Acute pancreatitis. It is a disease of etiopathogenesis not yet completely clarified and with a worrying severity, since around 20% evolve with severe complications and a high mortality rate.
[ hide ]
- 1 Definition
- 2 History
- 3 Classification
- 4 Frequency
- 5 Etiology
- 6 Aetiopathogenesis
- 7 Clinical picture
- 8 Prognostic criteria
- 9 Diagnosis
- 10 Complications
- 1 Premises
- 2 Systemic
- 11 Treatment
- 12 Sources
It is defined as the more or less diffuse abrupt enzymatic destruction of the pancreatic parenchyma produced by the release of activated enzymes into the glandular tissue .
The pancreatitis acute (PA) was already known in antiquity, but the importance of the pancreas as organ intraabdominal and severity of the inflammatory changes do not appear until the function of that body as part of the digestive system was established in the middle of the nineteenth century . In 1886 Senn proposed that surgical treatment of pancreatitis should be indicated in patients with pancreatic gangrene or abscesses. After 3 years in 1889Reginald Fitz presented the classic signs and pathological description of pancreatitis and suggested that early surgical intervention was ineffective and very dangerous. In 1901 Opie, at the Johns Hoppkins Hospital, accurately described the pathogenic mechanism of biliary pancreatitis, documenting the presence of an impacted calculus in the ampulla of Vater at autopsy performed on a patient who died of biliary pancreatitis. The importance of acute pancreatitis as a cause of morbidity and mortality was evidenced by Moynihan, who described acute pancreatitis in 1925 as the most terrible of all the calamities that could occur in the abdominal viscera.
Many have been the proposed classifications for acute pancreatitis (AP); A simple one is the one that considers 3 clinical-pathological types, which represent different phases of the same disease :
- Acute interstitial or edematous pancreatitis .
- Acute hemorrhagic or necrotic pancreatitis.
- Acute suppurative pancreatitis.
It is observed in 1 out of every 500 patients admitted to medical or surgical wards and in 5 out of every 100,000 inhabitants, representing 1.5% of emergencies with abdominal causes. It is also offered, as an approximate average figure, of 10 cases per 100 000 inhabitants and per year. Although both sexes are equally susceptible to the disease , it varies according to the etiology. When associated with alcoholism , it is more frequent in men; in women if it is related to bile duct pathology. the pancreatitisAcute can be observed at any age, it is infrequent in children and generally of an infectious, traumatic or hereditary etiology. The most frequent is its appearance in adults aged between 30 and 65 years. Others point out the highest frequency in ages between 40 and 50 years. Feldman and Zer describe an extremely rare case of acute pancreatitis, observed in a young man (8-10 years old) as a complication of a vaccination for parotid disease ; what led them to laparotomy was the suspicion of perforated appendicitis . As conclusions, they point out that a similar case in childhood or older children has not been reported to date.
The etiological factors are several, since the specific mechanism of acute pancreatitis is not known , and the following causes are noted:
- Acute inflammatory stones or calculations in the bile ducts.
- Alcoholism .
- Hypercalcemia , hyperlipemia.
- Family heritage.
- Retrograde pancreatography.
- Hypotension .
- Cardiopulmonary by pass.
- Atheromatous embolism.
- Pancreatic duct obstruction:
- Tumor .
- Pancreas divisium.
- Ampullary stenosis.
- Ascaris infection .
- Duodenal obstruction.
- Viral infections.
- Scorpion venom .
- Vasculitis .
- Hepatitis .
- Hyperparathyroidism .
There is a tendency to suppose the simultaneous action of several mechanisms: partial obstruction of the ducts by epithelial metaplasia, added to activated pancreatic secretion, which causes digestion of pancreatic and peripancreatic tissues by increasing the intracanalicular pressure and breaking the small-gauge ducts. Blockage of a common duct by a stone or tumor would be another mechanism, since it increases the pressure within the duct system. The spirit to the produce edemaDuodenal can also raise pressure. At the same time, the reflux of bile into the pancreatic ducts can cause vasoconstriction leading to ischemia. The exit of pancreatic enzymes is followed by proteolytic destruction of the pancreatic parenchyma, necrosis of bleeding blood vessels , fat necrosis by lipolytic enzymes and concomitant inflammatory reaction.
The abdominal pain is the main symptom of acute pancreatitis, ranging from mild and tolerable discomfort to severe suffering, constant and disabling. Terebrating, continuous pain is characteristic, located in the epigastrium and periumbilical region and often spreading to the back, chest , flanks and lower portion of the abdomen . The pain tends to be more intense when the patient adopts the supine position and with some frequency it is alleviated when the patient flexes the trunk and gathers the knees. Nausea, vomiting, and bloating due to gastric and intestinal hypomotility and peritonitis are common.chemistry. Physical examination usually reveals a distressed and anxious patient. Low-grade fever, tachycardia, and low blood pressure can often be detected . The shock is not uncommon and is due to:
- Secondary hypovolemia due to exudation of plasma and blood proteins into the retroperitoneal space, behaving like a burn.
- Greater formation and release of kinin peptides which tends to vasodilation with increased vascular permeability.
- Due to systemic effects of proteolytic and lipolytic enzymes released into the circulation.
The jaundice is rare and usually appear to be due to the edema of the head of the pancreas compressing intrapancreatic portion of the bile duct. Erythematous skin nodules may appear due to fatty necrosis. 10 to 20% of patients may have pulmonary signs, such as basal rales, atelectasis, and pleural effusion (most often left).
Abdominal stiffness and hypersensitivity can be found, but when compared to severe pain, they can be pushed into the background. Decreased or absent bowel sounds. Upon palpation of the abdomen and its upper portion, a tumor area can be seen, which tends to be painful and reluctant and its translation can be framed as a pancreatic pseudocyst. As signs of BP, many point to the blue coloration of the navel region (Cullen’s sign), a consequence of the hemoperitoneum. Also, a blue-red-purple or green-brown coloration on the flanks (Turner’s sign), reflecting the tissue catabolism of hemoglobin . Cullen and Turner signs are infrequent and late and indicate the existence of severe necrotizing pancreatitis.
The pain at the beginning of the disease can be so intense that it alone aggravates the patient’s condition. The shock (hemorrhagic) is a typical sign in these patients and present in many patients. As the inflammatory process of acute pancreatitis develops and invasion into the peritoneal cavity by activated enzymes occurs, the patient is aggravated by absorption of toxins, bacteria, and necrotic tissues . The clinical diagnosis of a peritoneal syndrome due to acute pancreatitis is truly complex, resembling intra-abdominal processes such as: perforated gastroduodenal ulcer, acute cholecystitis, mesenteric thrombosis and intestinal occlusion..
The diagnosis of acute pancreatitis is suspected due to a history of lithiasic cholecystopathy or alcoholism , as well as the ingestion of copious, greasy beverages and foods and the characteristics of pain, the intensity of vomiting as well as the state of peripheral collapse.
Based on clinical and laboratory studies, the prognosis of an attack of acute pancreatitis can be assessed . The 11 criteria proposed by Ranson seem to be the most effective method for evaluating these patients. It is imperative that the patient with acute pancreatitis be studied using the criteria of this author in order to proceed to the rapid identification of severe pancreatitis in order to subject it to appropriate monitoring and apply the most intense support measures. By studying the prognostic factors identified by Ranson in 1974The severity of the pancreatitis attack and the general prognosis can be predicted using the available clinical and laboratory measurements and are clinically valuable in formulating the prognosis and as a therapeutic guide in each patient with pancreatitis. Patients with 1 or 2 prognostic signs do not present mortality and require only common supportive treatment. Patients with 3 or 4 signs, present a mortality between 15 and 40%, requiring intensive medical treatment. Those with five or six prognostic indices reach 100% mortality. The application of this scoring system allows the early identification of severity in these patients.
The diagnosis of pancreatitis is not given absolutely by laboratory results. The tests support the diagnosis which is complex and difficult through the clinic. Generally, the diagnosis is made by demonstrating serum amylase values that tend to triple normal levels in the absence of perforation or intestinal infarction or evident disease of the salivary glands. Thus, serum amylase and lipase have to be raised 3 times their normal value during the first day of the attack. After 48 to 72 h the amylase normalizes. Lipase and isoamylase can continue to be elevated for up to 2 weeks.
Simultaneous serum amylase and lipase enhance diagnostic sensitivity. The leukogram in these patients rises to figures between 12,000 and 20,000. Fluid loss towards the 3rd. space will be increased with hematocrit figures between 50 and 55% (hemoconcentration), indicating severe inflammation of the pancreas . Glycemia may be elevated depending on the degree of inflammation of the gland. The calcium serum appear decreased in the 1st period. day of the process, given by the formation of calcium soapsby the action of pancreatic lipase. Serum bilirubin will also be observed to be elevated, with figures higher than 20-25%, mainly due to edema of the pancreatic gland which tends to compress the common bile duct. Regarding Imaging, X-rays of the simple standing and lying abdomen may reveal images of stones in the pancreatic ducts. Its appearance is evidence of chronic pancreatitis.
Segmental distension of the ascending, transverse, and small intestine can also be observed by X-rays , which tends to be located in the left upper quadrant of the abdomen or in the periumbilical region. The X – ray of the chest can demonstrate, pulmonary or pleural effusion left atelectasis. Ultrasonography (ultrasound) is not only diagnostic in acute pancreatitis, but also raises its complications. Through it, it is possible to detect gallstones or duct dilation and pancreatic edema, although it is sometimes difficult to visualize due to the segmental ileus of the transverse colon and small intestine.
CT is an indication for severe pancreatitis or when hypotension or progressive leukocytosis and elevated temperature are present. In this situation, the severity assessment using APACHE II and TAC are useful throughout the process. Endoscopic retrograde cholangiopancreatography (ERCP), is an indication of sphincterotomy and stone extraction in patients who do not improve their clinical picture during the period of 24 to 48 hours of hospitalization.
- Necrosis and infection .
- Pancreatic abscess.
- Pancreatic pseudocyst.
- Hemorrhages .
- Cardiocirculatory failure (shock).
- Hydroelectrolytic and metabolic disorders.
- Hypocalcemia .
- Metabolic acidosis.
- Gastroduodenal hemorrhage .
- Impaired coagulation (disseminated intravascular coagulation).
- CNS (pancreatic encephalopathy).
- Eyepieces (Purtcher’s retinopathy).
- Digestive (paralytic ileus, stress ulcer).
In edematous pancreatitis , the first objective of treatment is to keep the patient in a fasted state until the manifestations of acute inflammation are reduced , such as pain relief, signs of peritoneal irritation, normalization of serum amylase, return of appetite and patient well-being. If the clinical picture is severe acute pancreatitis, treatment and care in intensive care may be determined by the following danger signs:
- Hypotension .
- Hemoconcentration with hematocrit greater than 50%.
In intensive care, vital signs and urine output must be monitored every hour. Measurement of central venous pressure (PVC) and the use of the Swan Ganz catheter. The gastric pH must be measured every 6 h with neutralization of the acid in its therapy.
Arterial gases, hematocrit, glucose and electrolytes measured every 6 or 8 h. Daily exams: complete coagulogram, serum proteins, creatinine, calcium, magnesium, amylase and lipase. Sometimes intubation or nasogastric aspiration is not necessary in a mild attack, but if the patient worsens, the Levin probe must be used, connected to a vial with aspiration every 3 h. The fast will be held for 2 to 4 weeks. Antacid blockers (cimetidine, ranitidine, omeprazole, or others) will be administered. No additional effort to reduce pancreatic secretion with drugs has proven beneficial, such as the use of anticholinergics, glucagon, or even octeotride, which is a synthetic derivative of somatostatin; neither the use of trasylol nor 5-fluoracil among others. The action of 5-fluoracil is to stop the synthesis of pancreatic proteolytic enzymes by inhibiting DNA formation. It produces relief of symptoms, although no significant decrease in mortality has been shown so far. Daily dose: 250 mg in 500 mL of 5% dextrose (1-3 doses).
Somatostatin has been introduced in the treatment of severe pancreatitis in recent years due to its potent inhibition of pancreatic exocrine secretion (Ranson> 3 criteria). Multiple studies have shown a decrease in trypsin and chymotrypsin activity and in blood amylase and lipase levels when administering somatostatin. It also reduces gastrointestinal motility and intraluminal secretions, an effect that has led to the evaluation of complications from pancreatic surgery, pancreatic fistulas, small intestine and acute pancreatitis. It also has activity on the endocrine secretion of the pancreas, with an inhibitory effect on the production of insulin and glucagon. The somatostatin dose should be 250 µg / h, in continuous infusion,
Treatment of acute pancreatitis with somatostatin should begin as soon as possible, in a period not exceeding 48 h of the disease since in this period, it is when the necrotic toxic picture of pancreatic and self-digestion enzymes occurs, which will mark the subsequent poor evolution of the disease. The duration of treatment with this drug will be: 48 to 72 h; Furthermore, it is recommended to avoid the contact of this medication with sunlight, not to use it through the venoclysis equipment for blood transfusions and to dissolve it in glucose serum. Fluid intake is essential in BP, being 8 to 10 L or more per day with an adequate electrolyte balance. Colloids may be required as well. Before the fall of the hematocrit due to hemorrhage, blood replacement will be necessary. If there is hypoxia, supply oxygen by mask or nasal catheter. If the patient does not respond adequately to treatment, ventilatory assistance may be required, especially if hypoxemia persists and wedge pressure of the pulmonary artery remains normal, leading to adult respiratory distress syndrome, so assisted ventilation should be performed. with positive expiratory pressure at the end of it.
Pain in acute pancreatitis can be treated with meperidine, 50 or 100 mg intramuscularly and provided that the renal function is normal. Other pain relievers can be: – Dipyrone. – Meperidine (Demerol). Pentazocine (Talwin). – Continuous epidural. Figures between 11 and 13 mmol / L of glycemia generally do not require treatment; Higher levels should be treated cautiously by simple, intravenous or subcutaneous insulin. Hypocalcemia generally should not be treated unless muscle irritability appears. Administer 10% calcium gluconate intravenously (iv), from 10 to 20 mL, in 1 L of physiological saline to pass in 6 h.
The use of antibiotics is controversial, but there is proven evidence that antibiotic prophylaxis with imiprene (beta-lactam) can prevent infection from pancreatic necrosis. Good results are also reported with cefuroxin, 2nd quinolones. generation or piperacillin plus metronidazole. Others report unsatisfactory results with the use of ampicillin. Antibiotics should be used to treat specific infections: pneumonia, biliary and urinary tract infections. If septic foci are suspected in the pancreatic gland, it is advisable to perform aspiration puncture guided by ultrasound or CT. If the culture or the Gram are positive for infectionBacterial, the specific antibiotic should be used as well as surgical debridement of the septic and necrotic focus. Peritoneal lavage without prior abdominal surgery is not recommended. Regarding the nutritional needs of the patient with severe acute pancreatitis, it will be done under strict calculations, so total parenteral nutrition will be used as nutritional support.
Surgical intervention is indicated under specific circumstances, which are as follows:
- Uncertain diagnosis: exploratory laparotomy will be performed with a view to excluding potentially fatal diseases that can be surgically corrected ( appendicitis , perforated ulcer , choleperitoneum, and others). Other times the diagnosis of pancreatitis surprises the surgeon during urgent laparotomy. With the availability of laparoscopy, videolaparoscopy, ultrasound, and CT, this attitude is less and less frequent.
- Pancreatic sepsis : pancreatic abscess develops in 50% of patients with acute pancreatitis and is more frequent the more severe the inflammatory process and pancreatic necrosis . Operationally, all the necrotic material should be debrided and then place drains or pack the debrided area.
- Correction of disease associated with the biliary tract: definitive biliary tract surgery will be performed in patients with pancreatitis associated with biliary lithiasis. In these cases ERCP should be evaluated as well as endoscopic cholecystectomy.
- Deterioration of the clinical state: it is the most controversial and very little accepted indication of surgical indication, ranging from wide debridement to total pancreatectomy.