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| {{SI}} | | __NOTOC__ |
| | {{Anoxic brain injury}} |
| | '''For patient information, click [[Anoxic brain injury (patient information)|here]]''' |
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| {{CMG}} | | {{CMG}}; '''Associate Editors-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S. |
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| '''Associate Editors-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.
| | {{SK}} Hypoxic brain injury; post cardiac arrest syndrome |
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| '''Synonyms and keywords:''' Hypoxic brain injury, post cardiac arrest syndrome
| | ==[[Anoxic brain injury overview|Overview]]== |
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| ==Overview== | | ==[[Anoxic brain injury pathophysiology|Pathophysiology]]== |
| '''Post-cardiac arrest:''' is defined as absence of pulses requiring chest compressions, regardless of location or presenting rhythm.
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| '''Post-cardiac arrest syndrome:''' is characterized by resumption of spontaneous systemic circulation after prolonged [[ischemia]] of whole body.<ref> Neumar RW, Nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark RSB, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT Jr, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Vanden Hoek T. Post– cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication: a consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation. 2008;118 DOI:10.1161/ CirculationAHA.108.190652 Published online on 27.10.2008 </ref> Anoxic or hypoxic brain injury is often seen after [[cardiac arrest]] as part of the post-cardiac arrest syndrome. Major efforts are underway to improve "The Chain of Survival" based upon early access to medical care, early defibrillation, early [[CPR]] and early hospital care. Therapeutic [[hypothermia]] may improve outcomes. Steroids, [[manitol]], [[diuresis]] and [[hyperventilation]] have not been documented to meaningfully improve clinical outcomes.
| | ==[[Anoxic brain injury causes|Causes]]== |
| | ==[[Anoxic brain injury differential diagnosis|Differentiating Anoxic brain injury from other Diseases]]== |
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| ==Epidemiology== | | ==[[Anoxic brain injury epidemiology and demographics|Epidemiology and Demographics]]== |
| In a 1990s study from the UK, resuscitation for cardiac arrest was attempted in 10,081 patients. Of these only 1476 (14.6%) survived to be admitted to the hospital <ref name="pmid15333549">{{cite journal |author=Lyon RM, Cobbe SM, Bradley JM, Grubb NR |title=Surviving out of hospital cardiac arrest at home: a postcode lottery? |journal=Emerg Med J |volume=21 |issue=5 |pages=619–24 |year=2004 |month=September |pmid=15333549 |pmc=1726412 |doi=10.1136/emj.2003.010363 |url=}}</ref><ref name="pmid8664715">{{cite journal |author=Cobbe SM, Dalziel K, Ford I, Marsden AK |title=Survival of 1476 patients initially resuscitated from out of hospital cardiac arrest |journal=BMJ |volume=312 |issue=7047 |pages=1633–7 |year=1996 |month=June |pmid=8664715 |pmc=2351362 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=8664715}}</ref>. Of these small number of patients who survived to admission, 59.3% died during that admission, half of these within the first 24 hours. 46.1% survived to hospital discharge (this is 6.75% of those who had been resuscitated by ambulance staff). Of those who were successfully discharged from hospital, 70% were still alive 4 years after their discharge.
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| In a review of 68 studies through 1997, the incidence of survival to discharge was higher at 14% with a wide range of 0-28%.<ref name="pmid9167565">{{cite journal |author=Ballew KA |title=Cardiopulmonary resuscitation |journal=BMJ |volume=314 |issue=7092 |pages=1462–5 |year=1997 |month=May |pmid=9167565 |pmc=2126720 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=9167565}}</ref>
| | ==[[Anoxic brain injury natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| ==Pathophysiology== | | ==Diagnosis== |
| The underlying mechanism of post cardiac arrest syndrome is a combination of: <ref>Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med. Sep 10 2001; 161(16): 2007-2012.</ref> <ref>van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. New England Journal of Medicine. Nov 8 2001;345(19): 1359-1367.</ref> <ref>Van den Berghe G, Wouters PJ, Bouillon R, et al. Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control. Crit Care Med. Feb 2003;31(2):359-366.</ref> <ref>Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288(7):862-871.</ref> <ref>Zandbergen EG, de Haan RJ, Stoutenbeek CP, et al. Systematic review of early prediction of poor outcome in anoxic-ischaemic coma. Lancet. Dec 5 1998; 352(9143): 1808-1812.</ref> <ref>Rello J. Risk factors for developing pneumonia within 48 hours of intubation. Am J Respir Crit Care Med. 1999;159:1742-1746.</ref> <ref>Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. New England Journal of Medicine. Jun 5 1997;336(23):1629-1633.</ref> <ref>Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease after cardiac arrest: a sepsis-like syndrome? Curr Opin Crit Care. Jun 2004;10(3):208-212.</ref> <ref>Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine. 2001;345(19):1368-1377.</ref> <ref>Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of hospital cardiac arrest with induced hypothermia. New England Journal of Medicine. Feb 21 2002;346(8):557-563.</ref> <ref>Hypothermia after Cardiac Arrest Study G. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. Erratum appears in N Engl J Med 2002 May 30;346(22):1756]. New England Journal of Medicine. Feb 21 2002;346(8):549-556.</ref>
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| * '''Systemic response to ischemia and reperfusion'''
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| :* Circulatory [[collapse]]
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| :* [[Hyperglycemia]]
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| :* [[Hypotension]]
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| :* [[Infection]]s
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| :* Multiorgan failure
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| :* Ongoing tissue [[hypoxia]] / [[ischemia]]
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| :* [[Fever]]
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| * '''Myocardial dysfunction'''
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| :* Circulatory [[collapse]]
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| :* [[Dysrhythmia]]s
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| :* [[Hypotension]]
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| :* Reduced [[cardiac output]]
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| * '''[[Brain injury]]'''
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| :* [[Brain death]]
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| :* Cognitive dysfunction
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| :* [[Coma]]
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| :* Cortical [[stroke]]
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| :* [[Myoclonus]]
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| :* Persistent vegetative state
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| :* Secondary [[parkinsonism]]
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| :* [[Seizure]]s
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| :* Spinal [[stroke]]
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| * '''Effects of persistent precipitating pathologies'''
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| :* Cardiovascular disease ([[Acute coronary syndromes]], [[cardiomyopathy]])
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| :* [[Chronic obstructive pulmonary disease]]
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| :* Central nervous system diseases (e.g. [[cerebrovascular accident]])
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| :* Thromboembolic disorders (e.g. [[pulmonary emboli]])
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| :* Drug / substance overdose, [[poisoning]]
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| :* [[Infection]]s ([[sepsis]], [[pneumonia]])
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| :* Volume loss ([[Hypovolemia]]: e.g. [[hemorrhage]], [[dehydration]])
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| ==Natural History==
| | [[Anoxic brain injury history and symptoms|History and Symptoms]] | [[Anoxic brain injury physical examination|Physical Examination]] | [[Anoxic brain injury laboratory findings|Laboratory Findings]] | [[Anoxic brain injury CT|CT]] | [[Anoxic brain injury MRI|MRI]] | [[Anoxic brain injury echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Anoxic brain injury electroencephalogram|Electroencephalogram]] | [[Anoxic brain injury other diagnostic studies|Other Diagnostic Studies]] |
| Patients with anoxic injury due to cardiac arrest are at risk of death from a variety of causes including recurrent [[sudden cardiac death]], [[congestive heart failure]], [[pneumonia]], [[sepsis]] from a variety of sources and [[pulmonary embolism]].
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| ==Signs and Symptoms==
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| Serial neurologic examinations are critical in the assessment of long term prognosis.
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| ===Assessment of the Brain Stem===
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| The brainstem is more resistant to hypoperfusion that the cerebral cortex, and if the brainstem does not recover, the cerebral cortex is not likely to recover. The presence of brain stem reflexes is therefore critical to recovery. Preservation of brainstem function is indicated by the presence of blinking, coughing, gagging, sneezing, and yawning.
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| ====Pupillary Size====
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| The presence of peristently dilated pupils is a poor prognostic sign <ref>Steen-Hansen JE, Hansen NN, Vaagenes P, Schreiner B: Pupil size and light reactivity during cardiopulmonary resuscitation. A clinical study. Crit Care Med 1988;16:69-70.</ref>. It should be noted that both [[catecholamines]] and [[atropine]], can affect pupillary size, and confound the assessment of pupillary size.
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| ==Laboratory Studies==
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| (In alphabetical order)<ref> Neumar RW, Nolan JP, Adrie C, Aibiki M, Berg RA, Böttiger BW, Callaway C, Clark RSB, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT Jr, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Vanden Hoek T. Post– cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication: a consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation. 2008;118 DOI:10.1161/ CirculationAHA.108.190652 Published online on 27.10.2008 </ref> <ref>Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, Reinhart K, Angus DC, Brun-Buisson C, Beale R, Calandra T, Dhainaut JF, Gerlach H, Harvey M, Marini JJ, Marshall J, Ranieri M, Ramsay G, Sevransky J, Thompson BT, Townsend S, Vender JS, Zimmerman JL, Vincent JL; International Surviving Sepsis Campaign Guidelines Committee; American Association of Critical-Care Nurses; American College of Chest Physicians; American College of Emergency Physicians; Canadian Critical Care Society; European Society of Clinical Microbiology and Infectious Diseases; European Society of Intensive Care Medicine; European Respiratory Society; International Sepsis Forum; Japanese Association for Acute Medicine; Japanese Society of Intensive Care Medicine; Society of Critical Care Medicine; Society of Hospital Medicine; Surgical Infection Society; World Federation of Societies of Intensive and Critical Care Medicine. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008 [published correction appears in Crit Care Med. 2008;36: 1394–1396]. Crit Care Med. 2008;36:296 –327.</ref> <ref>Gazmuri RJ, Nolan JP, Nadkarni VM, Arntz HR, Billi JE, Bossaert L, Deakin CD, Finn J, Hammill WW, Handley AJ, Hazinski MF, Hickey RW, Jacobs I, Jauch EC, Kloeck WG, Mattes MH, Montgomery WH, Morley P, Morrison LJ, Nichol G, O’Connor RE, Perlman J, Richmond S, Sayre M, Shuster M, Timerman S, Weil MH, Weisfeldt ML, Zaritsky A, Zideman DA. Scientific knowledge gaps and clinical research priorities for cardiopulmonary resuscitation and emergency cardiovascular care identified during the 2005 International Consensus Conference on ECC and CPR Science with Treatment Recommendations: a consensus statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Stroke Council; and the Cardiovascular Nursing Council. Resuscitation. 2007;75:400–411.</ref>
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| * [[Arterial blood gas]]es
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| * [[Blood glucose]]. Elevated blood glucose is associated with a poorer prognosis.
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| * [[Cardiac output]] monitoring with noninvasive methods or [[pulmonary artery]] catheter
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| * [[Chest x-ray]] to evaluate for aspiration pneumonia
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| * [[Complete blood count]]
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| * Continuous [[ECG]] monitoring to prompltly shock any recurrent arrhythmia.
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| * [[Echocardiography]] to evaluate LV function and assess for the presence of [[hypertrophic obstructive cardiomyopathy]] ([[HOCM]])
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| * [[EEG]] for early [[seizure]] detection and treatment
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| * [[Electrolytes]] to reat [[hyopkalemia]] and [[hypomagnesemia]]
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| * [[Cardiac enzymes]] to assess MI size
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| * [[Oxygen saturation]] by [[pulse oximetry]]
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| * Placement of an arterial catheter
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| * ScvO2
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| * Serum [[lactate]]
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| * Temperature
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| * Urine output
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| ===The Electroencephalogram (EEG)===
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| Most often the EEGs of patients in coma after cardiac arrest shows diffuse slowing of both the theta and delta waves, and periodic epileptiform firing. Severe slowing or a flat line appearance is associated with a poor prognosis.
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| ===Evoked-Response Testing===
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| If there is absence of bilateral [[somatosensory evoked potentials]], then it is unlikely that the patient will survive.<ref>Chen R, Bolton CF, Young B: Prediction of outcome in patients with anoxic coma: A clinical and electrophysiological study. Crit Care Med 1996;24:672-678.</ref><ref>Kaplan PW: Electrophysiological prognostication and brain injury from cardiac arrest. Semin Neurol 2006;26:403-412.</ref><ref>Young GB, Doig G, Ragazzoni A: Anoxic-ischemic encephalopathy: Clinical and electrophysiological associations with outcome. Neurocrit Care 2005;2:159-164.</ref> In particular, if there is no N20 response, there is a very highly likelihood of a vegetative state or death, with only 1 patient of 21 surviving in one study compared with survival in 11 of 26 patients surviving if the N20 response was positive.<ref>Young GB, Doig G, Ragazzoni A: Anoxic-ischemic encephalopathy: Clinical and electrophysiological associations with outcome. Neurocrit Care 2005;2:159-164.</ref>
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| ===Imaging Findings===
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| In the early hours and days after anoxic brain injury, there is often diffuse [[cerebral edema]] and blurring of the border between the grey and white matter. In some patients there may be discrete infarcts after a few days.
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| If there is irreversible bilateral medial tegmental [[brainstem]] injury, then patients do not survive.
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| ===Diagnosis of Brain Death===
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| If there is no longer brain activity, and there is 0% chance of the recovery of the patient, a patient is declared "Brain Dead". Brain death is diagnosed when all four of the following criteria are met:<ref>Ad Hoc Committee of the Harvard Medical School: A defi nition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical
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| School to examine the defi nition of brain death. JAMA 1968;205:337-340.</ref><ref>Walker A: An appraisal of the criteria of cerebral death. JAMA 1977;237:982-986.</ref><ref>Shemie SD, Pollack MM, Morioka M, Bonner S: Diagnosis of brain death in children. Lancet Neurol 2007;6:87-92.</ref>
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| 1. There is coma with a loss of cerebral reactivity.
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| 2. There is absence of spontaneous respiration.
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| 3. There is a loss of [[brainstem reflexes]] (pupillary, corneal, oculovestibular, and oculocephalic). In some definitions this is qualified by a requirement that the loss of reflexes exceeds 24 hours in duration.
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| 4. There is no activity on the electroencephalogram ("electrocerebral silence", a "flat electroencephalogram") for > than 12 hours. This last criteria requires that the patient is not hypothermic or on sedative drugs. In some definitions > 24 hours is required.
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| ==Treatment== | | ==Treatment== |
| ===Therapeutic Hypothermia (TMH) ===
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| Hypothermia has been associated with a reduction in ischemic brain injury in animal models <ref name="pmid8370299">{{cite journal | author = Kuboyama K, Safar P, Radovsky A, Tisherman SA, Stezoski SW, Alexander H | title = Delay in cooling negates the beneficial effect of mild resuscitative cerebral hypothermia after cardiac arrest in dogs: a prospective, randomized study | journal = [[Crit. Care Med.]] | volume = 21 | issue = 9 | pages = 1348–58 | year = 1993 | month = September | pmid = 8370299 | doi = | url = | issn = | accessdate = 2011-03-02}}</ref><ref name="pmid1389956">{{cite journal | author = Ginsberg MD, Sternau LL, Globus MY, Dietrich WD, Busto R | title = Therapeutic modulation of brain temperature: relevance to ischemic brain injury | journal = [[Cerebrovasc Brain Metab Rev]] | volume = 4 | issue = 3 | pages = 189–225 | year = 1992 | pmid = 1389956 | doi = | url = | issn = | accessdate = 2011-03-02}}</ref><ref name="pmid1412583">{{cite journal | author = Weinrauch V, Safar P, Tisherman S, Kuboyama K, Radovsky A | title = Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs | journal = [[Stroke]] | volume = 23 | issue = 10 | pages = 1454–62 | year = 1992 | month = October | pmid = 1412583 | doi = | url = http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=1412583 | issn = | accessdate = 2011-03-02}}</ref>.
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| While patients with a shockable rhythm such as [[VT]]/[[VF]] derive significant benefits from therapeautic hypothermia, patients with non-shockable rhythms such as [[PEA]] and [[asystole]] may not derive the same benefits<ref name="pmid21321156">{{cite journal | author = Dumas F, Grimaldi D, Zuber B, Fichet J, Charpentier J, Pène F, Vivien B, Varenne O, Carli P, Jouven X, Empana JP, Cariou A | title = Is Hypothermia After Cardiac Arrest Effective in Both Shockable and Nonshockable Patients?: Insights From a Large Registry | journal = Circulation | volume = | issue = | pages = | year = 2011 | month = February | pmid = 21321156 | doi = 10.1161/CIRCULATIONAHA.110.987347 | url = | issn = | accessdate = 2011-03-01}}</ref>. While 39% (274/708) of patients with VT/VF treated with TMH achieved an acceptable level of neurologic outcome (cerebral performance categories level 1 or 2) at discharge, only 16% (68/437) of patients with PEA/asystole treated with TMH achieved an acceptable outcome. In multivariate analyses, TMH was associated with increased odds of an acceptable neurological outcome (multivariate odds ratio = 1.90) in patients with VT/VF, while in contrast TMH was not associated with acceptable neurological outcome (multivariate odds ratio = 0.71) in patients with PEA/asystole.
| | [[Anoxic brain injury medical therapy|Medical Therapy]] | [[Anoxic brain injury surgery|Surgery]] | [[Anoxic brain injury cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Anoxic brain injury future or investigational therapies|Future or Investigational Therapies]] |
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| ==Prognosis== | | ==Case Studies== |
| ===Predictors of Survival===
| | [[Anoxic brain injury case study one|Case #1]] |
| ====Improved Prognosis with In-Hospital versus Out-of-Hospital Cardiac Arrest====
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| Out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% survival at discharge) than in-hospital cardiac arrest (15% survival at discharge).
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| ====Improved Prognosis with VT/VF versus PEA or Asystole==== | | ==Related Chapters== |
| A major determining factor in survival is the initially documented electrocardiographic rhythm. Patients with [[ventricular fibrilation]] ([[VF]]) or [[ventricual tachycardia]] ([[VT]]) (aka VT/VF) have a 10-15 fold greater chance of survival than patients with [[pulseless electrical activity]] ([[PEA]]) or [[asystole]]. VT and VF are responsive to [[defibrillation]], whereas asystole and PEA are not.
| | *[[Sudden cardiac death]] |
| | *[[Therapeutic hypothermia]] |
| | *[[Post cardiac arrest syndrome care pathway]] |
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| ====Rapid Defibrillation is Associated with Imporved Survival====
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| Rapid intervention with a [[defibrillator]] increases survival rates.<ref>{{cite journal |author=Eisenberg MS, Mengert TJ |title=Cardiac resuscitation |journal=N. Engl. J. Med. |volume=344 |issue=17 |pages=1304–13 |year=2001 |month=April |pmid=11320390 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11320390&promo=ONFLNS19}}</ref><ref name="pmid12826637">{{cite journal |author=Bunch TJ, White RD, Gersh BJ, ''et al'' |title=Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation |journal=N. Engl. J. Med. |volume=348 |issue=26 |pages=2626–33 |year=2003 |month=June |pmid=12826637 |doi=10.1056/NEJMoa023053 |url=}}</ref>
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| | | [[CME Category::Cardiology]] |
| ===Incidence and Predictors of Entering Into a Vegetative State versus Making a Full Neurologic Recovery===
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| Cardiac arrest is the third leading cause of [[coma]]. Approximately 80% of patients who suffered a cardiac arrest who survived to be admitted to the hospital will be in coma for varying lengths of time. Of these patients, approximately 40% will enter into a persistent vegetative state and 80% die within 1 year. In contrast, those rare patients who survive until discharge without significant neurological impairment can expect a fair to good quality of life.
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| The duration of hypoxia/ischemia determines the extent of neuronal injury i.e. in patients who suffer hypoxia for less than 5 minutes, are less likely to have permanent neurologic deficits, while with prolonged, global hypoxia, patients may develop [[myoclonus]] or a persistent [[vegetative state]].<ref name="pmid16363390">{{cite journal |author=Mellion ML |title=Neurologic consequences of cardiac arrest and preventive strategies |journal=[[Medicine and Health, Rhode Island]] |volume=88 |issue=11 |pages=382–5 |year=2005 |month=November |pmid=16363390 |doi= |url=}}</ref>
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| The duration of coma is an important predictor of the recovery of neurologic function. In a 1979 study of 181 cardiac arrest patients who survived to hospital admission, 84% were comatose for more than 1 hour and 56% were comatose for more than 24 hours<ref name="pmid442945">{{cite journal |author=Thomassen A, Wernberg M |title=Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units |journal=[[Acta Anaesthesiologica Scandinavica]] |volume=23 |issue=2 |pages=143–8 |year=1979 |month=April |pmid=442945 |doi= |url=}}</ref>. There was minimal neurologic deficit if coma lasted less than 24 hours. However, among the 85 patients who were comatose for more than 24 hours, only 7 of them were discharged alive. The severity of neurological impairment increased with increased duration of coma. Of the patients who were in coma for more than 7 days, none regained consciousness. It should be noted that 80 patients died in a coma.
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| A [http://jama.ama-assn.org/content/253/10/1420.full.pdf+html JAMA article] in 1985 attempted to identify the multivariate predictors neurologic prognosis in 210 patients with coma due to cerebral hypoxia. A total of 13% of patients regained neurologic function and independent function at some time during the first year.
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| '''Initial Neurologic Findings:'''
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| * Patients who had the initial absence of pupillary light reflexes did not recover independent functioning (52 patients, 25% of patients)<ref name="pmid442945">{{cite journal |author=Thomassen A, Wernberg M |title=Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units |journal=[[Acta Anaesthesiologica Scandinavica]] |volume=23 |issue=2 |pages=143–8 |year=1979 |month=April |pmid=442945 |doi= |url=}}</ref>.
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| * In contrast, patients who had the initial presence of pupillary light reflexes, the development of spontaneous eye movements that were roving conjugate or better, and the presence of either extensor, flexor, or withdrawal responses to pain had a 41% chance of regaining independent function (of the 27 patients in this group, 11 (41%) regained independence).<ref name="pmid442945">{{cite journal |author=Thomassen A, Wernberg M |title=Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units |journal=[[Acta Anaesthesiologica Scandinavica]] |volume=23 |issue=2 |pages=143–8 |year=1979 |month=April |pmid=442945 |doi= |url=}}</ref>.
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| * In a study by Snyder et al, the absence of corneal or pupillary light reflexes at 3 hours after [[cardiac arrest]] was associated with death in all patients <ref>Snyder BD, Loewenson RB, Gumnit RJ, et al: Neurologic prognosis after cardiopulmonary arrest: II. Level of consciousness. Neurology 1980;30:52-58.</ref><ref>Snyder BD, Gumnit RJ, Leppik IE, et al: Neurologic prognosis after cardiopulmonary arrest: IV. Brainstem refl exes. Neurology 1981;31: 1092-1097</ref>. By 6 hours, all the patients who survived had the presence of three brainstem reflexes: [[pupillary light response]], [[corneal reflex]], and reflex eye movements.
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| *The absence of spontaneous limb movements and the absence of withdrawal to pain in the early hours is a poor prognostic sign.
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| *The presence of either decorticate or decerebrate posturing is a poor prognostic sign.
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| *Frequent [[myoclonic jerking]] is associated with a poor prognosis.
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| *The presence of seizures in the initial 24 hours is modestly associated with outcomes: 53% of patients who seize survive compared to 70% of those who do not seize during the first day<ref>Roine RO: Neurological Outcome of Out-of-Hospital Cardiac Arrest [dissertation]. University of Helsinki, 1993.</ref>.
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| '''24 Hour Neurologic Findings:'''
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| * Most patients who survive become alert by 24-48 hours. In one series, of those patients who were in a coma through day 2, only 2 of the 27 (7%) survived.<ref>Snyder BD, Loewenson RB, Gumnit RJ, et al: Neurologic prognosis after cardiopulmonary arrest: II. Level of consciousness. Neurology 1980;30:52-58.</ref> In a second series, no patient who remained in a coma by the third day sirvived.<ref>Bell JA, Hodgson HJF: Coma after cardiac arrest. Brain 1974;97:361-372.</ref>
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| * Absent motor responses, the presence of posturing (extensor / flexor motor responses) and the lack of spontaneous eye movements that were either orienting or roving conjugate was associated with a lack of independent recovery in 92 of 93 patients. <ref name="pmid442945">{{cite journal |author=Thomassen A, Wernberg M |title=Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units |journal=[[Acta Anaesthesiologica Scandinavica]] |volume=23 |issue=2 |pages=143–8 |year=1979 |month=April |pmid=442945 |doi= |url=}}</ref>.
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| * In contrast, of the 30 patients who showed improvement in their eye-opening responses, obeyed commands or had withdraw to pain, 19 (63%) regained independent function.<ref name="pmid442945">{{cite journal |author=Thomassen A, Wernberg M |title=Prevalence and prognostic significance of coma after cardiac arrest outside intensive care and coronary units |journal=[[Acta Anaesthesiologica Scandinavica]] |volume=23 |issue=2 |pages=143–8 |year=1979 |month=April |pmid=442945 |doi= |url=}}</ref>.
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| *Seizures that occur after the initial 24 hours are associated with a poorer outcomes. In one study only 3 of 15 patients who seized recovered consciousness, and only one patient lived a year<ref>Roine RO: Neurological Outcome of Out-of-Hospital Cardiac Arrest [dissertation]. University of Helsinki, 1993.</ref>. The presence of [[status epilepticus]] at any time following cardiac arrest is associated with a very poor prognosis as all nine patients with status epilepticus died in one series.<ref>Roine RO: Neurological Outcome of Out-of-Hospital Cardiac Arrest [dissertation]. University of Helsinki, 1993.</ref>
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| *The absence of spontaneous eye opening and intermittent visual fixation by the end of the first day is associated with a poor prognosis. Although eye opening is necessary for a good outcomes, it alone is not sufficient, as many patients who have spontaneous eye opening still go on to have a poor prognosis. Roving eye movements in the absence of visual fixation is often indicative of extensive bilateral cerebral hemispheral damage and portends a poor prognosis. If the gaze is sustained in an upeard direction, this carries a poor prognosis as well.<ref>Keane JR: Sustained upgaze in coma. Annals of Neurolology 1981;9:409-412.</ref>
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| ==References==
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| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| [[Category:Neurology]] | | [[Category:Neurology]] |
| [[Category:Emergency medicine]] | | [[Category:Emergency medicine]] |
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| | [[Category:Up-To-Date cardiology]] |
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