Acute pancreatitis complicated by multiple organ damage in clinical analysis of 196 cases of_3078

By Wesley White,2014-10-30 08:25
7 views 0
Acute pancreatitis complicated by multiple organ damage in clinical analysis of 196 cases of_3078

    Acute pancreatitis complicated by multiple organ damage in clinical analysis of 196 cases of

     Key Words pancreatitis with multiple organ damage

     Acute pancreatitis (acute pancreatitis, AP) of the acute abdomen is a common clinical one. Authors from May 2001 to May 2007 study of 196 cases of AP observed in patients with clinical features of MODS, the report is as follows.

     A clinical data

     1.1 General Information

     This group of 196 cases in 123 cases of male and female 73 cases;

    aged 25 to 79 years old, with an average (42.6 ? 8.9) years of age. 143

    patients with mild AP, severe in 53 cases. Etiology: just 107 cases of gallstone pancreatitis, alcoholic in 18 cases, hyperlipidemia in 12 cases, bile source of sexual partners, alcohol in 13 cases, bile source of 10 cases of sexual partners, hyperlipidemia, alcohol, sexual partners, blood fat 8 cases of sexual disorders, eating and drinking, 14 cases of pancreatic cancer, 2 cases were 12 cases of unknown causes. The main clinical manifestations of acute upper abdominal pain, nausea, vomiting, fever, blood and urine amylase increased, B Chao, CT examination confirmed the pancreatic swelling, uneven texture, outside the inflammatory infiltration of the pancreas, suggesting that there are signs of

    pancreatitis, and to exclude other diseases. AP diagnostic criteria according to the Chinese Medical Association Society of Pancreatic Surgery Group in 1996 the 2nd program standards [1]. At the same time meet the criteria Panson if ? 3 and (or) APACHE-? ? 8 items, and <48h disease

    were diagnosed as having severe acute pancreatitis [2].

     1.2 Treatment

     Patients are therefore correspondingly the following conventional treatments: (1) fasting, gastrointestinal decompression, oxygen nasal

    catheter or mask; (2) to maintain effective circulating blood volume, correcting water, electrolyte and acid-base imbalance, and provide

    nutritional support; (3 ) Application proton pump inhibitors, somatostatin or octreotide inhibit such synthesis and secretion of trypsin; (4) severe acute pancreatitis to use the pancreas through the blood barrier potent broad-spectrum antibiotics such as quinolones, ?-generation

    cephalosporins class, metronidazole, etc.; (5), sedation, spasm, pain; (6) stomach tube infusion of rhubarb suspension; (7) major organ function monitoring and support.


     (1) cardiac function tests, including ECG and (or) myocardial enzymes: creatine kinase (CK), creatine kinase isoenzyme (CK-MB); (2)

    liver function tests, including serum total bilirubin (TBIL) , serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB) and γ-glutamyl-GGT (GGT); (3) Determination of renal function, including serum creatinine (Cr), serum urea ammonia (BUR) and urine

    protein, etc.; (4) pulmonary function test, including arterial partial pressure of oxygen (PaO2), oxygen saturation, etc.; (5) C-reactive protein

    (CRP), measured on admission CRP values, and to observe its continues to rise time.

     1.4 criterion

     Cardiac dysfunction manifested as ECG changes or myocardial enzyme changes, admission ECG were normal, 12 ~ 24h after the apparent ST-segment

    depression or non-specific changes (excluding past coronary heart disease history). Liver dysfunction manifested as TBIL, AST, ALT, GGT, etc. increased, ALB reduced. With impaired renal function expressed as Cr, BUN and the emergence of increased urinary protein and so on. The performance of the lung damage PaO2 / oxygen concentration (FiO2) ? 300mmHg, acute

    respiratory distress syndrome (ARDS), when, PaO2/FiO2 ? 200mmHg, chest X-

    ray shadow infiltration lungs. CRP value increased to "normal levels six-

    fold (100 ~ 200mg / L), 5d is still dropped after known as the CRP continues to rise.

     1.5 Statistical analysis

     Comparison of all count data are used χ2 test, P <0.05 for

    significant difference. Reposted elsewhere in the paper for free download http://

     2 Results

     2.1 mild pancreatitis and severe pancreatitis compared with multiple

    organ damage

     Table 1. Table 1 mild and severe pancreatitis complicated by pancreatic organ damage compared to other (slightly) Note: * P <0.05, # P <0.01

     2.2 AP with acute liver damage in other organ damage

     Table 2.

     Table 2 liver dysfunction associated with other organ damage (omitted) Note: * P <0.05

     2.3 gallstone and non-gallstone pancreatitis compared with other

    organ damage

     Table 3. Table 3 Biliary and non-gallstone pancreatitis compared with

    other organ damage (a little) Note: * P <0.05, # P <0.01

     2.4 CRP continues to rise and multi-organ dysfunction in the

    relationship between

     Table 4.

     Table 4 CRP continues to rise with multiple organ damage (a little) Note: * P <0.05, # P <0.01

     3 Discussion

     Acute pancreatitis (AP) clinical manifestations of severe acute pancreatitis, especially the risks of complications and early mortality is mainly due to heart, liver, kidney, lungs and other multiple organ dysfunction (multiple organ dgsfunction syndrgme, MODS), which led to MODS The key is systemic inflammatory response syndrome (Systemic inflammarory

    response syndrome, SIRS). AP acute phase response, due to a cascade of multiple cellular factors is an important factor in causing SIRS [3], many

    studies have confirmed that trypsin on pancreatic tissue damage and induction of cytokine release is an important part of pancreatitis.

     AP patients with MODS, the liver was first involved, is also common involved organs, liver dysfunction in patients with severe acute

    pancreatitis is more obvious when compared with the mild difference was significant. And gallstone pancreatitis complicated by liver damage up to see, OK retrograde cholangiopancreatography (ERCP) to lift biliary obstruction is conducive to recovery of liver function.

     Myocardial damage caused by the reason that the stress state of the body with adrenaline, norepinephrine is elevated, and the AP, when the release of myocardial depressant factor, a large number of trypsin and the

    peptides direct myocardial injury. Plasma epinephrine (ET) levels increased by a strong vasoconstrictive effect of increased cardiac burden and the inhibition of myocardial energy metabolism lead to myocardial damage.

     AP called the pancreatic renal damage caused by kidney disease, the pathogenesis of a lot of controversy, mainly that: (1) lack of circulating blood volume, lack of oxygen caused by kidney damage, AP in particular, severe pancreatitis, systemic inflammatory response obviously, a large

    number of liquid extravasation of an extent which rendered valid relative or absolute lack of circulating blood volume will enable renal ischemia, glomerular filtration rate has dropped, renal ischemia, hypoxia an extent which rendered renal function impairment; (2), renal hemodynamics abnormal, the blood concentration of trypsin to activate kallikrein -

    kinin system and release of vasoactive peptide, has a strong renal toxicity; (3) activity of trypsin can significantly activate the renin -

    angiotensin system biotin system [4], on the strong role of the renal vascular system caused by increased renal vascular resistance, glomerular filtration rate and effective renal blood flow decreased significantly leading to impaired renal function; (4) lead to impaired renal function,

    uric acid increased . Acute pancreatitis in high catabolism to accelerate the decomposition of the organization, increased serum uric acid, uric acid increased emission of Er Zhi impaired renal function.

     Severe acute pancreatitis than in mild lung injury more common mechanism may be activated complement kinin and trypsin into the blood stream directly damage the lung capillary endothelial cells, I, II alveolar epithelial cells in the pancreas release of phospholipase A2, the

    kinds of inflammatory mediators, neutrophils, and oxygen free radicals and lipid media, the role of endotoxin and cytokines in the role of microcirculation and blood coagulation abnormalities, as well as the role of platelets, leading to increased permeability of the lung, and lung damage with the severity of the AP, light damage after treatment of infection, with the disappearance of the original disease improvement [5].

     CRP was also determined the severity of pancreatitis, one of the

    important parameters, light pancreatitis at admission in patients with elevated CRP levels to the normal six-fold (100 ~ 120mg / l), sustained

    its level began to decline after 5d, and 5d in patients with severe acute pancreatitis continues to rise after, CRP levels increased with the patient's general condition and the extent of pancreatic necrosis related to AP in this group study found that CRP were significantly associated with MODS continues to rise, the more complications, the more dangerous

    disease, CRP values are higher authors believe that CRP reflects the severity of pancreatitis, is complicated by the better indicators of MODS.

     AP may appear MODS, the liver is one of the major organ damage, protect liver function and to block the damage, is essential to improving the cure rate pancreatitis.


     Surgical Society of Chinese Medical Association a study group of the pancreas. The clinical diagnosis of acute pancreatitis and the grading standards. Zhonghua Surgery, 1997,35 (12): 773 ~ 775.

     2 Chinese Medical Association pancreas surgery group. Draft diagnosis and treatment of severe acute pancreatitis. Pancreatic disease study, 2001,1 (1): 46 ~ 48.

     3 Kingsnorth A. Role of eytokines and their inhibitors in acute

    pancreatitis. Gut, 1997,40 (1): 1 ~ 4.

     4 Blameys L. Progonstic factor in acute pancreastitis.Gut, 1984,25 (12): 1340 ~ 1346.

     5 Cai, ZHANG Qun-hua, Yin Bao-bing, et al. Acute necrotizing

    pancreatitis in the pathogenesis of lung injury research. Chin J Dig, 1998,18 (3): 139 ~ 141. Reposted elsewhere in the paper for free Download Center http://

Report this document

For any questions or suggestions please email