Intestinal perforation is rare in neurosurgical population despite risk factors such
as surgical stress, concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs)
and corticosteroids, chemotherapy, and infection. We report fatal duodenal perforation
in a child and discuss the possible factors contributing to this complication.
A 4-year-old male child weighing 15 kg underwent re-exploration and decompression
of a recurrent ependymoma ([Fig. 1A]). The child received cefazolin 400 mg/day, pantoprazole 10 mg/day, and dexamethasone
8 mg/day during the perioperative period. He was operated earlier for a fourth ventricular
anaplastic ependymoma at 1 year and had received 6 cycles of chemotherapy and 31 cycles
of radiotherapy.
Fig. 1 (A) Recurrent posterior fossa tumor; (B) Radiographic image of free air under the diaphragm; (C) Exploratory laparotomy revealing duodenal perforation.
External ventricular drain was placed in view of neurological deterioration secondary
to hydrocephalus on the third postoperative day (POD), along with elective ventilation.
The child was started on enteral feeds on the second POD and tolerated the same until
seventh POD, when the child developed melena (preceded by a decrease in hemoglobin
to 9 g/dL the previous day) and coffee-ground aspiration with abdominal distension
and guarding, suggestive of acute abdomen. Neurological status further worsened with
subsequent onset of features of septic shock requiring change in antibiotics and noradrenaline
infusion. Emergent treatment was started and one unit of red blood cells was transfused.
Abdominal radiograph revealed free air under the diaphragm ([Fig. 1B]). An emergent exploratory laparotomy and primary repair were performed followed
by peritoneal lavage for duodenal perforation ([Fig. 1C]). Bilateral transverse abdominis plane block was performed for postoperative analgesia
to avoid opioids and NSAIDs. However, despite continued supportive measures, the child
succumbed 30 hours after surgery to multiorgan dysfunction.
A combination of surgical stress, corticosteroid use, and sepsis is the likely cause
for duodenal perforation in this previously asymptomatic child. As steroids can mask
inflammatory signs of peritonitis, diagnosis should be considered if patient has abdominal
discomfort, fever, leucocytosis, and melena or gastrointestinal bleeding with guarding
and rigidity of abdomen. Abdominal tenderness, the earliest sign of peritonitis, was
masked by the poor neurological status, and dexamethasone further delayed its manifestation,
leading to sepsis and poor outcome despite an emergency laparotomy. This emphasizes
the need for a daily auscultation for adequate bowel sounds in neurocritical care
patients, particularly if on prolonged steroids and have a high index of suspicion
of an abdominal emergency in the presence of the above-mentioned signs. Mortality
is high (85%) in patients receiving high-dose glucocorticoids.[1] Hence, strategies for prevention (early enteral nutrition, prophylactic H2 receptor
antagonists, and judicious use of corticosteroids and NSAIDs by daily scrutiny and
de-escalation) and prompt recognition of this complication by assessment of abdominal
tenderness and radiograph of the abdomen should be adopted early.
There are very few reports of intestinal perforation in neurosurgical population,
mostly subsequent to ventriculoperitoneal shunt surgery.[2] Perforation due to NSAIDs or corticosteroids is extremely rare. One study documented
intestinal perforation in 5/719 neurosurgical patients who received steroids as compared
with none in 3,749 patients who did not receive steroids. Age > 50 years and pre-existing
diverticular disease were identified as risk factors for perforation.[3] In pediatric population, fatal hemorrhage from duodenal perforation 10 days after
surgery was described in a 10-year-old child with medulloblastoma receiving high-dose
dexamethasone.[4] Authors of a recent report of two cases of brain stem anaplastic ependymomas attribute
duodenal ulceration to autonomic dysfunction-induced gut ischemia, gastric hypersecretion,
and adrenal cortical hormones-induced decreased gastric mucus secretion.[5] Perforation can complicate 2 to 14% of duodenal ulcers in general population,[6] contributing to approximately one-tenth of all acute abdomen diagnosis in medical
intensive care units.[7]
Despite perioperative steroids being routinely used in the perioperative period for
brain tumors, literature search reveals that guidelines for optimal treatment duration
of steroid therapy are lacking. A recent cohort study of 131 newly diagnosed neurosurgical
patients with glioblastoma provides evidence of scope for successful steroid tapering
within 2 weeks after surgery with improved survival rates.[8]
To conclude, steroids can mask the symptoms of peritonitis and hence close monitoring
and high degree of suspicion are essential. Perioperative steroids should be tapered
and discontinued as soon as possible. Safer alternatives to NSAIDs such as paracetamol
should be preferred for perioperative analgesia in patients receiving steroids.
