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Acute necrotising pancreatitis from ascariasis in a gravid patient
  1. Vernon Chuabio1,
  2. Maria Rina Lanoy2 and
  3. Mark Anthony De Lusong1
  1. 1Division of Gastroenterology, Department of Medicine, Philippine General Hospital, University of the Philippines Manila, Manila, Metro Manila, Philippines
  2. 2Department of Medicine, Philippine General Hospital, University of the Philippines Manila, Manila, Metro Manila, Philippines
  1. Correspondence to Dr Vernon Chuabio; chuabiovernon{at}gmail.com

Abstract

Rarer causes of acute pancreatitis may be considered in certain settings, such as parasitism in endemic regions. This report describes a pregnant female (second trimester) in her 20s who presented with 3-day steady epigastric pain radiating to the back and passage of worm from the mouth. She was diagnosed with mild acute pancreatitis, given a significantly elevated serum lipase and absence of organ failures. Fecalysis showed Ascaris lumbricoides ova; hence, she was treated with mebendazole. Plain MR cholangiopancreatography showed an 842 mL necrotic pancreatic fluid collection and tubular flow void foci within the gallbladder and duodenum consistent with helminthiasis. The patient was managed conservatively in the absence of indications for drainage. The abdominal pain remarkably improved, and she underwent eventual vacuum-assisted delivery to a healthy term baby 4 months after the bout of acute pancreatitis.

  • Pancreatitis
  • Hepatitis and other GI infections
  • Pregnancy
  • Radiology
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Background

Acute pancreatitis management depends on the disease severity, with supportive care, including appropriate intravenous hydration, instituted for patients. Another aspect of management involves determining the aetiology of pancreatitis to address it accordingly and prevent a recurrence. With gallstone disease being the most common cause of acute pancreatitis, planning for cholecystectomy is a cornerstone in several cases of acute pancreatitis.1 2 However, several other less common risk factors for acute pancreatitis exist that may have a bearing on treatment. This case report describes the course of acute necrotising pancreatitis from parasitism in a pregnant patient.

Case presentation

A 22-week pregnant female in her 20s presented to the emergency room with a 3-day history of steady epigastric pain radiating to the back, with associated nausea, vomiting and undocumented fever. Passage of worm from the mouth during a vomiting episode was noted. She had no jaundice, overt gastrointestinal bleeding or dyspnoea. Similarly, she did not have lower abdominal contractions, vaginal discharge or vaginal bleeding. She was known to have bronchial asthma since childhood; however, she did not have any allergies or past surgeries. An occasional alcoholic drinker, her last intake was before her current gestation. On physical examination, she had normal vital signs and was awake, calm and coherent, with no need for oxygen support. She had anicteric sclerae. Her abdomen was soft and gravid but with direct epigastric tenderness; no ecchymoses were noted. Pulses were full and regular.

Investigations

The patient’s blood tests showed the following results: haemoglobin 127 g/L (120–160 g/L), haematocrit 0.39 (0.38–0.47), white blood cells 28.2×109/L (95% neutrophils, 3% lymphocytes) (4.5–11×109/L), platelet count 382×109 /L (150–450×109/L), blood urea nitrogen 2.8 mmol/L (2.5–6.1 mmol/L), creatinine 50 µmol/L (estimated glomerular filtration rate 130.17 mL/min) (46–92 µmol/L), Na 135 mmol/L (137–145 mmol/L), K 4 mmol/L (3.5–5.1 mmol/L), Ca 1.98 mmol/L (corrected 1.96 mmol/L) (2.1–2.55 mmol/L), albumin 41 g/L (35–50 g/L), aspartate aminotransferase 37 U/L (14–36 U/L), alanine aminotransferase (ALT) 21 U/L (<35 U/L), alkaline phosphatase 162 U/L (38–126 U/L), total bilirubin 0.88 mg/dL (0.2–1.3 mg/dL), direct bilirubin 0.42 mg/dL (0–0.3 mg/dL), amylase 1917 U/L (30–110 U/L) and lipase 6803 U/L (23–300 U/L). Hepatobiliary ultrasound revealed high intensities of varying sizes within the gallbladder lumen, interpreted as cholecystolithiasis. There was no biliary tree dilation while the pancreas and distal common bile duct were obscured by overlying bowel gas. Given the clinical presentation, absence of organ failures and laboratory test results, particularly the degree of pancreatic enzyme elevations, the diagnosis at this point was mild acute pancreatitis. In addition, fecalysis showed the presence of Ascaris lumbricoides ova (figure 1). A fetal viability study was also performed, with the impression of a single live intrauterine pregnancy with good cardiac and somatic activities and normohydramnios.

Figure 1

Ascaris lumbricoides ova on faecal smear. The images show A. lumbricoides ova seen on direct faecal smear (wet mount examination).

The patient’s abdominal pain persisted in the next few days but without associated nausea or vomiting. Plain MR cholangiopancreatography (MRCP) was then performed, which showed a well-defined air-filled and fluid-filled cavity with thick and irregular border involving the tail of the pancreas and peripancreatic regions with surrounding fat stranding; its approximate volume was 842 mL (figure 2). T1W-hypointense and T2W-hyperintense soft tissues were seen along the cavity’s pancreatic side, likely representing necrotic pancreatic parenchyma. It compressed the splenic vein and left kidney posteriorly and the stomach superoanteriorly. Although no gallstones were detected on MRI, tubular flow void foci were imaged within the gallbladder lumen and descending duodenal segment (D2), consistent with gallbladder and duodenal helminthiasis (figures 3 and 4). The common bile, cystic and intrahepatic ducts were non-dilated and appeared unremarkable.

Figure 2

Necrotising pancreatitis with acute necrotic collection. These axial MRCP images show an 842 mL well-defined air-filled and fluid-filled cavity (yellow arrow) with thick and irregular border involving the tail of the pancreas and peripancreatic regions with surrounding fat stranding. MRCP, MR cholangiopancreatography.

Figure 3

MRCP images of gallbladder. The gallbladder is contracted, precluding adequate assessment. However, a tubular flow void (yellow arrow) is imaged within its lumen, as seen in these axial (left image) and coronal (right image) cuts. MRCP, MR cholangiopancreatography.

Figure 4

MRCP images of descending duodenal portion. A tubular flow void focus (yellow arrow) is seen within the descending segment of the duodenum (D2), as shown in these axial (left image) and coronal (right image) cuts. MRCP, MR cholangiopancreatography.

Additionally, an antinuclear antibody (ANA) test was done later, yielding a negative result. Along with a normal serum ALT level and negative ANA test, the MRCP and fecalysis findings established ascariasis as the cause of acute pancreatitis via an obstructive process.

Treatment

With the diagnosis of mild acute pancreatitis, management was mainly supportive, including intravenous hydration and diet progression. In addition, a single oral dose of mebendazole 500 mg, which was available in the local setting, was given and no other antimicrobial drugs were administered. Since the acute necrotic collection was detected less than 4 weeks from the onset of acute pancreatitis, conservative and supportive treatment, including pain management, was continued in the absence of other indications for drainage.

Outcome and follow-up

The patient recovered with conservative management and was eventually discharged. In the interim, abdominal pain markedly improved. Subsequent prenatal consultations were uneventful, with repeat fecalysis showing no parasite ova. Four months after the bout of acute pancreatitis, the patient eventually underwent vacuum-assisted delivery to a healthy-term baby. No specific management, such as intensive care, was done. The patient and her baby were discharged uneventfully. Household members, all asymptomatic, were also referred to the local health centre for screening and possible treatment for parasitism. Notably, the patient reported no recurrences of asthma symptoms for at least a year after antihelminthic treatment, raising the possibility that her previously diagnosed bronchial asthma was actually a manifestation of Loeffler syndrome.

Discussion

A. lumbricoides is the largest common nematode and is responsible for human ascariasis. Although it is silent in the majority of infected people, its clinical disease spectrum comprises pulmonary, intestinal, appendicular, hepatobiliary and pancreatic ascariasis.3 Transmission is via the faecal-oral route, such as when people ingest food or water contaminated by mature ova.3 4 Over one billion people worldwide are infected with A. lumbricoides, with higher prevalence in Southeast Asia.3 5 6 Hepatobiliary ascariasis, a manifestation of human ascariasis, is frequently seen in children in South Africa, whereas in the Philippines, 20% of all biliary diseases are due to live or dead worms.3 In a systematic review from India, the majority (78%) of cases of extraintestinal ascariasis involved the hepatobiliary-pancreatic system.7 With the jejunum as the natural habitat of ascaris worms, hepatobiliary and pancreatic ascariasis is initiated by proximal movement into the duodenum, of which heavy worm load is the main factor for such movement. In the duodenum, the adult worm repeatedly enters into and out of the ampulla of Vater orifice, which can result in obstruction of the bile and pancreatic ducts.6 Hepatobiliary and pancreatic ascariasis has a female preponderance with a female-to-male ratio of 3:1 and can lead to six distinct clinical presentations: biliary colic, acute cholangitis, acalculous cholecystitis, hepatic abscess, acute pancreatitis and recurrent pyogenic cholangitis. Patients with acute pancreatitis present with epigastric pain, which radiates to the back and vomiting; 90% would have mild edematous pancreatitis while 10% develop necrotising pancreatitis, as seen in this case.3 6

Acute pancreatitis is defined by meeting two of the following criteria: symptoms consistent with pancreatitis, serum amylase or lipase level greater than thrice the upper limit of the laboratory reference range and consistent radiologic imaging. It is physiologically characterised by an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. Abdominal pain is usually present at the onset of acute pancreatitis attacks. It frequently involves the entire upper abdomen, typically characterised as steady and boring, that may have band-like radiation to the back in half of patients. The severity of acute pancreatitis may be classified based on CT scan findings such as gland enlargement and the presence of peripancreatic inflammation or fluid collections. MRI gives similar information to CT scans regarding pancreatitis severity and is superior to CT in assessing fluid collections.1 In this case, the diagnosis of acute pancreatitis was made with the patient’s characterisation of abdominal pain and markedly elevated serum pancreatic enzymes.

The usual causes of acute pancreatitis in the majority of cases are gallstone disease and alcohol, with the former being more frequent in women, often after age 40.1 2 Laboratory tests may aid in distinguishing between these aetiologies, with a serum ALT>150 IU/L having a high specificity for gallstone pancreatitis.1 Notably, the patient in this case had a normal serum ALT level, which can justify consideration of alternative causes. Other conditions that may predispose to acute pancreatitis include metabolic abnormalities such as hypercalcaemia, infection, vascular disorders such as vasculitis, trauma and postendoscopic retrograde cholangiopancreatography (ERCP) state. Parasitic diseases such as ascariasis or clonorchiasis that may obstruct the pancreaticobiliary system are rarely associated with acute pancreatitis. However, biliary ascariasis may be a common risk factor in endemic areas, as shown in a hospital-based study by Bhattacharya et al, where ascariasis was the most frequent aetiology of acute pancreatitis in a locality in India.8 Thus, parasitism may be a relatively more common cause of acute pancreatitis in the Philippines, where a national survey of soil-transmitted helminthic infections showed endemic levels in the three regions of the country.9

Regarding pregnant patients, a review by Szatmary et al noted that the incidence of acute pancreatitis in pregnancy is higher than that in the general population, with gallstone-related diseases, alcohol and triglyceridaemia as the more common causes.2 A number of case reports have described pregnant patients who were diagnosed with acute pancreatitis from ascariasis.10–12 A review by Khuroo et al also mentioned that worms in pregnant women reach the gallbladder more frequently than in the non-pregnant population, owing to hormone-induced relaxation and dilation of the ampullary orifice.6 In this case, cholecystolithiasis was initially considered the aetiology of acute pancreatitis, which was corroborated by the hepatobiliary ultrasound reading. However, no description of posterior acoustic shadowing typical of stones was made in the detection of high-intensity echoes within the gallbladder lumen. The absence of posterior acoustic shadowing on ultrasound is actually a supportive feature of an ascaris worm.3 6 13 Although ultrasound biliary imaging is useful to visualise ascaris worms in the stomach, duodenal lumen, biliary tree, pancreatic duct and gallbladder, it is limited in detecting single worms in the duodenal lumen invading the ampullary orifice, reportedly missing up to 50% of hepatobiliary ascariasis cases.3 6 Another option for diagnosis is via an ERCP, which has the advantage of having therapeutic capabilities.3 6 13 In this case, since no therapeutic intervention was planned, ERCP was not considered. Eventually, MRCP indicated the presence of helminthiasis instead of stones, which, along with the fecalysis finding of A. lumbricoides ova, resulted in a revised diagnosis of acute pancreatitis from ascariasis. In addition, the negative ANA test and absence of prior bouts of acute pancreatitis virtually ruled out autoimmune pancreatitis and further supported parasitism as the culprit in this case.

Acute pancreatitis appears to have two distinct phases, with the first phase usually lasting a week and characterised by systemic symptoms that may be consistent with systemic inflammatory response syndrome.1 Pancreatic and peripancreatic ischaemia or oedema from the initial inflammatory state may resolve, head towards irreversible necrosis or develop fluid collections in and around the pancreas. The second phase often starts after 7 days and is mainly characterised by local complications, including infection of such local complications. Approximately 75%–80% of patients with acute pancreatitis do not enter a second phase, reflecting the resolution of the disease process characterised by interstitial pancreatitis. However, approximately 20% of patients may enter a second phase, which is a more protracted course that may last weeks to months, typically related to a necrotising process. Acute pancreatic fluid collections usually resolve in 4 weeks; some persist and develop a wall, as in cases of walled-off necrosis (WON). Although the MRCP in the present case suggested a well-defined wall in the peripancreatic collection, the patient was not considered to have WON given the timeframe of less than 4 weeks between the onset of the acute pancreatitis and the performance of the MRCP.

Initial management of acute pancreatitis, especially in the first week, is mainly supportive and involves fasting, intravenous hydration and close monitoring for organ failure. Interventional treatments such as cholecystectomy and ERCP are performed as appropriate, particularly for gallstone pancreatitis. Percutaneous drainage via endoscopic or percutaneous approaches may be indicated for persistent pancreatic fluid collections such as WON in the presence of infection, obstructive manifestations, persistently unwell state or a fistulous tract.1 2 In treating hepatobiliary and pancreatic ascariasis without suppurative cholangitis that would warrant emergent ERCP, conservative management is initiated, which includes the administration of antihelminthic drugs.3 5 6 13 Very effective drugs include pyrantel pamoate, mebendazole, albendazole and ivermectin.6 Conservative treatment may resolve symptoms in 68%–80% of patients.13 Endoscopic treatment is indicated for those who do not respond to conservative management, such as in situations where worms persist in the biliary tree for 3 weeks despite vermifuge.3 6 13 Surgical intervention is indicated for cases of endoscopic treatment failure and involvement of intrahepatic ducts by ascaris worms.13 In this case, the eventual diagnosis of acute pancreatitis from ascariasis allowed to defer plans for cholecystectomy, and the patient was treated appropriately with antihelminthic medication. A systematic review and meta-analysis showed that gestational treatment with albendazole had cure rates of up to 90% for ascaris and hookworm while treatment with mebendazole had an overall cure rate of at most 70%.14 Rates of pregnancy loss and haemoglobin concentration did not differ between albendazole or mebendazole vs placebo.14 In the present case, mebendazole was administered mainly for reasons of availability. Since the patient also did not have obstructive jaundice and had no persistent worms within the bile ducts, ERCP was not performed. In the absence of indications for drainage, her acute necrotic collection was also observed and managed conservatively until her unremarkable delivery at term. From a community perspective, improving sanitation, health education and mass chemotherapy are vital in controlling ascariasis and preventing reinfections.6 13

Learning points

  • In a patient with acute pancreatitis, although the more usual causes should be worked up first, other less common possibilities should be kept in mind.

  • Parasitic infestation, such as ascariasis, may cause pancreatitis, especially in endemic areas.

  • Conservative management of acute pancreatic collections in pregnant patients in the second trimester is possible.

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Patient consent for publication

References

Footnotes

  • Contributors The following authors were responsible for drafting of the text, sourcing and editing of clinical images, investigation results, drawing original diagrams and algorithms, and critical revision for important intellectual content: VC. The following authors gave final approval of the manuscript: MRL and MADL.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.