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พญ. อิศราภรณ์ พูน สวัสดิ์ พบ. AITSARAPORN PHUNSAWAT MD. DEPARTMENT OF ANESTHESIOLOGY, FACULTY OF MEDICINE NARESAUN UNIVERSITY HOSPITAL.

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Presentation on theme: "พญ. อิศราภรณ์ พูน สวัสดิ์ พบ. AITSARAPORN PHUNSAWAT MD. DEPARTMENT OF ANESTHESIOLOGY, FACULTY OF MEDICINE NARESAUN UNIVERSITY HOSPITAL."— Presentation transcript:

1 พญ. อิศราภรณ์ พูน สวัสดิ์ พบ. AITSARAPORN PHUNSAWAT MD. DEPARTMENT OF ANESTHESIOLOGY, FACULTY OF MEDICINE NARESAUN UNIVERSITY HOSPITAL

2 Anatomy of the cranium  Cranium is a rigid box containing 1. brain 80% (1300 ml) 2. blood 12% (110 ml) 3. CSF 8% (65 ml) All of these contents are maintained a balanced pressure referred to as intracranial pressure (ICP)

3 Intracranial pressure Best Practice & Research Clinical Anaesthesiology.2007;21: 517–38 The normal range for ICP varies with age Age group ICP normal (mmHg) Infant < 7.5 Child < 10 Adult < 15 ( cm H2O)

4 Intracranial pressure  Transient elevation with straining, coughing, or trendelenberg position  Sustained ICP ≥20: abnormal  ICP 20-40mmHg : moderate ICH (intracranial hypertension)  Sustained ICP ≥ 40 mm Hg indicate severe, life- threatening ICH Neurol Clin 2008;26: 521–41 Goal: Keep ICP≤ 20 mmHg

5 Monro-Kellie Doctrine (Compensatory mechanism) To maintain normal pressure in the skull, any increase in the size of one component initially will lead to a compensatory decrease in one or both of the other two.  The skull is a rigid bowl that offers little flexibility for changes in the size of the three intracranial components. To maintain normal pressure in the skull, any increase in the size of one component initially will lead to a compensatory decrease in one or both of the other two.

6 Brain  displaced to moderate degrees to accommodate an expanding mass.  Slow expansion  Rapid expansion Cerebral herniation 1.Subfalcine 2.Uncal transtentorial 3.Tonsillar 4.Trancalvarial 5.Transtentorial(Central) 6.Upward transtentorial

7 Adverse effect of ICH  Decreased CPP  Brain ishemia brain edema increase ICP  Brain herniation

8 Conditions Associated with Increased ICP  Subdural hematoma  Epidural hematoma  Brain tumor  Cerebral abscess  Intracerebral hemorrhage  Cerebral infarction  Global hypoxia-ischemia  Reye's syndrome  Acute hyponatremia Intracranial mass lesions Increased brain volume (cytotoxic edema)

9 Conditions Associated with Increased ICP  Hepatic encephalopathy  Traumatic brain injury  Meningitis  Encephalitis  Hypertensive encephalopathy  Eclampsia  Subarachnoid hemorrhage  Dural sinus thrombosis  Altitude-related cerebral edema  Communicating hydrocephalus  Noncommunicating hydrocephalus  Choroid plexus papilloma Increased blood and brain volume (vasogenic edema) Increased CSF volume

10 Extracranial cause (secondary) Prevent cause, Prevent ICH

11 Clinical Signs of Increased ICP

12  Signs which are almost always present  Depressed level of consciousness (lethargy, stupor, coma)  Hypertension, with or without bradycardia  Cushing triad: hypertension, bradycardia, and respiratory depression  Symptoms and signs which are sometimes present  Headache  Vomiting  Papilledema  Sixth cranial nerve palsies

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14 Neurogenic Patterns of Respiration Typelocation Cheynes - Stokes RespirationDiffuse forebrain injury Central neurogenic hyperventilation Midbrain,such as thalamus Apneustic (pause at full inspiration) Mid to caudal pontine, brainstem or Basilar a. occlusion Ataxic ( radom deep and shallow breaths) Medulla lesion (terminal stage) Cluster (irregular breaths and pause) Lower medulla

15 Powerpoint Templates

16 Page 16  Monitoring Clinical Status 1. Level of alertness and GCS; 2. Pupillary examination; 3. Ocular motor examination (with special attention to the third and sixth cranial nerves); 4. Motor examination with special attention for hemiparesis; 5. Presence of nausea or vomiting; 6. Complaints of headache; and 7. Current vital signs and the recent course. Best to Correlate with ICP

17 Powerpoint Templates Page 17  CT-brain  MRI

18 Powerpoint Templates Page 18

19 Powerpoint Templates Page 19  Measure basal arterial cerebral blood flow, ◦ 40 to 70 cm/s.  Diffuse Increase ICPcompress cerebral arteriesincrease flow velocity  TCD is insufficiently sensitive and specific to provide a noninvasive alternative to ICP monitoring.

20 Powerpoint Templates Page 20 Neurol Clin 2008;26: 521–41 1. Fontanometry 2. Epidural pressure monitoring 3. Subdural pressure monitoring 4. Parenchymal measuring 5. Ventricular pressure monitoring 6. Lumbar pressure monitoring

21 Powerpoint Templates Page 21 Direct ICP Monitoring

22 Powerpoint Templates Page 22  (1) the condition leading to ICP elevation  is amenable to treatment  (2) ongoing direct assessment of ICP will be of consequence in decisions regarding treatment interventions  (3) the risks of device placement do not outweigh the potential benefits. Neurol Clin 2008;26: 521– 41

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24 Treatment of increased ICP The goals of ICP treatment 1. Maintain ICP ≤ mmHg. 2.Maintain CPP ≥ 60 mmHg by maintaining adequate MAP. 3. Avoid factors that aggravate or precipitate elevated ICP. Neurol Clin 2008;26: 521–41 CPP=MAP-ICP CBF = CPP / CVR

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26 Management of  ICP  Head elevation 15 ˚ - 30 ˚  Hyperventilation  Control BP  Hyperosmolar therapy  Sedative and paralysis  Steroid  Decompressive craniectomy and lumbar drainage

27 Head elevation  venous out flow resistance  CSF from intracranial spinal compartment  Position above heart and prevent kinking or compression of jugular v.(c-spine precaution) The mean ICP was significantly lower when the patient's head was elevated at 30° than at 0° (14.1 ± 6.7 mm Hg vs ± 8.3 mm Hg). J Neurosurg 1992;76:207–11.

28 Head elevation  The anesthetized or hypovolemic pts may response to head elevation by developing systemic hypotension  Must treat to avoid adverse impact to CPP Neurol Clin 2008;26: 521–41

29 Oxygenation and Ventilation  Respiratory dysfunction is common esp in head trauma.  Hypoxia and hypercapnia can ICP  Adequate ventilation: Pao2 ≥60 mmHg Paco2:30-35 mmHg Neurol Clin 2008;26: 521–41

30 Oxygenation and Ventilation  intrathoracic pressure are transmitted directly through the neck to the intracranial cavity Increase intrathoracic pressure: increase ICP  decreased venous return to the right atrium and a rise in jugular venous pressure, increase in CBV and in ICP  Decreased venous return also leads to a drop in cardiac output and blood pressure, thereby reducing CPP PEEP

31 Oxygenation and Ventilation  The consequences of PEEP on ICP depend on  lung compliance,  ICP  MAP Minimal consequences for ICP are usually observed when lung compliance is low J Trauma 2005;58:571–6.

32 Hypercapnia and hypocapnia  Hypercapnia  Cerebral vasodilate  CBF and ICP   PaCO 2 1 mmHg  CBF 2 ml/100g/min  In situations of reduced intracranial compliance  Increased ICP and reduced CPP  In situations of reduced cerebral blood flow and oxygen delivery, where ICH is not a problem  improvements in cerebral blood flow

33 Hyperventilation  Hyperventilation PaCO2, which can induce constriction of cerebral arteries  Cerebral vasodilate  CBF and ICP  PaCO 2 1 mmHg  CBF 2 ml/100g/min  PaCO 2 1 mmHg  CBV 0.04 ml/100g/min  Aim: Paco mmHg  Hyperventilation may produce a decrease in CBF su ffi cient to induce ischemia.  Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often critically reduced. Neurol Clin 2008;26: 521–41

34 Hyperventilation  Most e ff ective use of hyperventilation is acutely  The vasoconstrictive e ff ect :11-20 hours  When hypocarbia is induced and maintained for several hours, it should be reversed slowly, over several days, to minimize this rebound hyperemia Prophylactic hyperventilation (PaCO 2 of 25 mm Hg or less) is not recommended. Crit Care Clin 1997;13:163–84.

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36 Decompressive Abd Pressure  intra-abdominal P.(abdominal compartment syndrome), can ICP by obstructing cerebral venous outflow.  Immediate reductions in ICP with decompressive laparotomy Neurol Clin 2008;26: 521–41

37 Decompressive Abdominal Pressure  17 pts with intractable ICH that is refractory to medical treatment (abdominal compartment syndrome is not present)  abdominal fascial release can e ff ectively reduce ICP (30.0± ±3.2) J Trauma 2004;57:687–93.

38 Hyperthermia  metabolic rate 10-13% per 1°C and is a potent vasodilator.  Induce dilation of cerebral vessels can CBF and ICP.  Fever during the post injury period worsens neurologic injury in TBI Neurosurgery 1996;38:533–41

39 Hypothermia  Prophylactic hypothermia  Not significantly associated with decrease mortality when compare with normothermic controle  Cochrane review in 2004  not find any evidence supporting the use of hypothermia during the treatment of TBI,  a statistically significant increased risk of pneumonia and other potentially harmful side-effects Although routine induction of hypothermia is not indicated at present,hypothermia may be an e ff ective adjunctive treatment of increased ICP refractory to other medical management

40 Hypertension  Common in pts who have ICH  Esp 2° to HI  Characterize by a SBP increase greater than diastolic increase.  Associate with sympathetic hyperactivity Neurosurgery 1996;38:533–41.

41 Hypertension  Not reduce BP in HT pts associated with untreated intracranial mass lesions  cerebral perfusion maintain by the higher BP.  In the absence of an intracranial mass lesion, controversy to treat HT Neurol Clin 2008;26:521–41

42 Hypertension  When autoregulation is impaired, common after TBI,  HT may CBF and ICP,cerebral edema,risk for post-op intracranial hemorrhage  Keep SBP mmHg Neurol Clin 2008;26:521–41

43 Hypertension  Vasodilating drugs e.g. nitroprusside, NTG, and nifedipine, can ICP and catecholamines  Sympathomimetic-blocking antiHT drugs,  β -blocking drugs ( esmolol)  α -central acting receptor agonists (clonidine) are preferred ( reduce BP without a ff ecting the ICP)  Agents with a short half-life have an advantage when BP is labile. Neurol Clin 2008;26:521–41

44 Treatment of anemia  Mechanism: CBF for maintain cerebral oxygen delivery when severe anemia.  Anemia has not been clearly shown to exacerbate ICP after TBI,  a common practice is to maintain Hb ≥ 10 g/dL. Neurol Clin 2008;26:521–41

45 Prevention of seizures  Seizure occur 15-20% in severe HI.  Seizures can CMR and ICP  In severe TBI, 50% of seizures may be subclinical and can be detected only with continuous EEG monitoring J Neurosurg 1999;91:750–60

46 Prevention of seizures  Significant risk factors for later seizures - brain contusion - subdural hematoma - depressed skull fracture - penetrating head wound - loss of consciousness or amnesia ≥1 day - age ≥ 65 years Neurol Clin 2008;26:521–41

47 Barbiturates  High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment.  Dose-dependent CBF and CMRO2  ICP by CBF and CBV  Neuroprotective effect  Hemodynamic stability is essential before and during barbiturate therapy.  Barbiturate coma: EEG shows a burst suppression pattern.

48 Barbiturate coma  Complications during treatment with barbiturate coma include - hypotension in 58%of patients - hypokalemia in 82% - respiratory complications in 76% - infections in 55% - hepatic dysfunction in 87% - renal dysfunction in 47% Acta Neurochir 1992;117:153–9

49 Propofol  recommended for the control of ICP, but not for improvement in mortality or 6 month outcome. High-dose propofol  Hypotension and propofol infusion syndrome

50 Propofol infusion syndrome Acute refractory bradycardia leading to asystole, in the presence of one or more of the following:  metabolic acidosis (base deficit > 10 mmol/l),  rhabdomyolysis,  hyperlipidaemia,  enlarged or fatty liver. propofol infusions at doses higher than 4 mg/kg/h for greater than 48 h duration

51 ICP BloodBrain Mannitol HTS Steroid CSF Drainage Drug

52 HYPEROSMOLAR THERAPY

53 Mannitol  onset 1-5 min  peak e ff ect min  Duration hrs depending on the clinical condition  Dose:Bolus g/kg  Urgent reduce ICP :initial dose of 1 g/kg  Can be repeated g/kg q 2-6 hrs. Neurol Clin 2008;26:521–41

54 Mannitol  Sosm optimal is mOsm and should ≤ 320 mOsm to avoid S/E e.g. hypovolemia, hyperosmolarity, and renal failure.  Attention to replacing fluid that is lost because of mannitol-induced diuresis, or intravascular volume depletion Neurol Clin 2008;26:521–41

55 Mannitol  Osmotic e ff ect of mannitol serum tonicity ( draws edema fluid from cerebral parenchyma) Neurol Clin 2008;26:521–41

56 Mannitol  Mannitol has rheologic ( Hct and blood viscosity ( o 2 delivery to the brain)  CSF production, lead to prolonged ICP  free radical scavenging e ff ects. Neurol Clin 2008;26:521–41

57 Loop diuretic Furosemide  Dose: mg/kg  Synergize with mannitol  Greater ICP, less brain edema, prolong elevation of plasma osmolarity  Effect from CSF formation via alter Na + transport across choroid plexus

58 Hypertonic saline  Concentration %,

59 Hypertonic saline  Osmotic force to draw water from the interstitial space of the brain parenchyma into the intravascular compartment in the presence of an intact BBB  intracranial volume and ICP.  augments volume resuscitation  circulating BV, MAP,and CPP  modulation of the inflammatory response by adhesion of leukocytes to endothelium  Effective to reduce refractory increased ICP Anesth Analg 2006;102:1836–46

60 Hypertonic saline  Adverse e ff ects - hematologic and E’lyte abnormalities  HypoNa + should be excluded before administering HTS, to reduce the risk for central pontine myelinolysis  Serum Na is maintained mmol/L in TBI.  repeated until ICP is controlled or Na 155 mmol/L  After 3–4 days of HTS therapy, boluses of furosemide to mobilize tissue Na. J Trauma 2001;50:367–83 Anesth Analg 2006;102:1836–46

61 Steroids  Common use for 1° and metastatic brain tumors  Decrease vasogenic cerebral edema.  ICH decreases in 2-5 days  The most commonly used regimen - Dexamethasone 4 mg q 6 hours IV.  Other neurosurgical disorders, such as TBI or spontaneous ICH - not have a benefit Curr Opin Oncol2004;16:593–600

62 CSF drainage  Decrease ICP immediately by reducing intracranial volume  If brain is di ff use swollen, the ventricles may collapse, limited usefulness  Special consideration - large hemispheric mass - infratentorial mass  Result in subfalcine herniation, upward trantentorial herniation Neurol Clin 2008;26: 521–41

63 Surgical interventions  Resection of mass lesions  Decompressive craniectomy - Failure of medical therapy - Persistent cerebral swelling or increase ICP - Prevent transtentorial herniation Anesthesiology Clin 2007;25:

64 Prevent secondary brain damaged  Avoid hyper or hypoglycemia  Maintain glucose level mg/dL  A relative reduction in mortality of around 30% in patients with severe HI after the introduction of protocol  Correct electrolyte imbalance  Infection control  Prevent other organs dysfunction

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