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Allison TayloeClinical Case Study: Acute PancreatitisManaging Common Acute and Emergent Health Problems I, NUR 7201WSU, CONHClinical Case Study: Acute PancreatitisSource: patient, reliable sourceChief Complaint: “Abdominal pain, nausea and vomiting x six hours”History of Present Illness: D.M. is52 year old year old female who presents to the emergency department with complaints of left upper quadrant abdominal and epigastric pain radiating to the back, nausea, and vomiting that began approximately six hours ago. She reports she woke up at 6:00 AM this morning with severe abdominal pain 8/10 that began in the left upper abdominal quadrant with radiation to her epigastric area and around to her back. She describes the pain as a constant sharp and burning pain that is aggravated by movement or lying down and is somewhat improved when she leans forward sitting up. She attempted to take TUMS tablets x 4 this morning without relief thinking the pain was due to an ulcer as she has had one in the past. She also admits to nausea and vomiting three times this morning with the onset of abdominal pain and states she has not eaten since last night. By 9:00 am, three hours after the onset of symptoms, the patient reports the pain became more severe increasing to rate 10/10, thus she decided to call 911. She denies any fevers, chills, diarrhea, constipation, bloody emesis or stools in addition to reported symptoms.Medical History: Anxiety, depression, hypertension, peptic ulcer diseaseSurgical History: cholecystectomy 1998, cesarean section 1984, 1986Social History: The patient currently lives at home with her boyfriend. She is currently unemployed. She denies any current exercise program. She admits to smoking 1PPD of cigarettes x 20 years and consuming two-three 24 oz. beers nightly with two 4 oz. shots of vodka or rum x 10 years. She denies any illicit drug use such as cocaine, heroin, or marijuana. She did not receive the flu vaccine for the past three years and she does not recall ever receiving the pneumococcal vaccine. She is up to date on all childhood vaccines. Family History: Her paternal grandmother died at age 88 from unknown causes and paternal grandfather died at age 50 in a car accident. Her maternal grandmother lived to age 85 and died from lung cancer. Her maternal grandfather died at age 68 from chronic obstructive pulmonary disease. Her mother died at age 72 from cirrhosis of the liver due to alcoholism and she is estranged from her father. She has one living sister who has a history of hypertension and diabetes. She has two living sons who are in their late twenties and have no known chronic medical condition. Medications: Alprazolam (Xanax?) 0.5 mg three times a day, Fluoxetine (Prozac?) 40 gm daily, amlodipine (Norvasc?) 5 mg daily, hydrochlorothiazide 25 mg dailyAllergies: No known allergiesReview of Systems ROS is positive for nausea, vomiting, and abdominal pain with radiation to back. Otherwise negative as listed below. General: Denies weight loss, malaise/fatigue, fever/chills, or decreased appetiteNeuro: Denies weakness, dizziness, syncope, or near syncope, headaches, seizures, or loss of consciousnessHEENT: Denies sore throat, changes in hearing or vision, nasal drainage, ear pain, or blurry vision.Respiratory: Denies cough, sputum production, hemoptysis, or shortness of breathCardiovascular: Denies chest pain, PND, orthopnea, leg swelling, or palpitations.Gastrointestinal: Denies diarrhea, constipation, or bloody stools. Genitourinary: Denies vaginal discharge, hematuria, or dysuria. Musculoskeletal: Denies joint or bone pain/tenderness. Denies any recent falls. Skin: Denies rashes, lesions, or scars. Psychosocial: +history of depression and anxiety, denies any recent depressive or anxious episodes while taking home medications. Denies suicidal thoughts or ideations. Denies any domestic violence.Physical Exam:Vitals: (in ED) B/P 138/82, RR 32, and HR 102 bpm, O2 sat: 96 % on room air, temp: 99.4 ?FGeneral: Appears older than stated age, anxious, pale, restless in bed gripping abdomenHEENT: Head normocephalic. Eyes, conjunctivae clear with no drainage. External ears symmetrical bilaterally. Mouth, nose, and throat, no significant lesions. No palpable tenderness over lymph nodes or sinuses. Mucous membranes dry, pink, no lesions or edema noted. No thyromegaly, trachea midline on palpation. No jugular venous distention. Skin: Diaphoretic, pale, warm. No appreciable rashes, lesions, or skin discoloration. No hair thinning.Neurological: Awake, alert, oriented x 3. Cranial nerves II-XII intact. Cardiac: The apex is nonpalpable. Pulses are 2+ in carotid, radial, femoral, posterior tibialis and dorsalis pedis bilaterally. Regular rhythm, tachy rate with no appreciable murmurs, rubs, or gallops. S1, S2 present. No carotid bruits. No palpable thrills. No tenderness on palpation of chest wall. Pulmonary: Shallow breathing, tachypenic. Symmetric thoracic expansion. No wheezing or rhonchi, or crackles. CTAB.Gastrointestinal: Hypoactive bowel sounds in all 4 quadrants. Mild distension. Unable to palpate pancreas. Liver size approximately 8 cm in length. Voluntary guarding to upper right quadrant. Tenderness to epigastric area and right upper quadrant on palpation. Mild tenderness to left upper quadrant, no tenderness to bilateral lower quadrants. No peritoneal signs. No Cullen or Grey Turner’s sign. Genitourinary: Urinary meatus normal, no edema or erythemaMusculoskeletal: Deep tendon reflexes intact any symmetrical bilateral upper extremities (BUE) and bilateral lower extremities (BLE). Motor and sensory function intact. Full range of joint motion to BUE and BLE and 5/5 muscle strength bilaterally. Table 1: Diagnostic Lab resultsDiagnostic Lab ResultsResultDiagnostic Lab ResultsResultGlucose (70-100 mg/dL)248 mg/dLWBC (k/mm3)14.4 k/mm3K (3.5-5 mEq/L)3.8 mEq/LRBC: (4.2-5.7 m/mm3)4.8 m/mm3Na (135-145 mEq/L)137 mEq/LHgb (12.0-14.8 g/dL)14.2 g/dLCreat (< 1.2 mg/dL)1.0 mg/dLHct (37.8-43.9%)43.9 %CO2 (22-28 mmol/L)23mmol/LPlt (150 -450 k/mm3)237 k/mm3Cl (96–107 mEq/L)98 mEq/L Troponin I (< 0.05 ng/mL)0.01 ng/mLBUN (5–18 mg/dL)18 mg/dLAlkaline Phophatase (25–160 IU/L) IU/LCa (8.5–10.5 mg/dL)8.2 mg/dLALT (1–45 IU/L) 78 IU/LGFR ( >70 mL/min)72 mL/min AST (7–42 IU/L )63 IU/LAmylase (0-100 U/L)468 U/LAlkaline phosphatase (40-117 U/L)264 U/LLipase (0-160U/L)2, 387 U/LUrinalysis: Color/clarity (clear/yellow)(clear/yellow)Trig (<150 mg/dL)329 mg/dL pH (5.0-9.0)6.0LDH 248mg/dL Specific gravity (1.005-1.030)1.025ABG: pH (7.35-7.45)7.42 Glucose (neg)negPaO2 (80-100 mm Hg)82 mm HgNitrates (neg)negCO2 (35-45 mm Hg)33 mm HgWBC (0)0-1BE (±2)0RBC (0)negHCO3 (22-26 mm Hg)24 mm HgProtein (neg)negO2 saturation96%Ketones (neg)negTable 2: Additional diagnostic testsEKGChest x-rayAbdominal x-rayAbdominal CT with IV contrastRhythm: STRate: 110 bpmPR interval: 0.12QRS: 0.08QT: 420 msecNo ST-T wave abnormalities, no q waves, normal axisCardiac silhouette is unremarkable. No active cardiopulmonary process, no pleural effusions or infiltrates visible. Minimal small bowel dilation concerning for possible ileus Diffuse pancreatic inflammation consistent with pancreatitis. No fluid collection, peripancreatic fat infiltration or pseudocysts visible. Differential Diagnosis The differential diagnosis for this patient could include various causes of sudden and severe abdominal pain and physical exam findings listed above such as: acute cholecystitis, acute cholangitis, acute pancreatitis, ruptured duodenal ulcer, pneumonia, acute myocardial infarction, renal colic, perforated viscous, small bowel obstruction, mesenteric ischemia, dissecting aortic aneurysm or diabetic ketoacidosis (Wu & Conwell, 2012). Probability of various diagnoses, presentation of symptoms, past medical and surgical history, physical exam findings, and diagnostic tests can all assist in differentiating appropriate diagnoses for patients who present to the emergency department. As noted in the surgical history of this patient, she has already had her gall bladder removed, helping to eliminate the diagnosis of acute cholecystitis as a cause of symptoms. Diabetic ketoacidosis is also a consideration with abdominal pain associated with nausea and vomiting, however, this patient describes a sudden onset of symptoms and has no history of diabetes, making this diagnosis less likely. Although this patient is hyperglycemia on presentation to the emergency department, anion gap is normal and there were no ketones present in the urine, also lessening the chance of diabetic ketoacidosis as a cause for her symptoms (Tierney, McPhee & Papadakis, 2014). Renal colic is also a consideration, but is unlikely given that renal calculi typically don’t cause elevations in serum amylase, lipase, and triglycerides, pain with renal colic is typically located in the flank area with radiation to the abdomen and groin, and urinalysis in this patient doesn’t show signs of infection, hematuria, or crystals concerning for urolithiasis (Kasper et al., 2012). Pneumonia is also an unlikely diagnosis, given the sudden onset of symptoms and absence of complaints of upper respiratory infection or shortness of breath on admission. Acute cholangitis, an infection in the biliary tract, is another possibility based on this patient’s presentation. Patients with acute cholangitis frequently present with symptoms known as Charcot triad, which includes fever, abdominal pain, and jaundice (Baillie, 2012). Although this patient did have a severe and sudden onset of abdominal pain and has a low grade fever with an elevated white blood cell count, she did not present with jaundice, which is almost always present in the sclera or sublingual area in patients with acute cholangitis (Baillie, 2012). Endoscopic ultrasound is considered the gold standard for diagnosing bile duct stones and may show dilation of biliary tree > 8 cm in patients with acute cholangitis, however magnetic resonance imaging (MRI) and computed tomography (CT) scan may give similar information if further testing is needed (Tierney, McPhee & Papadakis, 2014). This patient had no such findings noted on her CT scan or abdominal ultrasound, making acute cholangitis an unlikely diagnosis. Small bowel obstruction and mesenteric ischemia are also diagnoses that should be considered based on the patient’s presentation of symptoms, but can most likely be ruled out based on CT results not showing any areas of bowel dilation, or heterogeneous/homogenous low attenuation areas of bowel (Mortele, 2012). Mesenteric ischemic is more likely to occur in patients with a history of congestive heart failure, atrial fibrillation, unexplained weight loss, postprandial abdominal pain, or a recent myocardial infarction, none of which is mentioned in this patient’s presentation (Lo, 2010). This patient is also not noted to be anemic, which typically occurs from blood loss in patients with mesenteric ischemia related to coagulopathies causing lower GI bleeding and melena (Lo, 2010). This patient does have a history of previous history of peptic ulcer disease, as well as continued alcohol and tobacco use, further increasing her chances of having a ruptured duodenal ulcer (Kasper et al., 2012). However, a ruptured duodenal ulcer is typically associated with mild serum amylase elevation (< 2 times normal) and can be diagnosed with use of CT scan showing free air located in the abdominal cavity or below the left and right hemi diaphragm on chest x-ray, neither of which was noted to be present in this patient’s testing (McQuaid, 2014). In addition, perforated duodenal ulcers are rarely precipitated by nausea and vomiting and abdominal pain with radiation to the back is an uncommon finding, further decreasing the probability that this patient is experiencing a perforated ulcer (Doherty & Way, 2010).Although this patient did not present with symptoms of chest pain, syncope, or focal neurologic changes, an aortic dissection can present as severe abdominal pain with radiation to the back depending on the location of the dissection (Johnson & Prince, 2011). Chest x-ray in this patient did not show widening of the mediastinum or abnormal aortic contour which can frequently be seen in thoracic aortic dissection, but the diagnosis can’t be excluded based on the absence of this finding alone. Due to the severity of morbidity and mortality as well as hemodynamic instability associated with this diagnosis, a CT of the chest and abdomen should be performed with and without contrast to assess for aortic dissection if this diagnosis remains a concern (Johnson & Prince, 2011). An acute myocardial infarction, typically inferior, also needs to be considered as a possible diagnosis in a patient presenting with the above stated symptoms. In addition, women are more likely than men to present with atypical symptoms for acute myocardial infarction, such as epigastric pain (Boyle, 2014). To complicate matters more, conditions such as acute pancreatitis can mimic inferior myocardial infarctions for reasons thought to be related to increased vasovagal responses, electrolyte abnormalities, coronary vasospasm, or coagulopathy (Tejada et al., 2008). Therefore, electrocardiogram (EKG) findings alone may not be indicative of acute myocardial infarction. This patient was not noted to have any EKG ST-T wave abnormalities and troponin level was < 0.01, making the diagnosis of acute myocardial infarction unlikely (Tierney, McPhee & Papadakis, 2014). Troponin is a specific cardiac biomarker typically elevated within four to eight hours after initial injury and has a high sensitivity and specificity for cardiac ischemia and necrosis (Boyle, 2014). It is possible for a patient to be experiencing acute non ST elevated MI or unstable angina without subsequent EKG changes, but an acute ST elevated myocardial infarction can be ruled out based on the absence of EKG changes on this patient’s EKG (Boyle, 2014). This patient would need an additional one to two troponin levels checked eight hours apart to completely rule out myocardial ischemia or necrosis (Tierney, McPhee & Papadakis, 2014).The most likely diagnosis for this patient is acute pancreatitis related to alcohol consumption. The two most common causes of acute pancreatitis are alcohol exposure and biliary tract disease (Lippi, Valentino, & Cervellin, 2012). Furthermore, acute pancreatitis due to alcohol consumption is typically associated with chronic alcohol use of 5-15 years, which is described in this patient’s social history. This patient has had her gallbladder removed over a year prior to the onset of symptoms, lessening the chance of gallstones in the bile duct as a cause for her AP, and has no known vasculitis disorders that would cause acute AP (Kasper et al., 2012). Epigastric and left upper quadrant pain with radiation to the back with associated nausea and vomiting are the most common presenting symptoms in acute pancreatitis, which this patient is also described as experiencing (Atilla & Oktay, 2011). According to the American College of Gastroenterology, acute pancreatitis (AP) is diagnosed based on presence of two of the three following criteria: abdominal pain consistent with the disease, serum amylase and/or lipase elevations greater than three times upper normal limit, and findings characteristic of AP on abdominal imaging (Tenner, Baillie, DeWitt, & Swaroop Vege, 2013). This patient not only has characteristic abdominal pain as well as amylase and lipase levels three times upper limit of normal, but also has CT abdominal results revealing pancreatic inflammation consistent with acute pancreatitis. In addition, this patient is also noted to have elevated triglycerides, hyperglycemia, hypocalcemia, and elevated liver enzymes which are often seen in certain types of acute pancreatitis and help to classify the severity of acute pancreatitis diagnosis (Atilla & Oktay, 2011). Diagnostic TestingPatients admitted to the emergency department with complaints of severe abdominal pain should include laboratory testing and abdominal imaging in an effort to properly diagnose and treat the patient presenting with these symptoms. In cases of acute pancreatitis, like many other causes of acute abdomen, laboratory testing should include basic metabolic panel (BMP), complete blood count (CBC), amylase, lipase, liver function tests (LFT) including aspartate aminotransferase, serum alkaline phosphatase, and bilirubin levels, lactate dehydrogenase, triglyceride levels, urinalysis, and C-reactive protein levels (Atilla & Oktay, 2011). CBC is helpful in identifying leukocytosis often present in acute abdomen disorders, including acute pancreatitis. In addition, CBC revealing low hemoglobin may help differentiate diagnoses such as mesenteric ischemia, whereas patients with AP who yield high hematocrit levels above 44% have higher predictive value for pancreatic necrosis related to hemoconcentration and overall poorer prognosis (Tierney, McPhee & Papadakis, 2014). Serum amylase is primarily produced by the pancreas and salivary glands and rises rapidly (within 3-6 hours) with the onset of acute pancreatitis, making it an important diagnostic laboratory value for acute pancreatitis (Lippi, Valentino, & Cervellin, 2012). Even though amylase levels can be elevated in other disorders affecting pancreatic or salivary gland production or renal excretion such as renal failure, chronic alcoholism, pregnancy, appendicitis, and hepatitis, amylase levels elevated greater than three times the upper limit of normal with associated abdominal pain increased specificity of acute pancreatitis of ~95%, but sensitivity remains low at ~60% (Atilla & Oktay, 2011). Although lipase can also be affected by some abdominal processes and renal failure, lipase is solely produced by the pancreas and not salivary glands and stays elevated longer than amylase levels, making it a more accurate diagnostic test for the diagnosis of acute pancreatitis (Tierney, McPhee & Papadakis, 2014). Elevated fasting triglyceride levels ( > 1000 mg/dL) is associated with acute pancreatitis due to hypertriglyceridemia, a poor prognosis for patients with acute pancreatitis, and can inhibit serum amylase elevation in patients with acute pancreatitis masking elevated levels Tenner et al., 2013). Thus, fasting triglyceride levels are important diagnostic lab value when diagnosing acute pancreatitis, especially when gallstones or alcohol seems unlikely as potential cause (Tenner et al., 2013). On the same note, lactate dehydrogenase levels > 500 U/dL are also associated with a poorer prognosis (Atilla & Oktay, 2011). Elevated liver function tests and hyperbilirubinemia should be checked for degree of elevation and possibly underlying liver disease, although these levels are often mildly elevated in patients with AP and return to normal in approximately seven days (Kasper at al., 2012). In this patient, who is thought to have AP caused from continued alcohol use, liver enzymes are also useful for assessing chronic elevated liver enzymes which would occur with hepatitis or cirrhosis of the liver (Tierney, McPhee & Papadakis, 2014). C-reactive protein is an important inflammatory marker both in acute and chronic AP and should be checked within the first 72 hours to make assess for levels > 150 mg/L, which is associated with higher rate of pancreatic necrosis and increased severity of AP (Williamson & Williamson, 2010). Many other electrolyte and lab values such as calcium levels, blood urea nitrogen levels, and serum creatinine are not sensitive or specific for acute pancreatitis, but helpful in assessing severity of disease in those with AP to help guide appropriate treatment, thus should be obtained on all patients with AP (Kasper et al., 2012). For example, elevated creatinine > 1.8 mg/dL 48 hours after diagnosis of acute pancreatitis is associated with higher rates of pancreatic necrosis, whereas hypocalcaemia, for unknown reasons, is associated with poorer prognosis in those with acute pancreatitis (Tierney, McPhee & Papadakis, 2014). In patients diagnosed with acute pancreatitis that present with hypotension and elevated creatinine on admission, guidelines for treatment include more intense intravenous fluid volume management and admission to the intensive care unit for closer observation (Tenner et al., 2013). Diagnostic testing for acute pancreatitis also includes various forms of abdominal imaging. Abdominal x-ray is useful in identifying free air consistent with perforated peptic ulcer, but typically adds little assistance in diagnosing AP (Kasper et al., 2012). According to the American College of Gastroenterology guidelines, all patients presenting with AP should have a trans-abdominal ultrasound (Strong recommendation, low quality of evidence) (Tenner et al., 2013). Trans-abdominal ultrasound is useful in identifying cholelithiasis, but is often not helpful in diagnosing AP due to intervening bowel gas, therefore was not performed in this patient due to previous cholecystectomy (Tierney, McPhee & Papadakis, 2014). Contrast enhanced computed tomography (CECT) has > 90% sensitivity and specificity for diagnosing acute pancreatitis (Tenner et al., 2013). However, routine use of CECT is not necessary in mild AP cases due to typical exam and laboratory findings aiding in diagnosis. Rather, CECT should be completed in 48-72 hours after admission if patient does not improve to evaluate for pancreatic necrosis or initially if abdominal ultrasound is not completed or serum amylase levels are less than three times the upper limit of normal (Tenner et al., 2013). Magnetic resonance imaging (MRI) is comparable to CECT and can be used as an alternative to identify necrosis in patients who fail to improve within 48-72 hours after admission (Kasper et al., 2012). CECT imaging is also useful in assessing the severity of acute pancreatitis three to five days after diagnosis (Tenner et al., 2013). CECT images on admission in patients with mild AP can’t always predict the progression to severe AP in these patients and are often reserved for AP patients who fail to show improvement in 48-72 hours, therefore, CT images of this patient would need to be repeated in three days in order to assess severity index and associated mortality for AP based on CT results (Tierney, McPhee & Papadakis, 2014).There are also several severity scoring systems for severity of AP based on presenting signs and symptoms and whether or not there is improvement in 48 hours of admission. Such scoring systems include the Atlanta classification scoring system and the Ranson criteria. The Ranson criteria are especially useful in patients who present with acute alcoholic pancreatitis. Ranson criteria includes factors such as age> 55 years and presenting white blood cell count (> 16, 000/mm3), blood glucose levels (>200 mg/dL), LDH levels (>350 U/L), and AST levels (>250 U/L) and is associated with higher mortality if score ≥ 3or if other factors such as drop in hemoglobin (>10%), BUN rise (>5 mg/dL), PaO2drop (<60 mm Hg), serum calcium (<8 mg/dL), increased base deficit (> 4 mEq/L) or increased fluid restoration (> 6L) develops within 48 hours (Sargent, 2006). Atlanta scoring system divided into mild AP, moderately severe AP or severe AP. Severe AP is diagnosed based on findings of organ failure in at least one organ which would be defined as systolic blood pressure < 90 mm Hg, PaO2 < 60 mm Hg, creatinine > 2mg/dL, > 500 mL blood loss related to gastrointestinal bleeding within 24 hours, or local complications such as peripancreatic fluid collections or pseudocysts (Tierney, McPhee & Papadakis, 2014). Moderately severe AP includes definitions of severe AP, but with only transient organ failure < 48 hours. Mild AP, associated with the best prognosis and typically only requiring a short hospital stay of 72-96 hours, is defined by absence of organ failure or local complications on abdominal imaging (Tenner et al., 2013). The Bedside Index for Severity in Acute Pancreatitis (BISAP) and Acute Physiology and Chronic Health Evaluation (APACHE II) assess mortality risk of AP patients within the first 24 hours of admission. BISAP score includes levels of BUN (> 25 mg/dL), mental status impairment, systemic inflammatory response syndrome (SIRS) criteria , evidence of pleural effusion, and age (> 60 years) as criteria with scores ≤ 2 associated with mortality < 2% (Tierney, McPhee & Papadakis, 2014). Based on the above findings, this patient is classified as having mild AP. However, review of the literature regarding various scoring systems notes that severity scores usually take greater than 48 hours to become accurate and may not be able to accurately predict patients with mild AP who can quickly progress to severe AP (Tenner et al., 2013). Therefore, clinicians caring for these patients need to continue to assess diagnostic labs such as amylase and lipase and daily renal function panels to appropriately assess for hemodynamic stability and improvement of symptoms over the first 48-72 hours (Tierney, McPhee & Papadakis, 2014). Prioritized planPrioritized plan for the patient with acute pancreatitis includes assessing for level of severity, intravenous fluid resuscitation and early oral diet/enteral feeding initiation, analgesic medication administration, and treatment of underlying cause. In this patient’s case, treatment of AP would include all of the above as well as monitoring and treatment for alcohol withdrawal. Thus, this patient will be admitted to the hospital in a ICU-step down bed with continuous cardiac and pulse oximetry monitoring and receive treatment for acute pancreatitis.Treatment of the patient presenting with AP always includes early aggressive intravenous (IV) fluid hydration within the first 12-24 hours (strong recommendation, moderate quality of evidence) due to the underlying inflammatory processes of AP causing decreased pancreatic blood flow, as well as volume losses through nausea/vomiting, poor oral intake, and third spacing (Tenner et al., 2013). Although IV fluid replacement hasn’t shown to be effective with late AP presentation, this patient presented within six hours of symptom onset and therefore will be given an initial bolus of two liters lactated ringers (LR) solution (20 ml/kg over 1-2 hours) while in the emergency department (Marino, 2014). LR is the isotonic solution of choice for patients with AP due to several studies showing decreased risk of systemic inflammatory response syndrome with LR versus normal saline administration and overall decreased morbidity (Tenner et al., 2013). Thus, following initial two liter fluid bolus, the patient will be continued on LR on a continuous rate of 150 mL/hr up to 250 mL/hr to maintain mean arterial pressure > 65 mm Hg and urine output of 0.5 mL/kg/hr since this patient does not have any known underlying cardiac or renal disorders (Marino, 2014). A BMP will be checked every six hours with pancreatic enzyme levels including amylase and lipase every 24 hours with the goal of hydration to decrease BUN and hematocrit levels while maintaining normal creatinine levels (strong recommendation, moderate quality of evidence) (Tenner et al., 2013). As states above, CT scans are unnecessary and not cost effective in patients with mild AP, but if patient fails to improve within 47 hours ( low urine output < 0.5 mL/kg/hr or MAP < 65 mm Hg despite adequate fluid resuscitation), a CT scan should be performed to evaluate for possible pancreatic necrosis or pseudocyst formation. If necrosis is discovered, surgical intervention may be needed and antibiotic therapy may be warranted (Tierney, McPhee & Papadakis, 2014). Pain in AP is caused by leakage of inflammatory exudates into retroperitoneal spaces (Sargent, 2006). Furthermore, generalized pain with any illness increases metabolic activity which in turn increases production and secretion of pancreatic enzymes, thus increasing pain for patients with AP. Meperidine used to be the drug of choice for analgesia in acute pancreatitis due to thoughts that other narcotics caused spasm in the sphincter of Oddi, but morphine is now the analgesic of choice due to harmful metabolites of meperidine that can accumulate and potentiate seizures (Tierney, McPhee & Papadakis, 2014). Patient controlled analgesia (PCA) has also showed improved pain control in patients with acute pancreatitis, therefore, this patient will be given 4 mg morphine IV in the emergency department every one-two hours and started on a morphine PCA with demand dose of 1 mg every 15 minutes with a lockout of 4 mg every hour and 20 mg lockout in four hours (Lexi-comp, 2014). Continuous end pulse oximetry and cardiac monitoring will be applied to this patient as well as every four hour full nursing assessments to monitor for central nervous system depression. If the PCA is ineffective at controlling the patient’s pain, consideration of increasing morphine to 2 mg every 15 minutes or a bolus of morphine 2 mg every two hours through the PCA should be considered (Sargent, 2006). Once the patient is pain free, usually in 48-72 hours with mild AP, IV pain medications can be weaned. Non-steroidal anti-inflammatory agents have been shown to be ineffective in treatment of AP (Doherty & Way, 2010). This patient will also be given an antiemetic, such as zofran, 4 mg IV every four hours as needed for nausea and vomiting in the initial acute period of AP (Lexi-Comp, 2014). Based on current recommended guidelines, patients admitted with AP no longer are required to have nothing by mouth (NPO) to allow the pancreas to “rest” (Williamson & Williamson, 2010). Furthermore, patients being maintained on an NPO diet causes bowel atrophy due to nonuse (Tenner et al., 2013). Because this patient only shows mild AP on admission to the hospital, a low-fat solid diet should be initiated within 12-24 hours as early oral nutrition is associated with decreased hospital stay and overall morbidity and mortality (Willamson & Williamson, 2010). Current evidence supports idea that initiation of solid low fat diet is just as safe as initiation of clear liquid diet in patients with mild AP (conditional recommendation, moderate quality of evidence) (Tenner et al., 2013). However, oral nutrition should not be started until nausea/vomiting has abated and the patient’s pain has subsided (Tierney, McPhee & Papadakis, 2014). In addition, if pain or vomiting reoccurs after starting an oral diet, the patient should be made NPO again and may require placement of an oral gastric tube for ileus release and control of symptoms (Kasper et al., 2012). Should this patient fail to show improvement within 48-72 hours, enteral nutrition through placement of a nasojejunal or even nasogastric tube with usual enteral nutritional formulas should be considered (Williamson & Williamson, 2010). Enteral nutrition should include 25-35 kilocalories/kg, 1-2g fat/kg, 3-6 g/kg of carbohydrate and 1.2-1.5grams of protein/kg (Holcomb, 2007). Parenteral nutrition should only be used if enteral nutrition is not tolerated or not meeting caloric requirements (strong recommendation, high quality of evidence) (Tenner et al., 2013). Patients who present with AP are frequently hyperglycemic on admission and treatment of AP should include blood glucose levels as well as insulin therapy to maintain adequate glucose control. Current recommendations of the American Diabetes Association includes blood glucose monitoring every four hours in non-ICU hospitalized patients who are NPO admitted and noted to have hyperglycemia (Magaji & Johnston, 2011). Blood glucose monitoring should be changed to prior to meals and at bedtime when the patient is eating. Current recommendations also support basal and sort acting insulin for goal of blood glucose control of ≤ 140 mg/dL premeal glucose and random blood glucose goal of ≤180 mg/dL (Marino, 2014). Therefore, this patient will be started on basal insulin and short acting insulin in the dose of 0.3 units/kg/ day to be divided up as 50% basal insulin once daily subcutaneously and the other 50% divided up into three doses of short acting insulin to be given prior to meals subcutaneously (Magaji & Johnston, 2011). In addition, the patient will be placed on sliding scale coverage for addition short acting insulin to be given subcutaneously premeal and before bedtime or every four hours for blood glucose levels ≥ 140 mg/dL. A fasting hemoglobin A1C should be obtained during the hospital admission to assess for underlying insulin resistance or diabetes (Magaji & Johnston, 2011). As the patient recovers from acute pancreatitis, basal insulin may need to be reduced as blood glucose levels return to normal, but blood glucose monitoring should continue while the patient is hospitalized. If the patient requires transfer to the intensive care unit, an insulin drip with regular insulin should be initiated for blood glucose levels > 180 mg/dL (Magaji & Johnston, 2011). Although this patient is noted to have leukocytosis on admission, prophylactic antibiotic treatment is not recommended due to the lack of evidence showing improved outcomes on patients with AP, even when pancreatic necrosis develops, therefore antibiotics will not be started (strong recommendation, moderate quality of evidence (Tenner et al., 2013). Treatment of this patient with suspected alcoholic acute pancreatitis will include management of alcohol withdrawal while in the hospital to prevent possible seizures. Thus, this patient will be monitored with the clinical institute withdrawal assessment protocol (CIWA) with Ativan IV in increments of 0-4 mg every two hours will be ordered based on CIWA scores (Kasper et al., 2012). Doses will then be tapered over three-five days. A behavioral assessment consult will also be placed to assess for underlying chronic alcohol abuse as well as depression/anxiety medication adjustments needed on discharge. Chronic alcohol use is associated with multiple vitamin deficiencies, therefore this patient will be treated with thiamine 100 mg IV daily for three days followed by 50 mg per day by mouth as this is the recommendation for any patient with acute alcohol withdrawal (Lexi-Comp, 2014). Due to the patient’s chronic alcohol use, it would not be inappropriate to draw a hepatitis panel, especially if the liver enzymes remain elevated (Kasper et al., 2012). Scheduled alprazolam, which the patient was taking prior to admission, should be continued as soon as the patient is able to tolerate oral diet with 0.5 mg twice daily by mouth. As such, the patient’s Fluoxetine (40 mg daily by mouth), hydrochlorothiazide (25 mg daily by mouth), and amlodipine (5 mg daily by mouth) should be restarted when the patient is able to tolerate oral intake. Blood pressure will be monitored every one-two hours in the first twenty four hours with goal blood pressure < 140/90 mm Hg and mean arterial pressure > 65 mm Hg (Marino, 2014). Treatment for this patient should also include measures to aide in smoking cessation and nicotine replacement, if needed while in the hospital, which could be accomplished with Nicoderm CQ transdermal patch 21 mg/day which should be continued after discharge for a total of six weeks, then tapered down to 14 mg/day for two weeks and 7 mg/day for two weeks (Lexi-Comp, 2014). This patient will be counseled during the hospitalization regarding the importance of smoking cessation and readiness to quit will be assessed. Health Promotion/Follow-upIn follow-up for patients admitted with acute pancreatitis, management focuses on prevention of recurrent AP as well as managing complications of the disease (Wu & Conwell, 2012). In this patient with presumed alcoholic acute pancreatitis, alcohol cessation and abstinence will help prevent future AP occurrences as well as development of chronic pancreatitis. Therefore, this patient will be given contact information on outpatient treatment centers and outpatient group therapy sessions such as alcoholics anonymous (AA), which have been shown to decrease alcohol consumption in as little as one to four sessions (Williamson & Williamson, 2010). Follow-up with this patient’s primary care physician should include assessment for continued alcohol use through questionnaires such as CAGE (cutting down, annoyed by drinking, feel guilty, eye opener) (Kasper et al., 2012). Follow-up should also include continued appointments with the patient’s primary care physician to assess smoking cessation progress and if the patient has relapsed. The patient’s willingness to quit should be reassessed at every visit if the patient continues to smoke. Furthermore, holistic care, in the form of counseling should be used in addition to medical treatments such as bupropion or varenicline if patient is willing to quit (Lexi-Comp, 2014). The patient should be encouraged to continue a low fat diet, as well as continue his medications for management of underlying chronic conditions with yearly vaccinations and diagnostic labs including fasting lipid levels, hemoglobin A1C, and baseline BMP and CBC. Following discharge from the hospital, the patient should follow-up with his PCP within a week to discuss hemoglobin A1C results if greater than 6.5% for potential treatment options as well as assess liver enzymes, BMP, and amylase to ensure return to normal levels. If the patient’s hepatitis panel comes back positive for hepatitis C or liver enzymes remain elevated, further treatment may be recommended (Kasper et al., 2012). Measures such as yearly vaccinations (influenza and pneumococcal), continued diet, and daily rigorous exercise of 30 minutes or more should be encouraged in this patient in addition to smoking and alcohol cessation to decrease this patient’s chance of recurrent AP episodes.ReferencesAtilla, R. & Oktay, C. (2011). Chapter 82. Pancreatitis and Cholecystitis. In Tintinalli, J.E., Stapczynski, J., Ma, O., Cline, D.M., Cydulka, R.K., & Meckler, G.D. (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, (7th ed.). Retrieved from , J. (2012). Chapter 157. Biliary Disease: Jaundice, Obstruction, and Acute Cholangitis. In McKean, S.C., Ross, J.J., Dressler, D.D., Brotman D.J. & Ginsberg, J.S. (Eds), Principles and Practice of Hospital Medicine. Retrieved from , A.J. (2014). Chapter 8. Acute Myocardial Infarction. In Crawford M.H. (Eds), Current Diagnosis & Treatment: Cardiology, (4th ed.). Retrieved from , G.M. & Way, L.W. (2010). Chapter 23. Stomach & Duodenum. In Doherty, G.M. (Eds), CURRENT Diagnosis & Treatment: Surgery, (13th ed.). Retrieved from , S. (2007). Stopping the destruction of acute pancreatitis. Nursing, 37(6): 42-48.Johnson, G.A. & Prince, L.A. (2011). Chapter 62. Aortic Dissection and Related Aortic Syndromes. In Tintinalli, J.E., Stapczynski, J., Ma, O., Cline, D.M., Cydulka, R.K., & Meckler G.D. (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, (7th ed.). Retrieved from et al. (Ed). 2012. Principles of Internal Medicine. (18th ed.). New York: McGraw Hill.Lexi-Comp, Inc. (2014). Lexi-Drugs. Retrieved from , G., Valentino, M., & Cervellin, G. (2012). Laboratory diagnosis of acute pancreatitis: in search of the Holy Grail. Critical Reviews In Clinical Laboratory Sciences, 49(1): 18-31. doi:10.3109/10408363.2012.658354Lo, B.M. (2011). Chapter 79. Lower Gastrointestinal Bleeding. In Tintinalli, J.E., Stapczynski, J., Ma, O., Cline, D.M., Cydulka, R.K. & Meckler, G.D. (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, (7th ed.). Retrieved from , V. & Johnston, J.M. (2011). Inpatient management of hyperglycemia and diabetes. Clinical Diabetes, 29(1): 3-9. doi: 10.2337/diaclin.29.1.3 Marino, P. (2014). The ICU Book. 4th ed. Philadelphia: Williams & Wilkins.McQuaid, K.R.(2014). Chapter 15. Gastrointestinal Disorders. In Papadakis, M.A., McPhee, S.J. & Rabow, M.W. (Eds), CURRENT Medical Diagnosis & Treatment 2014. Retrieved from , K.J. (2012). Chapter 9. State-of-the-Art Imaging of the Gastrointestinal System. In Greenberger, N.J., Blumberg, R.S. & Burakoff, R. (Eds), CURRENT Diagnosis & Treatment: Gastroenterology, Hepatology, & Endoscopy, (2nd ed.). Retrieved from , S. (2006). Gastrointestinal nursing. Pathophysiology, diagnosis and management of acute pancreatitis. British Journal Of Nursing, 15(18), 999-1005.Tejada, J., Hernández, F., Chimeno, J., Alonso, M., Martin, R., & Bastante, T. (2008). Acute pancreatitis mimicking acute inferior myocardial infarction. Angiology, 59(3), 365-367. doi:10.1177/0003319707304533Tenner, S., Baillie, J., DeWitt, J., & Swaroop Vege, S. (2013). American college of gastroenterology guidelines: Management of acute pancreatitis. The American Journal of Gastroenterology, 1-16. doi:10.1038/ajg.2013.218Tierney, L., McPhee & Papadakis, M. (2014). Current medical diagnosis and treatment. (53rd ed.). CT: Appleton & Lange.Williamson, J., & Williamson, R. (2010). Alcohol and the pancreas. British Journal Of Hospital Medicine (17508460), 71(10): 556-561.Wu, B.U. & Conwell, D.L. (2012). Chapter 156. Acute Pancreatitis. In McKean, S.C., Ross, J.J., Dressler, D.D., Brotman, D.J. & Ginsberg, J.S. (Eds), Principles and Practice of Hospital Medicine. Retrieved from . ................
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