acute pancreatitis
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MEDICAL MANAGEMENT OF THE ACUTE ABDOMEN FERNANDO URRUTIA M.D. ST LUKE’S EPISCOPAL HOSPITAL, METHODIST HOSPITAL HOUSTON, TEXAS CLINICAL DEFINITION OF ACUTE ABDOMEN CLINICAL SCENARIO CHARACTERIZED BY SEVERE PAIN, OFTEN OF RAPID ONSET, THAT PREVENTS BODILY MOVEMENTS. PAIN FOR LONGER OF 6 HOURS, USSUALLY REQUIRES SURGICAL INTERVENTION. ACUTE ABDOMINAL PAIN COMMON COMPLAINT 1 IN 20 VISITS TO AN ER IS FOR ABDOMINAL PAIN ½ OF THE PATIENTS WILL HAVE NON-SPECIFIC FINDINGS ½ OF THE PATIENTS WILL HAVE A SERIOUS DISORDER FEW PATIENTS WILL HAVE LIFE-THREATENING DISORDERS. THEREFORE • EVALUATION TO BE EFFICIENT • ACCURATE EARLY DIAGNOSIS • AVOID DELAYS' IN THE EVALUATION • AVOID OVER INVESTIGATIONS IN PATIENTS WITH SELLLIMITED DISORDERS. APPROACH TO ACUTE CARE 1) 2) RAPID ASSESSMENT OF THE PATIENT OVERALL PHYSIOLOGIC STATE THE “ ABC “ RULE AIRWAY IS THE PATIENT ABLE TO MAINTAIN AN AIRWAY ? IS ASPIRATION AT RISK ? CAN THE PATIENT MANAGE ORAL SECRETIONS ? BREATHING TACHYPNEA USE OF ACCESSORY MUSCLES CIRCULATION 1) IS THE PATIENT IN SHOCK ? PALLOR CYANOSIS HYPOTENSION TACHYCARDIA 2) IV ACCESS 3) EVIDENCE OF ACTIVE BLEEDING ? HEMODYNAMIC INSTABILITY SURGICAL CONSULT STAT RESUSCITATION OF THE PATIENT PROTECTION OF AIRWAYS ( INTUBATION ) DEATH BEGINS IN RADIOLOGY ADAGE IN ACUTE CARE SURGERY REMAINDER RESUSCITATION PROCEED WITH DIAGNOSTIC IMAGINE C D Severity B A Time IMAGING STUDIES COMPUTED TOMOGRAPHY CHANGED THE EVALUATION OF ACUTE ABDOMINAL PAIN CT WITH RENAL CALCULUS PROTOCOL CT ARTERIOGRAPHY ABDOMINAL SERIES ULTRASONOGRAPHY MRI HIDA SCAN ABDOMINAL PAIN IN THE E.R. CAUSE PATIENTS (%) NONSPECIFIC ABDOMINAL PAIN 35 APPENDICITIS 17 BOWEL OBSTRUCTION 15 UROLOGIC DISEASE 6 BILIARY DISEASE 5 DIVERTICULAR DISEASE 4 PANCREATITIS 2 VASCULAR 1 MEDICAL OR METABOLIC 1 EXTRA-ABDOMINAL CAUSES OF ACUTE ABDOMINAL PAIN CARDIAC MYOCARDIAL ISCHEMIA, MYOCARDITIS, ENDOCARDITIS THORACIC P.E, PLEURITIC PAIN HEMATOLOGIC HEMOLYTIC ANEMIA, LEUKEMIA METABOLIC UREMIA, DIABETIC KETOACIDOSIS, PORPHYRIA EXTRA-ABDOMINAL CAUSES OF ACUTE ABDOMINAL PAIN TOXINS INSECT BITES, LEAD POISONING INFECTIONS HERPES ZOSTER, TYPHOID FEVER, OSTEOMYELITIS NEUROLOGIC RADICULOPATHY, ABDOMINAL EPILEPSY MISCELLANEOUS FAMILIAL MEDITERRANEAN FEVER, PSYCHIATRIC DISORDERS CAUSES OF NONSURGICAL PERITONITIS SPONTANEOUS BACTERIAL PERITONITIS CHRONIC AMBULATORY PERITONEAL DIALYSIS MYCOBACTERIUM TUBERCULOSIS AIDS CHLAMYDIA TRACHOMATIS NEISSERIA GONORRHEA (FITZ-HUGH-CURTIS SYNDROME) RARE CAUSES POLIARTERITIS NODOSA SLE SCLERODERMA FAMILIAL MEDITERREAN FEVER PHARMACOLOGIC MANAGEMENT DO NOT DELAY NARCOTICS SIR ZACHARY COPE: “MORPHINE DOES LITTLE OR NOTHING TO STOP SERIOUS INTRAABDOMINAL DISEASE, BUT IT PUTS AN EFFICIENT SCREEN IN FRONT OF THE SYMPTOMS” PHARMACOLOGICAL MANAGEMENT EARLY ADMINISTRATION OF ANALGESIA: 6 STUDIES HAVE CONCLUDED: (ANALGESIA VS PLACEBO) MORE COMFORT FOR THE PATIENT NO DELAY IN DIAGNOSIS ANTIBIOTIC TREATMENT CLINICAL SCENARIOS CLINICAL SCENARIO #1 A PREVIOUSLY HEALTHY 45-YEAR OLD MAN PRESENTS WITH SEVERE LOWER ABDOMINAL PAIN, WHICH STARTED 36 HOURS EARLIER. HE REPORTS NAUSEA, ANOREXIA, AND VOMITING ASSOCIATED WITH ORAL INTAKE. ON PHYSICAL EXAMINATION, HIS TEMPERATURE IS 39 C AND HIS HEART RATE IS 110 BEATS PER MINUTE. HE HAS GENERALIZED ABDOMINAL TENDERNESS MOSTLY IN THE LEFT SIDE WITH PERITONEAL SIGNS. CLINICAL SCENARIO # 1 CBC WBC 17,000 WITH LEFT SHIFT LFT, AMYLASE, LIPASE ARE NORMAL URINE NEGATIVE ABDOMINAL CT SCAN ACUTE DIVERTICULITIS RELEVANCE OF THIS CASE I. PRESENTATION OF ACUTE ABDOMINAL PAIN II. MANAGEMENT COULD BE MEDICAL OR SURGICAL III. EARLY RECOGNITION IMPORTANT TO AVOID SURGERY CLINICAL STAGES OF DIVERTICULAR DISEASE CLINICAL STAGE ASYMTOMATIC DIVERTICULAR DISEASE SYMTOMATIC UNCOMPLICATED DIVERTICULAR DISEASE (STAGE 1,2a) COMPLICATED DIVERTICULAR DISEASE SYMPTOMS/SIGNS PRESENCE OF COLONIC DIVERTICULI,NO CLINICAL SYMPTOMS L.L.Q. ABDOMINAL PAIN CHANGE IN BOWEL HABITS NO LEUKOCYTOSIS,FEVER,OR PERITONEAL SIGNS PERFORATION OF DIVERTICULUM FEVER,ELEVATED WBC OBSTRUCTION PERITONITIS FISTULA ABSCESS FORMATION BLEEDING HINCHEY’S CLASIFFICATION INITIAL ASSESSMENT SEVERITY OF DIVERTICULITIS HINCHEY’S CRITERIA RISK OF DEATH > 5% FOR STAGE 1 OR 2 13% FOR STAGE 3 43% FOR STAGE 4 ARCH SURG 2000; 135-558-62 MEDICAL MANAGEMENT DEPENDS ON CLINICAL STATUS MILD ATTACK WITH GOOD ORAL INTAKE ( 7 TO 10 DAYS OF ANTIBIOTICS) HOSPITALIZATION POOR ORAL INTAKE SEVERE PAIN ILEUS OR EVIDENCE OF OBSTRUCTION HINCHEY STAGE 2-3-4 HOSPITALIZED PATIENT FOLLOW-UP NO IMPROVEMENT OF PAIN,FEVER,OR LEUCOCYTOSIS IN 3 DAYS. PHYSICAL EXAM WITH NEW FINDINGS OR EVIDENCE OF WORSENING REPEAT CT SCAN PERCUTANEOUS OR SURGICAL INTERVENTION NATURAL HISTORY OF DIVERTICULITIS 85% ARE EFFECTIVELY MANAGED MEDICALLY < 10% WILL REQUIRE SURGICAL MANAGEMENT AFTER THE FIRST EPISODE 33% REMAIN ASYMTOMATIC 33% EPISODIC DISCONFORT WITHOUT DIVERTICULITIS (SPASTIC DIVERTICULAR DISEASE) 33% WILL HAVE A SECOND EPISODE. NATURAL HISTORY OF DIVERTICULITIS SECOND ATTACK 1. MORBIDITY INCREASES FROM 25% TO 50% 2. MORTALITY INCREAES FROM 1.3% TO 5% FACTS OF DIVERTICULITIS PERCUTANEOUS DRAINAGE > THAN 4 CMS PERCUTANEOUS DRAINAGE MAY BE BENEFITIAL. MAY ALLOW ELECTIVE RATHER THAN EMERGENCY SURGERY. GROSS FECULENT MATERIAL TEND TO RESPONDE POORLY. ACUTE DIVERTICULITIS ABSCESS ACUTE DIVERTICULITIS DRAINED ABSCESS CLINICAL SCENARIO #2 59 YEAR OLD FEMALE, PRESENTS TO THE E.R. WITH A SUDDEN ONSET OF SEVERE ABDOMINAL PAIN, GENERALIZED ASSOCIATED TO A FORCEFUL BOWEL EVACUATION, WITHOUT FEVER, NAUSEA, OR EMESIS. ON PHYSICAL EXAMINATION, HER TEMPERATURE IS 37.8 C AND HER HEART RATE IS 150, REGULAR-IRREGULAR. SHE HAS SOME ABDOMINAL TENDERNESS, DIFFUSE, WITHOUT PERITONEAL SIGNS. CLINICAL SCENARIO #2 INITIAL ASSESSMENT: CBC AMYLASE LIPASE LIVER PROFILE U/A WBC COUNT OF 11,000 HG 13.0 250 (90-140) 150 (100-300) NORMAL NEGATIVE EKG ATRIAL FIBRILLATION WITH RAPID V.R. ABDOMINAL SERIES MILD ILEUS PLAIN FILM OF THE ABDOMEN ILEUS CLINICAL SCENARIO #2 RELEVANT DATA ON INITIAL ASSESSMENT: - SUDDEN ONSET OF SEVERE PAIN - MINIMAL ABDOMINAL FINDINGS ON EXAM - NON-SPECIFIC FINDINGS ON ABDOMINAL SERIES - NO FINDINGS ON BLOOD WORK - IRREGULAR HEART RATE (ATRIAL FIBRILLATION) INTESTINAL ISCHEMIA MEDICAL EMERGENCY SUPERIOR MESENTERIC ARTERY ANGIOGRAM EMBOLUS OCCLUDING THE SMA INTESTINAL ISCHEMIA 1)- ONSET 2)- DURATION OF SYMPTOMS 3)- CAUSE OF THE INJURY 4)- AREAS AND LENGTH OF BOWEL AFFECTED 5)- VESSEL INVOLVED 6)- DEGREE OF COLLATERAL BLOOD FLOW TREATMENT AND PROGNOSIS CELIAC AXIS SUPERIOR MESENTERIC ARTERY INFERIOR MESENTERIC ARTERY COLLATERAL AND ANASTOMIC CIRCULATION ABUNDANT IN STOMACH, DUODENUM AND RECTUM. LIMITED IN SPLENIC FLEXURE AND SIGMOID COLON. ISCHEMIC COLITIS PATHOPHYSIOLOGY OF INTESTINAL ISCHEMIA REDUCTION OF MESENTERIC BLOOD FLOW (UP TO 75% REDUCTION) OCCLUSION OF A MAYOR VESSEL 1)- VASOCONSTRICTION 2)- PRESSURE ELEVATION 3)- REDUCTION OF FLOW BOWEL ISCHEMIA ISCHEMIA ISCHEMIC INJURY IS DUE FROM HYPOXIA AND REPERFUSION REACTIVE OXIGEN RADICALS: SUPEROXIDE HYDROGEN PEROXIDE HYDROXYL RADICALS TISSULAR DAMAGE NUCLEIC ACIDS MENBRANE LIPIDS ENZYMES CELL LYSIS AND NECROSIS ISCHEMIA REPERFUSION OXIGEN RADICALS XANTHINE OXIDASE (XO) MESENTERIC ISCHEMIA ACUTE MORE PREVALENT CHRONIC ARTERIAL MORE PREVALENT SMA EMBOLOUS (SAME) NON-OCLUSSIVE MESENTERIC ISCHEMIA (NOMI) SMA THROMBOSIS (SMAT) FOCAL SEGMENTAL ISCHEMIA (FSI) VENOUS ACUTE MESENTERIC VENOUS THROMBOSIS (MVT) FOCAL SEGMENTAL ISCHEMIA (FSI) INCIDENCE OF AMI SMAE 40 TO 50% NOMI 20 TO 30% SMAT 10 TO 20% AGING WIDESPREAD USE OF ICU SURVIVAL OF CV CONDITIONS REF 4 CLINICAL FEATURES AMI - HIGH INDEX OF SUSPICION CHF ARRHYTMIAS HYPOTENSION RECENT M.I. VASOACTIVE MEDICATIONS (COCAINE) HEMATOLOGICAL DISORDERS (THROMBOPHILIA) X-RAYS IN AMI • PLAIN FILMS OF THE ABDOMEN NORMAL BEFORE INFARCTION ILEUS PNEUMATOSIS PORTAL-MESENTERIC VASCULAR GAS X-RAYS IN AMI PREDICTORS OF MORTALITY 29% IN PAT WITH NORMAL ABDOMINAL SERIES 78% IN PAT WITH ABNORMAL FINDINGS J VASC SURGERY 2007;46:467-74 CT SCAN IN AMI MOST IMPORTANT STUDY ASSESMENT OF OTHER CAUSES OF ABDOMINAL PAIN IDENTIFY ARTERIAL AND VENOUS THROMBOSIS ASSESMENT OF ISCHEMIC BOWEL COLON DILATION BOWEL WALL THICKENING LACK OF ENHANCEMENT OF ARTERIAL VASCULATURE INTRAMURAL GAS VASCULAR GAS COMPUTED TOMOGRAPHY (CT) ACUTE MESENTERIC ISCHEMIA GAS IN THE PORTAL VEIN COMPUTED TOMOGRAPHY (CT) ACUTE MESENTERIC ISCHEMIA PNEUMATOSIS INTESTINALIS LATE SIGN OF ISCHEMIC INJURY BOWEL NECROSIS EXPLORATORY LAPAROTOMY OTHER MODALITIES CT ANGIOGRAPHY MAGNETIC RESONANCE ANGIOGRAPHY AND VENOGRAPHY DOPPLER FLOWMETRY LAPAROSCOPY SELECTIVE MESENTERIC ANGIOGRAPHY MAINSTAY IN DIAGNOSIS OF OCCLUSIVE-NONOCCLUSIVE M.I. INITIAL TREATMENT PAPAVERIN INFUSION SELECTIVE MESENTERIC ANGIOGRAPHY DIFFICULTIES: - CRITICALLY ILL PATIENTS IMPRACTICAL DELAYS IN SURGERY ADVANTAGES: - EARLY DIAGNOSIS - ROADMAP FOR REVASCULARIZATION TREATMENT OF AMI BASED ON 4 OBSERVATIONS: 1)- DELAYS IN THE DIAGNOSIS - MORTALITY RATE IS 70% TO 90% 2)- ANGIOGRAPHY IS USEFULL IN OCLUSSIVE AND NONOCLUSSIVE DISEASE 3)- VASOCONSTRICCION CAN PERSIST EVEN AFTER SUCCESFULL TX 4)- VASOCOSTRICTION CAN BE RELEEVED BY VASODILATOR INFUSION. INITIAL MANAGEMENT AMI RESUSCITATION BROAD-SPECTRUM ANTIBIOTICS (LEVOFLOXACIN, METRONIDAZOLE, PIPERACILLIN-TAZOBACTAM) PRE-OPERATIVE ANGIOGRAPHY MESENTERIC VASOCONSTRICTION RELIEF OF MESENTERIC VASOCONSTRICTION IS ESSENTIAL INFUSION OF THE PHOSPHODIESTERESE INHIBITOR PAPAVERINE (30-60 MG/HOUR) ACUTE MESENTERIC ISCHEMIA CT SCAN RESUCITATE THE PATIENT CORRECT PRECIPITATING FACTORS NO SIGNS OF PERITONITIS OBSERVE PERITONITIS LAPAROTOMY OR LAPAROSCOPY NORMAL HISTORY OF DVT OR HYPERCOAGULA BLE STATE CT VENOUS PROTOCOL CT SCAN ABNORMAL ABDOMINAL ANGIOGRAM ACUTE MESENTERIC ISCHEMIA ABDOMINAL ANGIOGRAM NO PERSISTEN SIGNS OF PERITONITIS HEPARIN / THROMBOLYTIC AGENTS MESENTERIC VENOUS THROMBOSIS PERSISTENT SIGNS OF PERITONITIS LAPAROTOMY OR LAPAROSCOPY SHORT ISCHEMIC SEGMENT EXTENSIVE ISCHEMIC INVOLVEMENT NO PERSISTENT SIGNS OF PERITONITIS ANGIOGRAPHIC EVIDENCE OF COLLATERALS GOOD FILLING OF SMA OBSERVE MAJOR ARTERIAL OCCLUSION (NONEMBOLIC) PERSISTENT SIGNS OF PERITONITIS NO ANGIOGRAPHIC EVIDENCE OF COLLATERALS ABSENT OR POOR FEELING OF SMA CONTINUOUS PAPAVERINE INFUSION, IF POSSIBLE LAPAROTOMY OR LAPAROSCOPY , ARTERIAL RECONSTRUCTI ON, AND/OR BOWEL RESECTION SECOND-LOOK IF APPROPRIATE MINOR ARTERIAL OCCULUSION OR EMBOLUS NO PERSISTENT SIGNS OF PERITONITIS PERSISTENT SIGNS OF PERITONITIS CONTINUOUS PAPAVARINE INFUSION OBSERVE CONTINUOUS PAPAVARINE INFUSION LAPAROTOMY OR LAPAROSCOPY AND LOCAL RESECTION THROMBOLYTIC AGENT OR HEPARIN REPEAT ANGIOGRAM OBSERVE NO PERSISTENT SIGN OF PERITONITIS MAJOR EMBOLUS PERSISTENT SIGN OF PERITONITIS SELECTED CASES: CI TO SURGERY GOOD PERFUSION OF THE DISTAL MESENTERIC VASCULAR BED AFTER BOLUS OF A VASODILATOR CONTINUOUS PAPAVERINE INFUSION PREOPERATIVELY CONTINUOUS PAPAVERINE INFUSION EMBOLECTOMY AND/OR RESECTION REPEAT ANGIOGRAM CONTINUOUS PAPAVERINE INFUSION POSTOPERATI VELY THROMBOLYTIC AGENT REPEAT ANGIOGRAM AND CONSIDER A SECONDLOOK OPERATION NO PERSISTENT SIGNS OF PERITONITIS CONTINUOUS PAPAVARINE INFUSION SPLANCHNIC VASOCONSTRI CTION (NO OCCLUSION) PERSISTENT SIGNS OF PERITONITIS CONTINUOUS PAPAVARINE INFUSION OBSERVE LAPAROTOMY OR LAPAROSCOPY +/- RESECTION REPEAT ANGIOGRAM CONTINUOUS PAPAVARINE INFUSION POSTOPERATIVELY REPEAT ANGIOGRAM AND CONSIDER A SECONDLOOK OPERATION Stents & Angioplasty National Inpatient Sample Database Admissions from 2005-2009 with a diagnosis of Acute Mesenteric Ischemia. Factors for consideration: Age Gender Comorbidities Open Procedure 1499 patients Endovascular 502 patients Outcomes (weighted) Open (n=1495), No. (%) Endovascular (n=502) No. (%) P value 587 (39.3) 125 (24.9) 0.010 Bowel resection 500.5 (33.4) 72.5 (14.4) <.001 TPN 365.4 (24.4) 68.6 (13.7) .025 Length of stay*, day 17.1 + 1.07 12.9 + 1.11 .006 Mortality TPN, Total parenteral nutrition *Mean + standard deviation Beaulieu R.J; Arnaoutakis K.D; Abularrage C.J: Efron D. T; Schneider E; Black III J.H. (2014). Comparison of open and endovascular treatment of acute mesenteric ischemia. Journal of Vascular Surgery, 59 (1) 159-164. Conclusion Endovascular intervention has increase significantly Decrease mortality Shorter length of stay Lower rate of bowel resection Decrease need for TPN use ANGIOGRAM 54 HOURS POST-EMBOLECTOMY-PAPAVERIN INFUSION IN SMA CASE # 3 A 56-YEAR-OLD WOMAN PRESENTS WITH SEVERE EPIGASTRIC ABDOMINAL PAIN AND VOMITING OF 14 HOURS DURATION, SYMTOMS THAT HAD DEVELOPED SHORTLY AFTER DINNER THE PREVIOUS NIGHT.SHE HAS NOT HISTORY OF ALCOHOL USE, TAKES NO MEDICATIONS, AND HAS NOT FAMILY HISTORY OF PANCREATITIS. ON PHYSICAL EXAMINATION, SHE HAS A HEART RATE OF 110 BETAS PER MINUTE AND MODERATE EPIGASTRIC ABDOMINAL TENDERNESS WITH PERITONEAL SIGNS. THE WHITE-CELL COUNT IS 16,500 PER CUBIC MILLIMETER, AND THE HEMATOCRIT IS 49 %. THE SERUM AMYLASE LEVEL IS 1450 IU PER LITER, AND THE SERUM LIPASE LEVEL IS 3200 IU PER LITER, THE SERUM ALT IS 280 IU PER LITER, AND THE SERUM LDH LEVEL IS 860 IU PER LITER. CALCIUM, ALBUMIN,TRIGLYCERIDES, AND ELECTROLYTES VALUES ARE NORMAL. ABDOMINAL CT SCAN: PANCREATITIS ACUTE PANCREATITIS ETIOLOGY OF THE PANCREATITIS DETERMINE THE SEVERITY OF THE DISEASE MEDICAL MANAGEMENT SURGICAL OUTCOME OF ACUTE PANCREATITIS 75-80% will present will mild pancreatitis. Interstitial Pancreatitis OUTCOME OF ACUTE PANCREATITIS 20 % of patients with acute pancreatitis will present with a severe course 10 to 30 % of this group will died. The rate of death has not decline. Br J Sur 2004;91;1243-4 RELEVANT IN THIS CASE LIVER ENZYMES Elevated AST/ALT in non-alcoholic patients is the best predictor of biliary pancreatitis. AST/ALT > 3 times the upper limits of normal. Positive predictive value of 95% of gallstone pancreatitis. Am J Gastro 1194;89;1863-6 ENDOSCOPIC RETRAOGRADE CHOLANGIOPANCREATOGRAPHY ERCP ERCP Persistent biliary obstruction worsens the outcome and increases the severity of acute pancreatitis, and predisposes the patient to bacterial cholangitis. NIH state of the science statement on ERCP 2002 ERCP IN BILIARY PANCREATITIS 3 Randomized trial with a total of 511 patients. Dx of biliary pancreatitis. Conservative Management VS ERCP ERCP IN BILIARY PANCREATITIS Lower risk of pancreatitis-associated complications in the ERCP groups. No significant ERCP complications. Cochrane Database Syst Rev 2004;4;CD003630 PREDICTING SEVERE ACUTE PANCREATITIS Identify high risk Patients. ( Close MONITORING ) Laboratory Values Clinical Parameters Findings on Imaging Studies. Obesity. ( BMI > 30 ) Genetic factors(MCP-1) SEVERITY SCORES RANSON’S SCORE Ranson’s Score 0-2 3-4 5-6 7-8 ICU > 7 days 1% 24% 53% 75% Death 3% 16% 40% 100% APACHE II SCORE Physiologic Variables Rectal temperature. Mean blood pressure. Heart rate. Respiratory Rate. Oxygenation. Arterial PH Serum Sodium. Serum Potassium. Serum Creatinine. Hematocrit. White Blood Count. PREDICTING SEVERE ACUTE PANCREATIS Atlanta Criteria Systemic complications Disseminated intravascular coagulation. Metabolic disturbances.( Acidosis ) Local Complications Pancreatic Necrosis. Pancreatic Abscess. Pancreatic Pseudo cyst. FACT PREVENT MORBIDITY- MORTALITY PANCREATIC NECROSIS CLINICAL SCENARIO # 4 36 YEAR OLD FEMALE, PRESENTS TO THE ER DEPARTAMENT COMPLAING OF 48 HOUR HISTORY OF SEVERE ABDOMINAL PAIN, ASSOCIATED TO ABDOMINAL DISTENSION AND FEVER. WAS WELL UNTIL 3 WEEKS PRIOR TO HER ER VISIT, WHEN SHE DEVELOPED SEVERE DIARRHEA WITH MUCUS AND BLOODY STOOLS, ON AN AVERAGE RANGE OF 8 TO 10 STOOLS A DAY ON EXAM, THE PATIENT IS LETHARGIC, TACHYCARDIC, WITH A BP OF 90/60 IN DISTRESS, DEHYDRATED, FEBRILE. ABDOMEN IS DISTENDED, TENDER TO PALPATION WITH MILD REBOUND, AND DECREASED BOWEL SOUNDS. CLINICAL SCENARIO # 4 CBC WBC 17,000 HG 9.0 GMS STOOLS NEGATIVE FOR C. DIFF NEGATIVE FOR O/P +++ OCCULT BLOOD ELECTROLYTES K+ 2.9 MEQ/L Toxic Megacolon TOXIC MEGACOLON DEFINITION: ACUTE COLONIC DILATATION WITH A TRANSVERSE COLON DIAMETER OF GREATER THAN 6 CMS (RADIOLOGY),AND LACK OF HAUSTRATION OF THE COLON IN A PATIENT WITH A SEVERE ATTACK OF COLITIS. DIFFERENTIAL DIAGNOSIS: INFECTIOUS PSEUDOMEMBRANOUS COLITIS CAN BE THE INITIAL PRESENTATION IN U.C. (5%) MEDICAL MANAGEMENT OF TOXIC MEGACOLON 1. TREATING THE UNDERLYING INFLAMMATION 2. RESTORING COLONIC MOTILITY 3. PREVENTING COLONIC PERFORATION 4. SYSTEMIC ANTIBIOTICS Hospitalization; oral glucocorticoids or IV glucocorticoids GOOD RESPONSE Taper glucocorticoids maintenance therapy with 5ASA; consider adding 6-MP or AZA SUCCESSFUL TAPER Continue maintenance therapy POOR RESPONSE IV glucocorticoids UNSUCCESSFUL TAPER More prolonged taper; add 6-MP or AZA maintain with 6MP or AZA 9 GOOD RESPONSE Convert to oral glucocorticoids followed by tapering; add 5-ASA; consider adding 6-MP or AZA UNSUCCESSFUL TAPER Longer glucocorticoid taper; maintain with 6-MP or AZA SUCCESSFUL TAPER Maintain with 6-MP or AZA POOR RESPONSE IV cyclosporine or IV infliximab POOR RESPONSE Surgery GOOD RESPONSE Oral cyclosporine and oral glucocorticoids; or maintain with infliximab Taper glucocorticoids add 6MP or AZA Maintain on 6-MP or AZA; discontinue cyclosporine within 6 mo. FACTS IN TOXIC MEGACOLON MORTALITY: 44% WITH EMERGENT COLECTOMY WITH PERFORATION 2% WITH COLECTOMY WITHOUT PERFORATION 50% RESOLVES WITH MEDICAL THERAPY 48 – 72 HOURS (CRITICAL IN ASSESMENT) 50% OF SUCCESSFUL TREATMENT WILL REQUIRE COLECTOMY CONCLUSSION THE PATIENT IS THE PRIORITY BE A TEAM PLAYER MEDICAL RADIOLOGICAL SURGICAL THE MAIN GOAL SHOULD BE TO AVOID MORBIDITY AND MORTALITY ACUTE ABDOMINAL PAIN CAN BE CATASTROFIC EARLY DIAGNOSIS AND INTERVENTION ARE CRITICAL MANAGEMENT OF SEVERE ACTIVE ULCERATIVE COLITIS ACUTE PANCREATITIS FERNANDO URRUTIA, M.D. ASSISTANT PROFESSOR OF MEDICINE UNIVERSITY OF TEXAS HOUSTON, TX 09-01-2007 CASE VIGNETTE 56 year old women Presents with severe abdominal pain and vomiting for 14 hours duration No Hx of alcohol or medication use. No family Hx of pancreatitis. CASE VIGNETTE On Physical examination: HR 110 per minute, with moderate epigastric abdominal tenderness without peritoneal signs. WBC is 16,500 Hematocrit is 49 % Amylase is 1450 IU, Lipase 3200 IU AST is 860 IU Ca,Triglycerides,Albumin,electrolytes are normal. RISK FACTORS Gallstones Excessive Alcohol intake However, clinically induce pancreatitis, almost never develops in most patients. Lankisch PG. Pancreas 2002;25;411-2 CAUSES OF PANCREATITIS Hypertriglyceridemia Duct obstruction (Tumor or P.D. ) Medications:(azathioprine,thiazides,estrogens,furosemide,pen tamidine,sulfas) Trauma 20% idiopathic Genetic predisposition Environmental susceptibility Whitcomb DC Gut 2004;53;1710-7 Pathology of Acute Interstitial Pancreatitis PATHOLOGY OF NECROTIZING PANCREATITIS STRATEGIES AND EVIDENCE 1- Diagnosis 2- Determine the cause: Prevent recurrence 3- Management DIAGNOSIS Characteristics of abdominal pain and nausea. Elevation of pancreatic enzymes. Elevation of liver enzymes. Levels of trypsinogen activation peptide. Levels of trypsinogen-2 CT scan,MRI,Ultrasound.(May help in determine the cause,r/o other causes of intraabdominal pathology or complications) ABDOMINAL PAIN Gallstone pancreatitis (Pain is sudden, epigastric, radiates to the back, described as a knife-like pain) Metabolic causes (Less abrupt pain, poorly localized) PANCREATIC ENZYMES Serum amylase > 3 times upper limits of normal ACUTE PANCREATITIS. Lipase levels are in parallel with amylase. Elevation means ongoing pancreatic inflammation. Amylase normalizes faster than lipase. Trypsinogen-2 levels Kemppainen E Gut 1997,41;690-5 DIAGNOSIS OF ACUTE PANCREATITIS PHATOGENESIS Inappropriate activation of trypsinogen to trypsin. Lack of prompt elimination of active trypsin inside the pancreas. Activation of pancreatic enzymes causes pancreatic injury. INFLAMMATORY RESPONSE. Tissue damage in the pancreas Progression beyond the pancreas Systemic inflammatory response syndrome Multiorgan failure or even DEATH. IMAGING STUDIES CT SCAN. MRI. Abdominal ultrasound. MRCP. Endoscopic ultrasonography EUS ERCP. IMAGING STUDIES CONCEPTS MRI better than CT for early duct disruption. Ultrasound more sensitive that CT or MRI for detection of gallstones or sludge. EUS best test for biliary pancreatitis. EUS may guide the use of emergent ERCP. Hyperdense focus in distal common bile duct Endoscopic view of an impacted common bile duct stone Endoscopic view of sphincterotomy and basket extraction Endoscopic view of sphincterotomy and basket extraction Endoscopic view of sphincterotomy and basket extraction Endoscopic view of sphincterotomy and basket extraction Balloon extraction of common bile duct stones after sphincterotomy Prospective endoscopic trials in gallstone pancreatitis HOSPITALIZATION Severe Pain. Vomiting, Dehydration Signs of severe acute Pancreatitis. TREATMENT Primarily Supportive Medications Lexipafant(Inhibitor of platelet activating factor) Somatostatin. Protease inhibitors Johnson CD Gut 2001;48;62-9 SUPPORTIVE THERAPY NPO. IV Pain medication Aggressive Hydration to prevent hemoconcentration.(250-500 ml of crystalloid solution per hour) Pulse oximetry. PREDICTING SEVERE ACUTE PANCREATITIS Laboratory Inflammatory Markers: Interleukin-6 levels. C-Reactive protein levels. PMN elastase. Urinary TAP. ( Trypsinogen A.F ) PREDICTING SEVERE ACUTE PANCREATITIS Clinical Parameters Clinical Findings Thirst Poor urine output Progressive tachycardia Tachypnea Hypoxemia Agitation Confusion Lack of improvement of Pain in 48 hours PREDICTING SEVERE ACUTE PANCREATITIS Ranson’s Score At Presentation: Age > 55 yr Blood glucose. > 200 mg White Cell Count. LDH > 350 IU AST > 250 IU > 16,000/mm PREDICTING SEVERE ACUTE PANCREATITIS Ranson’s score: Within 48 hours Hematocrit. >10% decrease Serum Calcium. < 8 mg/dl Base deficit. >4 mEq/Lt Blood Urea Nitrogen.> 5 mg/dl Fluid secuestration. > 6 Liters Arteria Oxygen <60 mm Hg PREDICTING SEVERE ACUTE PANCREATITIS Ranson’s Score: Indicated by a positive Score > 3 with one point for each positive factor. APACHE II SCORE 12 Physiological Variables. Patient Age. Previous history of severe organ system insufficiency or inmunocompromised state. Acute Pancreatitis Role of CT scan Diagnosis in doubt Prognosis Severe or worsening course Contrast-Enhanced CT Rapid bolus Dynamic sequential scanning Does not appear to make pancreatitis worse (Arch.Surg 2000) CT WITH PANCREATIC PROTOCOL Hyperdense focus in distal common bile duct INTERSTITIAL PANCREATITIS PANCREATIC NECROSIS PANCREATIC GAS PSEUDOCYST FLUID COLLECTION Pancreatic Fluid Collections • ACUTE FLUID COLLECTION • PSEUDOCYST • ABSCESS • PANCREATIC NECROSIS • INFECTED NECROSIS PANCREATIC-FLUID COLLECTIONS 57 % of hospitalized Patients, will have fluid collection. 39% will have 2 areas involved. 33% will have 3 or more. Resolves spontaneously 50%. FLUID COLLECTIONS ANALYSIS Pancreatic Enzymes Pancreatic Duct Disruption. Pseudocyst Ascites Pleural effusions FLUID COLLECTIONS Initially are ill-Defined. Tend to evolved over time. Management is conservative. However… ANY CHANGE ? FLUID COLLECTIONS WARNINGS Continues to enlarge Causes Pain Became Infected as suggested by fever, leucocytosis. or gas in fluid collection. Compress adjacent organs: MEDICAL-ENDOSCOPIC-SURGICAL THERAPY MAY BE NEEDED. PANCREATIC NECROSIS Important Complication. Means nonviable pancreatic parenchyma. Can develop during first few days. Associated with late complications and Death. Necrotic Tissue very susceptible to infection. NECROSIS Infected necrosis can occur within first week of illness © 2006 Current Medicine Group Ltd PANCREATIC NECROSIS Suspect if Fever Leukocytosis Failure to Improve Unexpected Deterioration PANCREATIC NECROSIS Diagnosis Loss of tissue perfusion on contrast-enhanced CT scan. Gas Bubbles within necrotic tissue. Fine-needle aspiration of necrotic area by either CT or US guided. Gram’s stain and culture. NECROSIS SCORE CT Severity Index Necrosis Score No Pancreatic necrosis Necrosis of one third of Pancreas Necrosis of one Half of Pancreas Necrosis of >one Half of Pancreas INFECTED PANCREATIC NECROSIS 1. CULTURE POSITIVITY OF TISSUE. 2. 36-71% OF PANCREATIC NECROSIS. 3. 2ND-3NR WEEK FOLLOWING ONSET. 4. TYPICALLY POLYMICROBIAL. 5. CT GUIDED ASPIRATION. Guide lines for FNA in ANP SYSTEMIC TOXICITY ABSENT ? FNA NO DECREASING NO PERSISTING OVERWHEALMING YES NO INCREASING YES FNA in ANP CT US 96% SENSITIVITY SPECIFICITY 99% 88% 90% TENNER S.W.J SUR 97 USE OF ANTIBIOTICS No antibiotics for mild cases Prophylactic antibiotics ? ROLE OF ANTIBIOTICS Prophylactic antibiotics ( Imipenen ) Reduced infectious complications (Line sepsis,Pulmonary,UTI,and infected pancreatic necrosis) Pederzoli P Surg Gyne-Obstet 1993;176;480-3 ROLE OF ANTIBIOTICS Trial by Nathems AB ( Pro Am Thorac Soc 2004;1;289-90 ) Failed to demonstrate difference in outcome among patients TX with cipro and metronidazole VS placebo Prophylactic Antifungal antibiotics ? TX ? Antibiotics for Acute Necrotizing Pancreatitis: Cochrane Database of Systematic Review: 4 prospective randomized trials ANTIBIOTICS IN ASP Cochrane Database of Systematic Review: ( Antibiotics for 10-14 days ) Decreased the risk of superinfection. Imipenen-cilastin- Excelent pancreatic tissue penetration. NUTRITIONAL SUPPORT Very important in severe Pancreatitis. Best way to do it ? Parenteral ? Enteral ? NUTRITIONAL SUPPORT Al-Omran (Cochrane Database Syst Rev 2003;1;CD002837 ) 70 pat in 2 small trials. Enteral VS Parenteral nutrition in severe acute pancreatitis. No Advantage. No difference in outcome. NUTRITIONAL SUPPORT Metha analysis: 6 randomized trails involving 263 pat ( BMJ 2004;328;1407 ) Better outcome with Enteral nutrition. Decreased rate of Infections. Decreased Surgical interventions. Reduced Length of hospital stay. Reduced Cost. NUTRITIONAL SUPPORT Ileus Some patients can not obtain adequate caloric intake with enteral feeds. Failure to maintain enteral access. THE TEN COMMANDMETS FOR SURGERY IN ACUTE PANCREATITIS Commandments: I-V Not operate on clinically mild AP Accept broad spectrum antibiotics to reduce infection rates in CT confirmed PN FNA to determine sterile from infected necrosis Infected necrosis in the setting of clinical sepsis is an indication for surgical drainage Not operate on sterile necrosis Commandments: VI-X Not operate within 14 days of onset except for selected cases Limit debridement to preserve organs Remove gallbladder in mild gallstone pancreatitis Do not remove gallbladder in severe gallstone pancreatitis until after recovery Accept sphincterotomy as an alternative to cholecystectomy in unfit patients DISCHARGE PLANNING Determine the cause of pancreatitis. Cholecystectomy should be done before D/C in mild cases. ERCP/sphinterotomy in poor surgical candidates. Control of lipids. Cessation of alcohol intake. Weight reduction. DISCHARGE PLANNING Hypercalcemia – Hyperparathyroidism or CA Discontinue Medications. Recurrent Pancreatitis: Ductal strictures Pancreas Divisum Mass Autoimmune pancreatitis Genetic Susceptibility Idiopathic Pancreatitis ( Dragnov P. Gastro 2005;128;756-63 ) DISCHARGE PLANNING Small low fat meals. Enteral feeds in persistent pain or large pseudocyst. SUMMARY Enteral nutrition better if possible. No consensus with prophylactic antibiotics. Fast assessment of severity on admission. Emergent ERCP has an important role in biliary pancreatitis. Reserve antibiotics to patients with pancreatic necrosis of more the 30% of the pancreas. THANK YOU GALLSTONE PANCREATITIS Increased among with women > age of 60 Highest with small stones Less than 5 mm. Microlithiasis Levy P Pancreatology 2005;5;450-6 ALCOHOLIC PANCREATITIS More common among men than women. Appears to be dose dependent NIH publication 1998. PANCREATIC NECROSIS • 1 OR MORE AREAS OF NO ENHANCING GLAND • WITH RETROPERITONEAL FAT NECROSIS. COMPLICATION OF PANCREATIC NECROSIS DEATHS. • • MAY APPEAR UP TO 48 HS AFTER ONSET. ACCOUNT FOR 70-80% OF PANCREATIC PSEUDOCYST Asymptomatic – Conservative Tx Symptomatic -- Drainage Endoscopic Intervention Radiological intervention Surgically PANCREATIC NECROSIS Associated with: Pancreatic Inflammation Hypovolemia Hypotension LACK OF IMPROVEMENT Failure to improve in 2-3 days CT of the abdomen with pancreatic protocol. Fluid collections Pancreatic necrosis Other complications LACK OF IMPROVEMENT Consider Antibiotic therapy Nutritional support ACUTE PANCREATITIS Necrotizing pancreatitis accounts for nearly all morbidity and mortality IMAGING STUDIES Tumors. Gallstones. Local complications of pancreatitis. Pancreas divisum. Early duct disruption. Dilated pancreatic duct. OTHER SCORING METHODS APACHE II SCORE: The Acute Physiology and Chronic Health Evaluation PROGNOSIS OF ACUTE PANCREATITIS ACUTE PANCREATITIS RELEVANT FACTORS COMMON CAUSE OF SEVERE ABDOMINAL PAIN 220,000 HOSPITAL ADMISSION PER YEAR 80 % HAVE A BENIGN COURSE MANAGED MEDICALLY 20% HAVE A SEVERE COURSE 10 TO 30% MORTALITY ACUTE PANCREATITIS INTESTINAL ISCHEMIA ACUTE ISCHEMIC INJURY TO THE GUT CHRONIC IMAGING COMPUTED TOMOGRAPHY (CT) ANGIOGRAPHY OTHERS COLONOSCOPY MRA mesenteric ischemia CAUSES OF ACUTE MESENTERIC ISCHEMIA CAUSE FREQUENCY (%) SMA EMBOLUS 50 (%) NONOCCLUSIVE MESENTERIC ISCHEMIA 25 (%) SMA THROMBOSIS 10 (%) MESENTERIC VENOUS THROMBOSIS 10 (%) FOCAL SEGMENTAL ISCHEMIA 5 (%) SPRECTRUM OF BOWEL INJURY 1. TRANSIENT ALTERATION OF BOWEL INJURY 2. TRANSMURAL GRANGRENE TYPES AND FREQUENCIES OF INTESTINAL ISCHEMIA TYPE FREQUENCY (%) COLON ISCHEMIA 75% ACUTE MESENTERIC ISCHEMIA 25% FOCAL SEGMENTAL ISCHEMIA < 5% CHRONIC MESENTERIC ISCHEMIA < 5% CONCLUSION Acute Pancreatitis HOW SHOULD THE PATIENT BE FURTHER EVALUATED ? ACUTE ABDOMINAL PAIN POSTRATION: ACUTE ABDOMINAL PAIN HEMODINAMICALLY RLQ PAIN(GRADUAL ONSET) CT APPENDIX PROTOCOL RUQ PAIN UNSTABLE RESUSCITATION URGENT SURGICAL CONSULT Acute Pancreatitis HOW SHOULD THE PATIENT BE FURTHER EVALUATED ? DIFERENTIAL DIAGNOSIS ACUTE APPENDICITIS INFLAMMATORY BOWEL DISEASE (CROHN’S DISEASE) PELVIC INFLAMMATORY DISEASE TUBAL PREGNANCY CYSTITIS ADVANCED COLONIC CANCER INFECTION COLITIS COMMON CAUSES OF ACUTE ABDOMINAL PAIN o Appendicitis o Cholecystitis o Pancreatitis o Diverticulitis o Perforated peptic ulcer o Small bowel obstruction o Mesenteric ischemia o Ruptured abdominal aortic aneurysm o Pelvic inflammatory disease---Ectopic pregnancy CT FINDINGS IN DIVERTICULITIS 1. INCREASED SOFT TISSUE DENSITYWITHIN PERICOLONIC FAT (98%) 2. COLONIC DIVERTICULI (84%) 3. BOWEL WALL THICKENING (70) 4. SOFT TISSUE MASS, PHLEGMON,FLUID COLLECTION,ABSCESS (35%) 5. SENSITIVITY 97% 6. SPECIFICITY 100% 7. POSITIVE PREDICTIVE VALUE 100% 8. NEGATIVE PREDICTIVE VALUE 98% 9. ALWAYS REMEMBER COLON CANCER AS INITIAL PRESENTATION Anti-inflammatory agents PEER-VIEW SLIDE 2.6 PAG 12 CLINICAL STAGES OF DIVERTICULAR DISEASE STAGE 1 STAGE 2 DEVELOPMENT OF DIVERTICULI a. Pericolitis b. Pericolic phlegmon c. Pericolic abscess d. Pelvic or intra-abdominal abscess e. Bowel obstruction f. Fistulization g. Bacteremia and sepsis h. Bleeding Pathophysiology: Diverticulitis as a Fiber Deficiency Disorder Most evidence suggest that diverticular disease is a fiber deficiency disorder Theoretical Progression From Diverticula Formation to Diverticulitis Low-fiber diet Diverticula formation Change in flora (+ altered immune response) Diverticulitis Colitis CLINICAL HISTORY CHARACTER OF THE PAIN ONSET LOCATION DESCRIPTION RADIATION INTENSITY PAST MEDICAL HISTORY PREVIOUS ABDOMINAL PAIN RECURRENT PROBLEM INTESTINAL OBSTRUCTION NO PRIOR SURGERY HISTORY OF SYSTEMIC ILLNESS S.L.E PHYSICAL EXAM POSITION IN BED TACHYPNEA HYPOTENSION IRREGULAR HEART RHYTHM ABDOMINAL EXAM RECTAL EXAM METABOLIC ACIDOSIS EKG SPECIAL CIRCUMSTANCES EXTREMES OF AGE PREGNANCY IMMUNOCOMPROMISED HOST CLINICAL MANIFESTATIONS ACUTE DIVERTICULITIS VARIES WITH THE EXTENT OF THE DISEASE PROCESS. THE CLASSIC CASE: OBSTIPATION, DISTENSION, ABDOMINAL PAIN MOSTLY IN THE LEFT LOWER QUADRANT. LOW GRADE FEVER LEUKOCYTOSIS THE PATIENT WITH SEVERE ABDOMINAL PAIN FREE PERFORATION PERITONITIS CLINICAL SCENARIO # 1 DIAGNOSIS SEVERE ACUTE DIVERTICULITIS CT SCAN IN AMI EARLY SIGNS ARE NONSPECIFIC LATE SIGNS REFLECT NECROTIC BOWEL SENSITIVITY 92% SPECIFICITY 100% Acute Pancreatitis HOW SHOULD THE PATIENT BE FURTHER EVALUATED ? THE CLINICAL PROBLEM 220,000 hospital admissions per year. Similar frequency among age groups. The cause and likelihood of death varies according to age, race, body-mass index, and other factors. PREDICTING SEVERE ACUTE PANCREATITIS Is Defined by: The presence of organ failure. Local complications. Both. Knaus WA Crit Care Med 1985;13:818-29 PREDICTING SEVERE ACUTE PANCREATITIS A. LABORATORY PARAMETERS B. CLINICAL PARAMETERS C. RANSON’S SCORE D. APACHE II SCORE E. ATLANTA CRITERIA F. CT SCAN FINDINGS. INFLAMMATORY MARKERS CT-GRADE CT Severity Index CT Grade Normal pancreas (Grade A) Focal or diffuse enlargement (Grade B) Intrinsic changes; Fat stranding (Grade C) Single;ill defined Collection of fluid (Grade D) Multiple collection of fluid or gas in or adjacent to pancreas (Grade E) SEVERITY SCORE CT Severity. Index 0-3 4-6 7-10- Complication 8% 35% 92% Death 3% 6% 17% FACTS OF DIVERTICULITIS OPERATIVE INTERVENTION < THAN 10% OF PATIENTS REQUIRE SURGERY INDICATIONS FOR EMERGENCY SURGERY GENERALIZED PERITONITIS UNCONTROLLED SEPSIS UNCONTAINED VISCERAL PERFORATION LARGE, UNDRAINABLE ABSCESS LACK OF IMPROVEMENT OR DETERIORATION WITHIN 3 DAYS CLINICAL EVALUATION 1) CAREFUL CLINICAL HISTORY 2) ADEQUATE PHYSICAL EXAMINATION 3) PERTINENT IMAGING STUDIES LABORATORY DATA COMPLETE BLOOD COUNT ELECTROLYTES, BUN, CREATININE, GLUCOSE URINALYSIS PREGNANCY TEST LIVER PROFILE AMYLASE, LIPASE STOOL EXAMINATION EKG GENERAL MANAGEMENT OF DIVERTICULAR DISEASE UNCOMPLICATED STAGE 1 HIGH-FIBER DIET +/- ANTISPASMODICS AND ANTIBIOTICS MESALANINE (0FF-LABEL) PROBIOTICS (UNCONTROLLED STUDIES) COMPLICATED STAGE 2 NPO,LIQUID DIETS, ON-LIQUID DIETS, OR REGULAR DIETS ANTIBIOTICS, MESALANINE (OFF LABEL) PROBIOTICS (UNCONTROLLED STUDIES) BLOOD FLOW REGULATION SYSTEMIC HUMORAL LOCAL SYMPATHETIC NERVOUS SYSTEM BY ALFA ADRENERGIC RECEPTORS VASOACTIVE SUBSTANCES ANGOTENSIN II VASOPRESSIN PROSTAGLANDINS CLINICAL FEATURES HIGH INDEX OF SUSPICION o SUDDEN ONSET OF SEVERE ABDOMINAL PAIN o RAPID AND FORCEFULL BOWEL EVACUATION o MINIMAL OR NO ABDOMINAL SIGNS o LOCALIZED ABDOMINAL PAIN AND BLEEDING (ISCHEMIC COLITIS) o ALTERED MENTAL STATUS (SEPSIS, METABOLIC ACIDOSIS) LABORATORY FEATURES o LEUKOCYTOSIS o METABOLIC ACIDOSIS o ELEVATED PHOSPHATE o ELEVATED LACTATE o ELEVATED AMYLASE > 15,000 MILD ELEVATION INTESTINAL ENZYMES o DEAMINE OXIDASE o HEXOAMINIDASE o GLUTATHIONE o S TRANSFERASE o INTESTINAL FETAL-ACID BINDING PROTEIN LACK OF SPECIFICITY/SENSITIVITY (LATE-STATE DISEASE) ENDOSCOPIC RETROGARDE CHOLANGIOPANCREATOGRAM ROLE IN ACUTE BILIARY PANCREATITIS ? Outcome Mortality Length of stay Need for bowel resection Use of TPN Measurements of acute illness severity in treatment groups Lactic acidosis Hypertension ARDS Open (n=1499) No. (%) Endovascular (n=502) No. (%) P value 404 (30.0) 57 (11.4) .0018 99 (6.6) 25 (4.9) .54 472 (31.5) 35 (7.0) <.001 ARDS, Acute respiratory distress syndrome Beaulieu R.J; Arnaoutakis K.D; Abularrage C.J: Efron D. T; Schneider E; Black III J.H. (2014). Comparison of open and endovascular treatment of acute mesenteric ischemia. Journal of Vascular Surgery, 59 (1) 159-164. ERCP in Acute Pancreatitis Conclusions Consider only for gallstone pancreatitis Cholangitis or significant biliary obstruction Clinically severe but without ongoing biliary obstruction, controversial Consider EUS or MRCP J Gastrointestinal Surgery 2001 PREDICTING SEVERE ACUTE PANCREATITIS Atlanta Criteria: Ranson Score > 3 APACHE II Score > 8 Organ Failure Shock: SBP < 90 mm Hg Pulmonary Insufficiency: pO2 < 60 Renal Failure: Creat. > 2 mg/dl GI Bleed: 500 ml/24 hr
