Paediatric Nephrology Journal of Bangladesh

: 2022  |  Volume : 7  |  Issue : 1  |  Page : 37--40

Renal replacement therapy (hemodialysis) in acute pancreatitis with acute tubular necrosis following injury by a cricket ball

Tahmina Ferdaus1, Shireen Afroz2, Sukrity Baroi1, Umme Tanjila1, Farhana Yasmin1, Mohammod Hanif2,  
1 Critical Care Nephrology & Dialysis, Department of Pediatric Nephrology, Bangladesh Shishu (Children) Hospital & Institute, Dhaka, Bangladesh
2 Department of Pediatric Nephrology, Bangladesh Shishu (Children) Hospital & Institute, Dhaka, Bangladesh

Correspondence Address:
Dr. Tahmina Ferdaus
Critical Care Nephrology & Dialysis, Department of Pediatric Nephrology, Bangladesh Shishu (Children) Hospital & Institute, Dhaka


Acute pancreatitis (AP) with severe acute kidney injury (AKI) is rare in children and is associated with high morbidity and mortality rates. We report a case of a 12-year-old boy who presented with upper abdominal pain, vomiting, and anuria following injury by a cricket ball. After resuscitation and investigation of the child, AP with AKI was diagnosed. This severe AKI needs renal replacement therapy (RRT). RRT is used to augment normal kidney function to rapidly remove toxic metabolites. We obtained central vascular access which is appropriate for his body size. We prepared a dialysate solution containing standard bicarbonate-buffered dialysate. Priming the circuit with dilute packed red blood cells was done due to his low hematocrit level. A beneficial effect of using RRT to facilitate recovery of renal function to RRT independence and reduce the long-term risk of chronic kidney disease was observed when used as initial supportive modality. Ultrasound-guided renal biopsy reported acute tubular necrosis and it was performed after recovery from his critical period.

How to cite this article:
Ferdaus T, Afroz S, Baroi S, Tanjila U, Yasmin F, Hanif M. Renal replacement therapy (hemodialysis) in acute pancreatitis with acute tubular necrosis following injury by a cricket ball.Paediatr Nephrol J Bangladesh 2022;7:37-40

How to cite this URL:
Ferdaus T, Afroz S, Baroi S, Tanjila U, Yasmin F, Hanif M. Renal replacement therapy (hemodialysis) in acute pancreatitis with acute tubular necrosis following injury by a cricket ball. Paediatr Nephrol J Bangladesh [serial online] 2022 [cited 2023 Oct 4 ];7:37-40
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Full Text


Acute pancreatitis (AP) is an inflammatory condition, and severe form of AP is associated with multiorgan failure and poor outcome. Acute kidney injury (AKI) has long been recognized as a common and important complication of AP.[1] It has been increasingly diagnosed in children in recent decades. A variety of etiologies can result in AP in children, including structural/anatomical, obstructive/biliary, trauma, infections, toxins, metabolic, systemic illness, inborn errors of metabolism, and genetic predispositions.[2] The revised Atlanta Criteria classified AP according to the type, severity, and phase of the disease.[3] Imaging plays an important role in the diagnosis and staging of AP, establishing the cause and identifying its complications. Contrast-enhanced computed tomography is the most useful imaging technique especially when performed after 72 h to assess the extent of the disease.[4] Systemic inflammatory response syndrome is the main cause of AKI in AP.[5] Earlier initiation of renal replacement therapy (RRT) can improve overt complications of AKI.[6] So, any patient who had acute abdomen should be evaluated for AP, and RRT can be provided safely to children of all age groups.

 Case Report

A 12-year-old boy of non-consanguineous parents hailing from Shatkhira admitted in the Critical Care Nephrology and Dialysis unit at Bangladesh Shishu Hospital and Institute (BSH & I) presented with sudden onset of severe abdominal pain for 6 days. He had history of trauma by someone throwing a cricket ball which forcefully hurt his abdomen 7 days back. Initially, pain was diffuse in nature, not radiating, and aggravated on lying position after 24 h of blunt injury. It was also associated with several times of vomiting containing non-bilious food particles. For this reason, he was admitted in Satkhira Sadar Hospital and treated with i.v. fluid, multiple antibiotics, and pain killers. Two days later, he developed pallor with facial puffiness which became generalized along with scanty normal colored urine. He had also developed anuria for the last 24 h and renal function (serum creatinine 12.8 mg/dL) was impaired. So, he was referred to BSH&I for further evaluation and management. He had no history of fever, jaundice, loose motion, bleeding manifestation, sore throat, skin infection, trauma, burning sensation during micturition, multiple joint pain, photosensitivity, oral ulceration, convulsion, or loss of consciousness. He had no family history of such type of illness or previous history of kidney diseases. Our patient was conscious, had rapid hurry breathing, severely pale, puffy, anthropometrically well thrived, normotensive (90/60 mmHg) (50th centile). He was tachypnic and had high volume pulse. There was acidotic breathing and vesicular breath sound without any added sound. Apex beat was located at the left fifth intercostal space just medial to mid-clavicular line. Abdomen was distended, and flanks were full. Muscle guarding and diffuse tenderness were present, especially at the upper epigastric region. Murphy’s sign, McBurney’s point, and rebound tenderness could not be elicited. Genitourinary system was normal except ascites were evident by fluid thrill. Catheterization was done, and only 50 mL urine was in a uro bag. Urine color was normal, 3+ proteinuria on boiling test. Capillary blood glucose was 6 mmol/L. So, we diagnosed as acute abdomen with AKI.

Initially managed with nothing per oral, oxygen inhalation, i.v. line establishment, maintained fluid, and packed red blood cells (RBCs) had been transfused. Immediately central vascular access had been inserted and we arranged for dialysis equipment. The dialyzer was chosen according to his weight and intermittent hemodialysis started with priming the circuit with dilute packed RBCs due to his low hematocrit values. Heparinized normal saline was used to prime the circuit and non-heparinized normal saline was used to reprime. Three courses of i.v. pulse methylprednisolone had been prescribed. His blood gas analysis showed severe metabolic acidosis (pH 7.14) and had managed with sodium bicarbonate drip.

He had Coombs-negative severe anemia (hemoglobin 5.4 g/dL) with normal platelet (280,000) and reticulocytosis (8%). Peripheral blood film showed normocytic normochromic anemia. Urine routine and microscopic examination showed hematuria with 3+ proteinuria, pus cell present. Spot protein creatinine ratio was raised (7.9). There was no urinary eosinophil, liver function test was normal, and there was no coagulopathy. There was also hypoalbuminemia (26 mg/dL) and hypercholesterolemia (335 mg/dL). His Lupus profile was negative. Ferritin, D-dimer, and LDH level were 2574 ng/mL, >10 mg/L, and 1650 U/L, respectively, with normal complement and antineutrophil cytoplasmic antibodies (ANCA) and P-ANCA level. His pancreatic enzyme serum lipase was markedly increased (643 U/L) along with amylase level (774 U/L). Ultrasound showed swollen pancreas, and there was no pancreatic cyst. Both kidneys were enlarged in size with normal shape and position. Right kidney was 10.8 cm and left kidney 11.6 cm. Cortical echogenicity of both kidneys was increased. But cortico-medullary differentiation was poor. The pelvicalyceal system was not dilated. Blood and urine culture sensitivity was sterile.

Renal biopsy report showed mild mesangial proliferation, increased matrix, and mild infiltration of polymorphs in glomerulus. Mild focal tubular atrophy, necrosis, and hyaline cast were present in tubules. There is edema in interstitium, which is a thick blood vessel wall [Figure 1] and [Figure 2]. No deposition of any antibody seen in direct immunofluorescence.{Figure 1} {Figure 2}

We had continued carbohydrate-based diet, and i.v. methylprednisolone 20 mg/kg was initiated for 3 days following oral prednisolone 1 mg/kg for 4 weeks with subsequent taper. Both antibiotics with pancreatic enzyme supplementation were continued. We had monitored glycemic level and intake–output chart. He got fourth intermittent HD session daily, subsequently EAD. After reaching a peak of 3.8 mg/dL on day 12, serum creatinine started to decline, reaching baseline on day 25. His urine output was progressively increasing on day 15 and he passed 2 mL/kg/h. We had been withdrawn of temporary angio access and discharged with oral prednisolone. One month later, the patient had come for follow-up and his serum creatinine continued to be normal and urine sediment findings showed signs of resolution. So, our final diagnosis was AP with acute tubular necrosis. RRT (hemodialysis) brought good outcome for AKI in AP with acute tubular necrosis patients.


AP is an acute condition presenting with abdominal pain usually associated with raised pancreatic enzymes as a result of pancreatic inflammation. It have three categories—AP, acute recurrent pancreatitis, chronic pancreatitis. There are 3.6 to 13.2 pediatric cases in 100,000 individuals per year.[7] The American College of Gastroenterology 2013 guidelines expressed clinical definition of AP—an acute condition presenting with abdominal pain usually associated with raised pancreatic enzymes as a result of pancreatic inflammation. The JPGN guidelines 2012 proposed diagnostic criteria: (1) abdominal pain suggestive of/or compatible with AP (abdominal pain specially in the epigastric region); (2) serum amylase and/or lipase activity at least three times greater than the upper limit of normal (IU/L); (3) imaging findings characteristic of or compatible with AP (using USG, CT, MRI). Patients who present with at least two of the above three manifestations are diagnosed as AP.[8] The Pediatric Acute Pancreatitis Severity (PAPS) score also proposed three of the following eight criteria: (1) age <7 years, (2) weight <23 kg, (3) WBC >18,500 cells/mm3, (4) LDH >2000 U/L, (5) 48 h trough calcium <8.3 mg/dL, (6) 48 h trough albumin <2.6 g/dL, (7) 48 h fluid sequestration >75 mL/kg per 48 h, and (8) 48 h rise in BUN >5 mg/dL.[9] The most common locations of pain are as follows: epigastric (62–89%), diffuse (12–20%), in the back (< 10%), and, in about 5% of cases, with radiation to the dorsal region. Nausea and vomiting are found in 40–80% of cases. Abdominal distention is found in 21–46% of the cases. Biomarkers of AP—amylase: increased level 2–12 h, peak 12–72 h, normal 3–4 days and lipase: increased 4–8 h, peak level 24 h, level decreased 8–14 days—remain elevated longer than amylase. Trypsinogen—both serum and urinary trypsinogen 2 levels—rises to high levels within a few hours and declines within 3 days.[10] AP parenchymal inflammation release of activated enzymes and protease occurs. In the first 24 h of pancreatic inflammation, histamine, activated kallikrein kinin, bradykinin, high prostaglandin E releases cause increased vascular permeability and hypovolemia, hypotension, increased vascular coagulation which aggravates AKI. After 24 h of inflammation, direct nephrotoxin (trypsin, chymotrypsin, elastase, phospholipase A2, platelet activating factor) releases which increase abdominal pressure. Inflammatory markers TNF-α, IL-8, IL-6 aggravate kidney tubular cell apoptosis, which activated renin–angiotensin system.[8] So, there is increased kidney vascular resistance. Current management strategies and early enteral nutrition should be instituted in severe AP due to prevention of bacterial stasis in the gut, lower rates of infection, and decreased mortality. Parental nutrition should be limited to cases when enteral feeds are not tolerated or contraindicated. Early aggressive fluid resuscitation in the 24 h of hospitalization, followed by initiation of enteral nutrition between 24 and 48 h after hospitalization, is associated with better outcomes and decreased mortality.[11] Acute tubule-interstitial nephritis/acute tubular necrosis presented as rapidly progressive glomerulonephritis. Immediately, we had started inj. methylprednisolone daily 20 mg/kg for 3 days and then oral prednisolone 1.5 mg/kg daily up to 4 weeks. Then gradual tapering of doses occurs for 2 weeks. If renal function impaired with continuation of steroids, use of immunosuppressive agents is recommended.[12] Despite supportive therapy, kidney function might be lost and RRT might be indicated. Early initiation of RRT in critical illness before onset of overt complications of AKI can improve outcomes.[13]

Our patient needs both supportive and RRT (hemodialysis) modalities for his early recovery, which reduces his long-term risk of chronic kidney diseases. After 2-month follow-up, his renal function was within the normal range with good urine volume.


Any patient presenting with acute abdominal symptoms should be evaluated for AP. Acute tubular necrosis is a serious complication of severe form of AP. So, early recognition of multisystem involvement is important to prevent severe complications. Acute dialysis is currently the most effective therapy for the management of AKI and can be safely provided to children of all age groups. It facilitates renal recovery rather than as the last resort.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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