1 / 128

NEUROSURGICAL ANESTHESIA part 2

NEUROSURGICAL ANESTHESIA part 2. ma_attari@med.mui.ac.ir.

vesta
Télécharger la présentation

NEUROSURGICAL ANESTHESIA part 2

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. NEUROSURGICAL ANESTHESIA part 2 ma_attari@med.mui.ac.ir

  2. A and B, The sitting position. The patient is typically semirecumbent rather than sitting. In A, the head holder support is correctly positioned such that the head can be lowered without the need to detach the head holder first. The configuration in B, with the support attached to the thigh portion of the table, should be avoided.

  3. Venous Air Embolism The common sources of critical VAE are the major cerebral venous sinuses, in particular, the transverse, the sigmoid, and the posterior half of the sagittal sinus, all of which may be noncollapsible because of their dural attachments.

  4. Venous Air Embolism The most common situation involve tumors Most often parasagital or falcinmeningiomas and craniosynostosis. Pin sites and trappped gas can lead to VAE. The common sources of critical VAE are the major cerebral venous sinuses.

  5. Detection of Venous Air Embolism The monitors employed for the detection of VAE should provide • a high level of sensitivity, • a high level of specificity, • a rapid response, • a quantitative measure of the VAE event, • an indication of the course of recovery from the VAE event. The combination of a precordial Doppler and expired CO2 monitoring meet these criteria and are the current standard of care.

  6. Detection of Venous Air Embolism Doppler placement in a left or right parasternal location between the second and third or third and fourth ribs has a very high detection rate for gas embolization, and when good heart tones are obtained, maneuvers to confirm adequate placement seem to be unnecessary. TEE is more sensitive than precordial Doppler to VAE and offers the advantage of identifying right-to-left shunting of air.

  7. The relative sensitivity of various monitoring techniques to the occurrence of venous air embolism (VAE). BP, blood pressure; CO, cardiac output; CVP, central venous pressure; ECG, electrocardiogram, ET-CO2, end-tidal carbon dioxide; PAP, pulmonary arterial pressure; physiol, physiological; T-echo, transesophageal echo.

  8. Venous Air Embolism Rate of occurrence: • Procedure Posterior fossa • Position Sitting • Detection method Doppler precordial 40% TEE 76% In cervical spine procedure 25% Posterior Fossa, Doppler, Nonsitting 12% VAE in nonsitting Position has Smaller volume.

  9. Management Of Acute Air Embolic Events

  10. Electrocardiogram (ECG) configurations observed at various locations when a central venous catheter is used as an intravascular ECG electrode. The configurations in the figure are observed when “lead II” is monitored and the positive electrode (the leg electrode) is connected to the catheter. P indicates the sinoatrial node. The heavy black arrow indicates the P wave vector. Note the equi-biphasic P wave when the catheter tip is in the mid right atrial position. 

  11. Right Heart Catheter Essentially all patients who undergo sitting posterior fossa procedures should have a right heart catheter. Although catastrophic, life-threatening VAE is relatively uncommon, a catheter that permits immediate evacuation of an air-filled heart occasionally is the sine qua non for resuscitation.

  12. Which Vein Should Be Used for Right Heart Access? Although some surgeons may ask that neck veins not be used, a skillfully placed jugular catheter is usually acceptable.

  13. Positioning the Right Heart Catheter A multi-orificed catheter should be located with the tip 2 cm below the superior vena caval–atrial junction, and a single-orificed catheter should be located with the tip 3 cm above the superior vena caval–atrial junction.

  14. Paradoxical Air Embolism There has been much concern about the possibility of the passage of air across the interatrial septum via a patent foramen ovale (known to be present in approximately 25% of adults).

  15. Fluid Therapy The intraoperative fluid management of neurosurgical patients presents special challenges for the anesthesiologist. Neurosurgical patients often experience: • Rapid changes in intravascular volume caused by hemorrhage • The administration of potent diuretics • Or the onset of diabetes insipidus.

  16. Intravenous Fluid Management • The general principles 1.Maintenance of normovolemia 2.Avoidance of a reduction in serum osmolarity. • Half-normal salineis probably a reasonable choice for maintenance fluid • To replace blood and third-space loss: Normal saline(308 mOsm/L )and lactated Ringer's solution (273 mOsm/L)[plasma (295 mOsm/L)].

  17. Intravenous Fluid Management (cont.) • In situations: multiple trauma, aneurysm rupture, cerebral venous sinus laceration, fluid administration to support filling pressure during barbiturate coma, combination ofisotonic crystalloid and colloidmay be appropriate. (Albumin to be a reasonable choice as a colloid solution)

  18. Fluid Therapy Intracranial hypertension secondary to cerebral edema is now known to be one of the most common causes of morbidity and mortality in the intraoperative and postoperative periods.

  19. Fluid Therapy We examine: • Some of the physical determinants of water movement between the intravascular space and the central nervous system. • Specific clinical situations and make suggestions for the types and volumes of fluids to be administered.

  20. Fluid Therapy For physiologic solutions, osmolality is commonly expressed as milliosmoles (mOsm) per kilogram of solvent, whereas the units of measure for osmolarity are milliosmoles per liter of solution.

  21. Fluid Therapy Water has a tendency to move from the solution of lower osmolality, across the membrane, and into the solution of higher osmolality.

  22. All act to draw fluid from the capillaries and into the extracellular space of the tissue: • Capillary pressure • Tissue pressure (negative in nonedematous tissues) • Tissue oncotic pressure.

  23. In peripheral tissues, the only factor that serves to maintain intravascular volume is the plasma oncotic pressure, which is produced predominantly by albumin and to a lesser extent by immunoglobulins, fibrinogen, and other high-molecular-weight (HMW) plasma proteins.

  24. The clinical effects of altering one or more of the variables in the Starling equation may frequently be observed in the operating room. Many patients who have been resuscitated from hemorrhagic hypovolemia with large volumes of crystalloid solutions demonstrate pitting edema, caused by a dilution of plasma proteins.

  25. Fluid Movement between Capillaries and the Brain The brain and spinal cord are unlike most other tissues in the body in that they are isolated from the intravascular compartment by the blood-brain barrier. Morphologically, this barrier is now thought to be composed of endothelial cells that form tight junctions in the capillaries supplying the brain and spinal cord.

  26. Fluid moves in and out of the central nervous system according to the osmolar gradient (determined by relative concentrations of all osmotically active particles, including most electrolytes) between the plasma and the extracellular fluid.

  27. Administration of large volumes of iso-osmolar crystalloid results in peripheral edema caused by dilutional reduction of plasma protein content but does not increase brain water content or intracranial pressure (ICP).

  28. Osmolarity is the primary determinant of water movement across the intact blood-brain barrier. The administration of excess free water (either iatrogenically or as a result of psychogenic polydipsia) can result in an increased ICP and an edematous brain.

  29. Hyperosmolar solutions are used daily in operating rooms throughout the world as standard therapeutic agents to treat intracranial hypertension.

  30. What occurs when the brain is injured with disruption of the barrier?

  31. In patients at risk for intracranial hypertension. The infusion of colloids is often recommended to maintain intravascular volume in such patients, implying that maintaining or increasing plasma oncotic pressure reduces cerebral edema.

  32. In the case of the intact blood-brain barrier, neither theoretical nor experimental evidence suggests that colloids are more beneficial than crystalloids for either brain water content or ICP.

  33. SOLUTIONS FOR INTRAVENOUS USE These fluids may be categorized conveniently on the basis of: • Osmolality • Oncotic pressure • Dextrose content.

  34. Osmolarity of Commonly Used Intravenous Fluids

  35. The term colloid denotes solutions that have an oncotic pressure similar to that of plasma. Some commonly administered colloids are: • 6% hetastarch (Hespan) • 5% and 25% albumin • The dextrans (40 and 70) • Plasma

  36. Dextran and hetastarch are dissolved in normal saline, so the osmolarity of the solution is approximately 290 to 310 mOsm/L with a sodium and chloride ion content of about 145 mEq/L.

  37. Hyperosmolar Solutions Although an acute beneficial effect has been demonstrated, the longer-term (24-48 hours) effect of such hyperosmotic fluid therapy remains unknown.

  38. Acute increases to values that exceed 170 mEq/L sodium are likely to result in a depressed level of consciousness or seizures.

  39. 30 mL of 23.4% saline brought prompt and sustained decreases in ICP.

  40. Despite these impressive results, it is unclear why hypertonic saline should be more effective than mannitol.

  41. In clinical studies, hyperglycemia has been associated with worsened neurologic outcome after traumatic brain injury (glucose > 200 mg/dL), acute ischemic stroke, and subarachnoid hemorrhage.

More Related