Evaluation of hyperbilirubinemia in acute inflammation of appendix: a prospective study of 45 cases.Kathmandu Univ Med J (KUMJ) 2006 Jul-Sep; 4(3):281-9KU
Hyperbilirubinemia is the result of imbalance between production and excretion of bilirubin by the liver. It may be because of hepatocellular, cholestatic or haemolytic diseases. Liver receives blood mainly through portal venous system, which receives blood from abdominal organs. Portal blood carries nutrients and other substances absorbed from gut including bacteria and its product (toxins). In small percentage, even in normal healthy people, bacteria are found in portal blood. It is commonly cleared by detoxification and immunological action of reticuloendothelial (RES) system of liver that act as first line defence in clearing toxic substances, bacteria and it's products. But when bacterial load overwhelms the Kuffer cell function, may cause dysfunction or damage to the hepatocytes (liver parenchyma). It reflects, rise in serum bilirubin (SB) alone or in combination with liver enzymes depending upon the type, severity and site of lesion. Recently, another substance known as Cytokines e.g. IL-6, Tumour necrosis factor (TNF), have also been labelled to be responsible for depressed excretory function of liver and may lead to increase in SB level without rise in liver enzymes.
To evaluate hyperbilirubinemia associated in acute inflammation of appendix (acute appendicitis and its complication).
MATERIAL AND METHODS
This is a prospective study conducted at NGMC Teaching hospital Nepalgunj, Nepal during Oct.2004-Oct.2005. 45 Consecutive cases of acute appendicitis admitted in surgical unit III, were recruited for this study. Clinically suspected cases were subjected to investigations to confirm the diagnosis. Investigations included total leucocytes count, differential leucocytes count, urine analysis and ultrasound. These cases were also subjected to routine liver function tests. Subsequently these cases were operated and clinical diagnosis was confirmed per-operatively and post operatively by histopathological examination of the specimen. Their clinical and investigative data were compiled and analyzed and following observations were obtained. Routine liver function test results were compared with laboratory reference values given in Table- 1, 2 and 3.
Case with acute appendicitis and its complication with test negative for HBSAg and no past history of jaundice.
Case with acute appendicitis and its complication with test positive for HBSAg and /or past history of jaundice.
Total number cases were 45. Of 45, 25 were males and 20 were females. Their age ranged from 11 years to 60 years. The average was 27.2 years. Duration of symptoms ranged from 5 hours to maximum 9 days. Among 45 cases diagnosed as acute appendicitis clinically (preoperatively), per operatively, 36 cases had inflamed appendix, 3 cases had gangrene, 5 cases had perforation with peritonitis (4 localized and 1 generalized peritonitis) and only a single case was noted to be of normal appendix (Table 4). Liver function tests (LFT) analysis revealed following results, Among 45 cases, SB was raised in 39 cases where as 6 cases had normal SB level. The raised SB ranged from 1.2 mg/dL to 8.4 mg/dL. The average level of SB was 2.38 mg/dL. All the cases had indirect fraction of SB above 15%. (Table 4). The rise in SB was without concomitant much rise in liver enzymes.
Following conclusion can be drawn from the present study. Firstly, There was Hyperbilirubinemia in 86.6% of the patients of acute inflammation of appendix (i.e. acute appendicitis and its complications). Secondly, Raised SB ranged from 1.2mg/dL - 8.4 mg/dL. Thirdly, The rise in SB was mixed in type (both indirect and direct). Finally, The hyperbilirubinemia was intra hepatic cholestatic in type due either to abnormality in permeability of hepatocyte or ductular membrane enzyme inhibition as the liver enzymes were not much elevated.