g/min in adults and 1.06+0.03 ml/100g/min in children. </li></ul><ul><li>Normal cerebral metabolic rate(CMRO2) of oxygen is 1.5micro mol/g/min. </li></ul><ul><li>After head injury CMRO2 is reduced by approx 50% </li></ul>
  17. 18. Measurement of cerebral perfusion in the ICU <ul><li>Cerebral perfusion pressure </li></ul><ul><li>simplest measure </li></ul><ul><li>MAP minus ICP </li></ul><ul><li>Normal lower limit of autoregulation for CPP is 50mm Hg </li></ul><ul><li>Ability to auto regulate may be impaired, CBF may decrease with CPP values<50mm Hg </li></ul><ul><li>Assess only ischemia caused by increased ICP or decreased BP </li></ul>
  18. 19. <ul><li>Transcranial Doppler ultrasonography (TCD) </li></ul><ul><li>Reduction in middle cerebral artery flow velocity-a useful marker </li></ul><ul><li>As ICP increases CPP decreases and highly pulsatile flow velocity pattern is seen. </li></ul><ul><li>Pulsatality index-describes waveform pattern </li></ul><ul><li>Cerebral vasospasm- TCD velocity. </li></ul>
  19. 20. <ul><li>Cerebral blood flow </li></ul><ul><li>Kety - Schmidt technique. </li></ul><ul><li> Inhaled Xenon technique </li></ul><ul><li>Both these methods are intermittent technique and requires the patient to be haemodynamically stable </li></ul><ul><li>Thermal diffusion method </li></ul><ul><li>Laser doppler method </li></ul>
  20. 21. <ul><li>Jugular venous saturation </li></ul><ul><li>To monitor cerebral hypoxia and ischemia </li></ul><ul><li>Right jugular venous oximetry -to assess the adequacy of CBF in head injury </li></ul><ul><li>Reductions in sjvo2 provide an useful marker of inadequate CBF </li></ul><ul><li>Measured with a fiberoptic oxygen saturation catheter </li></ul>
  21. 22. <ul><li>Near infrared spectroscopy </li></ul><ul><li>Measures cerebral oxygen saturation. </li></ul><ul><li>Reflects changes in oxygenated, deoxygenated and total hemoglobin. </li></ul><ul><li>Absorbance of NIRS light by extra vascular blood  used to identify intracranial hematomas </li></ul>
  22. 24. <ul><li>Medical management of head injury </li></ul><ul><li>Surgical lesion should be ruled out by CT scan whenever </li></ul><ul><li>Unexpected severe intra cranial hypertension develops. </li></ul><ul><li>When it is accompanied by neurological deterioration. </li></ul><ul><li>Refractory to medical management. </li></ul>
  23. 25. <ul><li>General measures </li></ul><ul><li>Head elevation- elevating the head & keeping the head in neutral position have been standard practice for management of ICP in past. </li></ul><ul><li>Treatment of systemic hypertension </li></ul><ul><li>common with head injury. </li></ul><ul><li>SBP>DBP </li></ul><ul><li>Hyperdynamic state including tachycardia & increased cardiac output. </li></ul><ul><li>Autoregulation is impaired in severe head injury, systemic hypertension may increase CBP & ICP and may exacerbate cerebral edema . </li></ul>
  24. 26. <ul><li>Often resolves with sedation </li></ul><ul><li>Hydralazine & nitroprusside </li></ul><ul><li>Beta & alpha blockers. </li></ul><ul><li>Fever </li></ul><ul><li>common during recovery from head injury. </li></ul><ul><li>potent cerebral vasodilator & increase ICP and cerebral metabolic requirements. </li></ul>
  25. 27. <ul><li>Prevention of seizures </li></ul><ul><li>Occurs early (<7 days) or late (>7 days) after head injury. </li></ul><ul><li>More common after 7 days. </li></ul><ul><li>Phenytoin & carbamazepine. </li></ul>
  26. 28. <ul><li>Specific measures </li></ul><ul><li>Target CPP values >60-70mmHg . </li></ul><ul><li>Ventilatory support & use of hypocapnia for ICP reduction </li></ul><ul><li>Patients with GCS<8 </li></ul><ul><li>Hyperventilation </li></ul><ul><li>Constricts cerebral blood vessels </li></ul><ul><li>Decreases CBV </li></ul><ul><li>Decreases ICP </li></ul>
  27. 29. <ul><li>Accompanied by reduction in global cerebral blood flow. </li></ul><ul><li>Hyperventilation has only short lived effectiveness in decreasing ICP </li></ul>
  28. 30. <ul><li>Neuromuscular blockade & sedation </li></ul><ul><li>Currently the subject is of debate. </li></ul><ul><li>Prevents rise in ICP produced by coughing & bucking on the tube. </li></ul><ul><li>Increased respiratory complications. </li></ul><ul><li>Long term neuromuscular blockade </li></ul><ul><li>Continued paralysis. </li></ul><ul><li>Acute myopathy. </li></ul>
  29. 31. <ul><li>Intravenous anesthetic agent preserve pressure auto regulation & cerebrovascular response to CO2 </li></ul><ul><li>Barbiturates less commonly used now. </li></ul><ul><li>Propofol </li></ul><ul><li>Midazolam in combination with propofol & fentanyl. </li></ul>
  30. 32. <ul><li>Fluid therapy & feeding </li></ul><ul><li>Accurate fluid management may be complicated by continuing or concealed hemorrhage but every effort must be made to restore normovolemia & prevent hypertension. </li></ul><ul><li>By clinical & laboratory assessment of volume status and invasive hemodynamic monitoring. </li></ul>
  31. 33. <ul><li>30-40ml/ kg of maintenance fluid per day. </li></ul><ul><li>Hypotonic & dextrose containing fluids should be avoided. </li></ul><ul><li>Increase in plasma oncotic pressure in blood brain barrier disruption. </li></ul><ul><li>Colloids effective. </li></ul><ul><li>High nutritional requirements and feeding should be instituted early (<24hrs) </li></ul>
  32. 34. <ul><li>Hyper osmolar therapy </li></ul><ul><li>Mannitol traditionally used to elevate plasma osmolarity & to decrease brain edema ( 20% solution) </li></ul><ul><li>Reduces ICP by improving CPP & microcirculatory dynamics. </li></ul><ul><li>Secondary increase in ICP when BBB is disrupted, fluid overload and renal toxicity. </li></ul>
  33. 35. <ul><li>Cerebral metabolic suppressants </li></ul><ul><li>IV barbiturates </li></ul><ul><li>cardiovascular depression </li></ul><ul><li>prolonged ICU stay </li></ul><ul><li>pulmonary infection </li></ul><ul><li>Excitatory amino acid antagonist </li></ul><ul><li>Calcium channel blockers( Nimodipine) </li></ul><ul><li>Antioxidants </li></ul><ul><li>Corticosteroids </li></ul><ul><li>Hypothermia </li></ul>
  34. 36. <ul><li>References </li></ul><ul><li>Text book of Neuroanaesthesia & critical care, 1 st edition. </li></ul><ul><li>Anaesthesia & neurosurgery, Cotrel, 2005 edition. </li></ul>
  35. 37. Thank you

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