Isolated Acute Rheumatic Pancreatitis- A Case Report
Ramachandran Muthiah *
Morning Star hospital, Marthandam, Kanyakumari District, India
*Corresponding Author: Ramachandran Muthiah
Citation: Ramachandran Muthiah, (2023). Isolated Acute Rheumatic Pancreatitis- A Case Report. Journal of Clinical and Medical Reviews. 2(1). DOI: 10.58489/2836-2330/014
Aim: To emphasize the role of antibiotics in acute pancreatitis as prophylactic and therapeutic benefits. Case Report: A 32-year-old obese male was admitted with acute abdomen in the emergency room. He was supported with intravenous fluids and the blood chemistry revealed elevated amylase and lipase levels, raised ESR and a positive ASO titer test. CT abdomen suggested interstitial edematous pancreatitis (IEP) and no fluid collection. Patient was treated with IV cefotaxime and metronidaziole and his condition remarkably improved with therapy and blood parameters returned normal at the end of 4 weeks and follow up CT revealed no abnormal findings and symptom free thereafter. Conclusion: Acute pancreatitis is usually a sterile inflammatory process caused by chemical autodigestion of pancreas. The edematous form of acute pancreatitis needs to correct its etiological factor to avoid recurrence. It is observed as an initial manifestation of group A beta hemolytic streptococcal infection in this patient and antibiotics play a role as curative and prophylactic in selected cases.
Introduction
Acute pancreatitis is a condition where the pancreas becomes inflammed (swollen) over a short period of time. Most people with acute pancreatitis start to feel better within about a week and have no further problems. It is sometimes associated with a systemic inflammatory response that can impair the functions of other organs, can go on to develop serious complications. Thus, there is a wide spectrum of disease from mild (80%), where patients recover within a few days, to severe (20%) with prolonged hospital stay, the need for critical care support, and 15-20% risk of death if patients have organ failure during the first few weeks of illness [1].
It occurs with an estimated incidence of 10-40 per 100,000 per year in the UK [2]. An increase in the annual incidence for acute pancreatitis has been observed worldwide varies between 4.9 and 73.4 cases per 100,000 [3],[4]. Every year, there are 275,000 hospitalisations for acute pancreatitis in the United States. In 2009, it is the most common gastroenterology discharge diagnosis with a cost of 2.6 billion dollars.
The evolving issues of antibiotics, nutrition, endoscopic, radiologic, surgical and other minimally invasive interventions will be addressed on early management to decrease morbidity and mortality.
Some studies have suggested that the administration of prophylactic antibiotics reduces the risk of pancreatic necrosis becoming infected [5]. Abdominal pain is the presenting manifestation of acute rheumatic fever [6], usually precedes the other rheumatic signs and it is the consequence of rheumatic inflammatory process affecting the pancreas in this patient and so this case had been reported.
Case Report
A 32 years old male was admitted with sudden onset of severe abdominal pain and he was found to be toxic and emaciated. His pulse rate was 114 bpm, blood pressure 90/60 mmHg and temperature 100.4∙F. Physical examination revealed distended abdomen with tenderness in the epigastric region. He had a history of alcoholic drinks occasionally. He was on anticonvulsants (phenytoin sodium 100mg twice daily) for the past 4 years as he suffered 2 to 3 episodes of seizure attacks before and his CT brain revealed normal earlier. On admission, his serum amylase was 548 IU/L (normal 10 to 96 IU/L). The total leukocyte counts 7190 cells/cumm blood (normal 4000 to 10000/cumm of blood), neutrophils 65.8% (normal 40 to 75%), lymphocytes 26.3% (normal 25 to 35%), monocytes 4% (normal 3.5 to 11.5%), eosinophils 3.5% (normal 2 to 6%), basophils 0.4% (normal 0 to 1%). ESR (Erythrocyte sedimentation rate) 26 mm in one hour (normal 0 to 14 mm per hour). Serum bilirubin (total) 1.2mg/dl (normal 0.4 to 1.2mg/dl). Random blood glucose 98mg/dl (normal 60 to 125 mg/dl). Total cholesterol 180mg/dl (normal 150 to 220 mg/dl), serum triglycerides 270mg/dl (normal 50 to 150 mg/dl). Serum SGOT (AST) 88 IU/L (normal 5 to 41 IU/L, SGPT (ALT) 78 IU/L (normal 5 to 50 IU/L). The renal parameters and serum electrolytes were within normal range. Serum lipase was highly raised as 1476 IU/L (normal < 60>Figures 1 and 2, with normal pancreatic parenchyma and no significant ductal dilatation and calcification. The liver and gallbladder appear normal, no evidence of gallstones and no fluid collections. The abdominal distension subsided on 4th day and the patient was advised to resume semisolid liquid diet, tendor coconut water, fruits and smashed vegetables without chillies slowly. The milk products were avoided. His condition began to improve thereafter. After one week of treatment, the amylase level decreased to 303.1 IU/L and lipase level becoming 240.4 IU/L, AST 84 IU/L, ALT 80 IU/L. Then one week thereafter, the amylase level reduced to 151.2 IU/L, lipase level 128.4 IU/L, AST 49 IU/L and ALT remaining high as 89 IU/L. At 3rd week, AST 36 IU/L, ALT 51 IU/L, amylase 148 IU/L, lipase 115 IU/L and ASO titer 288.5 IU/ml.
The treatment continued and at the end of 4 weeks, the amylase 69 IU/L, lipase 31 IU/L and ASO titer became negative. The CT abdomen revealed no fat stranding and the pancreas appeared normal. The patient get discharged to home and advised to avoid alcohol and fatty foods thereafter. The patient was symptom free and healthy on one year follow up, advised lifelong penicillin prophylaxis with oral penicillin V 250mg twice daily to prevent recurrent attacks of pancreatitis. Since he is obese with body mass index (BMI 32%), regular exercise programmes and diet control were advised for weight reduction with periodic medical check-up.
The RT PCR for COVID 19 infection (reverse transcriptase polymerase chain reaction test) was negative at present and it was not done initially since unknown at the time of presentation.
Figure 1 showing the mild increase in densities of ‘fat stranding’ as ‘mistiness’ or ‘hazy streaky densities’ representing the inflammatory changes in the peripancreatic fat near the uncinate process of pancreas. extending towards tail region and perinephric area suggesting “acute interstitial edematous pancreatitis (IEP)”
Figure 2 showing the ‘mistiness’ (fat stranding) in the tail region of the pancreas
Discussion
Etiopathogenesis
The pancreas is a secretory organ with both endocrine and exocrine functions and the main functional unit is the acinar cell, which comprises the parenchyma of the gland. Exocrine products from the acinar cells are secreted into a tubular system and the digestive enzymes are released via the pancreatic duct into the small intestine where they are activated to break down the fats and proteins. The digestive hormones (insulin & glucagon) produced by the pancreas are released into the blood stream where they help to regulate the blood glucose level.
Normally, digestive enzymes released by the pancreas are not activated to break down fats and proteins until they reach the small intestine. Trypsin is a digestive enzyme produced in the pancreas in an inactive form and ethanol molecules affect the pancreatic cells, triggering them to activate trypsin prematurely. When the digestive enzymes are activated in the pancreas, inflammation and local damage as ‘acinar cell destruction’ histologically occurs, leading to pancreatitis. Neutrophil polymorphs and macrophages infiltrate the pancreas and release their own proteases, free radicals, and cytokines which compound the vicious cycle of tissue damage and inflammation, inducing an ‘acute systemic inflammatory response syndrome (SIRS)’ and organ damage. The patient may become dehydrated and then heart, lungs, kidney fail. In very severe cases, pancreatitis can result in bleeding into the gland, leading to shock, serious tissue damage, infection, fluid collections and sometimes death.
There are many causes of pancreatitis as obstruction of the secretory tree or direct parenchymal cell damage. The gallstones, infection and alcoholism are the most common causes of acute pancreatitis. In recurrent acute pancreatitis, Oddi sphincter manometry is performed and a basal sphincteric pressure > 40 mmHg [7] is the most common abnormal finding described in 30-40% of cases. DIP (drug induced pancreatitis), which is an overlooked diagnosis in the clinical setting, must be rigorously considered whenever patients are on a set of new drugs and presenting with even, minimal symptoms and signs of acute pancreatitis.
The disease takes a mild course in most patients and the severe form carries a hospital mortality rate of 15%. Infection occurs in 20-40% of cases, contribute to 80% of deaths in acute pancreatitis [78] and it is associated with worsening organ dysfunction in < 5>
Case analysis
This 32 years old male was presented with acute abdomen as an initial manifestation of rheumatic fever due to Lancifield group A beta hemolytic streptococci [82] as evidenced by raised ASO titer and ESR. Elevated amylase and lipase with CT features of peripancreatic inflammatory changes as ‘mistiness’ (fat strandings) suggesting acute interstitial edematous pancreatitis (IEP) as in Figures 1 & 2 and these inflammatory changes are responded to antibiotic therapy. The patient improved dramatically within few days and resumed oral intake without any further complications. Cefotaxime showed good penetration into the pancreas to eradicate the infective process [83].
Presence of obesity, history of alcoholism, use of anticonvulsants and moderately raised triglyceride levels are the risk factors to trigger the pancreatic infection by streptococcus in this case. Periarteriolar connective tissue inflammation caused by the organism causes vasculitis and the resultant ischemia in the pancreas as an isolated event, may predisposes to further infection and so penicillin prophylaxis is indicated.
Preventive measures
a) A healthy lifestyle can reduce the chances of developing acute pancreatitis.
Hypertriglyceridemia causes 2 to 5 % of cases of pancreatitis and is associated with inherited disorders of lipoprotein metabolism, congenital type1, II and V without a precipitating factor in children [84]. Chylomicrons are triglyceride-rich lipoprotein particles believed to be responsible for pancreatic inflammation. They usually present in the circulation when serum triglyceride levels exceed 10 mmol/L. These largest of lipoproteins might impair circulatory flow in capillary beds; if this occurs in the pancreas, the resulting ischemia might disturb the acinar structure and expose these triglyceride-rich particles to pancreatic lipase. The pro-inflammatory non-esterified free fatty acids generated from the enzymatic degradation of chylomicron-triglycerides (ie, the release of free fatty acids by lipase) may lead to further damage of pancreatic acinar cells and microvasculature. Subsequent amplification of the release of inflammatory mediators and free radicals may ultimately lead to necrosis, edema, and inflammation. Hypertriglyceridemia was the cause of 56
Conclusion
GAS pharngitis and invasive infections are more common as seasonal trends, “a wave of airborne infection” with close ‘person-to-person contacts’ and predisposing to viral infections [113]. Mucosal hygiene (nasal, oral cavity and genitals) is an important measure to prevent it [114]. COVID 19 is similarly presenting and amenable to antibiotics in mild cases and vaccine development remains as a challenge for both conditions since seroconversions occurring frequently as noticed in the United Kingdom due to new outbreaks of corona virus with different strains recently. Live attenuated vaccine similar to oral polio vaccine as “drops” at the exposed mucosal surfaces of the body (mucosal vaccine) to induce immunity (both ‘humoral’ or serum immunity and local immune response) is a better option to control the outbreaks.
Acute abdomen, as pancreatitis and acute lung damage, as ARDS are the presenting manifestations of both of these infections. Penicillin prophylaxis is indicated in endemic areas to prevent it’s unexpected outbreaks and, serum ASO titer screening and PCR tests are advised to identify these infections.
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