C ASE REPO RT

Paralytic Ileus in Vegetarian with Pneumonia Infection

Khaira Utia Yusrie*, Nina Kemalasari**, C Martin Rumende***,
Marcellus Simadibrata****, Ari Fahrial Syam****
*Department of Internal Medicine, Faculty of Medicine,
University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital
**Division of Geriatri, Department of Internal Medicine, Faculty of Medicine,
University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital
***Division of Pulmonology, Department of Internal Medicine, Faculty of Medicine,
University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital
****Division of Gastroenterology, Department of Internal Medicine, Faculty of Medicine,
University of Indonesia/Dr. Cipto Mangunkusumo General National Hospital

ABSTRACT
Paralytic ileus which is commonly found in clinical practice is referred to clinical syndrome of
transportation disturbance of the intestinal lumen content due to various etiology and underlying condition.
It has been considered a transient gastrointestinal syndrome with good prognosis. Most cases respond well
to conservative management. However, inappropriate diagnostic approach and management will result in
severe complication leading to death such as septicemia and perforation. We reported a case of paralytic
ileus in young male who is vegetarian with pneumonia infection as the suspected underlying etiology.
Radiological examination of the abdomen in three position (upright, supine and lateral) showed dilated
gaster and duodenum with minimal air fluid level, no herring bone appearance and absent of free
intraperitoneal air. The laboratory result also showed low level of vitamin B12 which might be due to his
lactovegetarian diet habit. Management including supportive therapy such as decompression, fasting,
adequate parenteral nutrition, fluid balance and treatment of pneumonia as the underlying cause of
paralytic ileus had been resulted in good clinical response.

Keywords: Paralytic ileus, pneumonia, treatment

INTRODUCTION perforation is 3 percent, with an attendant mortality rate

Paralytic ileus is a clinical syndrome caused by acute of 50%. Most cases respond to conservative
and transient disturbance of transportation of management.4.5 However, diagnostic and management
the intestinal lumen content due to cessation of smooth approach based on guidelines have not been available
muscle motor activity in the small intestines and colon, yet.
with is potentially be returned to normal.1,2 Compared to Underlying conditions that could induce paralytic
obstructive ileus, paralytic ileus is more common ileus are intraabdominal (peritonitis, retroperitoneal
encountered by physicians. However, we still do not have processes, disturbance in oxygen supply) and extra
statistical data on incidence of paralytic ileus, possibly abdominal causes (metabolic disturbances such as ele
because it has been considered a transient ctrolyte imbalance, drugs, pneumonia, sepsis and whole
gastrointestinal syndrome with satisfactory prognosis.2 body infection). 2,3,6 Several conditions may create
Acute intestinal pseudo-obstruction consists of massive problems in the management of paralytic ileus such as
dilatation of the intestine in the absence of mechanical hypovolemic shock, septicemia, septic shock and
obstruction.3,4 The approximate risk of spontaneous malnutrition.1,2

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 C ASE REPO RT

Careful history and physical examination are of neostigmine should be considered before colonoscopy
important initial steps in assessing peritoneal signs and is performed in patients with acute colonic pseudo-
other evidence of a primary intra-abdominal obstruction who have not had a response to
inflammatory process or mechanical obstruction that conservative management.4 Surgical exploration is
may require surgical intervention.3 Clinical findings of reserved for acute cases with peritoneal sign, ischemic
paralytic ileus may take form of: bowel or other evidence of perforation.4
• gassiness, metereorismus (flatulence), reduced or di Vegetarian diets can be classified as either
minished bowel sounds lactovegetarian, ovovegetarian, lactoovovegetarian, or
• nausea, vomiting, generally constipated but diarrhea vegan if they include, respectively, dairy products, eggs,
is possible both dairy product and eggs, or no animal products at all.
• may be accompanied by fever (sub febrile or Vegan diets have a very low cobalamin (vitamin B12)
febrile) content.8
• the patient’s general condition mild to severely ill, The main source of dietary cobalamin for humans is
may be accompanied by loss of consciousness food of animal origin.9 Vitamin B12 is produced in nature
• shock may occur only by vitamin B12 producing microorganism. That is
• accompanying disease/conditions that may cause the reason why human must obtain vitamin B12 solely
increased risk: trauma, surgical procedures from the diet. Dhopeshwarkar et al observed that
(particularly in the abdomen), acute pancreatitis, bile lactovegetarians had distinctly lower serum vitamin B12
stone, diabetes mellitus, electrolyte imbalance, concentrations than did nonvegetarians.8 Measurement
spasmolytic agents, pneumonia and whole body of vitamin B12 levels can be helpful for diagnosing
infections.2,7 vitamin B12 deficiency. Generally, normal serum B12
levels range from 200 to 900 pg/mL.10 Clinical features
Decreased or absent of bowel sound indicates acute of vitamin B12 deficiency involve the hematopoetic,
intestinal obstruction, pseudo-obstruction or paralytic the gastrointestinal tract, and the nervous system.
ileus. Further examinations that support the diagnosis are Clinical manifestation may occur without abnormality in
very important. Conventional laboratory studies may help other systems.5,11,12
to assess electrolyte abnormalities or intra-abdominal Gastrointestinal manifestations reflect the effect of
infectious/inflammatory process. Supine, upright and cobalamin deficiency on rapidly proliferating
lateral abdominal X-rays determine the distribution of gastrointestinal epithelium. Anorexia with moderate
intestinal gas and asses for the presence of free weight loss may also be evident, possibly accompanied
intraperitoneal air.3 by diarrhea and other gastrointestinal symptoms. These
Most cases respond to conservative management, non latter manifestations may be caused in part by
operative continuous decompression and adequate megaloblastosis of the small intestinal epithelium, which
treatment of the primary disease.4,5 In protracted cases, results in malabsorbtion.12
gastric decompression eliminates upper GI secretions and On physical examination, the patient with cobalamin
decreases vomiting and gastric distention. Rectal tubes deficiency is pale with mild jaundice. Elevated serum
necessitate colonoscopic decompression, especially when bilirubin levels are related to high erithroid cell turnover
the cecal diameter approaches 9-10 cm. In most in the marrow.12 Management of cobalamin deficiency
patients with acute colonic pseudo-obstruction, is related to the underlying disorder. If the deficiency is
conservative management will result in the resolution of caused by malabsorbtion, initial parenteral treatment of
colonic distention within three days.3 Basic supportive 1,000 µg cobalamin per week for 8 weeks, followed by
measurements consist of fasting, fluid replacement, 1,000 µg cyanocobalamin injected intramuscularly
and correction of electrolyte imbalance. Prompt every month. However, cobalamin deficiency can also
antimicrobial therapy is indicated if infection is suspected. be managed very effectively by oral replacement therapy
Medications that slow GI motility (adrenergic agonists, of 2 mg crystalline B12 per day.12
sedative, narcotic analgesics) should be withdrawn or
dose reduced. Total parenteral nutrition may be required CASE ILLUSTRATION
in protracted cases.3 Male, 18 years old, was admitted to Cipto
Ponec RJ et al., found that treatment with Mangunkusumo hospital in March 7, 2004 with chief
neostigmine was effective to decompress the colon in complaint of nausea and vomiting since 3 days prior to
patients with acute colonic pseudo-obstruction. The use
110 The Indonesian Journal of Gastroenterology Hepatology and Digestive Endoscopy
 Paralytic Ileus in Vegetarian with Pneumonia Infection

admission. Since one month prior to admission, The abdomen was distended, liver and spleen were not
the patient also complained of cough, sometimes with palpable, and the bowel sound decreased. Epigastric pain
blood streak and shortness of breath, weight loss, loss of was felt on abdominal palpation. The extremities were
appetite and fluctuating fever, but he did not have night warm and there was no edema or clubbing finger digital
sweat. The patient went to Medika Lestari Hospital and rectal examination found weakness of anal sphincter
was given some medicine from the doctor which was muscle, ampula of rectum did not collapsed, no
not known by the patient. According to the patient, the tenderness, no mass, smooth inner surface of rectum
doctor said that he was suffering from typhoid fever and and no feces or blood on hand gloves.
was suspected to have lung tuberculosis. After he The previous laboratory results from Medika Lestari
completed the medications, he found no improvement at hospital on 4th March 2004 revealed hemoglobin level
al. Since 3 days prior to admission he suffered from 11.1 g/dL, hematocryte 33%, leukocyte 17,600/µL and
nausea and vomiting. He also complained about abdominal platelet count 325,000/µL, blood glucose 125 mg/dL, AST
discomfort and constipation for 3 days. There was no 114 µ/L and titer of serologic widal test were paratyphi
history of diarrhea. He went back to Medika Lestari BO 1/160, AH 1/160, BH 1/80.
hospital, and underwent abdominal X-ray and some On laboratory examination at the emergency room
others laboratory examination. He had been hospitalized revealed hemoglobin 11.3 g/dL, hematocryte 33%,
in Medika Lestari for 3 days and got some medications leukocyte 14,600/µL and platelet count 149,000/µL, blood
(ceftriaxone 2 g daily, ranitidin and metoclopramide glucose 99 mg/dL, liver function tests showed elevated
injection 3 times daily). Nasogastric tube (NGT) was ALT 135 µ/L and AST 183µ/L, BUN 51 g/dL,
inserted also but there was not any improvement of his creatinine 0.5 g/dL, serum electrolyte were normal with
condition at all. The doctor suggested that he should be sodium 144 mmol/L, potassium 4.1 mmol/L and chloride
referred to Cipto Mangukusumo hospital for exploration. 105 mmol/L. There were slightly elevated levels of
So he went to Cipto Mangunkusumo hospital, and the amylase 110 U/L and lipase 97 U/L. Three positional
doctor in emergency room said that he was suffering abdominal X-ray showed dilated gaster and duodenum
from gastrointestinal disorder and lung infection, but with minimal air fluid level at intralumen, no herring bone
because the wards were occupied, he went to Usada appearance, minimal air distribute to distal, and absent
Insani hospital. According to the patient, the doctor at of free intraperitoneal air. Chest X-ray showed infiltrates
the Usada Insani hospital suggested that he undergo in both of the lung, especially at the right lung.
operation because of intestinal perforation. The patient Based on all data above, the problems of this patient
and his family rejected the procedure decided to bring were: (1) Paralytic ileus; (2) Pneumonia; (3) Jaundice.
him back to Cipto Mangunkusumo hospital. Paralytic ileus was based on symptoms of nausea,
From the past medical history, the patient denied vomiting, abdominal discomfort, sign of decreased bowel
suffering from hepatitis, malaria, and he has no history sound, leukocytosis and slightly elevated levels of
of traveling out of town. He also denied using neither amylase-lipase enzymes, and on three positional
intravenous drugs nor free sex. He was a senior high abdominal X-ray showed dilated gaster and duodenum
school student, and had low social economic background. with minimal air fluid level at intralumen, no herring bone
On physical examination, the patient was moderately appearance, minimal air distribution to distal, and absent
ill, alert and fully oriented but looked underweight. Blood of free intraperitoneal air. Acute pancreatitis was
pressure was 100/60 mmHg, pulse rate was regular at suspected of the etiology of paralytic ileus, with
110 beats per minute, temperature was 37.7 oC and differential diagnosis of obstructive ileus and peritonitis.
respiratory rate was 24 per minute. His height was 165 Pneumonia was based on cough for one month, with
cm and the body weight was about 40 kg. Conjunctiva bloody streak, weight loss, loss of appetite, fluctuating
was not pale and his sclera was icteric. JVP was 5-2 fever, rales at both of the lung, leukocytosis, and
cmH2O, and there were no palpable lymph nodes. Lips infiltrate at both of the lung on chest X-ray. Differential
and tongue was dry. Nasogastric tube (NGT) had diagnosis was lung tuberculosis. Jaundice was detected
already been inserted for gastric content drainage. NGT on the sclera accompanied by leukocytosis and elevated
drainage was 200 cc greenish fluid. On chest levels of ALT and AST suggested possible causes like
examination, the heart sounds were normal without any cholecystitis and cholelythiasis with differential
murmur or gallop, the breath sound was vesicular with diagnosis of leptospira infection and acute hepatitis.
rales at both of the lungs, and no wheezing.

Volume 5, Number 3, August 2004 111

Khaira Utia Yusrie, Nina Kemalasari, C Martin Rumende, Marcellus Simadibrata, Ari Fahrial Syam

Our management included decompression of examine of vitamin B12 serum at the laboratory because
gastrointestinal, fasting with adequate parenteral of his life style. Unfortunately, the patient’s family
nutrition by giving triofusin E 1,000 each 12 hours, refused to do the examination because it was
normal saline and dextrose in saline 1,500 cc per day, considered too expensive.
2 liters oxygen, 1 gram of cefotaxime 3 times daily, On the 12th day the patient had defecation, jaundice
1 ampoule pantoprazole once daily and fluid balance for disappeared, minimal rales at the right lung, and he started
24 hours and consulted to Surgery Department. to have soft diet.
The result of the consultation, they suggested that On the 15th day the patient was discharged from
the patient be rehydrated, decompressed, were given total hospital, given some medications (cefixime 100 mg 2
parenteral nutrition and at that time no surgical times daily, lanzoprazole once daily, and hepatoprotector).
intervention was indicated but need further evaluation. We still motivated him to check his vitamin B12 serum
We planned to perform abdominal ultrasonography, level to confirm diagnosis vitamin B12 deficiency. We
repeat amylase-lipase test, liver function test, serologic also educated the patient to change his vegetarian
marker of hepatitis such as HbSAg and Anti HCV, acid lifestyle.
fast bacilli stained and sputum culture with Two weeks after being discharged, he underwent the
microorganism resistance test. examination of vitamin B12 serum and chest X-ray for
On the third day of hospitalization, the patient’s evaluation. The concentration of vitamin B12 serum was
condition was moderately ill, blood pressure 120/80 175 pg/mL (normal value: 179-1132 pg/mL) and
mmHg, pulse rate 100 times per minute, respiratory rate appearance of chest x-ray was improved. We suggested
20 times per minute, no fever, but icteric sclera and the patient to undergo bronchoscopic examination to help
decreased bowel sound. We continued to decompress establish the diagnosis of pulmonary infection.
with fasting and nasogastric tube, total parenteral March 7, 2004: Three positional abdominal X-ray
nutrition, 1 g cefotaxime 3 times daily, 1 ampoule showed dilated gaster and duodenum with minimal air
pantoprazole once daily, and twice daily alinamin fluid level at intralumen, no herring bone appearance,
F. Production of gastrointestinal secretion observed from minimal air distribute to distal, absent of free
NGT was 500 cc greenish fluid per 24 hours. We intraperitoneal air. On March 9, 2004, leptospirosis was
consulted to surgical department for further evaluation. negative. March 11, 2004. Culture of sputum was
On the fourth day we reexamined the levels of positive Pseudomonas sp.
amylase-lipase enzymes because production of NGT was
300 cc per 8 hours contained greenish fluid. We
DISCUSSION
examined the liver function test and scheduled for
abdominal ultrasonography. The results of the level of Diagnosis of paralytic ileus is based on the complaint
amylase-lipase enzymes were slightly increased of nausea, vomiting, abdomen discomfort, with decreased
with amylase: 129 U/L and lipase 128 U/L. bowel sound, there were leukocytosis and slightly elevated
On the fifth day, bowel sound started to improve, and amylase-lipase enzymes, and on three positions
we planned to administer liquid diet started from 50 cc, abdominal X-rays dilated gaster and duodenum were
if there were no complain of abdominal pain we planned found with minimal air fluid level at intralumen, no
to increase the volume of liquid diet on the following herring bone appearance, minimal air distribute to distal,
day. Anamnesis on diet lifestyle revealed that he had and absent of free intraperitoneal air.
been vegetarian since he was 6 years old. Paralytic Before all the data were available, we suspected
ileus might be correlated with his vegetarian lifestyle. the etiology of paralytic ileus in this patient was acute
We also suspected diagnosis of vitamin B12 deficiency pancreatitis with differential diagnosis tuberculosis
in this patient. peritonitis or leptopsirosis because of normal
On the 9th day lung condition were improved, with concentration of electrolyte serum. But after we repeated
minimal rales at both of the lung, and we changed some amylase-lipase enzymes, the result did not support the
medications to oral preparation (lanzoprazole once daily diagnosis of acute pancreatitis because the enzymes
and oral alinamin F two times daily and hepatoprotector). increased less than 2 times than normal value.
On the 10th day the patient underwent abdominal Leptospirosis was also negative. One of the clinical
ultrasound and the conclusion were chronic hepatitis conditions that may cause increased risk of paralytic
appearance, no obstruction, and was suggested to check ileus in this patient was pneumonia infection. Sepsis and
serologic marker of viral hepatitis. He was suggested to all infections of the body could induce paralytic ileus.2,3

112 The Indonesian Journal of Gastroenterology Hepatology and Digestive Endoscopy

 Paralytic Ileus in Vegetarian with Pneumonia Infection

But clinical status of pneumonia infection was not obstruction were found. But intestinal dilatation, had to
severe in this patient, so we tried to explore other be suspicion of intestinal perforation. If dilatation more
conditions that may aggravate paralytic ileus. After we than 12 cm or no resolution of colonic distention after six
asked the patient about his diet, we found that he was days, surgical exploration like caecostomy may be
lactovegetarian. From the literature we know that indicated. Risk of colonic perforation was reported higher
lactovegetarian has cobalamin deficiency compared to if the caecal diameter exceeds 12 cm and if distention is
non vegetarian. present for more than six days.2Surgical intervention is
The patient was lactovegetarian. He still consumed required if there is clinical suspicion of mechanical
milk for his diet, but did not consume egg, meat and fish. obstruction3
That indicated he could be suffering from vitamin B12 Gastric decompression would help to eliminate upper
deficiency. Clinical manifestation of vitamin B 12 GI secretions and decreases vomiting and gastric
deficiency are various, one of them gastrointestinal distention. The resolution of distention will be reached
disorder. Unfortunately, vitamin B12 serum could not be within 3 days. Ponec RJ recommended the use of
examined at that time when the symptoms and sign of neostigmine if conservative treatment shows no
paralytic ileus appeared. response.4 Supportive management like fluid replacement,
Pneumonia infection was suspected of the etiology temporary or total parenteral nutrition, is an important
of paralytic ileus, aggravated by vitamin B12 deficiency, thing for successful conservative management.
because all the data we collected did not support other Pneumonia infection may cause paralytic ileus, thus
causes like acute pancreatitis or electrolyte antibiotics should be administered according to the type
abnormalities. He was suggested to check vitamin B12 of infection and the results of the antibiotic sensitivity
serum level to confirm the diagnosis. test to achieve satisfactory outcome.
Determining the underlying disease in paralytic ileus The levels of bilirubin, ALT, AST, phosphatase
is not easy. Thus, conservative management must be alkaline and gamma GT increased in this patient might
given if clinical symptoms suggests diagnosis of be caused by cholestasis syndrome. We suspected that
paralytic ileus, while identify the etiologic diagnosis. he was infected by hepatitis A virus, but unfortunately
Causal therapy can immediately be initiated when due to financial limitation the diagnosis could not be
the underlying disease/condition has been identified.2 established. This condition could be attributed to the
Decisions about management and selecting parenteral feeding that might mimicked cholestasis
supporting examinations such as colonoscopy should be syndrome. The prognosis is usually good if the patient
based on the patient’s clinical status. 3 From responds to conservative management, although
the abdominal X-ray, dilated gaster and duodenum were sometimes the etiology remains undetermined.2,3 This
found with minimal air fluid level at intralumen, no case was presented as demonstration case of paralytic
herring bone appearance, minimal air distribute to distal, ileus in vegetarian due to pneumonia infection with
and absent of free intraperitoneal air. No sign of total vitamin B12 deficiency.

Volume 5, Number 3, August 2004 113

REFERENCES Informasi dan Penerbitan Ilmu Penyakit Dalam FKUI Jakarta
1999.p.32-4
1. Summer RW, Lu CC. Approach to the patient with ileus and 8. Antoby AC. Vegetarianism and vitamin B12 deficiency. Am J
obstruction. 2nd ed. Gastroenterology. Philadelphia: JB Clin Nutr 2003;78:3-6
Lippincott Co 1995.p.796-812 9. Dusseldorp M, Schneede J, Refsum H, Ueland PM, Thomas
2. Wintery EM, Syam AF, Simadibrata M, Manan C. PM, Boer E, et al. Risk of persistent cobalamin deficiency in
Management of paralytic ileus. Indonesian J Gastroenterol adolescents fed a macrobiotic diet in early life. Am J Clin Nutr
Hepatol 2003;4(3):80-8 1999;69:664-71
3. Prakash C. Gastrointestinal disease. In: Ahya SN, Flood K, 10. Snow CF. Laboratory diagnosis of vitamin B12 and folate
Paranjothi S, editors. The Washington Manual of Medical deficiency. Arch Intern Med 1999;159:1289-98
Therapeutics.30th ed. USA: Lippincott Williams & Wilkins 11. Rasmussen SA, Fernhoff PM, Scanlon KS. Vitamin B12
2001.p.365-66 deficiency in children and adolescents. J Pediatr 2001;138:10-17
4. Ponec RJ, Sauders MD, Kimmey MB. Neostigmine for 12. Babior BM, Bunn HF. Megaloblastic anemias. In: Braunwald E,
the treatments of acute colonic pseudo-obstructions. N Engl J Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL,
Med 1999;341(3):137-41 editors. Harrison’s Principles of Internal Med. 15th ed. USA:
5. Silen W. Acute Intestinal obstruction. In: Braunwald E, Mc Graw Hill Co 2001.p.451-54
Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL,
editors. Harrison’s Principles of Internal Medicine. 15th ed. USA:
McGraw Hill Co 2001.p.1703-05
6. Kumar D. Obstruction of small and large bowel and ileus.
In: Bouchier, Allan, Hodgson, Keighley, editors.
Gastroenterology clinical science and practice. Vol 2. 2nd ed.
Philadelphia: WB Saunders Co;1997.p.1033-44
7. Daldiyono H, Abdullah M. Ileus paralitik. Dalam: Pedoman
diagnosis dan terapi di bidang Ilmu Penyakit Dalam. Pusat

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