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DISPONIBILI
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ART
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ARTICLES IN THE BOOK

  1. Acute abdomen
  2. Acute coronary syndrome
  3. Acute pancreatitis
  4. Acute renal failure
  5. Agonal respiration
  6. Air embolism
  7. Ambulance
  8. Amnesic shellfish poisoning
  9. Anaphylaxis
  10. Angioedema
  11. Aortic dissection
  12. Appendicitis
  13. Artificial respiration
  14. Asphyxia
  15. Asystole
  16. Autonomic dysreflexia
  17. Bacterial meningitis
  18. Barotrauma
  19. Blast injury
  20. Bleeding
  21. Bowel obstruction
  22. Burn
  23. Carbon monoxide poisoning
  24. Cardiac arrest
  25. Cardiac arrhythmia
  26. Cardiac tamponade
  27. Cardiogenic shock
  28. Cardiopulmonary arrest
  29. Cardiopulmonary resuscitation
  30. Catamenial pneumothorax
  31. Cerebral hemorrhage
  32. Chemical burn
  33. Choking
  34. Chronic pancreatitis
  35. Cincinnati Stroke Scale
  36. Clinical depression
  37. Cord prolapse
  38. Decompression sickness
  39. Dental emergency
  40. Diabetic coma
  41. Diabetic ketoacidosis
  42. Distributive shock
  43. Drowning
  44. Drug overdose
  45. Eclampsia
  46. Ectopic pregnancy
  47. Electric shock
  48. Emergency medical services
  49. Emergency medical technician
  50. Emergency medicine
  51. Emergency room
  52. Emergency telephone number
  53. Epiglottitis
  54. Epilepsia partialis continua
  55. Frostbite
  56. Gastrointestinal perforation
  57. Gynecologic hemorrhage
  58. Heat syncope
  59. HELLP syndrome
  60. Hereditary pancreatitis
  61. Hospital
  62. Hydrocephalus
  63. Hypercapnia
  64. Hyperemesis gravidarum
  65. Hyperkalemia
  66. Hypertensive emergency
  67. Hyperthermia
  68. Hypoglycemia
  69. Hypothermia
  70. Hypovolemia
  71. Internal bleeding
  72. Ketoacidosis
  73. Lactic acidosis
  74. Lethal dose
  75. List of medical emergencies
  76. Malaria
  77. Malignant hypertension
  78. Medical emergency
  79. Meningitis
  80. Neuroglycopenia
  81. Neuroleptic malignant syndrome
  82. Nonketotic hyperosmolar coma
  83. Obstetrical hemorrhage
  84. Outdoor Emergency Care
  85. Overwhelming post-splenectomy infection
  86. Paralytic shellfish poisoning
  87. Paramedic
  88. Paraphimosis
  89. Peritonitis
  90. Physical trauma
  91. Placenta accreta
  92. Pneumothorax
  93. Positional asphyxia
  94. Pre-eclampsia
  95. Priapism
  96. Psychotic depression
  97. Respiratory arrest
  98. Respiratory failure
  99. Retinal detachment
  100. Revised Trauma Score
  101. Sepsis
  102. Septic arthritis
  103. Septic shock
  104. Sexual assault
  105. Shock
  106. Simple triage and rapid treatment
  107. Soy allergy
  108. Spinal cord compression
  109. Status epilepticus
  110. Stroke
  111. Temporal arteritis
  112. Testicular torsion
  113. Toxic epidermal necrolysis
  114. Toxidrome
  115. Triage
  116. Triage tag
  117. Upper gastrointestinal bleeding
  118. Uterine rupture
  119. Ventricular fibrillation
  120. Walking wounded
  121. Watershed stroke
  122. Wilderness first aid
  123. Wound

 

 
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THE BOOK OF MEDICAL EMERGENCIES
This article is from:
http://en.wikipedia.org/wiki/Acute_pancreatitis

All text is available under the terms of the GNU Free Documentation License: http://en.wikipedia.org/wiki/Wikipedia:Text_of_the_GNU_Free_Documentation_License 

Acute pancreatitis

From Wikipedia, the free encyclopedia

 

Acute pancreatitis is a rapidly-onset inflammation of the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures or laparoscopy, severe cases require invasive surgery (often more than one intervention) to contain the disease process.

Symptoms and signs

Common symptoms include:

  • Severe abdominal pain often radiating through to the back.
  • Nausea, vomiting, diarrhea and loss of appetite.
  • Fever
  • Shock, hemodynamic instability

Common signs include

  • Grey Turner sign (hemorrhagic discoloration of the flanks), Cullen sign (hemorrhagic discoloration of the umbilicus)
  • Recovery may be followed by development of pancreatic pseudocyst, pancreatic dysfunction (malabsorption due to exocrine failure) or diabetes mellitus.

Causes

Most common causes

A common mnemonic for the causes of pancreatitis spells "I get smashed", an allusion to heavy drinking (one of the many causes):

  • I - idiopathic
  • G - gallstone. Gallstones that travel down the common bile duct and which subsequently get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis.
  • E - ethanol (alcohol)
  • T - trauma
  • S - steroids
  • M - mumps (paramyxovirus) and other viruses (Epstein-Barr virus, Cytomegalovirus)
  • A - autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)
  • S - scorpion sting - Tityus Trinitatis - Trinidad/ snake bite
  • H - hypercalcemia, hyperlipidemia/hypertriglyceridemia and hypothermia
  • E - ERCP (Endoscopic Retrograde Cholangio-Pancreatography - a form of endoscopy)
  • D - drugs (SAND - steroids & sulphonamides, azathioprine, NSAIDS, diuretics such as furosemide and thiazides, & didanosine) and duodenal ulcers

Less common causes

  • pancreas divisum
  • long common duct
  • carcinoma of the head of pancreas, and other cancer
  • ascaris blocking pancreatic outflow
  • ischemia from bypass surgery
  • fatty necrosis
  • pregnancy
  • infections other than mumps, including varicella zoster
  • repeated marathon running.

Causes by demographic

The most common causes of pancreatitis, are as follows :

  • Western countries - chronic alcoholism and gallstones accounting for more than 85% of all cases
  • Eastern countries - gallstones
  • Children - trauma
  • Adolescents and young adults - mumps

Pathogenesis

The exocrine pancreas produces a variety of enzymes, such as proteases, lipases and saccharidases. These enzymes contribute to food digestion by breaking down food tissues. In acute pancreatitis, the worst offender among these enzymes may well be the protease trypsinogen which converts to the active trypsin which is most responsible for auto-digestion of the pancreas which causes the pain and complications of pancreatitis.

Histopathology The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Photos at: Atlas of Pathology

Investigations

  • Blood Investigations - Full blood count, Renal function tests, Liver Function, serum calcium, serum amylase and lipase, Arterial blood gas
  • Imaging - Chest Xray (for exclusion of perforated viscus), Abdominal Xrays (for detection of "sentinel loop" dilated duodenum sign, and gallstones which are radioopaque in 10%) and CT abdomen

Amylase and lipase

  • Serum amylase rises 2 to 12 hours from the onset of symptoms, and normalises within 1 week
  • Serum lipase rises 4 to 8 hours from the onset of symptoms and normalises within 8 to 14 days.
  • Serum amylase may be normal (in 10% of cases) for cases of acute on chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia
  • Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia
  • If Lipase level is about 2.5 to 3 times that of Amylase, it is an indication of pancreatitis due to Alcohol[1].

CT abdomen

CT abdomen should not be performed before the 1st 48 hours of onset of symptoms as early CT (<48 h) may result in equivocal or normal findings.

CT Findings can be classified into the following categories for easy recall :

  • Intrapancreatic - diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
  • Peripancreatic / extrapancreatic - irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
  • Locoregional - Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus,

Balthazar scoring

Balthazar Scoring for the Grading of Acute Pancreatitis

  • Grade A - normal CT
  • Grade B - focal or diffuse enlargement of the pancreas
  • Grade C - pancreatic gland abnormalities and peripancreatic inflammation
  • Grade D - fluid collection in a single location
  • Grade E - two or more collections and/or gas bubbles in or adjacent to pancreas

Classification by severity

Progression of pathophysiology

Acute pancreatitis can be further divided in mild and severe pancreatitis. Mostly the Atlanta classification (1992) is used. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. About 20% of the acute pancreatitis are severe with a mortality of about 20%. This is an important classification as severe pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common ward.

Necrosis will be followed by a systemic inflammation response syndrome (SIRS) and will determine the immediate clinical course. The further clinical course is then determined by bacterial infection. SIRS is the cause bacterial translocation from the patients colon.

There are several ways to help distinguish between these two forms. One is the above mentioned Ranson Score.

Prognostic indices

Important biochemical markers for pancreatitis are serum amylase and lipase levels. Amylase and lipase levels can rise to more than a hundred times normal levels in cases of acute pancreatitis.

In addition, in predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson and APACHE (Acute Physiology, Age and Chronic Health Evaluation) II indices.

Ranson

Ranson's Criteria on Admission :

  • age greater than 55 years
  • a white blood cell count of > 16,000/µL
  • blood glucose > 11 mmol/L (>200 mg/dL)
  • serum LDH > 350 IU/L
  • serum AST >250 IU/L

Ranson's Criteria after 48 hours of admission :

  • fall in hematocrit by more than 10 percent
  • fluid sequestration of > 6 L
  • hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL))
  • hypoxemia (PO2 < 60 mmHg)
  • increase in BUN to >1.98 mmol/L (>5 mg/dL) after IV fluid hydration
  • base deficit of >4 mmol/L

The prognostic implications of Ranson's criteria are as follows :

  • Score 0 to 2 : 2% mortality
  • Score 3 to 4 : 15% mortality
  • Score 5 to 6 : 40% mortality
  • Score 7 to 8 : 100% mortality

APACHE

"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 12 points

  • Hemorrhagic peritoneal fluid
  • Obesity
  • Indicators of organ failure
  • Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
  • PO2 <60 mmHg
  • Oliguria (<50 mL/h) or increasing BUN and creatinine
  • Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>

Treatment

General measures

  • Antibiotics for infected necrosis and severe pancreatitis improves outcome. The drug of choice is imipenem.
  • Supportive for shock.
  • Pain relief

The following have no role in the management of acute pancreatitis

  • Enzyme inhibitors are not proven to work.
  • The use of octreotide has not been shown to improve outcome.

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest.

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early, post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN (such as fungemia). The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus, as well as reduced risk of aspiration. Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the bronchus even in intubated patients (contrary to popular belief, the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea).

ERCP

Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 hours of presentation, is known to reduce morbidity and mortality. The indications for early ERCP are as follows :

  • Clinical deterioration or lack of improvement after 24 hours
  • Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen

The disadvantages of ERCP are as follows :

  • ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis
  • The inherent risks of ERCP i.e. bleeding

It is worth noting that ERCP itself can be a cause of pancreatitis.

Surgery

Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii)complications. The most common cause of death in acute pancreatitis is secondary infection. Infection is diagnosed based on 2 criteria

  • Gas bubbles on CT scan (present in 20 to 50% of infected necrosis)
  • Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the pancreas.

Surgical options for infected necrosis include:

  • Conventional management - necrosectomy with simple drainage
  • Closed management - necrosectomy with closed continuous lavage
  • Open management - necrosectomy with planned staged reoperations at definite intervals (up to 7 reoperations in some cases)

Complications

Complications can be systemic or locoregional.

  • Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin producing beta cell damage)
  • Locoregional complications include pancreatic pseudocyst and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis

Epidemiology

  • Annual incidence in the U.S. is 17 per 100,000 population. [2]
  • Prevalence in the US is 80,000 cases per year.

See also

  • Chronic pancreatitis

Reference

  •   Gumaste VV, Dave PB, Weissman D, Messer J. Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis. Gastroenterology 1991;101:1361-6. PMID 1718808.

External links

  • Medical Information and Treatment of Acute Pancreatitis
Retrieved from "http://en.wikipedia.org/wiki/Acute_pancreatitis"