Editorials
in defining incompletely understood pathophysiology as well as the interactions between subject and machine. Gonducting such integrative, organ level work is an irreplaceable step toward perfecting clinical methods and correcting misleading assumptions that too commonly stem without modification from the normal physiology we better understand. Thoughtful physicians are slow to change entrenched practice except when the logic and evidence are consistent and compelling. In the case of FGME-aided ventilation, however, we seem to be building a convincing case rather quickly.
REFERENCES 1. McMullen SM, Meade M, Rose L, et al; Canadian Critical Care Trials Group (CCCTG): Partial ventilatory support modalities in acute lung injury and acute respiratory distress syndrome-A systematic review. PLoS Cne 201 2; 7:e40190 2. Langer T, Vecchi V, Belenkiy SM, et al: Extracorporeal Gas Exchange and Spontaneous Breathing for the Treatment of Acute Respiratory Distress Syndrome: An Alternative to Mechanical Ventilation? Crit Care Med 2014; 42:e211 -e220 3. Protti A, Andreis DT, Monti M, et al: Lung stress and strain during mechanical ventilation: Any difference between statics and dynamics? Crit Care Med 2013; 41:1046-1055 4. Gama de Abreu M, Güidner A, Pelosi P: Spontaneous breathing activity in acute lung injury and acute respiratory distress syndrome. Curr Cpin Anaesthesiol 2012; 25:148-155 5. Mead J, Takishima T, Leith D: Stress distribution in lungs: A model of pulmonary elasticity. J AppI Physiol 1 970; 28:596-608 6. Ferguson ND, Cook DJ, Guyatt GH, et al; CSCILLATE Trial Investigators; Canadian Critical Care Trials Group: High-frequency
oscillation in early acute respiratory distress syndrome. N EngI J Med 2013; 368:795-805 7 Young D, Lamb SE, Shah S, et al; OSCAR Study Group: High-frequency oscillation for acute respiratory distress syndrome. N EngI J Med 2013; 368:806-813 8. Terragni PP, Del Sorbo L, Mascia L, et al: Tidal volume lower than 6ml/kg enhances lung protection: Role of extracorporeal carbon dioxide removal. Anesthesiology 2009; 111:826-835 9. Bein T, Weber-Carstens S, Goldmann A, et al: Lower tidal volume strategy (=3 ml/kg) combined with extracorporeal CC^ removal versus 'conventional' protective ventilation (6 ml/kg) in severe ARDS: The prospective randomized Xtravent-study. Intensive Care Med 2013; 39:847-856 10. Richard JC, Lyazidi A, Akoumianaki E^et al: Potentially harmful effects of inspiratory synchronization during pressure preset ventilation. Intensive Care Wed 2013; 39:2003-2010 11. Otis A: The work of breathing. J Physiol 1954; 34:449-458 12. Whipp BJ, Ward SA: Determinants and control of breathing during muscular exercise. Br J Sports Med 1998; 32:199-211 13. Jones NL: Exercise testing in pulmonary evaluation: Rationale, methods, and the normal respiratory response to exercise. N EngI J Med 1975; 293:541-544 14. Lefrak EA, Stevens PM, Noon GP, et al: Current status of prolonged extracorporeal membrane oxygénation for acute respiratory failure. C/iesM973; 63:773-782 15. Gattinoni L, Agostoni A, Pesenti A, et al: Treatment of acute respiratory failure with low-frequency positive-pressure ventilation and extracorporeal removal of CO^. Lancet 1980; 2:292-294 16. Camboni D, Philipp A, Lubnow M, et al: Extracorporeal membrane oxygénation by single-vessel access in adults: Advantages and limitations. ASAIC J 201 2; 58:616-621
Catatonia in the ICU: Something Worth Knowing G. Bryan Young, MD, FRCPC Division of Neurology Department of Clinical Neurological Sciences University of Western Cntario London, ON, Canada
I
n this issue of Critical Care Medicine, Saddawi-Konefka et al (1) bring the presentation of catatonia in the IGU to the attention of intensivists. Although a diagnosis of
'See also p. e234. Key Words: benzodiazepine; catatonia; electroconvulsive therapy; ICU Dr. Young served as a consultant to GE Healthcare for electroencephalography (EEG) monitoring in the ICU, has patent for EEG seizure recognition algorithm with GE Healthcare, received royalties for reviews in UptoDate (electronic journal), and received support for article research from the Canadian Institute of Health Research. His institution served as consultant to GE Healthcare for EEG monitoring in the ICU. Copyright © 2013 by the Society of Critical Care Medicine and Lippineott Williams & Wilkins DOI: 10.1097/CCM.0000000000000079
760
www.ccmjournal.org
exclusion of other conditions (including sepsis-associated encephalopathy, various metabolic and drug-related encephalopathies and encephalitides who have dehrium and altered motor function, nonconvulsive seizures, serotonin syndrome, and neuroleptic malignant syndrome), catatonia differs markedly in management from these other conditions and is potentially fatal if not recognized and managed appropriately. Kahlbaum (2) first used the term "catatonia" in 1874 to refer to a silent, motionless state, in which the patient seemed to lack any volition and would not react to stimuli. This was sometimes accompanied by a resistance to a limb being passively moved (paratonia), but once the limb was displaced, the altered posture was sustained [flexibilitus cerea or waxy flexibility). Since then psychiatrists have broadened the definition to include excessive, purposeless, often stereotyped motor activity, sometimes accompanied by sympathetic nervous system overactivity, without influence by external stimuli (3). Although catatonia was first described in patients with psychoses, autism, and developmental disorders, it can also appear acutely from primary medical causes (4). Mareh 2014 • Volume 42 • Number 3
Editorials
Catatonia is a challenging diagnosis to make, especially in the ICU, but if one takes a pathophysiological approach, it can be more readily understood. Although catatonia is associated with altered mental status, it is also a derangement in a neuronal network that also involves the motor system, in particular the basal ganglia-thalamo-cortical circuit. In turn this system involves several distinct neurotransmitters and receptors. It appears that the activity of gamma-aminobutric acid-A receptors, or the portion of this receptor on which benzodiazepines act, is especially important. Two of the five cases presented by Saddawi-Konefka et al (1) developed catatonia after the abrupt withdrawal of long-term benzodiazepines. Further, the institution of benzodiazepines in three of the five cases was followed by a quick resolution of catatonic features. There is some evidence that glutamate, dopamine, serotonin, and even cholinergic systems may play secondary roles (5-7). Other authors have reported similar cases of catatonia with abrupt withdrawal of long-term benzodiazepines, especially in older individuals (8). It is of interest that the patients with benzodiazepine withdrawal-related catatonia in the article by Saddowi-Konefka et al (1) were over 75 years old. Other patients, who had not been withdrawn from benzodiazepines, responded to electroconvulsive therapy (ECT) (1), although it is best to try a small dose of benzodiazepines in all catatonic patients before resorting to ECT. ECT has multiple effects on the brain, including augmenting the release of various neurotransmitters and hormones, altering the activity of various networks, and even causing an increase in hippocampal neurogenesis and synaptogenesis (9). Its more immediate effect on catatonia probably involves the first two mechanisms. Readers are encouraged to carefully read the article by Saddawi-Konefka et al (1) to note the main criteria for the diagnosis of catatonia from Table 2 and to consider catatonia when
Critical Care Medicine
there is a sudden, unexpected change in behavior, with reduced interaction and either hypoactivity or hyperactivity. Remember to first exclude the more common conditions, and also be aware that catatonia might coexist with other conditions, for example, sepsis, that could alter brain function. A clue in some patients is the history of sudden withdrawal of benzodiazepines. Administering low doses of benzodiazepines maybe of diagnostic and therapeutic benefit. In other cases, where catatonia is suspected, a psychiatric consultation is indicated. Both ECT and benzodiazepines can be beneficial in catatonia but potentially harmful in other causes of ICU-encountered brain dysfunction.
REFERENCES 1. Saddawi-Konefka D, Berg SM, Nejad SH, et al: Catatonia in the ICU: An Important and Underdiagnosed Cause of Altered Mental Status. A Case Series and Review of the Literature. Crit Care Med 2014; 42:e234-e241 2. Kahlbaum KL: Die Katatonieoderdas Spannungsirresein: Eine Klinische Form Psuchischer Krankheit. Berlin, Verlag August Hirshwald, 1874 3. American Psychiatric Association: DSM 5 Implementation and Support. Available at: http://www.dsm5.org. Accessed Cctober30, 2013 4. Jaimes-Albornoz W, Serra-Mestres J: Catatonia in the emergency department. Emerg Med J 2012; 29:863-867 5. Kanemoto K, Miyamoto T, Abe R: letal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal. Seizure 1999; 8:364-366 6. Glover SG, Escalona R, Bishop J, et al: Catatonia associated with lorazepam withdrawal. Psychosomatics 1997; 38:148-150 7 Rosebush PI, Mazurek MF: Catatonia after benzodiazepine withdrawal. J Clin Psychopharmacol 1 996; 1 6:315-319 8. Carroll BT, Carroll TD, Lee JW, et ai: Why are some medications effective against catatonia? Int J Neuropsychopharmacol 2006; 9 (SuppI 1):S270 9. Bolwig TG: How does electroconvulsive therapy work? Theories on its mechanism. Can J Psychiatry 2011 ; 56:13-18
www.ccmjournal.org
761
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
in defining incompletely understood pathophysiology as well as the interactions between subject and machine. Gonducting such integrative, organ level work is an irreplaceable step toward perfecting clinical methods and correcting misleading assumptions that too commonly stem without modification from the normal physiology we better understand. Thoughtful physicians are slow to change entrenched practice except when the logic and evidence are consistent and compelling. In the case of FGME-aided ventilation, however, we seem to be building a convincing case rather quickly.
REFERENCES 1. McMullen SM, Meade M, Rose L, et al; Canadian Critical Care Trials Group (CCCTG): Partial ventilatory support modalities in acute lung injury and acute respiratory distress syndrome-A systematic review. PLoS Cne 201 2; 7:e40190 2. Langer T, Vecchi V, Belenkiy SM, et al: Extracorporeal Gas Exchange and Spontaneous Breathing for the Treatment of Acute Respiratory Distress Syndrome: An Alternative to Mechanical Ventilation? Crit Care Med 2014; 42:e211 -e220 3. Protti A, Andreis DT, Monti M, et al: Lung stress and strain during mechanical ventilation: Any difference between statics and dynamics? Crit Care Med 2013; 41:1046-1055 4. Gama de Abreu M, Güidner A, Pelosi P: Spontaneous breathing activity in acute lung injury and acute respiratory distress syndrome. Curr Cpin Anaesthesiol 2012; 25:148-155 5. Mead J, Takishima T, Leith D: Stress distribution in lungs: A model of pulmonary elasticity. J AppI Physiol 1 970; 28:596-608 6. Ferguson ND, Cook DJ, Guyatt GH, et al; CSCILLATE Trial Investigators; Canadian Critical Care Trials Group: High-frequency
oscillation in early acute respiratory distress syndrome. N EngI J Med 2013; 368:795-805 7 Young D, Lamb SE, Shah S, et al; OSCAR Study Group: High-frequency oscillation for acute respiratory distress syndrome. N EngI J Med 2013; 368:806-813 8. Terragni PP, Del Sorbo L, Mascia L, et al: Tidal volume lower than 6ml/kg enhances lung protection: Role of extracorporeal carbon dioxide removal. Anesthesiology 2009; 111:826-835 9. Bein T, Weber-Carstens S, Goldmann A, et al: Lower tidal volume strategy (=3 ml/kg) combined with extracorporeal CC^ removal versus 'conventional' protective ventilation (6 ml/kg) in severe ARDS: The prospective randomized Xtravent-study. Intensive Care Med 2013; 39:847-856 10. Richard JC, Lyazidi A, Akoumianaki E^et al: Potentially harmful effects of inspiratory synchronization during pressure preset ventilation. Intensive Care Wed 2013; 39:2003-2010 11. Otis A: The work of breathing. J Physiol 1954; 34:449-458 12. Whipp BJ, Ward SA: Determinants and control of breathing during muscular exercise. Br J Sports Med 1998; 32:199-211 13. Jones NL: Exercise testing in pulmonary evaluation: Rationale, methods, and the normal respiratory response to exercise. N EngI J Med 1975; 293:541-544 14. Lefrak EA, Stevens PM, Noon GP, et al: Current status of prolonged extracorporeal membrane oxygénation for acute respiratory failure. C/iesM973; 63:773-782 15. Gattinoni L, Agostoni A, Pesenti A, et al: Treatment of acute respiratory failure with low-frequency positive-pressure ventilation and extracorporeal removal of CO^. Lancet 1980; 2:292-294 16. Camboni D, Philipp A, Lubnow M, et al: Extracorporeal membrane oxygénation by single-vessel access in adults: Advantages and limitations. ASAIC J 201 2; 58:616-621
Catatonia in the ICU: Something Worth Knowing G. Bryan Young, MD, FRCPC Division of Neurology Department of Clinical Neurological Sciences University of Western Cntario London, ON, Canada
I
n this issue of Critical Care Medicine, Saddawi-Konefka et al (1) bring the presentation of catatonia in the IGU to the attention of intensivists. Although a diagnosis of
'See also p. e234. Key Words: benzodiazepine; catatonia; electroconvulsive therapy; ICU Dr. Young served as a consultant to GE Healthcare for electroencephalography (EEG) monitoring in the ICU, has patent for EEG seizure recognition algorithm with GE Healthcare, received royalties for reviews in UptoDate (electronic journal), and received support for article research from the Canadian Institute of Health Research. His institution served as consultant to GE Healthcare for EEG monitoring in the ICU. Copyright © 2013 by the Society of Critical Care Medicine and Lippineott Williams & Wilkins DOI: 10.1097/CCM.0000000000000079
760
www.ccmjournal.org
exclusion of other conditions (including sepsis-associated encephalopathy, various metabolic and drug-related encephalopathies and encephalitides who have dehrium and altered motor function, nonconvulsive seizures, serotonin syndrome, and neuroleptic malignant syndrome), catatonia differs markedly in management from these other conditions and is potentially fatal if not recognized and managed appropriately. Kahlbaum (2) first used the term "catatonia" in 1874 to refer to a silent, motionless state, in which the patient seemed to lack any volition and would not react to stimuli. This was sometimes accompanied by a resistance to a limb being passively moved (paratonia), but once the limb was displaced, the altered posture was sustained [flexibilitus cerea or waxy flexibility). Since then psychiatrists have broadened the definition to include excessive, purposeless, often stereotyped motor activity, sometimes accompanied by sympathetic nervous system overactivity, without influence by external stimuli (3). Although catatonia was first described in patients with psychoses, autism, and developmental disorders, it can also appear acutely from primary medical causes (4). Mareh 2014 • Volume 42 • Number 3
Editorials
Catatonia is a challenging diagnosis to make, especially in the ICU, but if one takes a pathophysiological approach, it can be more readily understood. Although catatonia is associated with altered mental status, it is also a derangement in a neuronal network that also involves the motor system, in particular the basal ganglia-thalamo-cortical circuit. In turn this system involves several distinct neurotransmitters and receptors. It appears that the activity of gamma-aminobutric acid-A receptors, or the portion of this receptor on which benzodiazepines act, is especially important. Two of the five cases presented by Saddawi-Konefka et al (1) developed catatonia after the abrupt withdrawal of long-term benzodiazepines. Further, the institution of benzodiazepines in three of the five cases was followed by a quick resolution of catatonic features. There is some evidence that glutamate, dopamine, serotonin, and even cholinergic systems may play secondary roles (5-7). Other authors have reported similar cases of catatonia with abrupt withdrawal of long-term benzodiazepines, especially in older individuals (8). It is of interest that the patients with benzodiazepine withdrawal-related catatonia in the article by Saddowi-Konefka et al (1) were over 75 years old. Other patients, who had not been withdrawn from benzodiazepines, responded to electroconvulsive therapy (ECT) (1), although it is best to try a small dose of benzodiazepines in all catatonic patients before resorting to ECT. ECT has multiple effects on the brain, including augmenting the release of various neurotransmitters and hormones, altering the activity of various networks, and even causing an increase in hippocampal neurogenesis and synaptogenesis (9). Its more immediate effect on catatonia probably involves the first two mechanisms. Readers are encouraged to carefully read the article by Saddawi-Konefka et al (1) to note the main criteria for the diagnosis of catatonia from Table 2 and to consider catatonia when
Critical Care Medicine
there is a sudden, unexpected change in behavior, with reduced interaction and either hypoactivity or hyperactivity. Remember to first exclude the more common conditions, and also be aware that catatonia might coexist with other conditions, for example, sepsis, that could alter brain function. A clue in some patients is the history of sudden withdrawal of benzodiazepines. Administering low doses of benzodiazepines maybe of diagnostic and therapeutic benefit. In other cases, where catatonia is suspected, a psychiatric consultation is indicated. Both ECT and benzodiazepines can be beneficial in catatonia but potentially harmful in other causes of ICU-encountered brain dysfunction.
REFERENCES 1. Saddawi-Konefka D, Berg SM, Nejad SH, et al: Catatonia in the ICU: An Important and Underdiagnosed Cause of Altered Mental Status. A Case Series and Review of the Literature. Crit Care Med 2014; 42:e234-e241 2. Kahlbaum KL: Die Katatonieoderdas Spannungsirresein: Eine Klinische Form Psuchischer Krankheit. Berlin, Verlag August Hirshwald, 1874 3. American Psychiatric Association: DSM 5 Implementation and Support. Available at: http://www.dsm5.org. Accessed Cctober30, 2013 4. Jaimes-Albornoz W, Serra-Mestres J: Catatonia in the emergency department. Emerg Med J 2012; 29:863-867 5. Kanemoto K, Miyamoto T, Abe R: letal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal. Seizure 1999; 8:364-366 6. Glover SG, Escalona R, Bishop J, et al: Catatonia associated with lorazepam withdrawal. Psychosomatics 1997; 38:148-150 7 Rosebush PI, Mazurek MF: Catatonia after benzodiazepine withdrawal. J Clin Psychopharmacol 1 996; 1 6:315-319 8. Carroll BT, Carroll TD, Lee JW, et ai: Why are some medications effective against catatonia? Int J Neuropsychopharmacol 2006; 9 (SuppI 1):S270 9. Bolwig TG: How does electroconvulsive therapy work? Theories on its mechanism. Can J Psychiatry 2011 ; 56:13-18
www.ccmjournal.org
761
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
