Ebook Solving critical consults: Part 2
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Ebook Solving critical consults: Part 2
6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2after cardiopulmonary resuscitation (CPR) and adequate resumption of spontaneous circulation. This is also one of the most difficult tasks. Cynics may argue that the neurologist may not be needed to assess the prognosis of a comatose patient one or two days after CPR—the patient’s chances for good r Ebook Solving critical consults: Part 2ecovery are poor. Unfortunately there is a misconception that is all there is to it. Hie rate of mortality and poor outcome in most recent studies ofEbook Solving critical consults: Part 2
surviving comatose patients after CPR however has remained at about 50%.4142 The key to successful outcome is having a bystander who not only is able 6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2eterization suite, and patients may benefit from urgent revascularization.For the neurologist seeing a patient for the first time, five main questions (as well as subsidiary questions) should be asked: (1) Is there any possibility that cardiac arrest was a consequence of an acute catastrophic intrac Ebook Solving critical consults: Part 2ranial hemorrhage, and what did the computed tomography (CT) scan of the brain show? (2) what is the patient’s cardiac reserve, and how advanced is cuEbook Solving critical consults: Part 2
rrent support? (3) when was hypothermia started, and what supportive medication and in what dose is being used? (4) Is there evidence of liver or kidn6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2eizures?Over the last decade, the practice of neurologic assessment of patients with acute severe brain injury after cardiac standstill has become more complicated as a result of cooling, the use of additional sedation and neuromuscular junction blockers, and especially the introduction of extracorp Ebook Solving critical consults: Part 2oreal membrane oxygenation (ECN4O).27-28-32 With all that noise and confounding, the hands of the neurologist may be tied, and they may just have to dEbook Solving critical consults: Part 2
eliberatively wait.78 SOLVING CRITICAL CONSULTSThis chapter provides three pieces of crucial information. First, current practices of targeted tempera6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2een used to set this procedure apart from accidental hypothermia or hypothermia associated with medical or neurologic disease. Now a new term Targeted Temperature Management seems to take hold. Cooling of unresponsive resuscitated patients has been considered the standard of care for patients with c Ebook Solving critical consults: Part 2ardiac arrest due to a shockable rhythm.45"17'61 Cooling of patients has also been recommended by specifically created councils and guideline committeEbook Solving critical consults: Part 2
es of US and European professional organizations.12 Hypothermia with various temperatures is likely effective through abating oxidative stress and red6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2 targeted temperature management, aiming at fever control or far more moderate hypothermia at 36°c. Second, this chapter concentrates on the more severely affected patient, one who has required extracorporeal support. Third, the tools of prognostication in comatose patients after CPR are reiterated Ebook Solving critical consults: Part 2here, but a more detailed discussion can be found in another volume of this series (Communicating Prognosis).Often, the pendulum has shifted toward thEbook Solving critical consults: Part 2
e more severely injured patient, who has a much lower probability of a good outcome, but one may still need to identify patients who have a fighting c6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2ents are given a fair chance and that withdrawal does not occur as a result of too-quick decision making or faulty perception.Predictors of poor neurologic outcome (with and without hypothermia) have been systematically reviewed. The guidelines recommended in 2006 by the American Academy of Neurolog Ebook Solving critical consults: Part 2y63 (discussed in greater detail later) remain valid after additional review of studies, emphasizing the reliability of myoclonus status epilepticus,Ebook Solving critical consults: Part 2
fixed pupils, and bilateral absence of N20 cortical responses on somatosensory evoked potentials (SSEP) for poor prognosis in most instances. The crit6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2 is more often seen in patients with the absence of several brainstem reflexes.53 After therapeutic hypothermia (33’C), one study found that only N20 cortical absence on SSEP, a nonreactive EEG after rewarming, absent oculocephalic responses, and extensor motor responses or worse were predictors wit Ebook Solving critical consults: Part 2h sufficient reliability.54To the reader it will become rapidly clear that studies on prognosis vary because patients vary and the neurologic acumen oEbook Solving critical consults: Part 2
f the assessing specialist may vary. The assessment and management of comatose patients after return of spontaneous circulation is a major clinical an6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2t core principle is to have an understanding of the limits of CPR. Cardiac arrest is the most profound injury to the brain, even worse than traumatic brain injury orPost-Cardiac Arrest Support and the Brain 79 central nervous system infection. If there is no global arterial supply to neurons, the br Ebook Solving critical consults: Part 2ain oxygen tension in brain tissue will decline in just a few minutes.3 This leads to dysfunction of cell membrane ion pumps and then to a rapid unravEbook Solving critical consults: Part 2
eling of the cellular machinery, resulting in opening of calcium channels and release of excitatory amino acids eventually, calcium overload and cellu6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2to reperfusion. There are many areas that are not reperfused (the no-flow phenomenon) as a result of endothelial edema due to ischemia, blood sludging, early intervascular coagulation, and leukocyte adhesion (Figure 6.1).714-34-36 In fact it may be more complex and because of the potent vasoparalysi Ebook Solving critical consults: Part 2s, a period of hyperperfusion followed by hypoperfusion may occur, resulting in a marked reduction of cerebral blood flow.24The cytopathology of ischeEbook Solving critical consults: Part 2
mia is impressive with nuclear hyperchromasia, nuclear pyknosis, cytoplasmic eosinophilia, cytoplasmic shrinkage, cytoplasmic microvacuolation, and ce6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2oration of circulation starts with manual compression, but this produces only a fraction (5%) of the normal cerebral blood flow. AngiographicCardiac arrestCerebral blood flow-zeroApoptosis H No reflow ■ ExcitotoxicityFigure 6.1 Mechanism of anoxic-ischemic injury to the brain.&3SOLVING CRITICAL CONS Ebook Solving critical consults: Part 2ULTSand echocardiographic studies have shown that chest compression sets in motion an increase in intrathoracic pressure that causes blood to flow froEbook Solving critical consults: Part 2
m the lung passively through rhe left side of the heart. The question of whether mechanical devices produce a better result was studied in the LUCAS i6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2n with defibrillation during ongoing compressions, did not improve survival or neurologic outcome when compared with manual CPR, although cerebral blood flow does seem significantly better with automated devices than with manual compression. Again, despite demonstrably better cortical cerebral blood Ebook Solving critical consults: Part 2 flow in animal experiments, (Figure 6.2) the sad reality is that this does not translate to improvement in outcome. This device (and others) providesEbook Solving critical consults: Part 2
a positive intrathoracic pressure with chest compression, which causes a recoil—an important step that secures cardiac preload (this recoil is less c6Post-Cardiac Arrest Support and the BrainA frequent reason for a neurology consult in the intensive care unit (ICƯ) is to assess a comatose patient a Ebook Solving critical consults: Part 2injury, rib fracture, cardiac rupture, and esophageal rupture, but not as much as with manual resuscitation.59The second core principle is that hypothermia may be the only effective therapy in patients who remain unresponsive after CPR. Targeted hypothermia does protect the brain but there is no evi Ebook Solving critical consults: Part 2dence that hypothermia after percutaneous coronary intervention reduces myocardial infarct size.23 Therapeutic hypothermia protocols have been developEbook Solving critical consults: Part 2
ed and differ little from institution to institution. Generally speaking, there is an induction phase that provides temperature controlFigure 6.2 CortGọi ngay
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