J Ped Surg Case Reports 6 (2016) 20e23

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Journal of Pediatric Surgery CASE REPORTS

Abdominal compartment syndrome associated with

a r t i c l e i n f o a b s t r a c t

Article history: Norovirus infection is a leading cause of infectious gastroenteritis and is typically self-limited. Abdominal
Received 20 November 2014 compartment syndrome is rare in the pediatric population. To date, there have been no reports of
Received in revised form abdominal compartment syndrome secondary to Norovirus infection. This patient is a 7-year old female
23 May 2015
who presented with abdominal compartment syndrome and fulminant sepsis attributed to acute
Accepted 23 May 2015
Available online 1 June 2015
Norovirus infection. The patient was successfully treated with decompressive laparotomy, delayed
abdominal closure, and supportive therapy. The patient’s post-operative course was notable for acute
hepatitis and pancreatitis, which resolved without further intervention. The patient was discharged
Key words:
Norovirus
home after a prolonged hospital stay in good condition.
Abdominal compartment syndrome Ó 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND
Decompressive laparotomy license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Pancreatitis
Hepatitis
Pediatric patient

Norovirus is a leading cause of infectious gastroenteritis and is could not be measured. The patient was emergently intubated due
usually a self-limited disease. Abdominal compartment syndrome to respiratory distress. Attempts at gastric decompression with
in the pediatric population is uncommon, and there are no reports placement of a nasogastric tube were unsuccessful due to tube
of abdominal compartment syndrome associated with Norovirus coiling in the esophagus. Serum laboratory studies were notable for
infection. a leukocytosis of 18,000 k/uL, glucose of 439 mg/dL, acute
transaminitis with AST 152 U/L and ALT 116 U/L, hyperlipasemia of
1. Case report 434 U/L, lactic acidemia of 12.36 mmol/L, and an arterial blood gas
pH of 6.9. Chest and abdominal x-rays demonstrated massive
The patient is a 7 year-old female born at 28 weeks gestation. gastric and small bowel distention (Fig. 1). Computed tomography
Her early medical history is significant for open Nissen fundopli- imaging demonstrated similar findings without a transition zone
cation in the first year of life for refractory gastroesophageal reflux. and gas distributed within the distal rectum; a nasogastric tube was
The patient was feeling well until the morning of presentation, at looped in the esophagus (Fig. 2). The patient was subsequently
which time she began to experience nausea, retching without transferred to our institution for further management.
vomiting, abdominal pain and distention. Over a period of hours Surgical evaluation confirmed the above findings as well as lack
she progressed to lethargy, acute mental status changes, and of palpable pulses in the lower extremities. Attempts at reposi-
cyanosis. Of note, three household members had overcome recent tioning and replacing an orogastric and nasogastric tube were
flu-like illnesses characterized by nausea, emesis, and lethargy. unsuccessful. Due to concern for abdominal compartment
The patient initially presented to an outside hospital syndrome (ACS), the patient was taken emergently to the operating
unresponsive and in respiratory distress. Examination revealed room. Esophagogastroduodenoscopy (EGD) revealed a normal
tachycardia, a severely distended and firm abdomen, and diffuse appearing esophagus, and intact Nissen fundoplication. There was a
cyanosis with mottling of her lower extremities. Blood pressures significant amount of dark succus within the stomach and there
was evidence of gastric mucosal sloughing. A decompressive
* Corresponding author. Cleveland Clinic Main Campus, Mail Code A100, 9500
orogastric tube was successfully placed under endoscopic guidance.
Euclid Ave., Cleveland, OH 44195, USA. Tel.: þ1 216 636 9297. Due to persistent abdominal distention, an exploratory laparotomy
E-mail address: lium@ccf.org (M.H. Liu). was performed. Laparotomy revealed a small amount of clear

2213-5766/Ó 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
http://dx.doi.org/10.1016/j.epsc.2015.05.012
 M.H. Liu et al. / J Ped Surg Case Reports 6 (2016) 20e23 21

Fig. 1. Chest (A) and abdominal (B) radiographs demonstrate prominent gastric and bowel distention.

ascites without evidence of peritoneal contamination. The small returned to the operating room on hospital day number two for a
bowel was markedly dilated and congested but without evidence of second look operation and repeat EGD. Endoscopy demonstrated
ischemia. Exploration of the abdomen revealed no additional congestion and erythema of the gastric mucosa with a large
abnormalities. The abdomen was temporarily closed with a quantity of undigested food or tissue in the fundus. The gastric
modified negative pressure wound therapy dressing. The patient effluent was sent for cultures, and biopsies of the gastric mucosa
demonstrated immediate improvement in perfusion as evidenced and mass were obtained. Abdominal exploration revealed minimal
by resolution of cyanosis and increased urine output. serous ascites. The small bowel appeared viable but remained
The patient was maintained on mechanical ventilation significantly dilated, precluding definitive closure. A liver biopsy
post-operatively and admitted to the intensive care unit. She was obtained due to worsening hepatitis and the abdomen was

Fig. 2. Coronal (A) and axial (B) computed tomography images demonstrate prominent gastric and bowel distention. (A) also demonstrates intra-esophageal looping of the
nasogastric tube.
22 M.H. Liu et al. / J Ped Surg Case Reports 6 (2016) 20e23

again temporarily closed with a modified negative pressure device. associated with benign seizures without any long-term neurologic
Definitive abdominal closure was ultimately obtained on hospital sequelae [5e7]. Among premature infants infected with Norovirus,
day 6 during the patient’s third operative exploration. The patient vomiting was less common and patients more frequently demon-
was subsequently extubated successfully. strated symptoms of abdominal distention, apnea, or tachypnea
The patient underwent extensive work-up to determine the requiring supplemental oxygen therapy; a sepsis-like appearance
cause of her severe enteritis. Blood testing did not find any culprit was also reported [8]. A more severe disease course has been
toxic agents. Infectious disease work-up, including shigella, observed in children with underlying medical conditions. In pedi-
salmonella, campylobacter, Escherichia coli, rotavirus, Hepatitis atric patients with inflammatory bowel disease (IBD), infection
A and B, CMV, EBV, and adenovirus were negative. A stool sample with Norovirus was associated with acute exacerbation of IBD,
obtained early in the patient’s hospital course tested positive for hematochezia, and prolonged viral shedding [9]. Similar results
Norovirus 2. Liver biopsy demonstrated non-specific portal have been demonstrated in immunocompromised pediatric
inflammation without any infectious component. Stomach biopsy patients. In a prospective study of patients with inherited immune
demonstrated reactive epithelial changes and lamina propria deficiencies, patients demonstrated prolonged viral shedding, with
hemorrhage/edema, while the gastric effluent demonstrated positive stool samples detected at a median of 9.5 months.
Candida albicans. The patient developed acute hepatitis with Shedding was also associated with gastrointestinal symptoms and
elevation of AST and ALT to 4831 U/L and 3026 U/L, respectively, viremia in a significant proportion of subjects [10]. Interestingly,
without evidence of elevated alkaline phosphatase or hyper- despite these reports of more severe disease courses following
bilirubinemia. She also developed pancreatitis, as evidenced by infection with Norovirus, there are no reports of associated
hyperlipasemia of 434 U/L. These abnormalities resolved during the abdominal compartment syndrome in the medical literature.
patient’s hospital course. The patient was ultimately discharged to Abdominal compartment syndrome (ACS) is defined as a
home on hospital day number 41 in good condition. The patient’s sustained elevation in intra-abdominal pressure (IAP) that results in
final diagnosis was acute Norovirus 2 infection causing abdominal end-organ damage, particularly to the cardiovascular, pulmonary
compartment syndrome. The patient returned for outpatient and renal systems [11]. Untreated, mortality from ACS is almost
follow-up at three and six months following her discharge. Gastric certain. The intra-abdominal pressure is influenced by intraluminal
emptying studies performed at follow-up were normal. The patient abdominal volume and, in turn, determines abdominal perfusion
had recovered fully and was without any identified sequelae from pressure (APP, APP ¼ mean arterial pressure  IAP). Recent updates
her disease process and interventions. issued by the World Society on Abdominal Compartment Syndrome
recommend assessing IAP through the use of bladder catheters and
2. Discussion advocate serial measurements in patients with risk factors for ACS
and elevated intravesical pressures [12].
Norovirus, an RNA virus, is amongst the most common causes of Similar definitions for ACS have been applied to pediatric
non-bacterial gastroenteritis. There are six recognized genogroups patients (age < 18 years). However, ACS is poorly described in the
of Norovirus, three of which affect humans. Norovirus has been pediatric population primarily due to its infrequency. An intra-
estimated to account for 47e96% of outbreaks of acute gastroen- abdominal hypertension threshold of 10 mm Hg has been sug-
teritis and 5e36% of sporadic cases of gastroenteritis [1,2]. Among gested, but this number disregards the large variability in MAP and
children less than 5 years of age, Norovirus is the second leading IAP within the pediatric population. Indeed, IAP as low as 4 mm Hg
cause of gastroenteritis, eclipsed only by Rotavirus. In a 2009e2010 has been associated with ACS in critically ill children [12]. The
prospective study of US children less than 5-years of age for whom physician must therefore demonstrate vigilance, relying on clinical
medical attention was sought due to gastroenteritis, Norovirus was judgment and on physical exam findings, in order to make an
detected in 21% of individuals with a rate of hospitalization of 7.2 expedient diagnosis and to avoid delayed treatment. Findings
per 1000 [2]. With improvements in Rotavirus vaccination, the suggestive of ACS include a tense abdomen, lack of distal pulses,
prevalence of Norovirus as a cause for gastroenteritis appears to be and cyanotic extremities. The presentation may include other
increasing [3]. The highly contagious nature of Norovirus infection secondary effects, including wheezing, tachypnea, elevated venti-
is in part due to its multiple modes of transmission, which include latory peak pressures, oliguria, low cardiac index, and other signs of
direct person-to-person fecal-oral route, ingestion of aerosolized hypovolemia. Further evaluation may be undertaken with labora-
vomit, and indirect transmission by means of contaminated sur- tory analysis of lactate measurement, renal function tests, diag-
faces, food, or water [4]. Additionally, the virus possesses a rela- nostic imaging, and intra-abdominal pressure measurements.
tively low infectious dose, demonstrates prolonged stability on Initial management should emphasize medical therapy to
inanimate surfaces, and is relatively resistant to conventional optimize fluid status, intra-viscus decompression, and increase of
cleaning agents. abdominal wall compliance. Although the incidence of ACS in
Infection with Norovirus is more common during the winter pediatric intensive care unit patients has been reported to be be-
months and commonly presents with symptoms that may include tween 0.6 and 4.9%, the observed mortality lies close to 60% [13].
nausea, emesis, diarrhea, abdominal pain, malaise, anorexia, fevers, Therefore, emergent decompression via laparotomy with the
and chills [2]. Confirmation of infection is typically performed via option of temporary abdominal wound closure is indicated. When
real-time reverse transcription-polymerase chain reaction assay, possible, fascial closure should be attempted within five to seven
which can be used on a variety of samples ranging from stool to days of laparotomy in order to reduce the associated mortality and
vomitus, foods, water, and environmental specimens. The length of morbidity. In a retrospective review of pediatric ICU patients, sur-
gastroenteritis is typically self-limited, lasting 1e3 days. Given the gical decompression was performed within the first 24 h of
typical self-limited course of infection, treatment is non-specific. If admission with clinical improvement [14]. The authors encourage
treatment is instituted, it is directed at treating signs and symptoms decompressive laparotomy for refractory oliguria, increased intra-
of dehydration. Unlike Rotavirus, there is currently no vaccine for abdominal pressures and ventilation pressures, lactic acidosis and
Norovirus. vasopressor requirements. Similarly, an earlier prospective study
Although infection with Norovirus is usually self-limited in confirmed that surgical intervention in pediatric ICU patients with
healthy children, more severe disease courses have been reported. IAP exceeding 15 mm Hg and accompanying kidney, lung or
In two observational studies, Norovirus infection was found to be cardiovascular compromise yields immediate clinical benefit [15].
 M.H. Liu et al. / J Ped Surg Case Reports 6 (2016) 20e23 23

Although there is no identifiable cause for the severe course of venting and thereby leading to progressive gastric and bowel
Norovirus infection described herein, the authors suspect a role for distention that resulted in ACS.
the patient’s previous Nissen fundoplication in exacerbation of the
infection. Nissen fundoplication, a three hundred and sixty degree Conflicts of interest statement
gastric fundus wrap around the gastroesophageal junction, serves The authors have no conflict of interest to declare.
to reinforce the function of the lower esophageal sphincter as a
barrier to gastric reflux in the setting of GERD. Although Nissen References
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