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Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome) in Progressive Supranuclear Palsy
Psychosomatics 2013:54:80 – 83
© 2013 The Academy of Psychosomatic Medicine. Published by Elsevier Inc. All rights reserved.
Case Reports Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome) in Progressive Supranuclear Palsy Ana Hategan, M.D., James A. Bourgeois, O.D., M.D., Usha Parthasarathi, M.B.B.S.
A
cute colonic pseudo-obstruction (ACPO), also known as Ogilvie syndrome, is an enteric dysmotility characterized by acute dilatation of the colon unrelated to any mechanical cause. In 1948, Ogilvie described two patients with colonic dilatation associated with malignant infiltration of the celiac plexus without evidence of a mechanical obstruction and attributed the syndrome to sympathetic deprivation.1 In 1958, Dudley et al.2 used the term “pseudo-obstruction” to describe the same clinical and radiographic appearance with no evidence of mechanical obstruction discovered during laparotomy. The pathophysiology of ACPO is not completely understood, but it is thought to be related, at least in part, to an alteration in the autonomic regulation of colonic motor function.3 Notably, the parasympathetic nervous system promotes enteric motility, while the sympathetic stimuli result in the inhibition of bowel motility and the contraction of sphincters. Therefore, an imbalance in the autonomic innervation appears to lead to a functional bowel obstruction. Medications that interfere with sympathetic and parasympathetic balance may be associated with ACPO; this model is a departure from the original formulation by Ogilvie of sympathetic deprivation. Multiple predisposing conditions and pharmacologic factors have been associated with ACPO4 – 6 (Table 1). Due to the functional relative hypocholinergic status in this condition, it is also suggested that anticholinergic pharmacotherapy may be associated with the presentation of ACPO.
Case Reports
Ms. R, a 74-year-old with a history of a major depressive episode that fully remitted after 2 months of treatment with mirtazapine 30 mg/d, presented to the emergency 80
www.psychosomaticsjournal.org
department (ED) with a 5-day history of mutism, worsening constipation, vomiting, and urinary retention. Her medical history also included progressive supranuclear palsy (PSP) with dementia and chronic urinary incontinence. The Montreal Cognitive Assessment (MoCA)7 score was 11 out of 30 (performed 4 weeks earlier), with notable deficits in verbal fluency, recall, and executive function. Her medications included furosemide (prescribed for a recent history of bilateral pedal edema), which was increased to 40 mg/d 10 days earlier. She also received docusate sodium 200 mg/d, lactulose 30 mL/d, bisacodyl 10 mg/d PRN, and sodium phosphate 130 mL/d PRN for severe constipation. Ms. R was not cooperative with a formal mental status examination. However, reduced motor activity and mutism were noted. Level of consciousness was intact; this initial mental status examination, while incomplete because of her lack of cooperation, appeared more consistent with dementia, although delirium could not be completely ruled out. Physical examination revealed a tense but nontender abdomen and distended bladder. Rectal examination revealed stool in the rectum. Electrolytes, inflammatory markers, complete blood count, and liver function profile were normal. Vital signs were normal except for pulse of 112 beats/minute. Abdominal X-rays showed extensively dilated loops of large bowel without any evidence of obstruction (Figure 1). Received March 3, 2012; revised March 29, 2012; accepted March 30, 2012. From Department of Psychiatry and Behavioural Neurosciences, Michael G. DeGroote School of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada (AH, JAB, UP); St. Joseph’s Healthcare Hamilton, West 5th Campus (AH, JAB, UP). Send correspondence and reprint requests to Ana Hategan, M.D., St. Joseph’s Healthcare Hamilton, West 5th Campus, 100 West 5th Street, Hamilton, ON, L8N 3K7, Canada; e-mail: [email protected] © 2013 The Academy of Psychosomatic Medicine. Published by Elsevier Inc. All rights reserved.
Psychosomatics 54:1, January-February 2013
Hategan et al.
TABLE 1.
Risk Factors Associated with the Development of ACPO
Post-surgical Abdominal/pelvic surgery Other surgical procedures Neurosurgery, thoracic, orthopedic, gynecologic, and urologic surgery Trauma Retroperitoneal trauma Spinal cord injury Medical Infectious diseases (e.g., herpes zoster, pneumonia, sepsis) Neurologic disorders (e.g., Parkinson disease, Alzheimer disease, multiple sclerosis) Endocrine disorders (e.g., hypothyroidism) Cardiac disorders (e.g., myocardial infarction, heart failure) Respiratory/renal insufficiency Malignancy (e.g., leukemia, retroperitoneal cancer, small cell lung cancer) Electrolyte imbalances (e.g., hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia) Medications Anticholinergics Opioids/opiates Clonidine Tricyclic antidepressants Phenothiazines Corticosteroids Advanced age Source: Edelman et al. 2010;4 Jetmore et al. 1992;5 Vanek and Al-Salti 1986.6
Ms. R was admitted to the surgery service for observation. A presumptive diagnosis of Ogilvie syndrome was made because of evidence of abdominal distension, obstipation, nausea, and vomiting in the absence of apparent mechanical cause on the abdominal radiographs. Mirtazapine and furosemide were continued. Dimenhydrinate 50 mg q4h PRN for emesis and morphine 30 mg q4h PRN for pain were initiated. On repeat examination, Ms. R was mute, drowsy, and falling asleep while physician talked to her. Ms. R could no longer eat on her own and required assistance with feeding, which represented an abrupt functional decline. Due to evidence of sudden changes in her cognitive and functional performance, as well as altered level of consciousness, a diagnosis of delirium was now given. Furthermore, conservative management with nasogastric suction, rectal tube, and positional changes failed. On day 3, she developed signs and symptoms of intestinal obstruction, as bowel sounds were absent. A repeat of abdominal X-rays confirmed the diagnosis of distal bowel obstruction without perforation. Colonoscopic decompression followed by surPsychosomatics 54:1, January-February 2013
gical resection of the sigmoid colon was required. Sudden death due to myocardial infarction occurred 3 weeks post-operatively.
Discussion
The emergence of ACPO in Ms. R with PSP was particularly interesting in context of a progressive neurodegenerative disorder and other plausible causal pharmacological factors. A clinical diagnosis of ACPO should be suspected in a history of abdominal distension, abdominal pain, nausea and/or vomiting, obstipation, and fever,6 and when confirmed by radiologic examination of dilated loops of bowel with no mechanical obstruction. Ms. R had no recent history of trauma, infection, malignancy, electrolyte imbalance, significant cardiac disease, or other systemic factors that might have further increased her risk for ACPO. PSP, a tauopathy, is a Parkinson-plus syndrome involving gradual deterioration of specific brain areas.8 Much support exists to suggest that the enteric nervous system is affected in multi-centric neurodegenerative processes, such as Parkinson disease, a synucleinopathy, leading to prolonged colon transit time and constipation.9 Yet, enteric dysmotility has not been formally explained in PSP, despite reports of spinal cord involvement that may exert some control of the bladder and bowel. Although micturition disturFIGURE 1.
Plain Supine Abdominal Radiograph Showing Extensive Colonic Dilatation
www.psychosomaticsjournal.org
81
Case Reports bance10 was reported in PSP, Ms. R developed an acute onset of urinary retention, possibly anticholinergic-related, overlapping on a chronic history of incontinence that may have been due to her PSP. Additionally, PSP may also predispose to constipation,11 which in itself can induce ileus states. Therefore, this case illustrates a plausible contribution of PSP in the onset of ACPO. Reports of ACPO were mostly associated with the surgical literature. Several cases were associated with tricyclic antidepressants (TCAs) and typical and atypical antipsychotics.12 Additionally, the chronic use of laxatives, as in Ms. R’s case, is associated with increased susceptibility to gastrointestinal side effects (such as constipation) of psychotropics. All agents with anticholinergic activity have the potential to contribute to paralytic ileus. Mirtazapine, a tetracyclic antidepressant, has mild anticholinergic effects, as does furosemide.13 However, concurrent use of such medications, or other medications affecting cholinergic function, could contribute to enteric dysmotility due to an additive effect.14 According to Anticholinergic Drug Scale scoring system,15 furosemide is potentially anticholinergic and dimenhydrinate, markedly anticholinergic. Mirtazapine and morphine both have a low anticholinergic activity.13 Notably, in our case, dimenhydrinate and morphine were added following a diagnosis of Ogilvie syndrome; this likely increased the anticholinergic burden and was temporally associated with worsening of the ACPO. Yet, the recent increase in furosemide may have caused a reduced hydration that could have worsened constipation, which in turn could explain a causal association between furosemide and ACPO. Additionally, morphine’s receptor agonist properties were likely contributing to Ms. R’s enteric dysmotility. Methylnaltrexone, a peripheral opioid antagonist approved for the treatment of opioid-induced constipation in critical care patients when response to ordinary laxatives have failed, may play an important role in restoration of bowel function and could be considered in such cases.16 Patients with dementia may be at particular risk for delirium.17 Delirium was considered in Ms. R because of sudden changes in her cognitive and functional performance. The highly anticholinergic agent, dimenhy-
drinate, and the CNS depressant, morphine, which likely added to the total anticholinergic burden, may have contributed to her delirium superimposed on her chronic dementia, while also causing progression of her ACPO. Even small increases in the anticholinergic burden in the elderly increase the risk of morbidity and mortality.15,18 A 30% mortality rate is reported in ACPO, which remains a difficult and sometimes delayed diagnosis.19 With early detection, ACPO may resolve in most patients, but when surgical intervention is required, as in this case, the subsequent mortality is reported to be much higher (57%).20
Conclusion
Psychiatrists in hospital practices routinely caution other medical teams about the use of anticholinergic and opioid medications, especially in neurologically/ cognitively impaired and/or elderly patients, out of concern that these medications may regularly precipitate an episode of delirium. Our case illustrates another physical complication of the use of these medications in patients at risk for enteric dysmotility. Beyond the familiar cautions of the use of significantly anticholinergic psychotropic medications (e.g., TCAs, clozapine) in patients at such risk, in some patients the medical/ surgical risks of anticholinergic and opioid medications need to be separately considered. Attention should be placed on concurrent medication use with varied degrees of anticholinergic effects, particularly in patients with potential predisposing factors for ACPO, such as PSP. Caution should be implemented when administering drugs such as dimenhydrinate and morphine, since both can induce enteric dysmotility and potentially worsen or prevent resolution of the condition. Disclosure: The authors disclosed no proprietary or commercial interest in any product mentioned or concept discussed in this article.
References 1. Ogilvie H: Large intestine colic due to sympathetic deprivation: a new clinical syndrome. BMJ 1948; 2(4579):671– 673 2. Dudley HAF, Sinclair ISR, Mclaren IF, McNair TJ, Newsam JE: Intestinal pseudoobstruction. J R Coll Surg Edinb 1958; 3(3): 206 –217
82
www.psychosomaticsjournal.org
3. Dorudi S, Berry AR, Kettlewell MGW: Acute colonic pseudoobstruction. Br J Surg 1992;79:99 –103 4. Edelman DA, Antaki F, Basson MD, Salwen WA, Gruber SA, Losanoff JE: Ogilvie syndrome and herpes zoster: case report and review of the literature. J Emerg Med 2010; 39(5):696 –700
Psychosomatics 54:1, January-February 2013
Hategan et al. 5. Jetmore AB, Timmcke AE, Gathright JB Jr, Hicks TC, Ray JE, Baker JW: Ogilvie’s syndrome: colonoscopic decompression and analysis of predisposing factors. Dis Colon Rectum 1992; 35(12):1135–1142 6. Vanek VW, Al-Salti M: Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of 400 cases. Dis Colon Rectum 1986; 29(3):203–210 7. Nasreddine ZS, Phillips NA, Bédirian V, Charbonneau S, Whitehead V, Collin I, et al: The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc 2005; 53(4):695– 699 8. Steele JC, Richardson JC, Olszewski J: Progressive supranuclear palsy: a heterogeneous degeneration involving the brain stem, basal ganglia and cerebellum with vertical gaze and pseudobulbar palsy, nuchal dystonia and dementia. Arch Neurol 1964; 10:333–359 9. Sakakibara R, Odaka T, Uchiyama T, Asahina M, Yamaguchi K, Yamaguchi T, et al: Colonic transit time and rectoanal videomanometry in Parkinson’s disease. J Neurol Neurosurg Psychiatry 2003; 74(2):268 –272 10. Sakakibara R, Hattori T, Tojo M, Yamanishi T, Yasuda K, Hirayama K: Micturitional disturbance in progressive supranuclear palsy. J Auton Nerv Syst 1993; 45(2):101–106 11. Brooks DJ: Diagnosis and management of atypical parkinsonian syndromes. J Neurol Neurosurg Psychiatry 2002; 72(Suppl 1): i10 –i16
Psychosomatics 54:1, January-February 2013
12. Nielsen J, Meyer JM: Risk factors for ileus in patients with schizophrenia. Schizophr Bull 2012; 8(3):592–598 13. PL Detail-Document, Drugs with Anticholinergic Activity. Pharmacist’s Letter/Prescriber’s Letter. December 2011 14. Pajouhi P, Bourgeois JA: Clozapine, fluoxetine, and benztropine-associated ileus: case report. Jefferson J Psychiatry 2007; 21(1):ISSN 1935-0783. Available at http://jdc.jefferson.edu/ jeffjpsychiatry/. Accessed February 26, 2012 15. Carnahan RM, Lund BC, Perry PJ, Pollock BG, Culp KR: The anticholinergic drug scale as a measure of drug-related anticholinergic burden: associations with serum anticholinergic activity. J Clin Pharmacol 2006; 46(12):1481–1486 16. Sawh SB, Selvaraj IP, Danga A, Cotton AL, Moss J, Patel PB: Use of methylnaltrexone for the treatment of opioidinduced constipation in critical care patients. Mayo Clin Proc 2012; 87(3):255–259 17. Inouye SK, Ferrucci L: Elucidating the pathophysiology of delirium and the interrelationship of delirium and dementia. J Gerontol A Biol Sci Med Sci 2006; 61(12):1277–1280 18. Rudolph JL, Salow MJ, Angelini MC, McGlinchey RE: The anticholinergic risk scale and anticholinergic adverse effects in older persons. Arch Intern Med 2008; 168(5):508 –513 19. Dudley HA, Paterson-Brown S: Pseudo-obstruction. Br Med J 1986; 292(6529):1157–1158 20. Tenofsky PL, Beamer L, Smith RS: Ogilvie syndrome as a postoperative complication. Arch Surg 2000; 135(6):682– 686
www.psychosomaticsjournal.org
83
© 2013 The Academy of Psychosomatic Medicine. Published by Elsevier Inc. All rights reserved.
Case Reports Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome) in Progressive Supranuclear Palsy Ana Hategan, M.D., James A. Bourgeois, O.D., M.D., Usha Parthasarathi, M.B.B.S.
A
cute colonic pseudo-obstruction (ACPO), also known as Ogilvie syndrome, is an enteric dysmotility characterized by acute dilatation of the colon unrelated to any mechanical cause. In 1948, Ogilvie described two patients with colonic dilatation associated with malignant infiltration of the celiac plexus without evidence of a mechanical obstruction and attributed the syndrome to sympathetic deprivation.1 In 1958, Dudley et al.2 used the term “pseudo-obstruction” to describe the same clinical and radiographic appearance with no evidence of mechanical obstruction discovered during laparotomy. The pathophysiology of ACPO is not completely understood, but it is thought to be related, at least in part, to an alteration in the autonomic regulation of colonic motor function.3 Notably, the parasympathetic nervous system promotes enteric motility, while the sympathetic stimuli result in the inhibition of bowel motility and the contraction of sphincters. Therefore, an imbalance in the autonomic innervation appears to lead to a functional bowel obstruction. Medications that interfere with sympathetic and parasympathetic balance may be associated with ACPO; this model is a departure from the original formulation by Ogilvie of sympathetic deprivation. Multiple predisposing conditions and pharmacologic factors have been associated with ACPO4 – 6 (Table 1). Due to the functional relative hypocholinergic status in this condition, it is also suggested that anticholinergic pharmacotherapy may be associated with the presentation of ACPO.
Case Reports
Ms. R, a 74-year-old with a history of a major depressive episode that fully remitted after 2 months of treatment with mirtazapine 30 mg/d, presented to the emergency 80
www.psychosomaticsjournal.org
department (ED) with a 5-day history of mutism, worsening constipation, vomiting, and urinary retention. Her medical history also included progressive supranuclear palsy (PSP) with dementia and chronic urinary incontinence. The Montreal Cognitive Assessment (MoCA)7 score was 11 out of 30 (performed 4 weeks earlier), with notable deficits in verbal fluency, recall, and executive function. Her medications included furosemide (prescribed for a recent history of bilateral pedal edema), which was increased to 40 mg/d 10 days earlier. She also received docusate sodium 200 mg/d, lactulose 30 mL/d, bisacodyl 10 mg/d PRN, and sodium phosphate 130 mL/d PRN for severe constipation. Ms. R was not cooperative with a formal mental status examination. However, reduced motor activity and mutism were noted. Level of consciousness was intact; this initial mental status examination, while incomplete because of her lack of cooperation, appeared more consistent with dementia, although delirium could not be completely ruled out. Physical examination revealed a tense but nontender abdomen and distended bladder. Rectal examination revealed stool in the rectum. Electrolytes, inflammatory markers, complete blood count, and liver function profile were normal. Vital signs were normal except for pulse of 112 beats/minute. Abdominal X-rays showed extensively dilated loops of large bowel without any evidence of obstruction (Figure 1). Received March 3, 2012; revised March 29, 2012; accepted March 30, 2012. From Department of Psychiatry and Behavioural Neurosciences, Michael G. DeGroote School of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada (AH, JAB, UP); St. Joseph’s Healthcare Hamilton, West 5th Campus (AH, JAB, UP). Send correspondence and reprint requests to Ana Hategan, M.D., St. Joseph’s Healthcare Hamilton, West 5th Campus, 100 West 5th Street, Hamilton, ON, L8N 3K7, Canada; e-mail: [email protected] © 2013 The Academy of Psychosomatic Medicine. Published by Elsevier Inc. All rights reserved.
Psychosomatics 54:1, January-February 2013
Hategan et al.
TABLE 1.
Risk Factors Associated with the Development of ACPO
Post-surgical Abdominal/pelvic surgery Other surgical procedures Neurosurgery, thoracic, orthopedic, gynecologic, and urologic surgery Trauma Retroperitoneal trauma Spinal cord injury Medical Infectious diseases (e.g., herpes zoster, pneumonia, sepsis) Neurologic disorders (e.g., Parkinson disease, Alzheimer disease, multiple sclerosis) Endocrine disorders (e.g., hypothyroidism) Cardiac disorders (e.g., myocardial infarction, heart failure) Respiratory/renal insufficiency Malignancy (e.g., leukemia, retroperitoneal cancer, small cell lung cancer) Electrolyte imbalances (e.g., hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia) Medications Anticholinergics Opioids/opiates Clonidine Tricyclic antidepressants Phenothiazines Corticosteroids Advanced age Source: Edelman et al. 2010;4 Jetmore et al. 1992;5 Vanek and Al-Salti 1986.6
Ms. R was admitted to the surgery service for observation. A presumptive diagnosis of Ogilvie syndrome was made because of evidence of abdominal distension, obstipation, nausea, and vomiting in the absence of apparent mechanical cause on the abdominal radiographs. Mirtazapine and furosemide were continued. Dimenhydrinate 50 mg q4h PRN for emesis and morphine 30 mg q4h PRN for pain were initiated. On repeat examination, Ms. R was mute, drowsy, and falling asleep while physician talked to her. Ms. R could no longer eat on her own and required assistance with feeding, which represented an abrupt functional decline. Due to evidence of sudden changes in her cognitive and functional performance, as well as altered level of consciousness, a diagnosis of delirium was now given. Furthermore, conservative management with nasogastric suction, rectal tube, and positional changes failed. On day 3, she developed signs and symptoms of intestinal obstruction, as bowel sounds were absent. A repeat of abdominal X-rays confirmed the diagnosis of distal bowel obstruction without perforation. Colonoscopic decompression followed by surPsychosomatics 54:1, January-February 2013
gical resection of the sigmoid colon was required. Sudden death due to myocardial infarction occurred 3 weeks post-operatively.
Discussion
The emergence of ACPO in Ms. R with PSP was particularly interesting in context of a progressive neurodegenerative disorder and other plausible causal pharmacological factors. A clinical diagnosis of ACPO should be suspected in a history of abdominal distension, abdominal pain, nausea and/or vomiting, obstipation, and fever,6 and when confirmed by radiologic examination of dilated loops of bowel with no mechanical obstruction. Ms. R had no recent history of trauma, infection, malignancy, electrolyte imbalance, significant cardiac disease, or other systemic factors that might have further increased her risk for ACPO. PSP, a tauopathy, is a Parkinson-plus syndrome involving gradual deterioration of specific brain areas.8 Much support exists to suggest that the enteric nervous system is affected in multi-centric neurodegenerative processes, such as Parkinson disease, a synucleinopathy, leading to prolonged colon transit time and constipation.9 Yet, enteric dysmotility has not been formally explained in PSP, despite reports of spinal cord involvement that may exert some control of the bladder and bowel. Although micturition disturFIGURE 1.
Plain Supine Abdominal Radiograph Showing Extensive Colonic Dilatation
www.psychosomaticsjournal.org
81
Case Reports bance10 was reported in PSP, Ms. R developed an acute onset of urinary retention, possibly anticholinergic-related, overlapping on a chronic history of incontinence that may have been due to her PSP. Additionally, PSP may also predispose to constipation,11 which in itself can induce ileus states. Therefore, this case illustrates a plausible contribution of PSP in the onset of ACPO. Reports of ACPO were mostly associated with the surgical literature. Several cases were associated with tricyclic antidepressants (TCAs) and typical and atypical antipsychotics.12 Additionally, the chronic use of laxatives, as in Ms. R’s case, is associated with increased susceptibility to gastrointestinal side effects (such as constipation) of psychotropics. All agents with anticholinergic activity have the potential to contribute to paralytic ileus. Mirtazapine, a tetracyclic antidepressant, has mild anticholinergic effects, as does furosemide.13 However, concurrent use of such medications, or other medications affecting cholinergic function, could contribute to enteric dysmotility due to an additive effect.14 According to Anticholinergic Drug Scale scoring system,15 furosemide is potentially anticholinergic and dimenhydrinate, markedly anticholinergic. Mirtazapine and morphine both have a low anticholinergic activity.13 Notably, in our case, dimenhydrinate and morphine were added following a diagnosis of Ogilvie syndrome; this likely increased the anticholinergic burden and was temporally associated with worsening of the ACPO. Yet, the recent increase in furosemide may have caused a reduced hydration that could have worsened constipation, which in turn could explain a causal association between furosemide and ACPO. Additionally, morphine’s receptor agonist properties were likely contributing to Ms. R’s enteric dysmotility. Methylnaltrexone, a peripheral opioid antagonist approved for the treatment of opioid-induced constipation in critical care patients when response to ordinary laxatives have failed, may play an important role in restoration of bowel function and could be considered in such cases.16 Patients with dementia may be at particular risk for delirium.17 Delirium was considered in Ms. R because of sudden changes in her cognitive and functional performance. The highly anticholinergic agent, dimenhy-
drinate, and the CNS depressant, morphine, which likely added to the total anticholinergic burden, may have contributed to her delirium superimposed on her chronic dementia, while also causing progression of her ACPO. Even small increases in the anticholinergic burden in the elderly increase the risk of morbidity and mortality.15,18 A 30% mortality rate is reported in ACPO, which remains a difficult and sometimes delayed diagnosis.19 With early detection, ACPO may resolve in most patients, but when surgical intervention is required, as in this case, the subsequent mortality is reported to be much higher (57%).20
Conclusion
Psychiatrists in hospital practices routinely caution other medical teams about the use of anticholinergic and opioid medications, especially in neurologically/ cognitively impaired and/or elderly patients, out of concern that these medications may regularly precipitate an episode of delirium. Our case illustrates another physical complication of the use of these medications in patients at risk for enteric dysmotility. Beyond the familiar cautions of the use of significantly anticholinergic psychotropic medications (e.g., TCAs, clozapine) in patients at such risk, in some patients the medical/ surgical risks of anticholinergic and opioid medications need to be separately considered. Attention should be placed on concurrent medication use with varied degrees of anticholinergic effects, particularly in patients with potential predisposing factors for ACPO, such as PSP. Caution should be implemented when administering drugs such as dimenhydrinate and morphine, since both can induce enteric dysmotility and potentially worsen or prevent resolution of the condition. Disclosure: The authors disclosed no proprietary or commercial interest in any product mentioned or concept discussed in this article.
References 1. Ogilvie H: Large intestine colic due to sympathetic deprivation: a new clinical syndrome. BMJ 1948; 2(4579):671– 673 2. Dudley HAF, Sinclair ISR, Mclaren IF, McNair TJ, Newsam JE: Intestinal pseudoobstruction. J R Coll Surg Edinb 1958; 3(3): 206 –217
82
www.psychosomaticsjournal.org
3. Dorudi S, Berry AR, Kettlewell MGW: Acute colonic pseudoobstruction. Br J Surg 1992;79:99 –103 4. Edelman DA, Antaki F, Basson MD, Salwen WA, Gruber SA, Losanoff JE: Ogilvie syndrome and herpes zoster: case report and review of the literature. J Emerg Med 2010; 39(5):696 –700
Psychosomatics 54:1, January-February 2013
Hategan et al. 5. Jetmore AB, Timmcke AE, Gathright JB Jr, Hicks TC, Ray JE, Baker JW: Ogilvie’s syndrome: colonoscopic decompression and analysis of predisposing factors. Dis Colon Rectum 1992; 35(12):1135–1142 6. Vanek VW, Al-Salti M: Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of 400 cases. Dis Colon Rectum 1986; 29(3):203–210 7. Nasreddine ZS, Phillips NA, Bédirian V, Charbonneau S, Whitehead V, Collin I, et al: The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc 2005; 53(4):695– 699 8. Steele JC, Richardson JC, Olszewski J: Progressive supranuclear palsy: a heterogeneous degeneration involving the brain stem, basal ganglia and cerebellum with vertical gaze and pseudobulbar palsy, nuchal dystonia and dementia. Arch Neurol 1964; 10:333–359 9. Sakakibara R, Odaka T, Uchiyama T, Asahina M, Yamaguchi K, Yamaguchi T, et al: Colonic transit time and rectoanal videomanometry in Parkinson’s disease. J Neurol Neurosurg Psychiatry 2003; 74(2):268 –272 10. Sakakibara R, Hattori T, Tojo M, Yamanishi T, Yasuda K, Hirayama K: Micturitional disturbance in progressive supranuclear palsy. J Auton Nerv Syst 1993; 45(2):101–106 11. Brooks DJ: Diagnosis and management of atypical parkinsonian syndromes. J Neurol Neurosurg Psychiatry 2002; 72(Suppl 1): i10 –i16
Psychosomatics 54:1, January-February 2013
12. Nielsen J, Meyer JM: Risk factors for ileus in patients with schizophrenia. Schizophr Bull 2012; 8(3):592–598 13. PL Detail-Document, Drugs with Anticholinergic Activity. Pharmacist’s Letter/Prescriber’s Letter. December 2011 14. Pajouhi P, Bourgeois JA: Clozapine, fluoxetine, and benztropine-associated ileus: case report. Jefferson J Psychiatry 2007; 21(1):ISSN 1935-0783. Available at http://jdc.jefferson.edu/ jeffjpsychiatry/. Accessed February 26, 2012 15. Carnahan RM, Lund BC, Perry PJ, Pollock BG, Culp KR: The anticholinergic drug scale as a measure of drug-related anticholinergic burden: associations with serum anticholinergic activity. J Clin Pharmacol 2006; 46(12):1481–1486 16. Sawh SB, Selvaraj IP, Danga A, Cotton AL, Moss J, Patel PB: Use of methylnaltrexone for the treatment of opioidinduced constipation in critical care patients. Mayo Clin Proc 2012; 87(3):255–259 17. Inouye SK, Ferrucci L: Elucidating the pathophysiology of delirium and the interrelationship of delirium and dementia. J Gerontol A Biol Sci Med Sci 2006; 61(12):1277–1280 18. Rudolph JL, Salow MJ, Angelini MC, McGlinchey RE: The anticholinergic risk scale and anticholinergic adverse effects in older persons. Arch Intern Med 2008; 168(5):508 –513 19. Dudley HA, Paterson-Brown S: Pseudo-obstruction. Br Med J 1986; 292(6529):1157–1158 20. Tenofsky PL, Beamer L, Smith RS: Ogilvie syndrome as a postoperative complication. Arch Surg 2000; 135(6):682– 686
www.psychosomaticsjournal.org
83