Explain your diagnosis for the patient, including your rationale for the diagnosis. Describe an appropriate drug therapy plan based on the patient’s history, diagnosis, and drugs currently prescribed.
Using the attached CASE STUDY PROVIDED BELOW
Write a 2-page paper that addresses the following:
Explain your diagnosis for the patient, including your rationale for the diagnosis.
Describe an appropriate drug therapy plan based on the patient’s history, diagnosis, and drugs currently prescribed.
Justify why you would recommend this drug therapy plan for this patient. Be specific and provide examples.
Consider an appropriate drug therapy plan based on the patient’s history, diagnosis, and drugs currently prescribed.
Consider whether the patient has a disorder related to the gastrointestinal and hepatobiliary system or whether the symptoms are the result of a disorder from another system or other factors, such as pregnancy, drugs, or a psychological disorder.
Use 6 APA reference within the last 5years to support your writing.
Requirements: 3 page
DC is a 46-year-old female who presents with a 24-hour history of RUQ pain. She states the pain started about 1 hour after a large dinner she had with her family. She has had nausea and on instance of vomiting before presentation.
DX: CHOLECYSTITIS OR PANCRATITIS SEFONDARY TO GALL BLADDER PROBLEM.
CONSIDER THE LABS AND ARTICLE INFORMATION GIVEN BELOW TO DETERMINE YOUR DIAGNOSIS.
HTN Temp: 98.8oF
Type II DM Wt: 202 lbs
Gout Ht: 5’8”
DVT – Caused by oral BCPs BP: 136/82
HR: 82 bpm
Current Medications: Notable Labs:
Lisinopril 10 mg daily WBC: 13,000/mm3
HCTZ 25 mg daily Total bilirubin: 0.8 mg/dL
Allopurinol 100 mg daily Direct bilirubin: 0.6 mg/dL
Multivitamin daily Alk Phos: 100 U/L
AST: 45 U/L
ALT: 30 U/L
GI:bNondistended, minimal tenderness
Skin:bWarm and dry
Neuro: Alert and Oriented
© Springer Nature Switzerland AG 2020C. de Virgilio, A. Grigorian (eds.), Surgery, https://doi.org/10.1007/978-3-030-05387-1_20227Severe Epigastric Pain with Nausea and VomitingAreg Grigorian, Matthew Y. C. Lin, and Christian de Virgilio20
22820 Diagnosis What Is the Differential Diagnosis for Epigastric Abdominal Pain? Case StudyA 41-year-old woman presents to the emer-gency department complaining of severe and continuous epigastric pain for the past 24-hours. The pain radiates straight through to her back. She has had progressive nausea with vomiting. The vomit is bile-stained and without blood. She has had similar but less severe episodes of abdominal pain in the past, usually after eating heavy meals, but they always resolved within a few hours. She is gravida two, para two, with last menses 2 weeks ago, and does not consume any alcohol. On exam, she is afebrile, heart rate is 115 beats/min, blood pressure of 128/86 mmHg, and respiratory rate is 18/min. Her abdomen is not distended. She has no surgical scars on her abdomen and no obvious masses visible. She has no bruising around her umbilicus or along her flank. Bowel sounds are hypoactive. She has marked tenderness to palpation in her epigastrium, without guarding or rebound. The remainder of her abdomen is soft and non-tender to palpation. No masses or organomegaly are appreciated. Laboratory examination reveals a white blood cell count of 17.2 × 103 cells/μL (normal 4.1–10.9 × 103 cells/uL), amylase of 1545 u/L (30–110 u/L), lipase of 1134 u/L (7–60 u/L), ALT of 245 u/L (7–56 u/L), AST of 263 u/L (5–35 u/L), serum glucose of 156 mg/dl (65–110 mg/dL), and LDH 180 u/L (0–250 u/L). An abdominal series demonstrates gas throughout the small and large bowel and a focal dilated loop of proximal small bowel without air fluid levels. There is no free air under the diaphragm. .Table 20.1ConditionHistory and physicalGastroenteritisNausea, extensive vomiting, diarrhea, myalgia, fever, mild abdominal tendernessAcute gastritisBurning/gnawing epigastric pain, NSAID use, mild abdominal tendernessAcute cholecystitisRight upper quadrant/epigastric pain radiating to around the right back, nausea, vomiting, fever, Murphy’s signPeptic ulcer disease (PUD)Intermittent burning epigastric pain that is better (duodenal ulcer) or worse (gastric ulcer) with food intake, nausea, Helicobacter pylori infection, NSAID use, steroidsPerforated ulcerInitial epigastric pain, followed by diffuse tenderness, abdominal rigidity, rebound tendernessPancreatitisEpigastric pain radiating to the back, nausea, vomiting, anorexia, fever, tachycardia, cholelithiasis, alcohol abuseAppendicitisPeriumbilical pain migrating toward the right lower quadrant (McBurney’s point), associated with nausea, vom-iting, anorexia, fever, Rovsing’s sign, psoas signSmall bowel obstructionAdhesions, hernia, neoplasms, dilated loops of bowel with air fluid levels, absence of distal colonic gas on plain radiographMesenteric ischemia“Severe abdominal pain out of proportion to physical exam,” nausea, most often cardiac embolus to superior mesenteric artery from atrial fibrillation, bloody diarrhea in severe casesRuptured AAASevere abdominal/back/left flank pain, pulsatile abdominal mass, hypotension, elderly male smokerReferred pain from myo-cardial infarctionAtypical presentation more common in women and diabetics, cardiovascular disease, obesity, hypercholester-olemiaNSAID nonsteroidal anti-inflammatory drugs What Is the Diagnosis for This Patient?Acute pancreatitis, most likely secondary to cholelithiasis. This patient has the classic presentation which consists of epi-gastric abdominal pain radiating straight through to the back with nausea and vomiting. She has had prior episodes of pain, which have resolved within a few hours, after eating heavy meals, which is characteristic of symptomatic gallstones. Since the vast majority of pancreatitis cases are due to gallstones or alcohol use and this patient does not consume alcohol, we can conclude that her symptoms are most likely related to gall-stones. Finally, the amylase and lipase are elevated. How Do You Diagnose Acute Pancreatitis?Acute pancreatitis is considered a clinical diagnosis. The Atlanta criteria were created for the diagnosis of acute pan-creatitis. They require two of the following three: 1. Sudden, severe, persistent epigastric pain radiating to the back
22920 2. Elevated lipase or amylase to three times greater than the upper limit of normal 3. Characteristic findings of acute pancreatitis on imaging (i.e., enlarged pancreas, sentinel loops [dilated small bowel], colon cutoff sign, etc.) History and Physical What Nonsurgical Conditions Can Mimic an Acute Abdomen?Gastroenteritis, acute adrenal insufficiency, sickle cell crisis, diabetic ketoacidosis, acute porphyria, pelvic inflammatory disease, kidney stones, and pyelonephritis. What Is the Significance of Bruising Around the Umbilicus, Flank, and Inguinal Ligament?They are all signs of retroperitoneal hemorrhage in associa-tion with acute hemorrhagic pancreatitis where methemal-bumin formed from digested blood tracks subcutaneously to different parts of the abdominal wall. Grey Turner’s sign refers to a blue-black discoloration in the flanks. Cullen’s sign is a blue-red discoloration at the umbilicus, and Fox’s sign is bruising over the inguinal ligament.Watch OutOnly about 10% of gallstones are radiopaque (visible on plain radiographs) versus 90% of kidney stones. An abdominal ultrasound is the first step in the evaluation for gallstones. What Are the Signs, Symptoms, and Findings of Acute Pancreatitis?Epigastric pain radiating to the back, worsened with food, nausea/vomiting (90% of cases), anorexia, or decreased oral intake. Physical exam frequently reveals fever, tachycardia, epigastric tenderness with localized guarding, and hypoac-tive bowel sounds secondary to reactive ileus. What Structures Are in the Retroperitoneum?One can remember these structures with the following mne-monic, “SAD PUCKER”: suprarenal (adrenal) glands, aorta/IVC, duodenum (2nd and 3rd part), pancreas (except tail), ureters, colon (ascending and descending), kidneys, esopha-gus, and rectum. Pathophysiology What Is the Pathophysiology of Pancreatitis?It initially occurs as a result of inappropriate activation of pancreatic enzymes leading to peripancreatic inflammation. Intraparenchymal extravasation of enzymes causes autodi-gestion of pancreatic parenchyma but primarily damages the peripancreatic tissues and vasculature. The inflammatory response is out of proportion to the insult and, with time, potentiates further damage leading to fluid sequestration, fat necrosis, vasculitis, and hemorrhage. What Are the Etiologies for Pancreatitis? 5“GET SMASHED” will help you remember the causes of acute pancreatitis 5G – gallstones (40%) 5E – ethanol (30%) 5T – tumors 5S – scorpion stings 5M – mycoplasma or mumps 5A – autoimmune (Lupus or polyarteritis nodosa) 5S – surgery or trauma 5H – hyperlipidemia/hypercalcemia 5E – ERCP or embolic/ischemic 5D – drugs or toxinsWatch OutThe 4 “F’s” for gallbladder disease are female, fat, forty, and fertile. Almost 40% of acute pancreatitis cases are caused by gallstones. However, only about 3–7% of patients with gallstones develop acute pancreatitis. What Medications Can Cause Pancreatitis? .Table 20.2Disease treatedMedicationsCardiovascular diseaseFurosemide, thiazidesInflammatory bowel diseaseSulfasalazine, 5-ASAImmunosuppressionAzathioprineSeizuresValproic acidDiabetesExenatideHuman immunodeficiency virus (HIV)Didanosine, pentamidine
23020 How Do Gallstones Cause Acute Pancreatitis?The most prevailing theory is that as a gallstone passes from the gallbladder down into the common bile duct, it causes transient impaction at the ampulla which causes a sudden rise in pancreatic duct pressure. In Patients with Gallstone Pancreatitis, How Often Does the Gallstone Remain Impacted in the Distal Common Duct?The gallstones that cause pancreatitis are usually small, and as such, in the majority of cases, the stone remains impacted very briefly, only transiently obstructing the ampulla of Vater, and soon after passes into the duodenum. As such, persis-tence of a common bile duct (CBD) stone is uncommon, and therefore ERCP is not usually needed. This differs from gallstones that cause acute cholangitis, where the stones are usually large and usually need ERCP for removal. What Are the Differences Between Acute and Chronic Pancreatitis?Watch OutThe first stage of pancreatitis involves the premature activation of trypsin within the pancreatic acinar cells. How Is the Severity of Pancreatitis Classified?The severity of pancreatitis is classified as mild, moderately severe, and severe. Most patients (80–90%) have mild pan-creatitis, which is characterized by the absence of multi-organ failure and local/systemic complications. It usually resolves in 2–5 days. Moderately severe includes transient organ failure lasting less than 48 hours and/or local or systemic complications. Severe pancreatitis is defined by organ failure that persists for more than 48 hours (worst prognosis). What Organ Systems Can Be Affected by Acute Pancreatitis?Cardiac, pulmonary, renal, and gastrointestinal. How Is Organ Failure Defined?Organ failure, as defined by the Atlanta Symposium, includes: 5Systolic blood pressure < 90 mmHg 5PaO2 ≤ 60 mmHg 5Creatinine >2.0 mg/L after rehydration 5Gastrointestinal bleeding > 500 cc/24 hours 5Disseminated intravascular coagulation 5Metabolic disturbances (calcium < 7.5 mg/dl) What Is the Mechanism of Hypotension in Pancreatitis?Inflammation and cytokine storm cause endothelial injury and increased permeability in the peripancreatic vascula-ture, leading to fluid leaking into the retroperitoneal space (known as third spacing). The cytokine storm also causes massive vasodilation, which along with a shrunken intravas-cular volume can cause severe hypotension. What Are the Main Pulmonary Complications of Acute Pancreatitis?Pleural effusions (the majority on the left side) and acute respiratory distress syndrome (ARDS) (. Fig. 20.1). These complications are thought to be due to cytokine-mediated vasodilation and pancreatic enzyme (e.g., phospholipase- A2)-mediated lung injury. .Table 20.3Acute pancreatitisChronic pancreatitisOnsetSevere and suddenRecurrent episodesEtiologyGallstone (40%), alcohol (30%)Alcohol (90%), anatomic defects (pancreas divisum), hereditaryPresenta-tionEpigastric pain radiating to the back, nausea, vomiting anorexiaRecurrent epigastric pain, weight loss, diabetes, steatorrheaLabsHigh amylase and lipase (more sensitive)Low fecal elastase levelsRadiologyDilated loops of bowel near pancreas (sentinel loop) on plain filmsPancreatic calcifica-tions on plain films
23120 What Are the Different Histopathologic Types of Acute Pancreatitis? What Are the Important Differences?The majority of patients (>80%) develop acute interstitial edematous pancreatitis, characterized by an enlargement of the pancreas due to inflammatory edema. Such patients have no inflammation or destruction of pancreatic cells. Less than 20% develop necrotizing pancreatitis characterized by necrotic pancreatic parenchyma which can lead to sepsis in over half the cases. Hemorrhagic pancreatitis is a type of necrotizing pancreatitis in which there is extensive bleeding into the pancreatic parenchyma and surrounding tissues. The type of pancreatitis is important because it determines both prognosis and management. Prognosis How Is the Severity of Pancreatitis Determined?Severity is determined by using one of various scoring sys-tems: Ranson (. Fig. 20.2), APACHE II, or based on clini-cal evidence of local or systemic complications. Recently, the BISAP (bedside index of severity of acute pancreatitis) score has been found to be simpler than and as accurate as APACHE II. BISAP score is determined by adding one point for each of the following: BUN >25 mg/dL, impaired mental status, systemic inflammatory response syndrome (SIRS), age >60 years, and pleural effusion. The Ranson criteria are the most commonly used tool and include five admission variables and six criteria that are assessed after 48 hours. Use “GA (Georgia) LAW” to remember the parameters used in determining prognosis on admission. Use “CHOBBS” to remember the latter parameters. Each variable gets one point.Watch OutThe degree of amylase and lipase elevation does not corre-late with the severity of acute pancreatitis and should not be used to influence management (i.e., timing of surgery). What Is the Main Drawback of Ranson Criteria?It takes 48 hours to measure all variables, and by then, the majority of patients have already declared themselves as to whether their course will be mild or severe and whether they need to be in a monitored bed. In addition, the variables can-not be repeatedly measured on an hourly or daily basis to monitor improvement or deterioration. Why Does One Get Hypocalcemia with Severe Pancreatitis?With severe pancreatitis, free fatty acids are generated by the action of pancreatic lipase. The free fatty acids chelate calcium salts that are present in the pancreas, leading to saponification (the deposition of calcium soaps in the retroperitoneum). .Fig. 20.1 Chest X-ray showing diffuse bilateral pulmonary infiltrates characteristic of ARDSAdmissionGlucose > 200 mg/dLAge > 55 yearsLDH > 350 IU/LAST > 250 IU/LScore0–22%mortality15%mortality40%mortality100%mortalityScore3–4Score5–6Score7–8Calcium < 8.0 mg/dLOxygen PaO2 < 60 mmHgBase deficit > 4mEq/LSequestration offluids > 6 LBUN increased by 5mg/dL or more despite fluidresuscitationHematocrit decrease > 10%WBC count > 16000cells/mmAfter 48 hours .Fig. 20.2 Ranson criteria
23220 What Is the Natural Disease Course of Acute Pancreatitis?The majority of patients with acute pancreatitis recover in less than 5 days without any complications. Close to 20% of patients have a severe presentation with local or systemic complications (including organ failure). What Is the Most Common Cause of Mortality in the First Week of Acute Pancreatitis? Beyond the First Week?In the first week, death is most often due to multiorgan failure as a result of severe systemic inflammatory response. After the first week, mortality is most commonly due to sepsis sec-ondary to pancreatic necrosis and peripancreatic abscesses (these most often develop in the third and fourth week of hospitalization). If a pancreatic abscess is not drained, mor-tality approaches 100%. Workup What Are the Most Important Laboratory Tests to Order when Suspecting Acute Pancreatitis?Serum amylase, lipase, liver function tests (AST, ALT, AP), electrolytes, complete blood count, and a lipid panel. Amylase and lipase are typically elevated. Amylase lev-els tend to be much higher (often >1000 u/L) in patients with gallstone pancreatitis as compared to other etiologies. Similarly, elevated ALT greater than three times the upper limit of normal is highly suggestive of gallstone pancre-atitis. However, close to 20% of patients will have normal LFTs. A lipid panel is important to rule out hyperlipidemic pancreatitis; usually due to hypertriglyceridemia (must be >1000 mg/dl). Which Laboratory Test Is Most Specific for Acute Pancreatitis?Lipase is most specific (and sensitive). Numerous other dis-eases can cause hyperamylasemia (. Table 20.4).Watch OutIn patients with hemorrhagic pancreatitis, the initial hematocrit is not a good indicator of blood loss. The hematocrit may take 1–2 days to equilibrate. In addition, if the patient is severely volume depleted, it may lead to hemoconcentration, giving a falsely elevated or normal hematocrit. What Is the Diagnostic Imaging of Choice on Admission for Acute Pancreatitis?Right upper quadrant ultrasound. Since the most common cause of acute pancreatitis is gallstones, this is the first etiol-ogy that should be ruled out. What Are the Classic Abdominal X-Ray Findings in Acute Pancreatitis?A sentinel loop (dilated loops of proximal small bowel in the left upper quadrant near the pancreas) and colon cutoff sign (distended proximal colon with abrupt collapse in the left upper quadrant at the splenic flexure). Both are due to local ileus (paralyzed, nonmotile bowel) as a result of the pancre-atic inflammation.Watch OutThe delayed development of an ileus in a patient with pancreatitis or following trauma may indicate retroperi-toneal bleeding. What Is the Classic Chest X-Ray Finding in Acute Pancreatitis? How Does This Finding Influence Prognosis?A pleural effusion, classically on the left side. In patients with severe pancreatitis, nearly 85% have evidence of pleural effu-sion on admission. In contrast, only 15% of patients with mild pancreatitis have a pleural effusion on plain films upon admis-sion. This finding is strongly associated with severe pancreatitis. What Is the Role of Abdominal CT Scan on Admission?CT scan should not be routinely ordered on admission, as it does not change management in the vast majority of cases. Though CT scan can help distinguish between mild and .Table 20.4 HyperamylasemiaConditionsSpecific diseasesPancreatic diseasePancreatitis, pancreatic pseudocyst, trauma, ERCP, pancreatic carcinoma, cystic fibrosisSalivary diseaseParotitis, radiation, ductal obstructionGastrointestinal diseasePeptic ulcer disease, perforated bowel, mesenteric ischemia, appendicitis, cholecystitis, celiac diseaseOtherAlcohol abuse, renal failure (amylase is renally cleared)
23320severe pancreatitis, clinical criteria are equally useful in mak-ing this distinction. Severe pancreatitis can cause a diffuse peritonitis-like exam, so a CT is useful when the diagnosis is in doubt. What Is the Role of Abdominal CT Scan During Subsequent Hospitalization?If the patient is not clinically improving after several days of conservative management, CT scan is helpful as it may explain the lack of improvement (such as whether there is pancreatic necrosis). Beyond the first week, CT scan is helpful in the situation where a patient develops worsening abdominal pain, fever, and sepsis, as it may demonstrate a pseudocyst or a pancreatic abscess (these local complications do not manifest on admission) (. Figs. 20.3, 20.4, and 20.5). What Is the Role of Urgent ERCP in Gallstone Pancreatitis?It is rarely needed – only if there is a suspected concomi-tant acute cholangitis. ERCP itself may cause pancreatitis. If ERCP is necessary, indomethacin rectal suppository reduces risk of pancreatitis. Management What Is the Initial Treatment for Acute Pancreatitis?Treatment is supportive, and patients are managed conser-vatively with vigorous intravenous fluid resuscitation, NPO, and analgesics. Routine nasogastric tube decompression is not recommended (only if there is ongoing vomiting). Similarly, routine use of antibiotics is not recommended. The majority of patients’ symptoms resolve within 3–5 days with this management.Watch OutAlthough not applied clinically, some test questions pre-fer meperidine over morphine for pain control in acute pancreatitis because in theory, meperidine does not cause contraction of the sphincter of Oddi (whereas morphine does) and may allow for quicker resolution of symptoms. However, meperidine increases the risk of seizures. What Is the Subsequent Management Plan? And How Does This Differ Between Gallstone and Alcoholic Pancreatitis?If gallstones were found on presentation (and there is no history of alcohol abuse), a cholecystectomy should be per-formed during the same hospitalization because recurrent gallstone pancreatitis risk is high within 30 days. The tim- .Fig. 20.3 Axial CT with a normal-appearing pancreas. (Black arrows: normal pancreas) .Fig. 20.4 Axial CT scan with peripancreatic fluid collections exhibiting thick irregular walls and marked fat stranding, consistent with abscesses .Fig. 20.5 Axial CT scan showing a thin-walled peripancreatic fluid collection consistent with pancreatic pseudocyst
23420ing of surgery depends on pancreatitis severity. Amylase and lipase levels should not influence timing of surgery. If alcohol is the etiology, counsel the patient on alcohol cessation, and provide referral for support groups. How Does the Severity of Acute Pancreatitis Affect Management?Pancreatitis severity assists in triage to a ward (mild pan-creatitis) or monitored step-down or ICU bed (moderately severe or severe pancreatitis). If severe pancreatitis is pre-dicted, it raises awareness to monitor the patient closely for local and/or systemic complications. For gallstone pancreati-tis, it assists in determining timing of cholecystectomy: early (within 48–72 hours) for mild pancreatitis versus delayed (weeks later after complete resolution) for moderately severe or severe pancreatitis. What Is the Management Algorithm for Acute Pancreatitis? . Fig. 20.6Classic case of pancreatitis: severeabdominal pain radiating to the back,nausea, vomiting, elevatedamylase/lipaseUltrasoundGallstones?Suspected acutecholangitis? (fever, RUQpain, jaundice)NoNPO, analgesics,IV fluidsWard, NPO,analgesics, IV fluids,cholecystectomywithin 48-72 hoursICU, NPO,analgesics, IV fluids,cholecystectomyweeks laterNoMildSevereRansoncriteriaYesYesUrgent ERCP .Fig. 20.6 Management algorithm for acute pancreatitis. (Based on the practice guidelines from the American College of Gastroenterology)
23520 Special Situations What Should You Suspect if a Patient with Severe Acute Pancreatitis Develops a Fever and Leukocytosis 4 Weeks into the Hospitalization?This presentation is concerning for a pancreatic abscess. The first step is to order a CT scan with contrast looking for necrotic tissue (i.e., areas that do not enhance) or a pancreatic abscess. If you find evidence of either, a CT or ultrasound- guided aspi-ration should be performed and sent for culture. If infection is present, antibiotics are administered. Infected pancreatic necrosis and pancreatic abscesses require surgical debride-ment using a step-up approach (sequential additional steps if needed): (1) percutaneous or endoscopic drainage, (2) video-assisted retroperitoneal debridement (VARD), and (3) open necrosectomy. These procedures are termed external drainage. What Should You Suspect If a Patient with a Recent Hospitalization for Pancreatitis Comes in 6 Weeks Later with Vague Abdominal Pain, a Palpable Epigastric Mass, and Persistently Elevated Serum Amylase?A pancreatic pseudocyst, a collection of pancreatic fluid sur-rounded by a wall without epithelium. It results from pancre-atic injury such as pancreatitis or trauma, which essentially disrupts a pancreatic duct. The pancreatic enzymatic fluid that leaks out is contained by surrounding fibrotic tissue. Although this most commonly appears in patients with chronic pancreatitis, it can also occur in the weeks follow-ing resolution of an acute pancreatitis. Patients often pres-ent with vague abdominal pain, elevated serum amylase, and possibly a palpable epigastric mass. The diagnostic test of choice is a CT scan, and most can be managed conser-vatively. Predictors of failure for conservative management include pseudocysts larger than 6 cm or those that have persisted for more than 6 weeks. Treatment of a symptom-atic, non- infected pseudocyst that fails to resolve is usually via internal drainage, by creating a connection between the cyst and the adjacent intestinal organ, usually the stomach (endoscopic cystogastrostomy). External drainage is not recommended as this may create a pancreatico-cutaneous fistula. A pseudocyst can erode into arteries, leading to a pseudoaneurysm and upper GI bleed (managed with angio-graphic embolization).Watch OutPancreatic cysts in the absence of a history of pancre-atitis should raise suspicion for a neoplasm; biopsy should be considered. What Are the Complications from Chronic Pancreatitis?Patients may develop diabetes mellitus secondary to the destruction of beta-islet insulin-producing cells in the pan-creas caused by chronic inflammation. This type of diabetes is termed type-3 diabetes and is very difficult to treat, and most patients require insulin. Patients may also develop steatorrhea due to poor absorption (particularly of fats and fat- soluble vitamins) from the digestive tract. These patients require pancreatic enzyme supplementation. Most patients also complain of severe and persistent chronic pain. Acute Pancreatitis After a Vascular ProcedureAlthough rare, patients who undergo an endovascular pro-cedure are at risk of atheroemboli (cholesterol embolism) dislodged by wires or stents. Cholesterol atheroemboli can lead to skin changes (e.g., blue toe, livedo reticularis) and/or gastrointestinal complications (e.g., acute pancreatitis, mes-enteric ischemia). Pancreatitis can also result from ischemia (such as after being on heart bypass). Acute pancreatitis that results from uncorrectable causes such as atheroembolism and ischemia should be managed with supportive treatment (e.g., IV fluids, analgesia). What Is the Most Common Indication for Surgical Management in Chronic Pancreatitis?The most common indication for surgical intervention is per-sistent and severe pain. The reason why chronic inflammation leads to constant pain is not fully understood, but the mecha-nism proposed includes nerve injury in the pancreatic head. Nonoperative management, providing temporary pain relief, includes placement of a stent in the pancreatic duct, allow-ing for improved anterograde flow of pancreatic juices. For definitive treatment, the Puestow procedure (lateral pancre-aticojejunostomy) is performed, in which the pancreatic duct is opened all the way from the head to the tail and sutured into the jejunum, allowing the free flow of pancreatic juices into the small intestine. Areas of Controversy Is Urgent ERCP Beneficial for Severe Pancreatitis?Only if there is suspicion of concomitant cholangitis. In the absence of cholangitis, the theoretical benefit of urgent ERCP is to remove a gallstone impacted in the distal common duct that might cause ongoing pancreatic inflammation. However, studies have failed to consistently show benefit in
23620using urgent ERCP in the absence of cholangitis. This may be a result of ERCP having a 5% risk of causing pancreatitis, related to over-injection of contrast medium into pancreatic ducts, and due to the fact that the majority of gallstones pass into the duodenum spontaneously. There is evidence to sup-port endoscopic removal of common bile duct stones with ERCP and papillotomy if cholangitis is also present. Some clinicians also choose to use ERCP in the setting of obstruc-tive jaundice as suggested by persistent and marked bilirubin elevation. Should Prophylactic Antibiotics Be Administered for Severe Acute Pancreatitis?There is no role for antibiotics for mild pancreatitis, as the disease is due to inflammation, not infection. Patients with severe pancreatitis have increased mortality as a result of subsequent infections, justifying a possible role for prophy-lactic antibiotics, anecdotally supported by its use in clini-cal practice over the past several decades. However, its role has been scrutinized by multiple studies in recent years, with most concluding that there is no decrease in mortality with prophylactic antibiotics. Areas Where You Can Get in Trouble Missing Hypercalcemia as the Cause of PancreatitisIn the absence of gallstones and alcohol abuse, the etiol-ogy of acute pancreatitis may be elusive. In a patient with hyperparathyroidism or hypertension controlled with hydrochlorothiazide, consider hypercalcemia as the etiol-ogy. Hydrochlorothiazide increases calcium reabsorption in the distal convoluted tubule. Hypercalcemia leads to a secretory block in the pancreatic duct. While hypercalcemia can cause pancreatitis, pancreatitis can cause hypocalcemia. Inflammation generates free fatty acids that avidly chelate insoluble calcium salts in the pancreatic bed, resulting in hypocalcemia. Thus, the predisposing hypercalcemia may be missed. Pseudohyponatremia in PancreatitisBe aware of pseudohyponatremia in patients with hyperlip-idemic pancreatitis. This is due to lipids displacing water, creating a measuring error. True sodium levels are normal. Nutritional SupportIf patients require being NPO greater than 7 days, nutri-tional support is needed. Enteral nutrition (not parenteral) is preferred, with the feeding tube placed past the ligament of Treitz to avoid activation of the pancreas. Summary of Essentials History and Physical 5Nonsurgical conditions that mimic an acute abdomen: gastroenteritis, acute adrenal insufficiency, sickle cell cri-sis, diabetic ketoacidosis, acute porphyria, pelvic inflam-matory disease, kidney stones, and pyelonephritis. 5Patients with pancreatitis typically present with epi-gastric pain radiating to the back, nausea, vomiting, anorexia, fever, and tachycardia. Pathophysiology 5The initial event in pancreatitis is the inappropriate acti-vation of pancreatic enzymes. 5Gallstones and alcohol are the most common causes of acute pancreatitis. Diagnosis 5Most cases can be diagnosed with just a history, physical, and abnormal amylase/lipase. 5Ranson criteria are used to predict severity based on parameters during initial admission and at 48 hours after. Workup 5Amylase/lipase levels do not correlate with severity of pancreatitis. 5In the absence of a history of alcohol abuse, start with a RUQ ultrasound to look for gallstones. Management 5Patients should initially be managed conservatively with IV fluids, NPO, and narcotic analgesia. 5Gallstones. 5Urgent ERCP rarely needed: 5Early cholecystectomy if mild pancreatitis. 5Late cholecystectomy if moderately severe or severe pancreatitis. 5If patients do not clinically improve after 3 days of con-servative management, get a CT scan with contrast to look for any underlying complications (i.e., necrosis). 5Begin enteral nutrition in patients with prolonged NPO status or in severe acute pancreatitis. 5Refractory persistent abdominal pain is the main indica-tion for surgery in chronic pancreatitis.
23720 Complications 5Systemic 5Early (first week) 5Multi-organ failure 5Local 5Late (3 weeks) 5Pancreatic abscess 5Pancreatic pseudocyst 5Pancreatic necrosisSuggested ReadingAboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B, Neville A, de Virgilio C. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010;251(4):615–9.Banks PA, Bollen TL, Dervenis C, Gooszen HG, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102–11.Chang L, Lo S, Stabile BE, Lewis RJ, Toosie K, et al. Preoperative versus postoperative endoscopic retrograde cholangiopancreatography in mild to moderate gallstone pancreatitis: a prospective random-ized trial. Ann Surg. 2000;231(1):82.Uhl W, Warshaw A, Imrie C, Bassi C, et al. IAP guidelines for the surgical management of acute pancreatitis. Pancreatology. 2003;3(2): 565–73.
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