|Year : 2015 | Volume
| Issue : 2 | Page : 261-263
Perforated duodenal ulcer in a child: An unusual complication of malaria
Neeraj K Dewanda, Manojit Midya
Department of General Surgery, Government Medical College and Associated Group of Hospitals, Kota, Rajasthan, India
|Date of Web Publication||13-Mar-2015|
Department of General Surgery, Government Medical College and Associated Group of Hospitals, Kota - 324 001, Rajasthan
Source of Support: None, Conflict of Interest: None
Gastrointestinal symptoms such as dyspepsia, vomiting, diarrhea, hepatitis, gastrointestinal bleed, abdominal pain, subacute intestinal obstruction like presentation and acute abdomen are common in acute malaria. However, perforated duodenal ulcer (PDU) complicating acute malaria in a child is a rare occurrence and uncommonly heard of. The exact mechanism of duodenal ulcer perforation in malaria is not clear due to the paucity of reported cases, and it may be multifactorial in etiology. The treatment of PDU in children is similar to adults that is surgical by omental patch repair of the perforation. We present an unusual case of PDU in a pediatric patient of malaria. The search of English literature revealed only one more reported case of PDU associated with malaria.
Keywords: Acute malaria complications, perforated duodenal ulcer, peptic ulcers in children, omental patch repair
|How to cite this article:|
Dewanda NK, Midya M. Perforated duodenal ulcer in a child: An unusual complication of malaria. Med J DY Patil Univ 2015;8:261-3
| Introduction|| |
Gastrointestinal symptoms are common in acute malaria.  These include dyspepsia,  vomiting, , diarrhea, , hepatitis, , gastrointestinal bleed, ,, abdominal pain,  subacute intestinal obstruction like presentation  and acute abdomen.  We present an unusual case of perforated duodenal ulcer (PDU) in a pediatric patient of malaria. The search of English literature revealed only one more reported case of PDU associated with malaria. 
| Case Report|| |
A 4-year-old male child was admitted to another hospital 6 days ago with complaints of fever for 4 days duration. His peripheral blood film report revealed high density of trophozoites of Plasmodium falciparum and he was diagnosed as a case of P. falciparum malaria (PFM) with severe anemia (hemoglobin-4.1 g/dl). He was treated there with injection quinine and multiple blood transfusion and was subsequently discharged after 3 days on syrup ibuprofen, tablet primaquine, tablet quinine, tablet rabeprazole and tablet domperidone.
Two days after discharge, he developed pain abdomen, abdominal distension and was admitted in emergency department of our hospital. There was no history of peptic ulcer disease (PUD) in a patient or a family. On examination, the child was drowsy with pulse rate of 130/min and respiratory rate of 36/min. There was no appreciable pallor or icterus. Cardiovascular and respiratory system examination were normal. Abdominal examination revealed generalized distension with tenderness but there was no demonstrable rigidity or guarding.
Routine hematological investigations showed hemoglobin −12.4 g/dl, total leukocyte count-19000/mm 3 with differential counts showing neutrophils as 70% and lymphocytes 20%. Malarial parasite smear test was negative. Other biochemical investigations were within normal limits. X-ray abdomen in an erect position showed multiple air fluid levels with no appreciable gas under diaphragm. Ultrasonography of the abdomen demonstrated free fluid in the peritoneal cavity.
The patient was taken up for exploratory laparotomy after resuscitation with a provisional diagnosis of intestinal obstruction. At surgery, a 0.7 cm × 0.7 cm size perforation was seen on the anterior wall of the first part of the duodenum [Figure 1] with about 200 ml of pyobilious collection in the peritoneal cavity. Omental patch closure of the perforation with thorough peritoneal lavage was done, and abdomen was closed in layers along with peritoneal drain placement. Gastric biopsy for Helicobacter. pylori (HP) testing was not done as facilities for HP testing was not available at our center at the time of operation. Postoperatively patient was given intravenous antimalarial agents, proton pump inhibitors (PPI) and later on shifted to oral medications. Child was discharged after 2 weeks on oral antimalarial drugs and PPI's and was doing well on further follow ups. At the time of discharge, a pediatric medicine reference was sought regarding the follow-up treatment and accordingly following medications were advised: Tablet quinine sulfate 100 mg thrice daily (TDS) for 5 days, tablet primaquine 7.5 mg once daily (OD) for 2 days, tablet rabeprazole 10 mg OD empty stomach for 3 months, tablet domperidone 5 mg TDS for 3 days, syrup paracetamol 125 mg/5 ml suspension, 5 ml maximum up to 4 doses/day SOS and iron and folic acid supplements. He was asymptomatic at subsequent follow-ups till 2 years after which he was lost to follow-up.
|Figure 1: Intraoperative photograph showing 0.7 cm × 0.7 cm sized perforation on the first part of the duodenum|
Click here to view
| Discussion|| |
Duodenal ulcer (DU) is an uncommonly diagnosed entity in children with an incidence of 1.55 cases/year reported in one Indian series.  Its diagnosis can be missed easily in the emergency settings because the symptoms are often vague and low index of suspicion on the part of the treating physician.
Peptic ulcer disease in children can be classified as primary or secondary based on etiology.  Primary ulcers are caused by alterations of the gastric functions (i.e., increased hydrochloric acid production and pepsin function) and are commonly associated with HP infections or conditions causing increased acid secretion like Zollinger Ellision syndrome. Secondary PUD is associated with stress, severe systemic illness and drugs including nonsteroidal antiinflammatory drugs (NSAIDs) and steroids. PUD is more commonly secondary in children under 10 years of age. 
Perforation of a duodenal stress ulcer is rare in children and if it occurs, is classically associated or as a complication of concomitant disease.  Patients of PDU usually present with an acute abdomen  but in a few cases signs can be masked due to poor abdominal tone of children. Although subdiaphragmatic gas on the right side on plain X-ray of the abdomen is pathognomonic of duodenal perforation,  but about 15-18% of cases no free gas under diaphragm is demonstrable. 
The other case of PDU with malaria reported by Goldman et al.  show similarity in being from a developing country (Ghana), with severe anemia and similar X-ray findings. In their case, the patient presented with blood in stools that was not seen in our case. This may be explained by the presence of concurrent bleeding from the posterior duodenal wall in their case.
The exact mechanism of DU perforation in malaria is not clear due to the paucity of reported cases, and it may be multifactorial in etiology. The increased levels of tumor necrosis factor, and free oxygen radicals, which have been implicated by Prasad and Virk  as a causative factor in diarrhea and intestinal bleeding seen in malaria may also have a role in the etiology of PDU. The other causative factors working alone or in combination may be stress of acute severe illness, severe anemia and oral NSAIDs intake particularly ibuprofen.
The treatment of PDU is similar to adults that is surgical repair. Various surgical procedures such as simple closure with omental patch, truncal vagotomy and drainage procedures, hemigastrectomy etc., have been described.  However, simple closure with omental patch buttress is the commonly used procedure in emergency settings.  Laparoscopic route has now been reported to be safe and effective in the treatment of children with perforated PUD. 
| Conclusion|| |
Peptic ulcer perforation should be kept in mind in a child of malaria presenting with acute abdominal symptoms. It may be multifactorial in etiology like direct effect of malaria, physiological stress of severe illness, associated severe anemia and oral NSAIDs intake. This can be adequately treated surgically by omental patch repair of the perforation. Postoperatively this has to be supported by medical treatment of PUD.
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