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    10 vizualizări9 pagini

    Acute Pancreatitis

    Încărcat de

    kitsilc
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    din 9
    ‘Michael Parker RN, DipHE, is an acting grade F charge nurse at the A&E, St James’ University, Hospital, Leeds This article has been subjected to double biind peer review 2% ACUTE PANCREATITIS MICHAEL PARKER provides an overview of fhe pancreos, its function and assessment, as well os the appropriale reaiments for pancreas and their rationale A ste since a common ener gency with potential devastating con- Seaquences, but recognising symptoms eary and good nursing and cincal assessment can benefit patents. Familarty wth the patho- physiology of the pancreas can provide an understanding of why acute pancreatitis can develop as well sts dina presentation Acute pancreatitis is pancreatic inflam. maton due to auto-dgestion. The condton is believed to develop when injury to the pancreatic duct alos protedytic pancreatic enzymes to be activated prematurely in pancreatic tissue. The inflarrmatory response this initiates produces varying degrees of pancreatic oedema, fat necrosis and haemorrhage. Toxic enzymes ae reeased into the bloodstream that can damage blood vesses and vital organs Most epsodes are mid and sling but up toa ith of patents have attacks that can be fatal (Wilson et af 1990). The overall mortality at of acute pancreatitis is between 5 and 10 per cent (Banks 1997, Bone et af 1995) but can increase to 35 per cent or moreif complications develop Ganese et al 1995, Ranson 1993). In view ofthis, an underying cause is usvlly Sought so that appropriate treatment canbe administered and recurentepiscces prevented In Europe and the US, gallstones and alcoho excess are the most Common cause of acute pancreatitis, accounting for between 64 and 80 per cent of cases {Neoptolemos eta! 1984). Figures suggest that in the UK gallstone disease is twice as likely a alcohol excess to be the cause (Beckingham and Bornman 2001). Drugs, metabolic abnormalities, viral in fections, trauma and various other rarer causes ae implicated in up to 10 per cent of cases, and in between another 10 and 20, per cet of casesrno abnormaliys detected despite comprehensive investigations and biochemical screening. In these cases patiemts are conventionally classified as having acute idiopathic pancreatitis (Venu et.al 1989). ‘THE PANCREAS AND ITS FUNCTIONS ‘The word pancreas comes from the Greek ‘meaning ‘all flesh’. tis along gland, which, because it resembles a bunch of grapes, i described as racemose: from the Latin word for a bunch of grapes, racernuse, It is situated behind the stomach, stretching fram the duodenum to the spleen (Borland 1994) (Fig. 1), and it has been described as the ‘hermit or ‘hidden organ! ‘of the abdomen because of its location bchind the peritoneum (Gore 1994). Its location also makes it virtually impossible t palpate so life threatening lesions often go undetected until they encroach on other nearby structures such as the intestines The pancreas is portioned into three ~ the head, body and tail and feeds into two pancreatic ducts: the principle duct, or duct ‘of Wirsung, and the accessory duct, or duct ‘of Santorini, These eventually join the ‘common bile duct (CBD) and ultimately the duodenum (Fg, 1). EXOCRINE AND ENDOCRINE ROLES The pancreas has roles as both an exocrine and endocrine gland. Exocrine cel’ form 98 per cent of pancreatic tisue and consis Of sim clusters called acini (Tortora et af 1996), collectively known as acinar cells. The acnar cels make digestive enzymes in their inactive state Box 1). As well a5 being a protein digesting enzyme ints on right, trypsin the catalyst for activating the other enzymes in the pancreas When trypsin is activated, there is a cascade of all the other enzymes and this, resuits in auto-digestion and consequently Fig. 1. The pancreas with duodenum, and islets of Langerhans all bladder Duct of Santorini ‘common bile duct. Duct of Wirsung produces symptoms of acute pancreatitis, The acini stop this from occurring by producing trypsin inhibitor. The endocrine function of the pancreas is {due to about a milion small Custers of cells, known collectively as the ists of Langerhans (Fg, 1) The sets are richly vasculrsed, which age > 55 years (non- 70 years (gallstone pancreatitis) > leucooyte count > 16,000 x 107, blood glucose > 1ommol. (if not diabetic) lactate dehydrogenase > 350 iu. > serum glutamic oxaloacetic transaminase levels > 100 ut. Within 48 hours of presentation: haematocrit decrease by > 10 percent > serum urea increase by > TOmmolA. despite adequate intravenous therapy brypocalcsemia: corrected serum concentrations of caium < 2meolL. ~ low arterial oxygen partial pressure: PO2 < Bkpa or 6OmmHg metabolic acidosis: base deficit» mai. > estimated fluid sequestration > BL (Ranson 1995) Pen ‘The modified Glasgow scoring system isa prognostic tool used to assess patient morbidity and mortality early. It has a sensitivity of 68 per cent and a specificity of ‘84 per cent, and is particularly popular in the UK. Criteria to be identified within 48 hhours of presentation. Severe disease is presenti more than thee factors are detected. ace > 55 years > white el count 215x107, > blood glucose > 1Ommolt tue > t6mmott > arterial oxygen partial pressure <80kpa > albumin < 22g > calcium <2mmollt lactate dehycrogenase > 600U ori (oe 1975) activating the enzymes, which stan to digest the pancreas PATIENT ASSESSMENT Patients typically present with sever, constant, epigastric pain cadiating into the centre of the back, with associated vomiting, They can be distressed due to the pain, sweating and pyrexial, and can show signs of hypovolaemia due to third space fluid loss. If there are signs of hypovolaemia, Urgent fluid resuscitation should be initiated ‘Abdominal tenderness is Ikely to be worst in the epigastrium, A blush discolouration in the loins, known asthe Grey-TumerS sign is not seen immediately but develops a few days after hypovolaemia and so is not a diagnostic tool in early presentation, CRITERIA Ranson’ criteria provide valuable inform: ation about the severity ofthe acute inf. matory process using 11 factors (Box 2), but the simplified eight-isk factor system with ‘modified Glasgow criteria, for use within the fist 48 hours, is more widely used (Box 3), The modified Glasgow crtera i the easiest ‘and quickest way to evaluate the seventy of pancreatitis, and to ensure that patients are ‘admitted to appropriate high denendency Cr intensive therapy uit, Morality is between about 10 and 20 per cent vuhen there are between three and five signs present, and 50 per cent when there ‘ate sx or mare signs (Banks 1997). A third set of criteria, Apache 11, has high sensitivity and specificity in differentiating ‘mld from severe pancreatitis, but it is time consuming and involves using a computer to ascertain values (Banks 1997). It is therefore rarely u Another method of investigation that is becoming more popular is computed ‘tomography (CT) scanning, Days, even hours after an acute pancreatitis attack, CT ng may offer better indications of prognosis than the more commonly used scoring systems and can show inflammation, fluid collection and changes consistent with necrosis. In general, the more complex the symptoms revealed by CT scans, the more likely patients will suffer 2 complicated course (Forsmark 2000) Fg. 2). Other, more ‘commonly used investigations and their rationales ae Isted in Box 4 TREATMENT ‘Oxygen delivery and fluid resuscitation Prowding adequate oxygen is essential when treating patients in hypowolaemic shock. The effectiveness of oxygen delivery should be judged against patients’ arterial oxygen partial pressure reading and titrated as necessary Close monitoring should be adopted to establish the effectiveness of tissue perfusion, with particular attention paid to pulse, blood pressure, capillary refill and ‘general cognitive state. t should be noted, however, that in the initial stage of hypovolaeric shock, and to some degree in compensated hiypowolaemic shock, the body Cften remains within normal physiological parameters (Adomat 1992). References in the literature to how often observations should be made are limited ‘most texts simply acknowledge that they take place, But frequency could start at a rate of once every five minutes and be adjusted according to clinical condition. Intravenous (IV) access is essential for administering fluids and analgesia, and should be gained as early as possible. Two wide-bore, 14-16fg peripheral lines should preferably be inserted in the eft and Tight antecubital fossae (American College of Surgeons 1993). Intravenous fluids should be given in accordance with the level of hypovolaemic shock (Wyatt 2001), The inflammatory exudates around the pancreas resemble those of internal burns and consequently fluid may be sequestered intro the retroperitoneal and peritoneal spaces. Its of paramount importance that this fluid is replaced, Choice of replacement fluid ~ blood, ‘arystallid or colloid ~ should be based on haemodynamic state and the resuits of tests, to ascertain levels of haemoglobin, haematocrit and serurn albumin, Resuscitation, however, is usually with ‘aystallod (Beckingham and Borman 2001) but colloids may be required to restore culating volume. Fluid resuscitation is monitored by ensuring that urine output exceeds 30 mUh Some texts advocate using normal saline to prevent hypotension and maintain sufficient hydration (McCance and Huether 1997) but others advocate IV fluids with electralyte replacement such as Hartrann’s fluid (Ruth-Sahd 1996). The volume of fluid being administered and rate of administration should be determined by blood pressure, centtal venous pressure and urine output, and patients should have indwelling urinary catheters 1o measure iwoluntary production of urine Ruth-Sahd 1996), ‘Morphine sulphate versus pethidine ‘Assessing and treating pain in patients with pancreatitis is vital. The most common method of assessing pain is using the Blood glucose concentration Serum amylase Serum lipase ‘chest X-ay Electrocardiogram ‘Arterial blood gas sampling Patients can show signs of hypoxia resulting from hypovolaemia due to third space fluid loss ulin production has decreased, patients can be expected to have higher dculating blood glucose levels because glucose can no longer enter muscle and adipose tissue ‘Amylase is an enzyme secreted by the pancreas. Serum concentrations are grossly elevated in patients with acute pancreatitis Test resuits are usually avaliable within an hhour but have low specificity: normally less than 70 per cent (Gorelick 1995). It should be noted that other conditions can also cause rises in serum amylase: perforated viseus, renal insufficiency and salvary land Inflammation. Amylase i a small molecule that is rapidly eared by the kidneys so large Serum concentrations tend to be short lived Testing serum lipase isthe test of choice, and can give results as quickly as serum amylase tests (Agarwal 1990), The simultaneous determination of amylase and lipase offers a sensitivity and specificity of between 90 and 95 per cont for detecting acute pancreatitis in patients presenting with acute abdominal pain (Calvien 1989). Serum lipase takes longer to clear from the bloodstream than amylase so isa more useful historical indicator This is used to rule out pleural effusion. Acute respiratory distress syndrome is common in severe attacks of acute pancreatitis (Burkit et a 1998) Pancreatitis can cause gross fluid and electrolyte disturbances induding hypocalcaemia. Electrocardiograms should therefore be taken to ensure that patients are in sinus rhythm (Burkitt eta! 1998) In the absence of insulin, large quantities of fatty acids are released into the circulation following the breakdown of stored ‘triglycerides. This raises the volume of fatty ‘acids in the liver. These are converted into _acetoacetc acd, which cannot be metabolised ‘and causes metabolic acidosis. Patients can show signs of hyperventilation as they try to ‘low off carbon dioxide. Pancreatitis also seduces levels of bicarbonate, the body's natural buffer. This causes blood pH to drop +t0.as low as 7, which can be fatal \When you have read the arte you should beable to answer the following questions: > Where isthe pancreas situated i the abdomen? > Wh has the pancreas been described asa hermit? > Name the principle pancreatic duct > Name the accessory pancreatic duct > Bxoctne cls form what percentage of the pancreatic tissue? > what is the active form of rypsinogen? > The endocrine function ofthe pancreas comprises around one milion smal clusters of eels, known collectively as what? > What do alpha cells secrete? What do beta cells secrete? > What to delta cells secrete? - What mechanical factors are sid to cause acute pancreatitis? > Name the two most common causes of acute pancreatitis > What dinical signs would you expect to see in patient with acute pancreatitis? > What sgn may be seen inpatients with pancreatitis afew days ater onset? > Name the two predictor systems used to identity morbidity and mortality rates in patients with acute pancreatitis > What analgesic is recommended for the treatment of acute pancreatitis? > What other drug mentioned is alo available for treating pain in patients with acute pancreatitis? ‘You should also: > be able to identify the main functions ofthe pancreas as an endocrine and exocrine gland > be aware ofthe altered pathophysiology in patients with acute pancreatitis > know the two most common causes of acute pancreatitis > know the most common presenting complaints of patients with acute pancreatitis, > understand what investigations are needed and why > understand the use and implications of the relevant predictive scoring systems > understand the drug therapy to treat acute pancreatitis ‘numeric ladder, on which patients are asked to score their pain from one to ten, where ‘one sno pain and tenis the worst pain they have ever experienced (Coyne 1997) Pain management for acute pancreatitis should begin with titration of opioids intravenously or through a patient controled analgesia system. Most texts and physicians advocate using pethidine rather than morphine (Ranson 1995) while some are reluctant to voice an opinion and refer merely to ‘analgesia’ (Beckingham and Bornman 2001), a However, the ‘pethidine is better than morphine sulphate’ debate is based on a common misconception that pethidine does not affect the sphincter of Odd. Infact, ke all opioids it can increase smooth muscle tone and so reduce bilary and pancreatic secretions and so increase bile duct pres This can lead to bilary spasm and constrict- {on ofthe sphincter of Oddi (Pasero 1998) There is no research evidence for using pethidine over morphine in patients with pancreas (Paulson 2002). Morphine, how ever, fs better than pethidine for severe pain ‘management in terms of duration British National Formulary 2003), and repeated ad: ‘ministration of pethidine can result in the ‘accumulation ofits metaboite, norpethiine, Which causes increased central nervous system irritability and possibly seizures (Paulson 2002), FUTURE OPTIONS FOR ANALGESIA More research into analgesic treatment is, needed, but preliminary clinica tals suggest that the long acting somatostatic analogue, ‘octreotide, can reduce pancreatitis pain that is umreleved by opios. Octreotide, lke somatostatin, is believed to wotk by suppressing the pancreatic secretions that cause auto-digestion. It is ‘given every 12 hours subcutaneously and has few adverse effects (Pasero 1998) The value of antibiotics in severe acute pancreatitis has been discussed for many years, Controlled trials suggest that there is 4 probable role for their use in preventing complications related to sepsis (Golub et al 1998). Current evidence shows that imipenem is better than other drugs such as. quinolones, which cannot penetrate pancreatic tissue (Bassi et al 1998). To reduce discomfort, patients should be sven il by mouth, have nasogastic tubes placed on free drainage inserted, and be Administered antiemetics such as cyclzine (wyatt 2001 CONCLUSION Acute pancreatitis is a life threatening condition with high moraty and morbicty rates, Patients typically present with severe epigastric pain that radiates to the back They may be vomiting or at least complain cof nausea, Depending on the severity of the attack, patients can also display signs of hypovolaemia that needs urgent fluid resuscitation. Patients should receive cxygen, and routine blood tess should be taken, Levels of serum amylase and serum lipase should be tested to enable diagnosis of acute pancreatitis within between 90 and 95 per cent specificity and sensitivity. Routine chest X-rays, electrocardiograms {and arterial blood gas sampling should be sought to rule out pleura effusion, cardiac arrhythmias and metabolic acidosis, Urinary catheters should be placed in situ, and urine output readings should be taken References ‘Adomat (1982) Understanding ‘hock Bt una of sing 1,3 pane Coyne P1897 Pancreatic cancer mercan Coleg of Sugeors (193) pa tame, ad tren ASP Paty 6,1, 4 Advanced Taums Ue Sgport ‘raga fr Psa Chan, Aanencan Coleg of Supers Abiering, Arata et (1984) Ocrectde saat dares parca ‘ermplcatens ater pancenic ‘eauna. eran Jara of Sager 168, 4345-347 Fexsmak 2000) Margie of ‘eat Fncets Foi Unie of For, rere Ao al 1995) uct faa acute parce Potacte ocala 77, 838,472 fons (1997 race ques seat pancretts Amencan Ju of Gasrontereay 92, 3, 327.380, Spe, Scent etn. Londen, Chal Uangatone Mekal Deter. Reet oth econ. Piha 28, 8 Sues hourly. Urine output should not fal below 30mUM, Intravenous opiates should be given for pain, although the drug of choice usually depends on the preferences of individual Clinicians. Patients should be given nil by mouth, prescribed antiemetics and have nasogastric tubes inserted Patients who score highly on the Ranson’ or modified Glasgow criteria should be moved 10 high dependency or intensive therapy units for dose monitoring tae CW (1975) rose ty faite pancratis Bah aunalot Spey 62.6, 490498, esha W195) Frente of rec: betes edn Cops led Pepecives 07 Pathog Phiadeonia FW MecCance Kl, Huger SE (1987) Pataphysoogy: The bg bas of dss acs and cen Thad ton St Ls MO, Mey Neptoemes t(1984) The Leger agro glo n ‘ce paneoits, tah ura of Suey 71, 3, 230-233, Goi Re 1998) of anodes in acute pancetta ot Gesroesta Suepy2 6496503, Gore (1988) Noma Aratary and baat Rens, Phinda BA, WB ounces. Per CL(1998 Fa cont. ‘Aeron sua of Nag. 5, Goreck 5 (1995) ace panceats, 4.18 bn Yanand Td Fok of Banks (1998) Acute and ric panera lla Ml cs) (Gastonia! and ver Does Paton, dor and rraeunpient Sth eden Prva PW Sauder as Ce 1998) Conte cca tml of pfloxcn vers iripener see preenit,Gasromtoo, eckrghn I Beran PC 2001) 1 of esis of he pncea, are ary ster: cate paresis, et Macca. 32. 7286, 5508, poco astoentrgy Second edo, Friatepha PA, ups Gore Spo HM (993) Pancreat Dros incl Gestoerneoby. Forth eon, Guyton Ac, Ha (1999 Fexbook ‘of Mekal Pky Furth eon, 15,6 191341517 london, Wa Saunders ashen © 2002 Mepis ‘morphine forthe treatment of Rarcon MC (1993 Acste parce: srgcal management (Gov alos The Pancreas Boy, patty and dase arson IC (1985) he cent rranagerert of ace pana, Hata ta 1989 Ci re sing anced Suey 28, 93.112 2 hos appro, Pada Pa rs ar Wik OF Nuig. 96,6, 3839, Imananeent of ads wh rss euch Non Farman 2003) ee Nationa Romy Mater 85 lendon, tah Media As arene Roya rama Sacey of Gat Stan Hearn B, Buck (1996) Nera ars tees uncinsof e ances, in lock Ld Patheysoloy Aptatrs and ateotons in fincon Furth eon, Paden PA, uppict raze (1958) Knowle base fer gutens vith getontesia

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