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 Table of Contents  
CASE REPORT
Year : 2012  |  Volume : 2  |  Issue : 2  |  Page : 85-87

Acute necrotizing pancreatitis leading to pancreatic encephalopathy in a patient undergoing long-term continuous ambulatory peritoneal dialysis


1 Department of Neurology, Max Superspecialty Hospital, Saket, New Delhi, India
2 Attending Consultant, Max Superspecialty Hospital, Saket, New Delhi, India

Date of Web Publication21-Sep-2013

Correspondence Address:
Ramnath Santosh Ramanathan
10 Pragati Apts, Bhairavnath Road, Maninagar, Ahmedabad - 380 028, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4855.118668

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  Abstract 

Acute Necrotizing Pancreatitis is not uncommon but pancreatic encephalopathy, which is a complication and a very rare as sparse are the published reports, linking the risk of continuous ambulatory peritoneal dialysis (CAPD) to acute necrotizing pancreatitis, especially in India. We report a rare case of pancreatic encephalopathy in a patient who was on long-term CAPD for end stage renal disease (ESRD) and developed acute necrotizing pancreatitis. This case suggests that the risk of acute necrotizing pancreatitis increases in patients on long-term peritoneal dialysis. It is also been seen in other studies, that the risk of acute necrotizing pancreatitis is significantly high in patients undergoing CAPD, when compared with the general population.

Keywords: Acute necrotizing pancreatitis, continuous ambulatory peritoneal dialysis, pancreatic encephalopathy


How to cite this article:
Ramanathan RS, Ahluwalia T. Acute necrotizing pancreatitis leading to pancreatic encephalopathy in a patient undergoing long-term continuous ambulatory peritoneal dialysis. J Acad Med Sci 2012;2:85-7

How to cite this URL:
Ramanathan RS, Ahluwalia T. Acute necrotizing pancreatitis leading to pancreatic encephalopathy in a patient undergoing long-term continuous ambulatory peritoneal dialysis. J Acad Med Sci [serial online] 2012 [cited 2019 May 21];2:85-7. Available from: http://www.e-jams.org/text.asp?2012/2/2/85/118668


  Introduction Top


Acute necrotizing pancreatitis may present with symptoms ranging from dysphoria, disturbance of orientation, lethargy, illusion, and even coma. [1]

Acute pancreatitis may manifest with mild disease to multi-organ failure and sepsis. It has numerous causes even as the pathogenesis remains obscure. There are few effective remedies, if any, and it often has an unpredictable outcome. [2]


  Mild Pancreatitis Top


Mild pancreatitis classified as pancreatitis without collections or necrosis (i.e., Balthazar grade A-C) is also referred to as "edematous or interstitial pancreatitis" (no pancreatic necrosis). In 80% of patients with acute pancreatitis, who have mild form of disease, the recovery is uneventful as it is a self-limiting disease. Extrapancreatic necrosis is an intermediate form of pancreatitis without pancreatic necrosis with an intermediate clinical course. Sometimes, the term exudative pancreatitis is also used. These patients have Balthazar grade D or E. The patients with exudative pancreatitis have a milder course of disease but have a higher morbidity than those patients with interstitial pancreatitis, as these latter patients have peripancreatic collections, which may become infectious.

Severe Pancreatitis or Necrotizing Pancreatitis

Severe pancreatitis, which is also known as "necrotizing pancreatitis," occurs in 20% of patients. In this entity, there is a protracted clinical course, a high incidence of local complications and a high mortality rate. It is very important to detect pancreatic necrosis in clinical practice because most life-threatening complications and higher mortality occur in patients with pancreatic necrosis. [3],[4]

Central Gland Necrosis

Central gland necrosis is a subtype of necrotizing pancreatitis. It represents necrosis between the pancreatic head and tail and there is a persistent collection as the non-necrotic pancreatic tail, which is viable, secretes pancreatic juices. There is also associated disruption of the pancreatic ducts. There is often poor response to endoscopic or percutaneous drainage. In such cases, definitive treatment usually requires distal pancreatectomy.

The major complications of continuous ambulatory peritoneal dialysis (CAPD) are peritonitis, catheter related non-peritonitis infections, weight gain and other metabolic complications like hypoprotienemia and hyperglycemia. Peritonitis is usually due to gram-positive cocci, like staphylococcus infection, which can generally be managed with antibiotics. However, if peritonitis occurs due to infection with gram-negative rods like Pseudomonas, then it mandates the removal of the Cather apart from the antimicrobial therapy. Acute necrotizing pancreatitis is indeed a rare complication related to CAPD.


  Case Report Top


A 53-year-old female known case of end stage renal disease (ESRD) - on regular CAPD, Diabetes Mellitus type II and hypertension was admitted with complaints of sudden onset jerky movements involving left upper-limb since morning on the day of admission and history of headache since one day. There was no history of fever, weakness of limbs or diplopia. On examination her blood pressure was 160/110 mmHg, pulse rate was 100/min and physical examination including CNS was unremarkable.

Her magnetic resonance imaging (MRI) brain showed multiple areas of signal alteration in cortical and sub cortical region in high right parietal and parieto occipital cortex. Her MRI also showed likely evidence of focal cerebritis and mild chronic deep white matter ischemic changes. Her MRI Venogram showed no evidence of cerebral venous thrombosis. Her serum Lipase was 2442 U/L (N 3 to 45 U/L) and serum amylase level was 1730 (N-20-90 U/L). Routine CSF study was normal and CSF culture sensitivity showed no growth. However, her CSF lipase raised. Her USG abdomen showed grade IV renal parenchymal disease and moderate ascites, but no gallstones. Blood and Urine C/S also showed no growth. Later the patient became drowsy and confused, and became deeply comatose and her TLC rose to 21.0 × 10 3 /μL (N 4 to 11 × 10 3 /μL) even on antibiotics with negative culture. Her CECT abdomen showed acute necrotizing pancreatitis [Figure 1]. In view of low GCS (GCS 3-E1M1V1) the patient was intubated and put on a ventilator support. She was managed with iv antibiotics and supportive care following ventilation. Patient was shifted from CAPD to Hemodialysis on Nephrologist's advice following which the patient showed remarkable recovery in her sensorium, following which she was extubated, and there was a progressive decline in the serum lipase levels.
Figure 1: Contrast enhanced axial tomographic section of the abdomen showing extensive hypointense non‑enhancing pancreatic body parenchyma with surrounding fat stranding and left paranephric fluid collection – suggestive of necrotizing pancreatitis

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  Discussion Top


The risk of acute pancreatitis in patients on long-term peritoneal dialysis has significantly increased compared with the general population. The mortality of acute necrotizing pancreatitis is 8-25% in the western world.

The underlying causal mechanisms are not definitely clear and remain to be elucidated. Overproduction of nitric oxide mediated by inducible NO synthase in the lung is required for the acute lung-inflammation and damage, secondary to acute necrotizing pancreatitis. [5] Pancreatic encephalopathy is a severe complication of acute pancreatitis. The role of pro-inflammatory cytokines in the development of multi-organ failure during pancreatitis cannot be denied, though, pathology remains obscure.

The most important interventions are rapid fluid resuscitation and analgesic therapy with opioids. Therapeutic agents specific to pancreatitis have failed to show any advantage so far. Prophylactic antibiotics in acute necrotizing pancreatitis are controversial. Prophylactic antibiotics were been considered, if Computed tomography (CT) scan demonstrates greater than 30% pancreatic necrosis. The role of antibiotic therapy and nutritional support in the therapeutic regimen has been profoundly reassessed during recent years. [6] Imipenem can be given for a duration of 10-14 days, if no systemic complications are present. In developing countries, the use of prophylactic antibiotics early on to the disease in selected cases can be beneficial as the cost of managing complications of pancreatitis can be a limiting factor for patients. [7] Low-molecular weight heparin is a safe and effective method for treatment of severe acute pancreatitis. [8]

Pancreatic encephalopathy has the potential for devastating neurological consequences, if recognition and treatment are delayed. [9] Surgery and endoscopic interventions may be necessary and beneficial.

A case of a 59-year-old man who developed acute pancreatitis and progressive cognitive impairment was reported by Boon et al. [10] Workup included CT scan which showed cortical atrophy; EEG was also done which showed bilateral theta activity and intermittent delta activity. An MRI done 3 weeks later revealed multiple small lesions in the white matter. Patient's neuropsychiatric status had normalized after 3 weeks.

A case of 51-year-old woman who developed acute pancreatitis with severe agitation and fatal multi-organ system failure was described by Guardia et al. [11] Later on pathological examination revealed petechial hemorrhages of the cerebrum, cerebellum, corpus callosum, basal ganglia, midbrain, pons, and medulla. In this case, the proposed mechanism of death was a cerebral fat embolism and pulmonary fat embolism that resulted in hypoxia.

Sjaastad et al. [12] reported an interesting case of relapsing pancreatitis. The patient was followed until her death at the age of 46. According to the report, in her last year, she developed fatigue, giddiness, amnesia, poor concentration, and aphasia. Her CT scan revealed diffuse cortical atrophy. Aminoacids were raised in her CSF and plasma, which suggested aberrant urea-cycle functioning.

A case of 43-year-old man who developed clouded consciousness, disorientation, auditory hallucinations, and eventually, coma within 2 weeks of the onset of acute pancreatitis was reported by Ruggieri et al. [13] CT scan and MRI were normal in this patient. He recovered from coma and upon recovery, he experienced disorientation, short attention span, amnesia, and aphasia, with persistent apathy. EEG revealed diffuse slowing with theta waves. A follow-up MRI showed cortical and subcortical atrophy after a second episode.

Seventeen cases of acute pancreatitis were studied prospectively by Estrada et al. [14] and they found encephalopathy (with visual and auditory hallucinations and time and place-disorientation) in six cases. They had reported a direct relationship between pancreatic encephalopathy and increased CSF lipase. The neuropsychiatric, EEG, and CSF lipase abnormalities reversed back to normal within 10 days.

Johnson and Tong [15] reported a case of 34-year-old man. The patient died from pancreatic encephalopathy with agitation, after seizures, within several hours of presentation. His pathological study had also revealed a cerebral fat embolism. The authors in this case too, like the above case, felt that the pathophysiological mechanism was a pulmonary fat embolism, leading to hypoxia, with also a possible role for cerebral fat metabolism.


  Conclusion Top


Thus, though peritoneal dialysis is an uncommon cause of pancreatitis, its suspicion should be high in such patients, where it might lead to rarer life-threatening complications like pancreatic encephalopathy.

 
  References Top

1.Qian ZY, Miao Y. Therapeutic strategy for severe acute pancreatitis and pancreatic encephalopathy. Zhonghua Wai Ke Za Zhi 2007;45:740-1.  Back to cited text no. 1
    
2.Steinberg W, Tenner S. Acute pancreatitis. N Engl J Med 1994;330:1198-210.  Back to cited text no. 2
    
3.Whitcomb N. Acute Pancreatitis. Engl J Med 2006;354: 2142-50.  Back to cited text no. 3
    
4.Werner J, Feuerbach S, Uhl W, Büchler MW. Management of acute pancreatitis: From surgery to interventional intensive care. Gut 2005;54:426-36.  Back to cited text no. 4
    
5.Cheng S, Yan WM, Yang B, Shi JD, Song MM, Zhao Y. A crucial role of nitric oxide in acute lung injury secondary to the acute necrotizing pancreatitis. Hum Exp Toxicol 2010;29:329-37.  Back to cited text no. 5
    
6.Teich N, Leinung S, Jonas S, Mössner J. Acute pancreatitis. Chirurg 2009;80:245-52.  Back to cited text no. 6
    
7.Khan A, Khan S. Antibiotics in acute necrotizing pancreatitis - Perspective of a developing country. J Pak Med Assoc 2010;60:121-6.  Back to cited text no. 7
    
8.Lu XS, Qiu F, Li YX, Li JQ, Fan QQ, Zhou RG. Effect of lower-molecular weight heparin in the prevention of pancreatic encephalopathy in the patient with severe acute pancreatitis. Pancreas 2010;39:516-9.  Back to cited text no. 8
    
9.Weathers AL, Lewis SL. Rare and unusual... or are they? Less commonly diagnosed encephalopathies associated with systemic disease. Semin Neurol 2009;29:136-53.  Back to cited text no. 9
    
10.Boon P, de Reuck J, Achten E, de Bleecker J. Pancreatic encephalopathy. A case report and review of the literature. Clin Neurol Neurosurg 1991;93:137-41.  Back to cited text no. 10
    
11.Guardia SN, Bilbao JM, Murray D, Warren RE, Sweet J. Fat embolism in acute pancreatitis. Arch Pathol Lab Med 1989;113:503-6.  Back to cited text no. 11
    
12.Sjaastad O, Gjessing L, Ritland S, Blichfeldt P, Sandnes K. Chronic relapsing pancreatitis, encephalopathy with disturbances of consciousness and CSF amino acid aberration. J Neurol 1979;220:83-94.  Back to cited text no. 12
    
13.Ruggieri RM, Lupo I, Piccoli F. Pancreatic encephalopathy: A 7-year follow-up case report and review of the literature. Neurol Sci 2002;23:203-5.  Back to cited text no. 13
    
14.Estrada RV, Moreno J, Martinez E, Hernandez MC, Gilsanz G, Gilsanz V. Pancreatic encephalopathy. Acta Neurol Scand 1979;59:135-9.  Back to cited text no. 14
    
15.Johnson DA, Tong NT. Pancreatic encephalopathy. South Med J 1977;70:165-7.  Back to cited text no. 15
    


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  In this article
Abstract
Introduction
Mild Pancreatitis
Case Report
Discussion
Conclusion
References
Article Figures

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