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Acute Pancreatitis PowerPoint Presentation

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This medical PowerPoint presentation talks about acute pancreatitis, a medical condition in which the pancreas, a gland located behind the stomach, becomes inflamed. The inflammation occurs when digestive enzymes that are normally released by the pancreas are activated prematurely and start attacking the pancreas itself.

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Published on : Apr 26, 2023 | Views : 829 | Downloads : 4

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Slide 1-

Acute Pancreatitis John Lieb II MD Assistant Professor of Clinical Medicine Division of Gastroenterology
Slide 2-

“Acute Pancreatitis is the most terrible of all the calamities that occur in connection with the abdominal viscera.” Sir Berkeley Moynihan Ann Surg 1925
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Outline Def Clinical presentation/Differential Epidemiol Pathophys Causes Complications Radiology Scoring systems/prediction Management: fluids, antibiotics, nutrition, ERCP Long term consequences (CP, DM, cysts, bleeds)
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Acute Pancreatitis Inflammation of the pancreas and associated adjacent organs without evidence of chronic pancreatitis Atlanta Symposium in 1992 defined acute pancreatitis clinically as 2 of 3 of the following Typical pancreatic type pain Radiographic findings of acute pancreatitis Elevations in blood chemistries (typically amylase and/or lipase >3x ULN)
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Causes of elevated: Amylase Renal insuf Salivary inflammation Ie vomitting, parotiditis Macroamylasemia Hereditary or from hetta starch Intestinal infarct/peritonitis Through transperit absorpt Chole’itis, Salpingitis, ectopic preg Ovarian cysts, lung inflamm Acidosis, ESLD Intest radiation, obstruction Colon, ovar, panc, brst, prst, lung, esoph CA MM, pheo, appendicitis, gastroenteritis Burns, normal pregnancy, FHF Lipase DU, renal insuff Small Intestinal ischemia/obstr Tuboovarian abscess Macrolipasemia (nonhodg, cirrh) Tylenol OD Hypotension/sepsis/DKA HIV, panc CA Gullo’s syndrome Cholecystitis False negative amylase/lipase: Hypertrigs, stoic person (vets) who presents late
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Working up false pos amylase/lipase If obvious other cause (vomitting, tub-ov abscess) then no further w/u needed Serum isoamylase (35-50% of serum amyalse usually pancreatic) Urinary amylase (beware of spitting in cup, munchausen) Serum trypsin (RIA, UF, NEJM 1984). Barely high levels: repeat the measurement in 6-12hr True elevations require workup, malig, CP, etc
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Acute Pancreatitis: Time course of enzyme elevations Amylase half life 10 hrs
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Acute Pancreatitis Presenting features Syncope! Rare Painless:post op, legionaire’s, DM, perit dialys
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Extraintestinal manifestations Arthritis (lipase laden fluid with leuks) Serositis (pericarditis, pleuritis) Panniculitis, subcutaneous fat necrosis, can look like e nodosum (1% of all cases, 10% have it at autopsy) Purtscher’s retinopathy (rare) Sudden blindness, post retinal artery occlusion
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Pain, Oh the pain “Worse than childbirth” “Worse than being shot” Starts fast within 10-20min reaches peak Third fastest pain onset in GI after perf and SMA thromb Does not usually undulate (not colicy) Lasts days (if no underlying chronic damage) Longer than biliary colic which is hours Radiate to back in 50% Sometimes diagnosed at autopsy (painless) Almost always causes ER visit/admission Capsaicin, glutamate, vanilloid, ppar-gamma
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Acute Pancreatitis: Epidem 5-35/100,000 Increasing incidence (detection?meds?iatrog?) Increases with increasing age Onset before 14-15 yrs unusual unless hereditary, traumatic, anatomic anomaly 250,000 admissions per year in U.S. (2nd GI) $2 billion in direct costs per year 6th costliest GI disease behind ESLD, cancers, IBD NIDDK funding is 11 out of 17 GI illnesses
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Acute Pancreatitis Pathophysiology Since starch and triglycerides are not stored in the pancreas, trypsin is the major catalyst for pancreatic autodigestion, not amylase or lipase (but later lipase gets to abd fat….) PREMATURE/INTRACELLULAR activation of trypsin. Leads to activation of chymotrypsinogen, more trypsinogen, elastase, phospholipase A2, complement, kinins ->>AUTODIGESTION!!
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Etiologies of Acute Pancreatitis Biliary (gallstones) *** Alcohol**** Triglycerides*** pERCP,* post surgical Drugs (except byetta and L-asparagenase and trigs **) Tumors/obstruction Trauma** Ischemia/embolic*** Infection (except mumps **) Hypercalcemia (hypPTH) Autoimmune/Sprue Hereditary Controversial (divisum/SOD) Scorpions *** Chemical: insecticide/MeOH Idiopathic: 30%!! Number of *’s denotes tendency to be severe
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Biliary anatomy GB Right lobe of Liver Left lobe Stomach Pancreas CBD PD Major papilla Duodenum Jejunum
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Biliary Gallstones or sludge, Microcrystals? Most common etiology in world. Still 35% in US. More in women Usually small ones that don’t obstruct cystic duct or most of CBD until right at major pap Usually pass on own, but don’t be complacent! Can be Necrotizing!! Biliary duct dil/LFT can occur late! (insensitive!) If fever, bili over 2, SIRS, (ie cholangitis) call adv endo immediately. ALT 3X ULN (>150) 50% sens and 90% specif. First ALT then bili then ductal dilation. ALT/AST can be 1000! NOTE MUST BE ON CHART FROM SURGERY BEFORE D/C !
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Biliary: who has extant CBD stone? Cholangitis—call even at 2am if look unwell, septic TBili over 3, esp if over 5 LFT not improve, esp if pt still has pain Pt looks unwell High (ERCP), moderate (MRCP), low risk (watch) Very personalized decision. Depends on local MRCP quality, surgical expertice in intraop cholangiogram, etc Call even on weekend MRCP can have false pos>>>false neg
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Biliary panc’itis Scenarios PT with fever, tbili 1.8, ALT 500, AP 250, tachy, WBC 20 with 20% bands, duct dil on US, looks unwell PT looks well but ALT still 100, AP 200 TB normal—sat nite at VA PT was very ill when they called you, fever, tachy, tachypnic, bili 3, AP 250, ALT 500, duct dil, but when you arrive suddenly pt feels great, looks better, stat labs bili now 6, AP300, ALT 640, WBC still 15 with left shift
Slide 18-

Biliary panc’itis scenarios Pt with pain of 6 hours duration now, bili 4.4, WBC 15, ALT 340, AP 300, t 100F, CT with mild AP and ductal dil No radiologist in house Sat 9pm at the VA You look at CT and inform the rad PGY2 at HUP that there is a CBD filling defect, likely stone, about 6mm in size. He agrees he must have missed it. Pt still not feeling well, writhing in pain
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Biliary panc’itis scenarios Pt with fever, WBC 11, bili 2.2, ALT 300, AP 300, AP, ER RUQ US shows gallstones, acute chole with duct dil 2am, pt does not look bad, feeling better than when first arrived, but still signif RUQ pain 2am surg PGY 2 says, “consult GI for urgent ERCP for cholangitis, discussed with surgery attdg” and that quote is on the chart. ER calls you at 230am.
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Alcohol TAKE A CAREFUL HISTORY Often after pt stops drinking (CCK is upregul and pts start to eat more fat/protein). “The night of the day after” a binge Typically a lot: >50g/day for years But no amount of ETOH is safe More in men; lipase 2X amylase? 1st or 2nd most common in US (31-40%) Mitochondrial toxin, lysosome instability Reactive oxygen species, proinflamm Increased lysosome and enzyme production Decrease panc blood flow, precipitate panc proteins Why only 10% of alcoholics get panc’tis? SPINK? Often have CP
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Triglycerides Usually >1000: an endocrine emergency! Can occur in 500 range In Children it is known that keeping trigs<200 prevents AP Alcohol raises trigs usually to 400-500 range, can be higher Can have normal amylase and lipase. What about post prandial trigs? Uncontrolled hyperglycemia can lead to high trigs Often have CP IV insulin works faster/better than SQ
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Trauma Disrupt PD as pancreas crosses spine in mid body ERCP needed once stabilized to “bridge” duct disruption with stent to prevent apoptosis of tail.
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pERCP Often mild/interstitial 5% of all ERCP But only 1/1000 of those are necrotizing pH of contrast dye? Osmolarity of contrast? Stent fell out? Mechanical swelling of papilla? Wire in duct? Bacterial reflux? Thermal effect of sphincterotomy? RFs: Pt, procedure (SOD, nondil ducts, no cancer, no stones, more cannul attempts, more panc dye injection (body, tail, acinarizat), pt with nml panc, pdivisum/ampullectomy, spincterotomy esp precut, dilating biliary orifice without sphincterotomy, <50 cases/year, <200 lifetime cases) Prophy: indocin PR? PD stents, wire guided cannulation
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Other endoscopic causes Diagnostic or therapeutic EUS Deep enteroscopy Duodenal adenoma resection even if lateral wall
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Post surgical 25% post CABG have high amylase 1% of CABG have necrotizing pancreatitis Mechanical stretch—Kocher maneuver? Ischemia? Anesthetics (propofol/trigs)? Cardioplegia? (CaCl during CABG) Note: amylase/lipase elevations in ICUs are common, most often not clinical pancreatitis
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Obstructive/Tumor Adenocarcinoma of pancreas/Acinar cell Ca P divisum? SOD? Long Common channel, Caroli IPMN, neuroendocrine, mets, lymphoma Ascariasis Ampullary tumors/diverticula (latter, controver.) Post acute pancreatitis with panc duct stricture Sprue or Crohns of duodenum ALL UNEXPLAINED PANCREATITIS PTS OVER AGE 50 OR EARLIER IF FHx OF RELEVANT CA’s (RCC, Breast CA, brain CA, uterine, etc) SHOULD HAVE A CT 6 week or so after the AP.
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IPMN
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Pdivisum from IU.
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Drugs AIDS— didanosine, pentamidine Antimicrobial— metronidazole, sulfonamides, tetracycline , INH, dapsone, nitrofurantoin Diuretics— furosemide, thiazides (sulfa?) Immunosuppressive/antimetabolite— L-asparaginase, azathioprine , 6MP, INFα?, sorafinib* Neuropsychiatric— valproic acid Antiinflammatory— sulindac, sulfasalazine, 5-ASA, salicylates Others— calcium, estrogen, tamoxifen, Byetta, TPN, propofol, accutane, vit A *sorafinib can raise lipase/amylase without p’itis
Slide 30-

Drug Induced AP by timing Early Within 30 days Reflects hypersenitivity or direct damage Rash, eosinophilia Azathiaprine/6MP, Sulfa, flagyl, ACE, salicylates Late Often after several months IgG or T cell related? Buildup of toxic metabolites? Didanosine, pentamidine, valproic acid
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Drug induced AP by mechanism HYPERTRIGLYCERIDEMIA Tamoxifin, estrogen, finasteride, beta blockers, vit A, thiazides ANGIOEDEMA ACE-I’s—Bradykinin? DIRECT TOXIC Sulfa, diuretics IMMUNOLOGIC Sulfa, 6MP/Imuran
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Infectious Viruses – Mumps, coxsackievirus, hepatitis B, cytomegalovirus, varicella-zoster, herpes simplex, HIV, atypical dengue Bacteria – Mycoplasma, Legionella, Leptospira, Salmonella, MAI/TB Fungi – Aspergillus, cryptococcus Parasites – Toxoplasma, Cryptosporidium, Ascaris, Pneumocystis carinii, leshmaniasis
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Exotics Scorpions (Trinidad/Mexico/India/Israeli) Brown Recluse (Sorry Santhi V, I cannot corroborate, maybe dapsone?) Snakes (very rare) African “killer” bees (very rare) Gila Monster
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Hereditary PRSS1 Auto dom. Incomplete pen. First attack by teens Calcif CP is inevitable. No Tx. 20% lifetime CA risk Islet cell autotransplant? SPINK –recessive. Not a cause, but a modifier CFTR—”atypical CF” “panc sufficient CF” Explains many “idiopathic” cases. Recess. 2 CF’s with two SPINKS: marked increase risk Chymotrypsin C (rare)
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Interstitial/edematous pancreatitis
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Necrotizing Pancreatitis
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Mortality Overall 2-5% and decreasing slightly Interstitial/mild pancreatitis (80% of all cases) ≤1% mortality Necrotizing/severe pancreatitis (20% of all cases) 20% mortality, long ICU stays (1-3 months) Infected necrotizing pancreatitis (occurs late) 50% mortality
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Interstitial pancreatitis
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Interstitial pancreatitis
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Necrosis
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Necrosis
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Pancreatic abscess/infected necrosis
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How pts die with AP?—Two Peaks Early within 1-2 weeks and often within 72 hours: multisystem organ failure (kidneys, lungs with ARDS) (can’t be ventillated/oxygenated even on vent), DIC, hypocalcemia, shock/hypotension, abd compartment synd, aspiration, cholangitis, acidosis, hemorrhagic pancreatitis, intest ischemia (clot in SV->SMV)) Late: pancreatic abscess/infected necrosis, usually by 2 weeks, secondary biliary obstruction, hypoalbuminemia, Hospital acquired (VRE, MRSA, line infect, aspirations), PE, gastric variceal bleeding, gut failure, neg nitrogen balance.
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Hemosuccus Pancreaticus
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Clues to send to ICU Tachypnea Oliguria <50ml/hr Hypotension/orthostasis Tachycardia >130 Tense, distended abd Grey-Turner’s/Cullen’s Pallor, cold extremities Jaundice esp if febrile Azotemia, hypoalbumin Age> 55, high fluid req’m First attack Mental status changes Uncontrol hyperglyc/hypo Cardiac ectopy (recurrent runs of NSVT/PVCs) QTc>440msec Obesity BMI>30, “apple” Baseline dec card/pulm fn Diastolic dysf Hemoconcentration WBC>15, bands/myelos Pleural effusion
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Clinical indices of severity RANSON APACHE ATLANTA BISAP Glasgow Delta HCT and/or Delta BUN
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Ranson At presentation Age >55 White blood cell count >16 Blood glucose >200 mg/dL LDH >350 U/L AST >250 U/L At 48 hours Hematocrit Fall by ≥10% BUN Increase by ≥5 mg/dL despite fluids Serum calcium <8 mg/dL pO2 <60 mmHg Base deficit >4 MEq/L Fluid sequestation >6 L 1-2 criteria - > <1% mortal 3-5 cirteria - > 15% mortal 6-8 criteria- > 60% mortal 9-11 -> >75% mortal .
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APACHE II Temp high or low MAP high or low HR high or low (HR 60 gets 2pts!) Na high or low K high or low Creat elev Age over 44 APACHE-O BMI>25 1 pt BMI>30 2pts WBC high or low Glasgow coma (low) pH or HCo3 High or low PaO2 Nonsurgical and emergency surgery More points Score <8 Mortal <4% Score >8 8-18%
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ATLANTA (1992) Mild vs severe (necrosis or organ failure) APACHE≥8 or RANSON≥3 Organ failure Systolic blood pressure <90 mmHg Pulmonary insufficiency PaO2 ≤ 60 mmHg Renal failure Creatinine ≥2 mg/dl after rehydration Gastrointestinal bleeding 500 ml in 24 h DIC: Platelets ≤100 fibrinogen <1·0 g/l and fibrin-split products >80 μg/l Calcium ≤7·5 mg/dl
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ATLANTA REVISED (2008) Early severity->organs fail Late severity->Structural (necrosis), esp infect PERSISTANT ORGAN FAILURE (>48 hrs) NEW DEFs of Radiographic/structural features of severity
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ATLANTA 1992 Interstitial vs necrotic Pseudocyst vs abscess Revised, 2008 Interstitial edematous panc Sterile necrosis Infected necrosis Acute Necrosis vs fluid, sterile vs infected Chronic Pseudocyst vs walled off necrosis Sterile vs infected
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BISAP SIRS T >38.5°C or <35.0°C, HR>90, RR >20 or PaCO2 <32 mm Hg WBC >12,000, <4000 or >10 percent immature (band) forms BUN>25 Age>60 Pleural effusion Altered mental status (glasgow CS < 15) 0-2 pts: <2% mortal 3-5pts: 22% mortal
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Glasgow Age >55 WBC >15 LDH>600 Glucose >180 Album <3.2 Calcium <8 PaO2<60 BUN>45 At admission and at 48hr Score 0 to 2: 2% mortality Score 3 to 4: 15% mortality Score 5 to 6: 40% mortality Score 7 to 8: 100% mortality
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Lieb’s Orderset Call for temp>100.5 or <97, HR>100 or <50, U/O <10cc/kg/hr, MAP<60, RR>12 FS q4hr. Call if >200 or <60 I/O check q4hr Dilaudid PCA, zofran/phenergan for N IV H2 blocker if not already on something. Good for first few dys, after that probably would not use esp if not on it on presentat. Hold ACEI NPO except comfort swab If neighbor not NPO, get private room. Repeat BMP/CBC in 4-6hrs after last one, consider LFT, mag, phos, cal/album repeat then too.
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Fluids: Theory and Data Principles/theory: Fluid prevents capillary microthrombi (necrosis?). Improves renal perfusion Can we prevent necrosis? First 12 hours maybe the key Once necrosis occurs, be careful with over resuscitation Often these pts have low albumins and have near abd compartment anyway Bolus, frequently. A pulse jet, not a hose! Think sepsis goal directed therapy Data: retrospective –more fluids are bad, classic causality bias Goal directed no better: classic referral bias (post hoc, LR better) China RCT: Colloid like heta starch (HESPAN)better? Really? But Large studies in all takers with shock show increased ARF, coagulopathy and death with heta starch
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Fluids, practical MD Stay in house until pt makes urine. Have night person in house check U/O, glucoses and f/u repeat BUN/creat/CBC Send to ICU NOW! if hemoconcentration, question of abd compartment, elev BUN, oliguria LR for first 1-2 L’s unless hypercal/kal. If no U/O may have to switch to NS AND BOLUS another 1-2L. Once second lytes back and OK and if urinating can do LR again Typically 250cc/hr or more for first 12 hr. Care with old age >75, diastolic dysf, CRI, baseline edema/hypoalbum, known necrosis (ie late presentation) When in doubt give more fluids, consider CVP monitoring
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Imaging now or later? RUQ US STAT anyone with no ETOH Hx and with intact GB and with elv transaminases/bili. CT: only those with questionable dx or maybe very ill about to be intubated or whisked to OR or >72 hrs into course. Is it a perf DU? But a KUB will help No CT post ERCP. MRCP can be done without gad! Future: 13NH3 PET
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Nutrition in acute pancreatitis—ideal world Goals: rest the pancreas/avoid bile flow Post Lig o Treitz, small volumes Can use elemental/MCT’s (medium chain trigs) Avoid aspiration Give with enzymes RCT comparing stomach feeds to TPN found stomach feeds superior if started within 48hr. RCT comparing post LOT feeds superior to TPN. Try to avoid TPN-- cost, infection, proinflam Dobhoff feed everyone with AP (DDW 2012)?!!
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Nutrition in acute pancreatitis—real world Most mild AP resolves in an few days, don’t need nutrition suppl. Most necrotizing panc have partial duodenal sweep obstruction so tough to pass dobhoff. Sedation for GI guided nasojej feed tube may require general due to aspiration risk. Long 1.5hour procedures at least. Most necrot panc are hypoalbum, hypoprotein.—no oncotic pressure to absorb enteral Ileus often present in necrotizing panc. Pts are high risk of aspiration of feeds. MCT’s, elemental feeds expensive, almost like TPN
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When to use antibiotics? Never for prophylaxis? If use antibiotics should be broad. Use if cholangitis suspected (amp/sul is all that is needed if no pancreatic necrosis) Meropenem (MRSA, anaerobes, GNR) or pip/tazo If PCN all, can use Vanco, levo and/or azactam, flagyl Don’t forget fungi if recent surg/intervention or if failing a carbepenem. Don’t forget VRE. Ecoli 51%, enterococcus 19%, staph 18%, klebs10%, proteus 10%, pseudomonas 10%, bacteriodes 6%
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When should IR drain a collection? Never?—Should only tap and send for culture, if grow a bug/bugs? In practice, IR tends to leave a drain—maybe bad! Typically surgery team should be aware of pt before you send to IR (you infect the surg bed!) If IR drain, should be retro approach
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Infected necrosis, new reality NEJM april 2010, Dutch group, 88pts, RCT, “PANTER” “Step up approach” Open laparotomy (bilateral subcostal) vs IR (12 Fr, multiple drains, only 2 endoscopic followed by retroperit debride (VARD) ) No mortal diff. 10% less cost in IR approach. Combined end point “death or major comlx” reduced from 69% to 40%. Open pts had more reoperations for sepsis 50% were not university hospitals, but were “tertiary” so were surgeons not as good? Why open approach, bilater subcostal? More of a test of VARD vs open not IR vs open
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Infected necrosis principles of mngmt Wait as long as you can before intervening Ideally at least 3-4 weeks Even if that means intubation, dobhoff feeds Let the bed mature/get walled off—this allows for IR/Endoscopic management New data suggest conserv mngmt for all necrosis has a 7% mortal Surgery series, 25-50% mortal (old studies) Newer surg series say 50% moral in first 14 dy, 15% at 30 or more days
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Endoscopic necrosectomy Must be within 1cm of stomach, walled off and mature Avoid if resp unstable, OK if intubated already If pseudoaneurism, must embolize in IR first. Endoscopic series 0 -7.5% mortality (2/96)—but these are sick pts, many “too sick” for surgery Median scopes: 5 Morbidity 25%, particularly bleeding, aspiration, abscess 80-90% successful F/u 43 mo Old teaching “not for infected necrosis”—no longer!
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When to call a surgeon? Pt unstable. Infected necrosis proven or suspected. They may not intervene until later, but let them know Abdominal compartment syndrome (ck foley pres) Pt with multiple poor prognostic signs, age, WBC, oliguria, SIRS ELECTIVELY WITH ANYONE WITH STRONG SUSPICION FOR GALLSTONE ETIOLOGY WITH GB STILL IN SITU. MUST HAVE CONSULT ON CHART AND F/U ARRANGED—HIGH RECURRENCE RATE W/O CHOLE Pt in ICU, can’t eat/tolerate enteral, not improving
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Scenarios Alcoholic, 3 attacks of AP from Sept to Feb with very similar CT findings, ER visit in April for same, but no CT done. Pt insists feels much worse sense april, early satiety, nausea Alcoholic presents to ED in extremis with acute onset abd pain 2 hours ago, AP, tachypnic, distended, not tense, ileus BS’s, hypotensive, creat 1.5 (was 0.8), BUN 50, was 5, afebrile—CT or no CT? what else to do? VA? 50 yo main line lawyer with unexplained AP neg US, nml trigs “I don’t want a CT, too many rads. MRI, cost ineffective”
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Scenarios 50 yo poorly controlled DM, obese, with 24 hrs abd pain, AP, after eating BarBQ/fries/cheesecake and two beers WBC 15, glucose 400, creat 2.2, on admit up from 1.2, trigs 400 after 36 hr fast Doing well on med floor, feels better, FS 250 CT now shows 10% necrosis and fluid collection about 3cm Pt wants to eat and “get outa here” Enthusiastic med resident calls, “hey GI/IR, please Drain collection?”
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Scenarios Alcoholic, severe presentation with SIRS, hypoxia, oliguria, gets intubated and then few days later, generally better. Initial CT on admit revealed “mild AP” with peripancreatic fluid Febrile on admit, deferversed after 2-3 days, now has few temps 100F in last 48 hours. You are called b/c ICU wonders why pt still distended, not tolerating dobhoff feeds, not weaning. You note initial WBC of 25, currently 15. What do you do next?
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Scenarios OSH doc (GI or gen surg) calls you at 2am on Sat nite from Poconos or S Jersey (200bed hosp) Pt with severe AP in their ICU same scenario as last one, with CT showing 50% gland necrosis with extensive peritoneal/retroperit necrosis, but doc asks—”this area has to be drained, I’m going to call in IR for perc drain and then we will send pt to you, OK? Do you accept pt?”
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Scenario You are the PGY4 on call New PGY6 starting an ERCP rotation (20th ERCP) ERCP done for intermitt dil CBD and RUQ pain with normal LFT, biliary sphinct done in this young female, age 20 with no alcohol history. Never had pancreatitis. Never had DM No stones found, no stent used,She smokes. She is 5’6” and weighs 190lbs, pt admitted for pain/AP post procedure. Floor nurse calls you for glucose on panel is 300. Worried? Not worried? What other questions should you ask? How to best manage this pt
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Scenario Same pt calls you from home, has pain, thinks it is gas pains. What should you do? Different pt just had “a small intestine polyp” removed by Dr. Ginsberg with PGY5 at 1pm, calling you with same at 8pm. She also “saw a plastic straw” in her BM just now. “Is that OK doc?” Ran out of her pec’s last week. “can you just get me a few more pec’s? I will be OK.” What do you do? Dr. Katzka’s IBS pt had a colonoscopy today and calling you with same. You note 20 calls in EPIC in the last month for various things. You note 3 CTs in the last 2 years in EPIC What do you do?
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Scenario 44 yo Main line lawyer with ideopathic Acute relapsing panc. Uncle had bad attacks of abd pain. Thin build, jogger, no other med problems. Calls you in ER “I’m waiting too long” “Can’t you do something?! I feel terrible. The pain is unbelievable” First attack was 9 months ago. Was in ICU with necrosis, ARF, tachypnea, but resolved. Two more attacks about every 3 mo since but not in ICU. Last CT 3 mo ago without necrosis or collections Worried? Not worried? Why? What do to next?
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Take home points AP Causes, presentation, labs (incl trigs!) CAN BE PAINLESS!!! Causes of false pos/false neg amylase/lipase (>3X ULN!!!) Predict the problem pt: age, abd obesity, SIRS, WBC, BUN, glucose, first attack etc Know the most severe etiologies, GET TRIGS EARLY/ADD ON!!!! Triage (scoring systems) Tiger or kitty (ie necrotic vs interstit)? Time will tell Hydrate hydrate hydrate for early disease by boluses, LR, consider colloid/heta starch if already necrosis Monitor Urine output, glucoses get 6 hr post CBC/BUN The first 12-24 hours should feel labor intensive—that means you are doing it right! Never hesitate to send to ICU if your gut is concerned Know how to recognize severe AP by CT criteria RUQ US first test of choice for unexplained (non con CT or noncon MR when US not available or when no GB) CT with contrast useful later (48 hrs or more) or if other diff dxs
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Take home points in AP CT more liberally later on (cyst or not) Know what a pseudoaneurism is and how to deal LFT abnml (esp ALT) predict biliary source (LABS are 12-24hr behind the pt!) ERCP for cholangitis in biliary pancreatitis Know when to MRCP (noncont if nec) vs ERCP Know who gets most severe pERCP pancreatitis (needle knife, SOD, ampullectomy, p divisum, etc) and RF’s for such Know 2 mortality peaks and the causes Nutrition (early dobhoff jejunal feeds if necro) Antibiotics only when infected necrosis or cholangitis/biliary pancreatitis Call Surgery for instability, abd compart, biliary, suspected abscess, pt failing “to fly” Do not call IR until after surgeon involved (ideally panc surg) If call IR, encourage VARD if possible (left retroperiton) If no clear cause, check panc protocol CT in 6wks
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John.Lieb@uphs.upenn.edu 215 823 5800 ext 3514