Stroke & Neurovascular Center of New Jersey. Jawad F. Kirmani, MD Director, Stroke and Neurovascular Center
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1 Stroke & Neurovascular Center of New Jersey Jawad F. Kirmani, MD Director, Stroke and Neurovascular Center
2 Past, present and future
3 Past, present and future Cerebral Blood Flow
4 Past, present and future Cerebral Blood Flow ICP monitoring
5 Past, present and future Cerebral Blood Flow ICP monitoring Cerebral oxygen monitoring
6 Past, present and future Cerebral Blood Flow ICP monitoring Cerebral oxygen monitoring Cerebral Metabolism
7 Past, present and future Cerebral Blood Flow ICP monitoring Cerebral oxygen monitoring Cerebral Metabolism
8 1940 s:polio Epidemic
9 Iron Lung Wards
10 Neurologists were making decisions regarding mechanical ventilation and various aspects of management of polio patients with respiratory failure.
11 Manual inflation of lungs
12 Manual inflation of lungs Prototype lung inflation device (Boston).
13 Manual inflation of lungs Prototype lung inflation device (Boston). Invention of PPV= Birth of Intensive care unit.
14 Generally applied for patient with respiratory failure in general medical and surgical ICUs.
15 Generally applied for patient with respiratory failure in general medical and surgical ICUs. Neurological patients with coma were often seen as non salvageable.
16 Generally applied for patient with respiratory failure in general medical and surgical ICUs. Neurological patients with coma were often seen as non salvageable. Neurologists gradually withdrew from critical care.
17 Focused exclusively on the care of postoperative patients. Monitoring = neuro checks to detect clinical deterioration as soon as possible
18 Often does not reveal changes in cerebral function until they are irreversible.
19 Our understanding about pathophysiology of outcome from severe TBI improves.
20 Primary Insult Local Immediate Cell bodies Axons Blood vessels Delayed Free radicals Ca+ influx K+ efflux
21 Primary Insult Local Immediate Cell bodies Axons Blood vessels Delayed Free radicals Ca+ influx K+ efflux Hematoma Inflammation Edema Ischemia Increased ICP
22 Primary Insult Local Systemic Stunned Myocardium Immediate Delayed Autonomic dysfunction Cell bodies Free radicals Hypovolumia Axons Ca+ influx Acute lung injury Blood vessels K+ efflux Hematoma Inflammation Edema Ischemia Increased ICP
23 Primary Insult Local Systemic Stunned Myocardium Immediate Delayed Autonomic dysfunction Cell bodies Free radicals Hypovolumia Axons Ca+ influx Acute lung injury Blood vessels K+ efflux Hematoma Inflammation Edema Ischemia Increased ICP Hypoxia Hypotension Hyperthermia Hyperglycemia Acidosis
24 ICP monitoring became more widespread
25 ICP monitoring became more widespread Advanced neuroimaging - Detection of structural lesion, mass effect, shift - CBF measurement with Xe-CT/PET scans
26 Transportation Expertise Static nature
27 Continuous and real time rather than static information. - Brain tissue O2 tension - Neurochemical analysis (microdialysis) - Continuous EEG monitoring - Ultrasound
28 Traditional Alarm the clinician when clinical deterioration has occurred. Reacting to harmful pyhysiologic events
29 Traditional Alarm the clinician when clinical deterioration has occurred. Reacting to harmful pyhysiologic events Multimodality Real time physiologic end points to detect secondary injury in its earliest phase Prevent harmful physiologic events altogether.
30 Past, present and future Cerebral Blood Flow ICP monitoring Cerebral oxygen monitoring Cerebral Metabolism
31 O2 contents of blood=1.34 x Hbx SaO2
32 O2 contents of blood=1.34 x Hbx SaO2 O2 delivery to any tissue=o2 contents x C.O.(flow)
33 Adequate oxygenation requires adequate flow.
34 Adequate oxygenation requires adequate flow. Normal CBF=50ml/100gm/min (20% of total C.O.)
35 Adequate oxygenation requires adequate flow. Normal CBF=50ml/100gm/min (20% of total C.O.) Amount + Duration
36 Adequate oxygenation requires adequate flow. Normal CBF=50ml/100gm/min (20% of total C.O.) Amount + Duration Ischemia=Low CBF Infarction=Neuronal death
37 CPP is driving force of CBF
38 CPP is driving force of CBF CBF = CPP/CVR
39 CBF = CPP/CVR
40
41
42 If volume of one compartment increases, other compartment must decrease, otherwise ICP will increase.
43
44 Compensatory Mechanisms Shift of CSF into spinal compartment. Reduction CBV
45 Compliance
46 Compliance
47 Kety-Schimdt Technique Thermodilution Xenon-CT SPECT/PET Perfusion Weighted MRI
48 Laser Flowmetry Thermal Diffusion (Bowman s Perfusion Monitor)
49
50
51
52
53 Past, present and future Cerebral Blood Flow ICP monitoring Cerebral oxygen monitoring Cerebral Metabolism
54 Headache, nausea, and vomiting, are impossible to elicit in comatose patients. Papilloedema is unreliable marker in acute settings. (Selhorst JB et al: Papilledema after acute head injury. Neurosurgery 1985;16: )
55 Headache, nausea, and vomiting, are impossible to elicit in comatose patients. Papilloedema is unreliable marker in acute settings. (Selhorst JB et al: Papilledema after acute head injury. Neurosurgery 1985;16: ) Pupillary dilatation and decerebrate posturing, can occur in the absence of intracranial hypertension.
56 Signs of brain swelling, such as midline shift and compressed basal cisterns, are predictive of raised ICP, but intracranial hypertension can occur without these findings. (Kishore PRS et al AJNR Am J Neuroradiol 1981;2: )
57 GCS of < 8 and Abnormal CT Scan OR
58 GCS of < 8 and Abnormal CT Scan GCS of < 8 and Normal CT Scan and One of following OR
59 GCS of < 8 and Abnormal CT Scan GCS of < 8 and Normal CT Scan and One of following 1) Age > 40 yrs. 2) Motor posturing 3) SBP < 90 mm Hg OR
60 ICP elevations after SAH result from - CSF outflow obstruction and. - Cerebral edema. (Rordorf G., Acta Neurochir (Wien) 139. (12): ;)
61 ICP control is essential before treatment of the aneurysm and is associated with more favorable outcome by - protection against cortical injury and - facilitation of surgical exposure of the aneurysm. (Rordorf G., Acta Neurochir (Wien) 139. (12): ;)
62 Microtransducers (Subdural/Epidural/Parenchymal) Intraventricular drains
63 Advantages Disadvantages Microtranducers Low infection rate Low risk of hemorrhage Considerable zero drift Cannot be rezeroed after insertion
64 Advantages Disadvantages Microtranducers Low infection rate Low risk of hemorrhage Conciderable zero drift Cannot be rezeroed after insertion Intraventricular Catheters More accurate Allow ICP control by CSF drainage Re-zeroed externally Higher complication rate
65
66 Risk of infection = 10%, which increase with longer duration of monitoring (Czosnyka M., Neurol Neurosurg Psychiatry 75. (6): ;)
67 Antibiotic coating of intraventricular drains may prevent or delay the onset of ventriculitis (Hamilton A.J Neurosurgery 40. (5): ;)
68
69
70 Plateau A Wave
71 Past, present and future Cerebral Hemodynamics ICP monitoring Cerebral oxygen monitoring Cerebral Metabolism
72 D Jugular Venous Oxygen saturation (SjvO2) Brain Tissue Oxygen Pressure (PBO2)
73 Retrograde placement of a catheter equipped with an oximeter. Dominant internal jugular vein Positioned in bulb
74 Indications Severe TBI with GCS < 8. High grade aneurysmal SAH. During neurosurgical procedures.
75 Absolute value in percentage. A-V difference in O2 supply. Hb x SaO2 x 1.34 Hb x SvO2 x 1.34
76 AVDO2 = CMRO2/CBF
77 Adequacy of balance between supply (Cerebral O2 delivery) & demand (Cerebral metabolic rate)
78 Real-time monitoring in NCCU can give immediate insight in the physiologic and metabolic state of brain regions at risk for ischemia and injury. NCCU enhances the potential of early effective interventions to reverse pathologic states in stroke patients.
79
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