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Table of Contents
Year : 2012  |  Volume : 16  |  Issue : 3  |  Page : 447-449

Ogilvie's syndrome in a case of myxedema coma

1 Department of Internal Medicine, Armed Forces Medical College, Pune, India
2 Department of Endocrinology, Command Hospital, Pune, Maharashtra, India

Date of Web Publication5-May-2012

Correspondence Address:
Narendra Kotwal
Department of Endocrinology, Command Hospital (Southern Command), Pune - 411 040, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2230-8210.95710

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Ogilvie's syndrome [acute colonic pseudo-obstruction (ACPO)] presents as massive colonic dilatation without a mechanical cause, usually in critically ill patients due to imbalanced sympathetic and parasympathetic activity. The initial therapy remains conservative with supportive measures (correction of metabolic, infectious or pharmacologic factors) followed by neostigmine and decompressive colonoscopy. Surgery is reserved for patients with clinical deterioration or with evidence of colonic ischemia or perforation. A 60-year-old lady presented with fever, altered sensorium, obstipation, bradycardia and abdominal distension. Investigation revealed hyponatremia and acute colonic pseudo-obstruction. Supportive measures and decompressive colonoscopy were not of great benefit. Thyroid profile was suggestive of primary hypothyroidism. Colonic motility was restored only on starting thyroxin. The case is illustrative of the need to consider hypothyroidism, a common endocrine disorder, in the differential diagnosis of Ogilvie's.

Keywords: Acute colonic pseudo-obstruction, hypothyroidism, myxedema, Ogilvie′s syndrome

How to cite this article:
Yanamandra U, Kotwal N, Menon A, Nair V. Ogilvie's syndrome in a case of myxedema coma. Indian J Endocr Metab 2012;16:447-9

How to cite this URL:
Yanamandra U, Kotwal N, Menon A, Nair V. Ogilvie's syndrome in a case of myxedema coma. Indian J Endocr Metab [serial online] 2012 [cited 2021 Feb 28];16:447-9. Available from: https://www.ijem.in/text.asp?2012/16/3/447/95710

   Introduction Top

Ogilvie described in 1948 [1] a syndrome of acute colonic obstruction associated with retroperitoneal malignancy. Dudley [2] in 1958 recognized the obstruction to be due to functional rather than mechanical causes and named it as acute colonic pseudo-obstruction (ACPO). It is postulated to occur due to imbalance between sympathetic and parasympathetic innervations of the large bowel. [3] It has been documented to occur with underlying medical and surgical disorders like recent surgery, general anaesthesia, medications, heart failure and electrolyte abnormalities. [4],[5] We present Ogilvie's syndrome in a patient with myxedema coma.

   Case Report Top

A 60-year-old lady with no previous co-morbidities presented with history of fever of 6 days, non-projectile vomiting, obstipation and altered sensorium of 2 days duration. Clinically, at admission, the patient had a pulse of 120/min, BP of 172/102 mm Hg and a temperature of 100 o F. The patient had pallor, with no icterus, cyanosis and pedal edema. Abdomen was distended; there was no guarding or rigidity. Bowel sounds were not heard, tympanitic note was present all over abdomen. Digital rectal examination did not reveal any impacted faeces. On neurological evaluation, the patient was conscious but drowsy, and was unable to recognize the relatives. Release reflexes or cranial nerve deficit were not present, gag reflex was preserved, the patient was moving all four limbs, cerebellum could not be assessed, there was no neck rigidity. Hematological investigations showed hemoglobin of 12.2 gm%, total lymphocyte count (TLC) of 7300/mm 3 with polymorphs 77%, and platelets of 2.24 × 10 5 /mm 3 . Serum electrolytes and arterial blood gas analysis showed hyponatremia (Na + 122 mEq/l) with potassium level of 4 mEq/l. Renal and liver functions were normal. Electrocardiogram (ECG) on Day 2 of admission revealed junctional rhythm [Figure 1]. Abdominal radiograph revealed gas-filled loops of large intestine [Figure 2]a. On contrast-enhanced computed tomography (CECT) abdomen, the colon appeared distended with maximum cecal diameter of 12 cm [Figure 2]b. Magnetic resonance imaging (MRI) brain and cerebrospinal fluid (CSF) studies were normal. Electroencephalogram (EEG) revealed diffuse slowing suggestive of a metabolic encephalopathy. An impression of encephalopathy secondary to hyponatremia was made. Intravenous 3% saline was instituted after calculating the deficit of sodium, with an aim to raise the serum sodium concentration by not more than 8-10 mEq/l per day. She was started on broad-spectrum antibiotics empirically due to the presence of fever; however, no focus of sepsis could be identified. Patient was kept nil per orally (NPO) and started on parenteral nutrition. Despite these measures, the altered sensorium and abdominal distension persisted. Gut decompression was attempted with colonoscope on Day 4 of hospitalization, but remained unsuccessful. A possibility of hypothyroidism was considered due to the presence of bradycardia, hyponatremia and altered sensorium. Thyroid profile was done and gave the following results: T3 0.37 ng/ml (0.6-1.8 ng/ml), T4 1.6 μg/dl (5.6-13.7 μg/dl) and thyroid stimulating hormone (TSH) 341.57 IU/l (0.35-5.5 IU/l). Anti-thyroid peroxidise (anti-TPO) antibodies were raised (86 U/ml with normal of 0.5-20 U/ml). She was started on replacement with thyroxin from Day 5. Ultrasonography (USG) thyroid revealed normal-sized thyroid and USG-guided fine needle aspiration cytology (FNAC) revealed lymphocytic thyroiditis. Abdominal girth was monitored for signs of peritonism on a daily basis. The abdominal distension regressed gradually and sensorium improved. By Day 11 , she was feeding orally and constipation was relieved. The ECG reverted to sinus rhythm. There were no distended bowel loops on abdominal radiograph on follow-up.
Figure 1: Electroencephalogram showing idioventricular junctional rythm

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Figure 2: Distended bowel loops on (a) plain X-ray abdomen and (b) coronal reformat

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   Discussion Top

We have described a patient of hypothyroidism presenting as Ogilvie's syndrome (ACPO). ACPO is diagnosed by excluding mechanical large bowel obstruction (LBO) characterized by more severe abdominal symptoms and signs. Other differential diagnoses include toxic mega colon and ischemic colitis. [5] ACPO can occur at any age, but occurs more frequently in the elderly. It usually presents in association with underlying medical or surgical disorders such as recent surgery, recent general anesthesia, medications, heart failure, infection, and electrolyte abnormality. [4] It mostly occurs in hospitalized patients who are frequently debilitated. [6]

The mechanism of Ogilvie's syndrome is poorly understood and likely to be multifactorial. The main theories involve an imbalance of autonomic influences, which produces a hypotonic bowel, either through increased sympathetic activity or through decreased parasympathetic activity. [3] Neostigmine improves bowel motility in patients with ileus, suggesting that parasympathetic deficiency causes colonic hypotonia producing stasis and dilatation by inefficient expulsion of gas and stool. [7],[8]

About 75% of cases resolve spontaneously with conservative therapy in a median of 4 days. In patients who do not resolve, intravenous neostigmine can be instituted. About 80% of patients with pseudo-obstruction respond to 2 mg neostigmine infused intravenously rapidly. [9],[10],[11],[12] Colonoscopic decompression relieves symptoms in up to 80% of cases. [13],[14],[15] Administration of polyethylene glycol after acute colonic decompression may help prevent relapse. [16] Precipitating conditions, particularly electrolyte abnormalities such as hypokalemia, hypomagnesaemia, and hypocalcaemia, are treated Supportive care includes NPO, intravenous hydration, and discontinuation of narcotic, sedative, or anticholinergic medications. Antibiotics are administered if sepsis is suspected. Ambulation, if possible, or frequent patient repositioning may help move intestinal gas. Laxatives are generally avoided because fluid tends to accumulate in the bowel. Conservative management is continued for 72 hours if cecal diameter is <12 cm and there are no signs of bowel or peritoneal complication. [17]

Hypomotility and atony of the gastrointestinal tract, mostly involving colon, occurs in myxedematous patients. Patients frequently have symptoms of bloating, flatulence, and constipation. As the hypothyroid state becomes more severe, intestinal hypomotility may progress to atony, ileus, prolapse or volvulus. [18] Chronic pseudo-obstruction has been described in hypothyroidism, [19] but de novo presentation as Ogilvie's syndrome (acute colonic pseudo-obstruction) has not been reported. One study on the prevalence of ACPO as a postoperative complication of hip arthroplasty recorded 3 out of 30 cases to have underlying hypothyroidism prior to surgery. [20] Possible mechanism of hypomotility in hypothyroidism is autonomic neuropathy and altered impulse transmission at myoneural junction, intestinal ischemia, intestinal myopathy and glycosaminoglycan (GAG) deposition. [21]

Our patient presented with altered sensorium and abdominal distension. The encephalopathy was thought to be resulting from hyponatremia. We considered diagnosis of ACPO as no mechanical cause could be identified as responsible for the obstruction and duration of disease was less than 6 days. The possible precipitants leading to ACPO could have been dyselectrolytemia and sepsis. Initial measures like administration of 3% saline and large bowel decompression with colonoscopy were not successful in improving her symptoms. Hypothyroidism was not recognized at presentation as it was masked by the sepsis and dyselectrolytemia. The bradycardia and junctional rhythm were unmasked only after treatment of the sepsis. Subsequently, when we diagnosed hypothyroidism and instituted thyroxin replacement, gut motility was restored and her sensorium improved. No previous case report has documented myxedema coma presenting as ACPO.

   Conclusion Top

We conclude hypothyroidism to be a cause of Ogilvie's syndrome. Ogilvie's syndrome should be diagnosed only after excluding mechanical causes for colonic obstruction. We emphasize the need to consider hypothyroidism in the differential diagnosis of any patient with acute onset LBO. If laparotomy is performed on the patient with ileus, the complications of myxedema coma and death may follow. Thus, it is important to consider the possibility of myxedema ileus in cases of marked colonic distension before subjecting them to surgery.

   References Top

1.Ogilvie H. Large-intestine colic due to sympathetic deprivation: A new clinical syndrome. Br Med J 1948;2:671-3.   Back to cited text no. 1
2.Dudley HA, Sinclair IS, Mclaren IF, Mcnair TJ, Newsam JE. Intestinal pseudo-obstruction. J R Coll Surg Edinb 1958;3:206-17.  Back to cited text no. 2
3.Turnage RH, Heldmann M, Cole P. Intestinal obstruction and ileus. In: Feldman M, Friedman LS, Brandt LJ, editors. Sleisenger and Fordtran's gastrointestinal and liver disease: Pathophysiology, diagnosis, and management. 8 th ed. Philadelphia: Elsevier Saunders; 2006. p. 2653-78.  Back to cited text no. 3
4.Wegener M, Borsch G. Acute colonic pseudo-obstruction (Ogilvie's syndrome): Presentation of 14 of our own cases and analysis of 1027 cases reported in the literature. Surg Endosc 1987;1:169-74.  Back to cited text no. 4
5.Batke M, Cappell M. Adynamic ileus and acute colonic pseudo-obstruction. Med Clin N Am 2008;92:649-70.  Back to cited text no. 5
6.Saunders MD, Kimmey MB. Systematic review: Acute colonic pseudo-obstruction. Aliment Pharmacol Ther 2005;22:917-25.  Back to cited text no. 6
7.Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie's syndrome): An analysis of 400 cases. Dis Colon Rectum 1986;29:203-10.  Back to cited text no. 7
8.Catchpole BN. Ileus: Use of sympathetic blocking agents in its treatment. Surgery 1969;66:811-20.  Back to cited text no. 8
9.Abeyta BJ, Albrecht RM, Schermer CR. Retrospective study of neostigmine for the treatment of acute colonic pseudo-obstruction. Am Surg 2001;67:265  Back to cited text no. 9
10.Mehta R, John A, Nair P, Raj VV, Mustafa CP, Suvarna D, et al. Factors predicting successful outcome following neostigmine therapy in acute colonic pseudo-obstruction. A prospective study. J Gastroenterol Hepatol 2006;21:459-61.  Back to cited text no. 10
11.Paran H, Silverberg D, Mayo A, Shwartz I, Neufeld D, Freund U. Treatment of acute colonic pseudo-obstruction with neostigmine. J Am Coll Surg 2000;190:315-8.  Back to cited text no. 11
12.Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med 1999;341:137-41.  Back to cited text no. 12
13.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;35:1135-42.  Back to cited text no. 13
14.Rex DK. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest Endosc Clin N Am 1997;7:499-508.  Back to cited text no. 14
15.Bode WE, Beart RW Jr, Spencer RJ, Culp CE, Wolff BG, Taylor BM. Colonoscopic decompression for acute pseudoobstruction of the colon (Ogilvie's syndrome). Report of 22 cases and review of the literature. Am J Surg 1984;147:243-5  Back to cited text no. 15
16.Shishido SM, de Oliveira MG. Polyethylene glycol matrix reduces the rates of photochemical and thermal release of nitric oxide from S-niroso-N-acetylcysteine. Photochem Photobiol 2000;71:273-80.  Back to cited text no. 16
17.Sloyer AF, Panella VS, Demas BE, Shike M, Lightdale CJ, Winawer SJ, et al. Ogilvie's syndrome: Successful management without colonoscopy. Dig Dis Sci 1988;33:1391-6.  Back to cited text no. 17
18.Bastenie PA. Paralytic ileus in severe hypothyroidism. Lancet 1946; 1:413-6.  Back to cited text no. 18
19.Abbasi AA, Douglass AC, Bissell GW, Chen Y. Myxedema ileus: A form of intestinal pseudoobstruction. JAMA 1975;234:181-3.  Back to cited text no. 19
20.Clarke HD, Berry DJ, Larson MS. Acute Pseudo Obstruction of the colon as a post operative complication of hip arthroplasty. J Bone Joint Surg 1997;79:1642-7.  Back to cited text no. 20
21.Dunet AL, Bastenie PA. Intestinal disorders in hypothyroidism: Clinical and manometric study. Am J Dig Dis 1971;16:723-7.  Back to cited text no. 21


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