Diane Byrum RN M SN CCRN CCNS FCCM Critical Care Clinical Nurse Specialist Presbyterian Hospital Charlotte, NC

Transcription

1 Diane Byrum RN M SN CCRN CCNS FCCM Critical Care Clinical Nurse Specialist Presbyterian Hospital Charlotte, NC

2 PANCREATITIS Pancreas is located in the retroperitoneal space with no capsule..inflammation can easily spread and lead to parenchymal edema with preservation of blood supply to pancreatic tissues. Definition: acute inflammation of the pancreas that may extend to local and distant extrapancreatic tissues. p Amylase (carbohydrates) and lipase (fats) active Trypsin, chymotrypsin (protien) inactive proenzymes Normally trysinogen can be released in small amounts..intrinsic mechanisms quickly inactivate to prevent damage to the acinar cells PSTI pancreatic secretory trypsin inhibitor **hereditary When acute pancreatitis occurs on two or more occasions (evidenced by elevation of the serum pancreatic enzymes), it is classified as acute recurrent pancreatitis. In some cases, acute recurrent pancreatitis progresses to chronic pancreatitis, implying the presence of parenchymal fibrosis and loss of glandular function. Types: - Acute edematous or interstitial: edematous pancreas, hypovolemia - Hemorrhagic or necrotizing: extensive necrosis of pancreas and peripancreatic tissue and fat, erosion into blood vessels, hemorrhage, SIRS often occurs 1

3 Causes of Acute Pancreatitis (% of Cases) Gallstones: 45% ( females > 60 years) Alcohol: 35% (> men than women) Other 10% omedications (thiazides, azathioprine, estrogens, corticosteroids, sulfonamides, furosemide, NSAIDS, mercaptopurine, methyldopa, tetracyclines) ohypercalcemia (calcium-mediated activation of trypsinogen and subsequent glandular autodigestion) ohypertriglyceridemia (> 1000 mg/u) oduct Obstruction opud opost-ercp ohereditary otrauma ovascular factors (ischemia or vasculitis) oviral infections (mumps, coxsackievirus, cytomegalovirus, hepatitis, Epstein-Barr, rubella obacterial infections (mycoplasma) oparacites (interstitial) opostcardiac bypass/abdominal bypass (self-limiting related to gland ischemia) Idiopathic: 10%-20% Tidbits: 220,000 hospital admissions/year - Acute: 19.5/100,000 - Chronic:8.3/100,000 Mortality of Acute Pancreatitis - Native Type Americans 4/100,000 Mortality Rate - White 5.7/100,000 - African Interstitial Americans AP 20.7/100,000 <1% with African Americans age at 10 times Necrotizing AP higher risk 20% have Sterile a severe course 10%-30% will die ***Despite Infected improvements in ICU 30% treatment rate of death is unchanged activation of trypsinogen to trypsin & lack of elimination of active trypsin inside the pancreas pancreatic injury and inflammatory response out of proportion to the response of other organs with a similar insult inflammation can cause substantial tissue damage and may progress beyond the pancreas to a systemic inflammatory response syndrome, multiorgan failure and death 2

4 Enhanced pancreatic ductal permeability allows enzymes to leak from duct start autodigestion Oxygen radicals cause inactivation of pancreatic secretory trypsin inhibitor (PSTI) Normal defenses overwhelmed **Intracellular Ca increases Increased trypsin leads to release of other pancreatic enzymes The continued destruction spreads in gland and into peripancreatic tissue Proinflammatory cytokines IL-1, IL-6, IL-8, TNF-α, arachchidonic acid metabolites (not limited to pancreatic tissue) Systemic Complications ARDS (lecithinase, pleural effusions Renal Failure Shock Myocardial depression ( vascular tone) Bacterial infection (30%) White Abdominal arrowheads: CT of Pancreatic acute pancreatitis abscess with Pancreatic Black pseudocyst arrowhead: Fluid formation collections Pancreatic (arrows). calcification Large Arrow: Peripancreatic fascial infiltration Acute fluid collections occur early in AP in the peripancreatic areas and are not encapsulated by a fibrous wall acute pseudocysts - well-developed collections of pancreatic juice encapsulated by a nonepithelialized wall of granulation tissue. Pseudocysts typically form 4 to 6 weeks after an episode of AP. Psuedocysts filled with very high levels of pancreatic enzymes and lead to ascites and pleural effusions pancreatic abscesses - pseudocytes that have become abscessed Pancreatic abscesses may also form through encapsulation of areas of infected pancreatic necrosis. 3

5 *** Intracellular calcium has been implicated in the development pancreatic autodigestion Intracellular free Ca+ is tightly controlled in acinar cells Increase in intracellular Ca+ mediates a variety of physiological functions Calcium is sequestered into pancreas, calcification begins Hematologic - DIC S/S - thrombocytopenia Neurological/Musculoskeletal Pain, shock, hypotension, hypocalcemia related to sequestration of Ca+ in fat necrosis S/S - restlessness Endocrine beta cell dysfunction S/S - hyperglycemia diffusely enlarged Diagnostic Studies: pancreas Contrast-enhanced CT of the pancreas is diagnostic and can show: Enlargement of pancreas due to edema with low Peripancreatic inflammation: density Fluid in the paracolic gutter from Fluid collections: A simple peripancreatic fluid collection will not edema. have a well-defined capsule Necrosis: On contrast enhanced phases the necrotic pancreatic parenchyma will show decreased or no enhancement when compared with normally enhancing viable tissue Pseudocysts: As liquifaction of necrotic pancreatic tissue progresses it will gradually take on the appearance of localized fluid collection...pseudocyst Abscesses: Diffusely enlarged pancreas with air pockets Hemorrhagic: Enlarged pancreas with increased density due to hemorrhage 4

6 Clinical Presentation Cardiovascular inflammation leads to capillary permeability, hemorrhage, shock, dehydration S/S - thirst, CO; urinary output, BP, CO, PAP, SVR, tachycardia, diminished pulses, delayed capillary refill Pulmonary pleural effusions (sequestered abdominal fluid), hypoventilation (pain), ARDS, emboli. S/S - or absent BS, crackles SOB; hypoxia, crackles, dyspnea, tachypnea Laboratory Findings Test/Normal values Amylase (blood) U/L Amylase (urine) 2 hr 2-34 U 24 hr U Lipase (blood) U/L Electrolytes Ca++ Total mg/dl Ionized mg/dl K Mg Significance acute pancreatitis 2-12 hrs. > 1000 U (return to base in < 5 days) Values lag 6-10 hrs. behind blood remain elevated for 14 days pancreatic damage remains elevated after amylase is normal more specific for pancreatitis levels < 8 not uncommon (bound to albumin which leaks into tissue) levels r/t vomiting, NG suctioning and F&E shifts Skin hemorrhage, shock, hypoperfusion, biliary tract disease S/S - grey-turner s sign (bluish-brown discoloration flank); cullen s sign (bluish discoloration around umbilicus); cool, sweaty skin; jaundice; cyanosis; skin turgor Gastrointestinal Ileus; inflammation leads to capillary permeability S/S - diminished or absent bowel sounds; N/V/D pain RUOQ (worse in supine position) Serum albumin g/dl Triglycerides mg/dl CBC WBC 5,000-10,000 Hbg g/dl Hct 40-54% Coagulation studies Platelets 150, ,000 mm 3 Fibrinogen mg% Fibrin split products (FSP) - Maintains oncotic pressure in pancreatitis, liver disease > 11,000 indicates inflammatory response hemorrhage dehydration Decreased related to bleeding Decgradation of clots r/t microthrommbi 5

7 ABG s ph ; pc ; p ; HC ; 02 sat 95% ECG Respiratory alkalosis; hypoxemia ST depression T wave inversion (shock of coronary spasms or trypsin and bradykinins on myocardium, Ca++ ST segment widening) Nutritional support Respiratory support Peritoneal lavage Parenteral feedings for healing in severe pancreatitis; compounds hyperglycemia which is common in pancreatitis give higher percentage of calories as fats; possibly a feeding J-tube Pulmonary congestion, pleural effusions and atlelectesis result in respiratory insufficiency; abdominal distention and fluid sequestration elevate diaphragm. Identify respiratory failure early continuous pulse ox; 02, intubation if in distress with positive pressure ventilation; IV fluids with caution Removes toxic waste can result in immediate improvement; 2 L of isotonic, balanced electrolyte solution infused over 15 minutesdwells for 20 mins drains for 20 mins. Fluid/Electrolytes Bed rest Suppression of pancreatic secretions Pharmacotherapy Pancreatic fluid collections, psuedocysts, necrosis Colloids or crystalloids to replace volume; large volumes of fluids sequestered needs lot of fluid replacement in acute phase; replace K+ and Ca++ if low (Ca++ cautiously as hypercalcemia is a cause of pancreatitis Decrease activity Reduce acidity H2 blockers Gastric suction should be used only with vomiting, abdominal distention) Pain PCA pump (Morphine) Antibiotics prophylactic use in severe disease 57% of patients have fluid collections, with 39% having two areas involved and 33% having three or more areas involved. These fluid collections can cause pain, become infected, compress other organs. If this occurs endoscopic drainage or surgery may be needed. Psuedocysts are fluid collections with very high levels of pancreatic enzymes and lead to ascites and pleural effusions. Necrotic areas can develop in the first few days and are usually associated with inflammation, hypotension and infection. It is usually diagnosed by fine needle aspiration of the necrotic area guided by CT with gram stain and culture. 6

8 Surgical Management Controversial Surgical management indicated in two clinical settings: infected pancreatic necrosis resection of all devitalized pancreatic and surrounding tissue is performed. Multiple reexplorations, continuous irrigation, or laparostomy formation may be required for adequate debridement ** Delayed approach to debridment improves outcomes by allowing time for seperation of necrosis and vital areas. Necrosectomy gallstone pancreatitis - Cholecystectomy is indicated to prevent recurrence of gallstone pancreatitis. In mild disease, an early cholecystectomy performed during the same hospitalization In severe gallstone pancreatitis, cholecystectomy may be delayed until clinical improvement or performed at the time of necrosectomy. Steve Parks, 43 year old man employed by a local textile mill has a long history of ETOH abuse with several previous admissions for GI bleeding and pancreatitis. He arrives at the ED with complaints of severe epigastric pain with nausea and vomiting following a weekend of binge drinking. Vital Signs: T= ; BP = 85/50; HR = 143; RR = 35 PA line inserted: PAP = 15/8; CVP = 1; PCWP = 2; CO = 3.8 On arrival he is hypotensive, and fluid resuscitation is begun. After initial stablization in the ED, he is tranferred to ICU. Ultrasound reveals a large edematous pancreas. Assessment: Oriented to person and place; anxious and uncooperative; diaphoretic; breath sound clear bilaterally; abdomen distended, bowel sounds absent; contines to complain of severe epigastric pain after meperidine given in the ED; foley inserted with 50 cc dark urine noted. Labs: K+=3.5; glucose = 180; Ca+ = 7.4; Amylase = 650; Lipase = 302; Hct = 48; Hbg = 16; WBC = 20,000; Albumin = 1.5; PT = 18; PTT = 28; ABG s = 7.35/33/90/25/91% Explain the picture beginning to emerge: Vigorous fluid resuscitation is continued with both colloid and crystalloid solutions. An NG tube is inserted, and 100 m Meperidine is given IM. 40 % face mask and serial labs are ordered. Check Point: Why were colloids and crystalloids both given? Ranson Criteria for Predicting Mortality in Acute Pancreatitis At Admission During Initial 48 Hours Age >55 yrs Hematocrit falls by >10 mg/dl WBC >16,000/cc BUN increases by >5 mg/dl LDH >350 IU/L Calcium <8 mg/dl AST >250IU/L PaO 2 <60 mmhg Glucose >200 mg/dl Base deficit >4 mg/dl Fluid sequestration >6 L WBC = white blood cell; BUN = blood urea nitrogen; LDH = lactate dehydrogenase; AST = aspartate aminotransferase; PaO 2 = partial pressure of carbon dioxide, arterial. Ranson score 0-2 minimal mortality rate Ranson score 3-5 has a 10%-20% mortality rate Ranson score > 5 has a 50% mortality rate amylase, lipase WBC s (inflammation) distended abdomen albumin (fluid collects around edematous pancreas pulling in albumin) Ca+ being sequestered into area around pancreas dehydrated CVP =1; wedge = 2; BP 85/50, HR

9 Labs 24 hours later: Na+ = 139; K+ = 3.2; Albumin = 2.2; Ca+= 7.8; Mg+ = 1.0; glucose = 203; lipase = 789; amylase = 575; Hct = 42; Hbg = 10.3; WBC s = 14,600 ABG s = 7.22/26/88/10/6/88% Vital Signs Bp 90/60; HR = 125; RR = 32; T = 103 Day 4, his PO2 falls to P02 falls with evidence on the chest x-ray. Over the next 48 hours worsening hypoxia develops with diffuse pulmonary infiltrates on chest x-ray. Check point: What is happening in the pulmonary system and how is it related to his original problem?? pulmonary system problem pleural effusions and early ARDS The End develop from large amounts fluid in abdomen 1. Why would a peritoneal lavage be performed? 2. What are the three most common causes of pancreatitis? 3. What is the mechanism of action for pancreatitis in the chronic alcoholic? Thank You! 4. What is Grey Turner s and Cullen s sign? When would you see these two signs? 5. Describe treatment parameters for decreasing pancreatic enzymes. 6. Identify nutritional support during acute pancreatitis. 8