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Clinical Case Study: Acute Pancreatitis

Aug 11, 2014

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Clinical Case Study: Acute Pancreatitis. By Nicole Vantress --- February 2013. Background. Medical Presentation. Patient C.P. transferred from Grossmont Hospital for gallstone pancreatitis Admitted to UCSD CCU January 13, 2013 with respiratory distress and sepsis

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• pancreatic rest
• low goal rate
• continuous renal replacement therapy

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Clinical Case Study: Acute Pancreatitis By Nicole Vantress --- February 2013

Medical Presentation • Patient C.P. transferred from Grossmont Hospital for gallstone pancreatitis • Admitted to UCSD CCU January 13, 2013 with respiratory distress and sepsis • Length of stay: 1/13/2013- present

Anthropometrics • C.P. 55 year old male • 6 ft. (72”) • 365# (166 kg) • BMI: 49.6 • Ideal Body Weight (IBW): 178# (81kg) • Percent IBW (%IBW): 205% • PMH: HLD, HTN, nephrolithiasis, BPH (benign prostatic hyperplasia), and morbid obesity

Prior to Admission • Symptoms • Back pain  upper abdominal pain • Pain worsened with food • Nausea and emesis • Fevers and chills • Decreased urine output • Social History/ Other History • Gallstones • 2 glasses of wine twice a week • No past history of pancreatitis • Lives with partner and daughter • Good job, no stressors

Medical Status at Admit to CCU • Gallstone pancreatitis with severe sepsis • AKI • Transaminitis • Plural effusion • Atelactasis vs developing PNA • Hyperglycemia • Hemodynamically unstable • NPO

Progress from Admit to Initial Nutrition Assessment • Pt intubated 1/14 • Sedated and started on 3 vasopressors (norepinephrine, phenylephrine, vasopresson) • Started CRRT 1/14 • Coretrack

Coretrack • Imaging note: “Coretrack placed with tip in atrum.” • Not appropriate with pancreatitis

Vasopressors • Patient on norepinephrine, phenylephrine and vasopressin. • Vasoconstriction and decreased oxygenation to the gut and microvili put the patient at higher risk for nonocclusive bowel ischemia. • 3 pressors hold • 2 pressors trophic feeds • 1 pressor advance TF slowly

Obesity in the ICU • Hypocaloric feeding when BMI >30 • 60-70% of target energy • If over age 65, Penn State Equation already factors this percentage in. • High protein needs • For ventilated, critically ill patients: • BMI<30: 1.2-2.0 gm/kg actual weight • BMI 30-40: 2.0 gm/kg IBW • BMI > 40: Greater than or equal to 2.5 gm/kg IBW • ~2 g/kg might not be indicated in liver and renal impairment • Patient on CRRT so not a concern.

Sepsis • Hypocaloric feeding the first week of sepsis • 55-65% of goal kcal • Then feed REE x 1.5 for calories • 1.5-2 g/kg protein • Increased needs can reamain elevated for up to 21 days even when sepsis has been treated.

CRRT (Continuous Renal Replacement Therapy) • CRRT removes water and wastes at a slow and steady rate (usually over 24 hrs). • Who gets CRRT?

CRRT cont. • Goals of CRRT • To correct electrolyte and metabolic imbalances associated with renal dysfunction • Maintain optimal fluid balance • Types/dialysate • SCUF (Slow Continuous Ultrafiltration) • CVVHDF (Continuous Venous-Venous HemoDiaFiltration) • CVVH (Continuous Venous-Venous Hemofiltraition) • CVVHD (Continuous Venous-Venous Hemodialysis • % glucose in dialysate ranges from 0.1%-2.5%. • UCSD uses 0.1%, which only provides 33 kcals.

CRRT Cont. • Nutrition goals • Oral and enteral diet does not usually need to be restricted for renal • Protein needs usually range from 1.5-2.5 g/g (more accurate estimate can be calculated from 24 hour data) • Renal MVI for water-soluble losses • Standard formula is appropriate • Insulin drip

CRRT Calculation for Protein Needs • In lab values, under filtrate tabs, find BUN ultrafiltrate. Start with lab value from day before and two others previous from that. Add up and take avg. • Only able to do calculation if all three values are within 10 points of each other. • Under CRRT flowsheet: • Make sure the is a number for each hour of the day yesterday 0000-2300. • Add up all the numbers from dialysate infused (1B) • Add up all the numbers in the patient fluid removal (3A)

CRRT Calculation Cont… • Take (1B) + (3A) = TOTAL • TOTAL x BUN Avg = XYZ • Take (XYZ/100/1000) + 4 + 1.5 (g of nitrogen lost per 24 hrs) = g nitrogen • G nitrogen x 6.25 (6.25g nitrogen in 1g protein) = g protein • Can add g nitrogen + 2, then multiply by 6.25 to make a protein range

Initial Nutrition Intervention

Significant Labs at Initial Assessment • No prealbumin or CRP • Elevated LFTs • K+/P/Mg WNL

Nutrition RequirementsEstimated Needs • Energy • REE per Penn State Equation: 3281 x 0.55-0.65 for sepsis/obesity = 1804-2133 kcal (22-26 kcal/81 kg IBW) • Protein • 162-203 gm protein (2-2.5 g/81 kg IBW) • 24 hr CRRT info not available • Maintenance Fluids • 500-1000 mL + UOP or per MD given CRRT

Nutrition Care Process • Diagnosis: PT with inadequate nutrient intake R/T NPO status, hemodynamic instability/sepsis AEB diet Rx and no nutrient intake since admission. • Intervention Goal: Pt to receive > 75% of estimated nutrient needs with acceptable tolerance.

Nutrition Plan/ Recommendations • Start senna/colace. • LBM prior to admission • D/C coretrack and place NJ tube via IR if/when possible. • pancreatitis • REC once on 2 pressors or less, start Peptamen AF @ 10 mL/hr x 24 hrs. • why the low goal rate? • Continue calcium gluconate. • Note low ionized Ca • REC check prealbumin along with CRP to get baseline, then weekly to trend and to better assess nutrition status. • Check weight daily to monitor trends/dry weight.

Acute Pancreatitis

Gallstone Pancreatitis • Gallstone pancreatitis is inflammation of the pancreas that results from blockage of the pancreatic duct by a gallstone.  • 15% of cases of acute pancreatitis are either idiopathic or from biliary disease. • Progression of disease • Obstruction blocks enzymes • Pancreatic enzymes • Amylase and lipase

LFTs • Obstructed outflow • Elevated alkaline phosphatase, ALT, AST, and bilirubin • ALT >150 IU/L • C.P. had these elevated liver enzymes • Progress note: • MD noted LFTs had begun to trend down, which suggests the gallstone had passed.

Risk Factors • Female gender • Obesity • Older age • High cholesterol levels • Rapid weight loss • Diabetes • Pregnancy

Severe acute pancreatitis • The mean hospital length of stay is approximately 1 month • Organ failure occurs in at least 16% to 33% of cases, and infection complicates the disease course in 30% to 50%. • Mortality alone is 19% to 30%, but may range up to as high as 80% if organ failure or sepsis complicates the disease process.

Treatment • Pancreatic Rest • Severe pancreatitis • Nutrition support • Fix underlying cause

PN vs EN • Need for pancreatic rest can still be achieved with EN • EN reduces: • infectious morbidity • hospital length of stay • cost for nutrition support • need for surgical intervention • multiple organ failure and mortality • Feeding the gut

Early Enteral Feeds • Feeding within 24-48 hours showed the most outcome benefits • EN should be initiated as soon fluid resuscitation is complete • Less gut permeability • Decreased release of inflammatory cytokines • Overall decrease in infectious morbidity and hospital length of stay

Tube Feed Placement and Formula • NJ preferred with severe acute pancreatitis • 40 cm or more below the Ligament of Treitz • Coretrackvs IR placement • Peptide based formula • Peptamen AF • Other options • Nepro • Standard formula (2 cal)

Nutrition Goals • Increased energy expenditure and protein catabolism • Calories: 22-47 kcal/kg or injury factor of 1.3-1.5 x REEProtein: 1.4-2 g/kg protein • End goal of low fat PO diet

Patient progress • Gallstone passed • Staged wounds • Stage 2 • REC nephrocaps • Feeding at goal rate • Peptamen @ 65 mL/hr + Prosource TID • Lipase back to normal

Complications • (1/26) Decreased goal rate to Peptamen @ 40 mL/hr • Diarrhea per MD; improved when tube feeds were held • Placement of FT still not optimal • (1/24) Imaging showed tip in duodenum, (1/25) imaging showed poorly visualized tip of the feeding tube • Left in duodenum because lipase, LFTs decreased • REC NJ for best tolerance • Couldn’t wean off ventilator, vasopressors or CRRT • Sepsis, necrotizing pancreatitis or both.

Patient Progress Cont. • Moved to SICU and put on surgical team service • Necrotizing pancreatitis • REC pancreatic enzymes-creon for better absorption • REC goal rate @ 65 mL/hr + Prosource TID • Necrosectomy (1/30) and repeat necrosectomy (1/31) • (2/4) Abdominal washout, debridement of necrotic pancreas, cholecystectomy, and temporary abdominal closure.

Monitoring/Evaluation • Labs • Prealbumin/CRP

Monitoring/Evaluation Cont • Labs • Lipase/amylase • Renal labs now switched to iHD • Wounds • Remains staged 2; improving • Wt/fluids • D/C CRRT, trending up

Weight and Fluid Trends

End Nutrition Goals • NJ feeding of Peptamen @ 65 mL/hr x 24 hrs + prosource TID • ADAT to PO low fat diet • Possible need for pancreatic enzymes, regular diet

References 1. The A.S.P.E.N. nutrition support core curriculum: A case-based approach-The adult patient. ASPEN. 2007. 2. Inotropes and vasopressors. Contemporary review in cardiovascular medicine. Circulation 2008. 3. Wells DL. Provision of enteral nutrition during casopressor therapy for hemodynamic instability: An evidence-based review. Nutrition in Clinical Practice. 2012; 27:521-526. 4. Choi Y, Silverman WB. Biliary tract disorders, gallbladder disorders, and gallstone pancreatitis. American College of Gastroenterology. 2013. 5. Norman JG. New approaches to acute pancreatitis: role of inflammatory mediators. Digestion. 1999;60(suppl 1): 57-60.

References Cont 6. Ed. Gottschlich, MM. The A.S.P.E.N nutrition support core curriculum: A case-based approach-The adult patient. ASPEN. 2007. 7. Petrov MS, Kukosh MV, Emelyanov NV. A randomized controlled trial of enteral versus parenteral feeding in patients with predicted severe acute pancreatitis shows a significant reduction in mortality and in infected pancreatic complications with total enteral nutrition. Dig Surg. 2006;23:336-344. 8. Eckerwall GE, Axelsson JB, Andersson RG. Early nasogastric feeding in predicted severe acute pancreatitis: a clinical, randomized study. Ann Surg. 2006;244:959-967. 9. Casas M, Mora J, Fort E, et al. Total enteral nutrition vs. total parenteral nutrition in patients with severe acute pancreatitis. Rev EspEnferm Dig. 2007;99:264-269.

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Acute pancreatitis is an important cause of acute upper abdominal pain. Because its clinical features are similar to a number of other acute illnesses, it is difficult to make a diagnosis only on the basis of symptoms and signs. The diagnosis of acute pancreatitis is based on 2 of the following 3 criteria: (1) abdominal pain consistent with pancreatitis, (2) serum lipase and/or amylase ≥3 times the upper limit of normal, and (3) characteristic findings from abdominal imaging. The sensitivity and specificity of lipase in diagnosing acute pancreatitis are undisputed. However, normal lipase level should not exclude a pancreatitis diagnosis. In patients with atypical pancreatitis presentation, imaging is needed. We experienced two cases of acute pancreatitis associated with normal serum enzyme levels. Both patients were diagnosed based on clinical and radiological evidence. They were successfully treated with intravenous fluids and analgesics with clinical and laboratory improvement. The importance of this case series is the unlikely presentation of acute pancreatitis. We believe that more research is needed to determine the exact proportion of acute pancreatitis patients who first present with normal serum lipase, since similar cases have been seen in case reports.

Acute pancreatitis (AP), an inflammatory disorder of the pancreas, is the leading cause of admission to hospital for gastrointestinal disorders in the USA and many other countries [ 1 ]. The diagnosis of AP requires 2 of the following 3 features: (1) abdominal pain characteristic of AP, (2) serum amylase and/or lipase ≥3 times the upper limit of normal, and (3) characteristic findings of AP on CT scan [ 2 ]. During AP, serum lipase increases within 4–8 h, peaks at 24 h, and remains elevated for 1–2 weeks, with a half-life between 7 and 14 h [ 3 ]. Lipase is more sensitive and specific than amylase in diagnosing AP, with a negative predictive value of 94–100% [ 4 ]. AP in the setting of normal amylase and lipase has been rarely described in the literature. However, the absence of elevated lipase should not exclude its diagnosis [ 5 ]. In patients with abdominal pain characteristic of AP and serum enzyme levels that are normal or <3 times the upper limit of normal, CT scanning provides an accurate confirmation of the diagnosis and offers an excellent anatomic and morphologic representation of the pancreas and peripancreatic tissue [ 2, 6 ]. We report a case series of two patients who presented with epigastric abdominal pain and were found to have AP by abdominal CT scan despite having normal serum amylase and lipase levels.

A 40-year-old white female with a past medical history of hypertension and bipolar disorder presented with a few hours of severe sharp epigastric abdominal pain radiating to the back associated with nausea and vomiting. The patient denied any history of pancreatitis, consuming alcohol, or illegal drug abuse. No new medication had recently been started, and there was no history of abdominal trauma. She had had a cholecystectomy in 2004. On physical examination, she was afebrile, had a heart rate of 105 beats/min, and a blood pressure of 132/84 mm Hg. She was in severe distress due to pain with severe epigastric tenderness. The remainder of her physical exam was normal.

Her laboratory tests on admission revealed a WBC of 22.1 × 10 3 /μL with neutrophils 87%, a hemoglobin level of 14.0 g/dL, and platelets 380 × 10 3 /μL. Her comprehensive metabolic panel was unremarkable except for a potassium level of 2.7 mEq/L. She had a negative pregnancy test and a normal urine drug screen. Her serum amylase was 31 IU/L (normal ref: 20–160) and lipase was 14 IU/L (normal ref: 8–78).

Since the patient was in severe pain with no clear diagnosis, a CT scan of her abdomen with intravenous contrast was done in the emergency room. The CT scan showed fat stranding in the pancreatic head consistent with pancreatitis and reactive thickening in the duodenum (Fig.  1 ). The patient was admitted to the floor and kept nothing by mouth. She was treated with intravenous fluids, analgesics, potassium supplement, and antiemetics. On the next morning, repeated measurements of her amylase and lipase were still within normal limits. We checked her triglyceride level and it was 53 mg/dL. Her symptoms continued to improve during her course of hospitalization, and her leukocytosis was resolved without the use of antibiotics. She was discharged home on day 3.

An abdominal CT scan of case 1 showed fat stranding in the pancreatic head consistent with pancreatitis and reactive thickening in the duodenum (white arrow).

A 45-year-old white male with a history of alcohol abuse presented with severe epigastric abdominal pain that lasted for approximately 12 h. The pain was sudden in onset, radiating to the back, and associated with nausea and vomiting. His last alcoholic drink was 1 day prior to presentation. He had had a cholecystectomy 4 years ago. On physical examination, his vital signs were within normal limits with epigastric tenderness.

His laboratory tests on admission revealed a WBC of 12.6 × 10 3 /μL, a hemoglobin level of 13.6 g/dL, and platelets 172 × 10 3 /μL. His comprehensive metabolic panel was remarkable for AST 98 IU/L (normal ref: 8–42) and ALT 43 IU/L (normal ref: 7–40). He had a negative viral hepatitis panel and a normal urine drug screen. His serum amylase and lipase levels were 55 IU/L and 28 IU/L, respectively. A CT scan of the abdomen with intravenous contrast showed a stranding edema within the peripancreatic fat suggestive of AP (Fig.  2 ). The patient was treated with intravenous fluid, analgesics, and antiemetics. His serum amylase and lipase levels were normal throughout the admission. Two days later, he was discharged home with complete resolution of his symptoms.

An abdominal CT scan of case 2 showed a stranding edema within the peripancreatic fat suggestive of acute pancreatitis (yellow arrow).

AP, an inflammatory disorder of the pancreas, is the leading cause of admission to hospital for gastrointestinal disorders in the USA and many other countries [ 1 ]. It has been estimated that in the United States there are 210,000 admissions for AP each year [ 2 ]. AP is a potentially fatal disease with a mortality rate of 5% in the United States. Given the dangers of misdiagnosing pancreatitis, awareness of unusual presentations is paramount [ 2, 5 ]. Alcohol use, gallstones, hypertriglyceridemia, hypercalcemia, medications, endoscopic retrograde cholangiopancreatography, and trauma account for most cases of AP; however, approximately 20% remain idiopathic [ 7 ]. Most patients with AP experience abdominal pain that is located generally in the epigastrium, and radiates to the back in approximately half of the cases. The onset may be swift with pain reaching maximum intensity within 30 min, frequently unbearable, and characteristically persisting for more than 24 h without relief. The pain is often associated with nausea and/or vomiting [ 2 ].

The diagnosis of AP requires the presence of 2 of the following 3 criteria: (1) characteristic abdominal pain, (2) serum amylase and/or lipase ≥3 times the upper limit of normal, and (3) CT scan findings compatible with AP [ 2, 7 ]. In AP, usually, serum lipase increases within 4–8 h after onset of symptoms, peaks at 24 h, and returns to normal after 8–14 days [ 3, 7 ]. The sensitivity and specificity of amylase and lipase are reported to be considerably dependent on the detection method used, ranging from 70 to 100% and from 33 to 89% for serum amylase, and from 74 to 100% and from 34 to 100% for serum lipase, respectively [ 6 ]. Several studies have reported the negative predictive value of serum lipase in diagnosing AP to be 94–100% [ 4, 7 ]. Factors that can lead to normal amylase and lipase values are hypertriglyceridemia, extensive pancreatic necrosis (acute fulminant or acute-on-chronic pancreatitis) [ 6 ], or very early pancreatitis when inflammation has not led to a lot of pancreatic acinar cell destruction yet (which was not the case in our patients as repeated measurements of the enzyme levels were still normal) [ 8 ]. Serum trypsinogen activation peptide and trypsinogen-2 are more specific early markers for pancreatitis but are expensive and not readily available [ 7, 8 ].

A contrast-enhanced CT scan is the best imaging technique to diagnose pancreatitis in patients with atypical presentations, exclude other etiologies of acute abdominal pain, evaluate the severity, and identify complications of AP [ 2, 6, 8 ]. The clinical severity of AP is stratified into 3 categories according to the revised Atlanta classification: mild (no organ failure), moderately severe (transient organ failure <48 h), and severe (persistent organ failure >48 h). The treatment of AP consists of fluid resuscitation, pain management, and nutritional support [ 1, 2, 7 ].

Relying solely on high serum lipase and/or amylase levels to establish the diagnosis of AP is reasonable, but increased awareness is needed in the setting of AP with normal enzyme levels. An abdominal CT scan is essential in establishing the diagnosis of AP in patients with atypical presentations.

The authors wish to thank the patients who kindly gave consent for their cases to be presented in this report.

The authors declare that none of them has a conflict of interest regarding the publication of this paper. There were no funding sources.

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• Management of Pancreatitis

Management and Treatment of Acute Pancreatitis

*Please note: This slide set represents a visual interpretation and is not intended to provide, nor substitute as, medical and/or clinical advice.

In acute pancreatitis, the digestive enzymes are activated prematurely and start to attack the pancreas. This causes inflammation, leading to symptoms that are often severe enough to require hospitalization.

Alcohol abuse and gallstones are the main triggers of acute pancreatitis.

Treatment options for acute pancreatitis depend on the severity of the condition. Initial treatment of acute pancreatitis is supportive. The focus is on resting the pancreas and managing the pain.

Since the pancreas is stimulated by eating, food and drinks are restricted and the patient is put on intravenous fluids to help maintain hydration. Medication for pain and vomiting may also be administered intravenously.

Most people who develop acute pancreatitis only require a few days of hospitalization.

However, about 1 in 10 cases are more serious and require treatment in the intensive care unit.

The kidneys and lungs can be affected, which may require dialysis or placement of a breathing tube.

Fluid-filled sacks (or pseudocysts) can also form inside the pancreas. If they become infected or cause symptoms like abdominal pain, gastric outlet obstruction (nausea and vomiting) or biliary obstruction (elevation in liver test), they will require drainage.

Surgery is sometimes needed to remove dead or infected pancreatic tissue or tissue around the pancreas.

Some specialised hospitals can drain fluid without surgery, using endoscopic methods where the drainage tube is inserted into the stomach or small bowel, or using a percutaneous procedure where a small drainage tube is inserted through the skin.

If gall bladder disease was the root cause of the pancreatitis, then the gall bladder may also be removed to prevent future attacks.

Most people recover from acute pancreatitis and are offered specific lifestyle advice to prevent future attacks, which can lead to a chronic, or on-going, form of the disease.

Patients are advised to avoid alcohol and high fat foods, stop smoking, eat a varied diet that is rich in fruits and vegetables, and keep triglyceride levels in the normal range. Medications that put stress on the pancreas must also be avoided.

However some people never recover fully from an attack. In rare cases, the pancreas becomes so damaged that it no longer functions properly. This is called pancreatic insufficiency.

In rare occasions, the pancreatitis can be so severe, that may lead to pancreatic insufficiency, diet is further restricted and life-long medication (pancreatic enzyme supplementation) is required.

Slide Show - Management and Treatment of Acute Pancreatitis

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Other Sections in this Module:

Management and Treatment of Chronic Pancreatitis

Other Modules:

Understanding Pancreatitis

Pancreatic Cancer

Nutrition and PERT

Nutrition and Chronic Pancreatitis

Pancreatic Surgery

Pancreatitis in Kids and Teens

Familial Chylomicronemia Syndrome

Caring for Caregivers

This educational activity has been developed by: The National Pancreas Foundation and Mechanisms in Medicine Inc.

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Pathophysiology and Clinical Presentation

(Miller, 2006)

Normal Physiology of the Pancreas

The pancreas is an endocrine and exocrine gland that produces hormones and digestive enzymes. It is located behind the stomach and between the spleen and duodenum, housing the Islets of Langerhans, which contain four types of hormone-secreting cells. These cells are responsible for the regulation of carbohydrate, fat, and protein metabolism, as well as the synthesis of insulin, glucagon, somatostatin, and pancreatic polypeptides (McCance & Huether, 2014).

Pathophysiology of Pancreatitis 

Pancreatitis is an obstructive disease in which the backup of pancreatic secretions causes the activation and release of enzymes within the pancreatic acinar cells. When these enzymes are activated, they cause the autodigestion of pancreatic cells and tissues, in turn, causing inflammation, fat and coagulative necrosis, the formation of pseudocysts, and vascular damage (McCance & Huether, 2014).

Classification: Acute or Chronic Pancreatitis

Pancreatitis can be classed in two forms: acute pancreatitis or chronic pancreatitis, which is the progressive form of untreated acute pancreatitis. In severe cases of acute pancreatitis, vasoactive peptides and pro-inflammatory cytokines are released into the bloodstream, activating leukocytes and causing injury to vessel walls, coagulation abnormalities, hypotension, and shock. These systemic effects can lead to acute respiratory distress syndrome (ARDS), systemic inflammatory response syndrome (SIRS), heart failure, renal failure, and coagulopathies. If the translocation of intestinal bacteria occurs, sepsis or peritonitis can result. As a response to the systemic inflammation, anti-inflammatory cytokines and specific cytokine inhibitors are produced, which can increase the body’s risk for infection. Without intervention, acute pancreatitis can cause pancreatic fibrosis, strictures, and duct obstruction, leading to chronic pancreatitis (McCance & Huether, 2014).

(Foto, 2014)

Clinical Manifestations

Epigastric or mid-abdominal pain radiating to the back

Fever and leukocytosis

Abdominal distension, nausea, and vomiting

Hypotension

Hyperglycemia

Tachycardia

Hypovolemia

Impaired renal function

Multi-system organ failure

Lab Markers

Serum Amylase above 140 U/L (Normal range: 23-85 U/L)

Serum Lipase above 160 U/L (Normal range: 0-160 U/L)

(Mymediasite365mymedi, 2017)

Mr. Walker’s Clinical Manifestations

• Pain: acute, sudden onset of epigastric pain, present after meals
• Strong family history of pancreas issues
• History of excessive drinking
• Vitals: tachycardia, fever, high pain
• Exam: abdominal rebound tenderness
• Labs: elevated WBC, amylase, lipase, C-reactive protein (CRP)
• Diagnostic imaging: showed generalized pancreatic inflammation and presence of gallstones

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Acute pancreatitis – case discussion.

Last modified: Jun 12, 2016

Cases of Acute Pancreatitis

32 years old male came to emergency department with complaint of:

• Upper abdominal pain X 3 days
• Vomiting X 2 episode (3 days back)
• Yellowish discoloration of urine and decreased urine output X 2 days

K/C/O hypertension and not under medication; Normal bowel habit; No h/o LOC/abnormal body movement; No fever; No cough/difficulty breathing

G/C: agonized

Icterus: Present

• Tenderness over epigastrium and right hypochondrium
• Bowel sound present

Chest: B/L NVBS, B/L equal air entry, no added sounds

CVS: S1 S2 M0

CNS: Grossly Intact

Lab Reports:

1. Serum Amylase: 1524 IU/L (Normal 40-140 IU/L ; Reference – Medscape)

2.  Serum Lipase: 396 IU/L (Normal 0-50 IU/L; Reference – Medscape)

3.  Serum Creatinine: 5.1 mg/dl (Normal 0.5-1.2 mg/dl; Reference – Medscape)

4. BUN: 18.9 mg/dl (Normal 3-20 mg/dl; Reference – Medscape)

5.  TLC: 19,900/cu.mm (Normal 4,000-12,000/cu.mm)

6.  DLC: Neutrophil 94% (Normal 40-60%) ; Lymphocyte 6% (Normal 20-40%)

7. Hemoglobin: 17.1 g/dl (Normal 13-18 g/dl)

8.  Platelets: 81,000/cu.mm (Normal 150,000-400,000/cu.mm)

Other Investigations:

1. INR: 1.07

2.  Na+: 138 mEq/L

3.  K+: 4.5 mEq/L

4.  Total Bilirubin: 6.6 mg/dl

5.  Direct Bilirubin: 2.2 mg/dl

6.  SGOT (AST): 34 IU/L

7.  SGPT (ALT): 20 IU/L

USG abdomen:

• Bulky pancreas with localized pancreatic collection likely pancreatitis
• Hepatomegaly and Splenomegaly
• Gall bladder sludge
• Bilateral increased cortical echo texture
• Left sided pleural effusion

CT Abdomen Revealed:

• Finding consistent with ascites with acute severe pancreatitis (modified CT Severity index 4+2+2=8 with moderate ascites)
• Mild hepatomegaly with fatty change in liver
• Minimal Left sided pleural effusion with Left lower lobe atelectasis

Severe Acute Pancreatitis (Alcoholic) with Acute Renal Failure

Disposition from ER:

Admitted to ICU after under following medications (after consultation from surgery and nephrology department):

• Inj. Imipenem 50mg iv stat then 250mg iv BD
• Inj. NS 3 pint IV over 24 hrs
• Inj. 5% dextrose 2 pint IV over 24 hrs
• Inj. Optineuron in 1 pint of NS OD
• Inj. Tramadol 50mg IV SOS
• Strict Renal Diet
• Inj. Tramadol replaced by Inj. Pethidine 50 mg IV SOS
• Regular vitals monitoring done
• Input/Output Charting done
• GRBS 4 hourly
• CVP Insertion done

Lab values some days later:

38 years old female came to ER with chief complaint of: Abdominal pain X 8 hours

Abdominal pain since 2 days – was intermittent but constant and more severe since last 8 hours. Pain was on Epigastric region and Left iliac fossa. There was a h/o 1 episode of non-bilious vomiting in the morning. There was a h/o decreased urinary frequency and passage of dark colored urine. Bowel habit was normal.

LMP: 2072/05/29

G/C: Agonized; Lying still on bed

Pallor: Present; Icterus: Absent

• Guarding present
• Tenderness Diffuse but more marked on Epigastric region and Left Iliac fossa
• Rebound tenderness and Epigastric region and Left Iliac fossa
• Bowel sound: Present

Chest, CVS, CNS: NAD

Provisional diagnosis:  Acute abdomen – to rule out hollow viscus perforation

Differential diagnoses:

• Acute Pancreatitis
• Acute Cholecystitis
• Inferior wall MI
• Peptic Ulcer Disease
• Serum Amylase: 2,399 IU/L
• TLC: 14,100/cu.mm
• DLC: Neutrophils 87%; Lymphocytes 12%; Eosinophil 1%
• Platelets: 3,05,000/cu.mm
• Urine R/E: All parameters within normal limits
• UPT: Negative
• Serum Calcium: 8.1 mg/dl
• LFTs: Total Bilirubin 2.1 mg/dl; Direct Bilirubin: 1.3 mg/dl; ALT: 117 U/L; AST 219 U/L; ALP 307 U/L

Abdominal X-ray showing both domes of diaphragms:

• No gas under diaphragm (perforation ruled out)
• No significant abnormalities detected
• Cholelithiasis (max 10 mm) with slightly distended Gall bladder
• Dilated proximal CBD (max 12 mm); Mild IHBD dilation
• Linear calcification in segment VIII of liver
• Bilateral minimal pleural effusion

Diagnosis:  Acute Mild Biliary Pancreatitis with Cholelithiasis with ? Choledocholithiasis

Management at ER:

• IV cannulation done
• Patient kept NPO
• Inj. Tramadol 50 mg IV Stat
• Inj. Ondem 4 mg IV Stat
• Inj. Pantoprazole 40 mg IV Stat
• Inj. Pethidine 50 mg and Inj. Phenargan 25 mg IM Stat (After 1 hour)
• Inj. NS 1 Pint over 1 hour
• Inj. NS 1 Pint over 2 hours

Admitted to Surgical ward after consultation with following advices:

• Counselling for probability of requirement of ICU support
• NPO and Foley catheterization
• Inj. NS 3 Pint and Inj. 5% DW 3 Pint over 24 hours
• Inj. Ceftriaxone 1 gm IV BD and Inj. Metronidazole 500 mg IV BD
• Inj. Pethidine 50 mg + Phenargan 25 mg IM TID
• Inj. Pantoprazole 40 mg IV BD
• Monitoring of Urine output

After Admission to Surgical Ward:

Added medications:

• 3 doses of Vitamin K
• Ketorolac instead of Pethidine

Lab Reports after few days:

• Amylase: 1408 IU/L
• Calcium: 8.3 mg/dl
• Total Bilirubin: 2 mg/dl; Direct Bilirubin: 1.1 mg/dl; AST: 77 IU/L; ALT 74 IU/L; ALP 191 IU/L

Cholecystectomy done:

• Due to poor visualization of the Calot’s triangle, Laparscopic cholecystectomy was converted into acute cholecystectomy
• Gall bladder distended
• Common Bile Duct dilated
• 2 stones – faceted 2X2 cm size

Definition of Acute Pancreatitis

Reversible process characterized by:

• Interstitial edema
• Infiltration by acute inflammatory cells
• Necrosis, apoptosis, and hemorrhage

Diagnosis of Acute Pancreatitis

Requires at least 2 of 3 of the following criteria:

• Acute Pancreatitis suggestive abdominal pain
• Serum amylase and/or lipase activity ≥ 3 X the upper limit of normal
• Acute Pancreatitis suggestive/compatible imaging

Diagnosis of Acute Recurrent Pancreatitis

Requires at least two distinct episodes of AP along with:

• Complete resolution of pain (≥1-month pain-free interval between the diagnoses of Acute Pancreatitis) OR
• Complete normalization of serum pancreatic enzyme levels (amylase and lipase), before the subsequent episode of Acute Pancreatitis is diagnosed, along with complete resolution of pain symptoms, irrespective of a specific time interval between Acute Pancreatitis episodes

Etiology of Acute Pancreatitis

Mnemonic: GET SMASHED

• G:  Gall stones *
• E:  Ethanol *
• T:  Trauma *
• S:  Surgical (Post-operative*), Scorpion sting (Tityus trinitatis)
• M:  Mumps and Coxsackie infection, Mysterious (Idiopathic *)
• A:  Autoimmune (Polyarteritis Nodosa)
• S:  SPINK-1 (Serine Protease Inhibitor Kajal Type 1), PRSS1 mutation (cationic trypsinogen) i.e. Genetic
• H:  Hypertriglyceridemia *, Hypercalcemia, Hypothermia
• D:  Drugs *(Corticosteroids, Thiazides, Valproate, Azathioprine, Estrogen, Sulfonamides, Tetracycline, 6-Mercaptopurine, anti-HIV medications)

How gallstones causes pancreatitis?

Theory 1: Reflux of bile into the pancreas due to obstruction at Ampulla of Vater

Theory 2: Intraductal hypertension due to outflow blockade at pancreatic duct and penetration of secretion into interstitial tissue

How alcohol causes pancreatitis?

Recommendations for Etiological Diagnosis:

Pathophysiology of Acute Pancreatitis

1st Phase:  

Premature activation of trypsin within pancreatic acinar cell leading to activation of varieties of injurious pancreatic enzymes.

Intrapancreatic inflammation

Extrapancreatic inflammation including ARDS

Co-localization theory (Pathogenesis at Cellular level):

• Ductal Obstruction
• Improper co-localization of lysosomal hydrolases (Cathepsin-B) with zymogens (Trypsinogen) into vacuolar structure within pancreatic acinar cell
• Activation of digestive enzyme zymogen (trypsinogen to trypsin)
• Activation of other digestive enzyme zymogens
• Initiation of auto-digestion within pancreas

Symptoms of Acute Pancreatitis

• L ocation: Upper abdomen/Epigastric
• L ength (Duration): Hours to a day
• I ntensity: Gradually becomes severe (not relieved by ordinary analgesics)
• Q uality: Constant and Dull
• O nset: Sudden
• R adiation: Back
• A ssociated symptoms: Nausea, Vomiting, Anorexia, Abdominal distension
• A ggravating factors: Eating or drinking (specially alcohol)
• A lleviating factors: Leaning forward, Curl up (Fetal position)

Signs of Acute Pancreatitis

General condition:  Distressed, Anxious

Vitals:  Fever, Tachycardia, Hypotension, Tachypnea

Cardinals:  Jaundice, Cyanosis, Dehydration

Respiratory:  Signs of pleural effusion – usually left sided (sometimes)

Abdominal:  Marked epigastric tenderness with voluntary and involuntary guarding +/- rigidity, Abdominal distension, Reduced bowel sound, Palpable pseudocyst (sometimes)

Uncommon signs associated with severe necrotizing pancreatitis:

• Cullen’s sign (Periumbilical discoloration due to peritoneal hemorrhage)
• Grey-Turner’s sign (Flank discoloration due to retroperitoneal hemorrhage)
• Fox’s sign (Discoloration below inguinal ligament or at the base of penis)
• Erythematous skin nodules (Subcutaneous fat necrosis)

Differential diagnosis of Acute Epigastric Pain

Some other eponymous signs

1.  Korte’s sign: painful resistance at a lumbar bar in a epigastric area on 6–7 cm above umbilicus (location of head of pancreas)

2.  Voskresynskyy’s sign: absence of pulsation of abdominal aorta in an epigastric area

3.  Mayo-Robson’s sign: left consto-vertebral angle (CVA) tenderness

4.  Rozdolskyy’s sign: percussion tenderness above pancreas

Frequency of signs and symptoms in Acute Pancreatitis

• Abdominal pain: 95–100%
• Epigastric tenderness: 95–100%
• Nausea and vomiting: 70–90%
• Low-grade fever: 70–85%
• Hypotension: 20–40%
• Jaundice: 30%
• Grey Turner/Cullen sign: <5%

Complications of Acute Pancreatitis

Local complications of acute pancreatitis.

Pancreatic necrosis is defined as diffuse or focal areas of nonviable pancreatic parenchyma > 3 cm in size or > 30% of the pancreas

Pancreatic fluid collections:

• Pancreatic abscess
• Pancreatic pseudocyst (Pain, rupture, hemorrhage, infection, obstruction of GIT)
• Pancreatic pseudoaneurysm (Erosion of adjacent artery by pseudocyst)

Pancreatic ascites

• Disruption of main pancreatic duct
• Leaking pseudocyst

Involvement of contiguous organs  by necrotizing pancreatitis

• Massive intraperitoneal hemorrhage
• Thrombosis of blood vessels (splenic vein i.e. sinistral portal HTN, portal vein)
• Bowel obstruction

Obstructive Jaundice

Systemic Complications of Acute Pancreatitis

Pulmonary:  Pleural effusion, Atelectasis, Mediastinal abscess, Pneumonitis, ARDS

Cardiovascular:  Hypotension (Hypovolemia), Sudden death, Pericardial effusion

Hematologic:  Disseminated Intravascular Coagulation (DIC)

Gastrointestinal hemorrhage:  Peptic ulcer disease, Erosive gastritis, Hemorrhagic pancreatic necrosis with erosion into major blood vessels, Portal vein thrombosis (Variceal hemorrhages)

Renal:  Oliguria, Azotemia, Renal artery/vein thrombosis, Acute Tubular Necrosis

Metabolic:  Hyperglycemia, Hypocalcemia, Encephalopathy, Sudden blindness (Purtscher’s retinopathy)

CNS:  Psychosis, Fat emboli

Timeline of complications in Acute Pancreatitis

Period 1 (Hemodynamic violations and pancreatogenic shock): Initial 2-3 days

Period 2 (Insufficiency of parenchymatous organs i.e. MODS): 3 rd -7 th days

Period 3 ( Postnecrosis dystrophic and festering complications): 1-2 weeks after disease onset i.e. Regenerative changes begin in the background of necrosis

• Parapancreatic infiltrate and cysts
• Cystic fibrosis of pancreas
• Aseptic retroperitoneal phlegmon
• Infection of pancreatic necrosis
• Erosive bleeding
• External and internal fistula

Lab Studies in Acute Pancreatitis

1.  Serum amylase and lipase:  ↑ by  3X  of upper-limit is diagnostic

• ↑ ALT and AST (ALT ↑ by around 3X i.e. > 150 IU/L  is diagnostic of gall stone pancreatitis)
• ↑ALP, ↑bilirubin, ↓albumin

3.  RFTs:  BUN and Creatinine (to rule out renal failure)

4.  CBC and HCt :

• Leukocytosis with shift to left (Inflammation or SIRS)
• ↑ HCt  (Hemoconcentration due to fluid sequestration)
• ↓ HCt  (Dehydration or Hemorrhage)

5.  Blood biochemistry:

• Blood sugar:  may ↑ due to insulin producing Beta-cell dysfunction
• Serum calcium:  ↓ (due to  hypoalbuminemia  or fat necrosis) or ↑ (if hypercalcemia is etiology)
• Lipid profile:  to rule out hypertriglyceridemia as the cause

6.  ABG:  every 12 hrs for 1st 3 days (to monitor oxygenation and  acid-base status )

7.  Other:  CRP, Trypsin, Trypsinogen-2, LDH, Phospholipase A

Lipase  is more specific than amylase (hence preferred). Lipase rises within 4-8 hours of pain onset. Amylase rises within 6 hours of pain onset. Amylase may be normal during acute inflammation due to significant pancreatic destruction. Amylase normalizes in blood by 3-5 days due to increased excretion in urine. Lipase remains elevated for 7-10 days. Other causes of ↑ amylase:   Macroamylasemia , Renal failure, Mumps parotitis , ERCP induced, Esophageal perforation, Pregnancy

Imaging Studies in Acute Pancreatitis

Plain Chest X-Ray:  Pleural effusion, ARDS (Atelectasis and Basal infiltrates), Elevation of left diaphragm

Plain Abdomina X-Ray (erect):

• To rule out perforated peptic ulcer
• Sentinel loop sign, Colon ‘cut-off’ sign, Renal halo sign
• May show gallstone, pancreatic calcification

Abdominal USG:  Can detect gallstones, biliary obstruction, pseudocyst formation

CT abdomen:  may be required if diagnosis uncertain, to rule out and find degree of: Peripancreatic collection; Necrosis and Abscess

CT Guidelines for Acute Pancreatitis

1. In the acute setting (<48–72 hours), CECT should not be performed when a typical clinical presentation and unequivocal elevations of amylase and lipase are present.

2. In the acute setting, CECT should be performed if the clinical presentation and amylase and lipase levels are equivocal.

3. Early (within the first 72 hours) imaging with CT may underestimate the full severity of the disease.

4. CECT after 48–72 hours will detect pancreatic and peripancreatic necrosis as well as acute pancreatic fluid collections.

5. Delayed CECT (>7–21 days after the onset of symptoms) is very effective in assessing severity and will guide management, including image-guided aspiration and/or drainage as well as other forms of minimally invasive drainage.

6. CECT should be performed when there is a significant deterioration of the patient’s condition, including an acute drop in hemoglobin and hematocrit, tachycardia, and hypotension, an abrupt change in fever, or leukocytosis.

Colon Cut-off sign

• Distended proximal colon + Splenic flexure narrowing +  Collapse of descending colon starting from region of pancreatic inflammation
• Extra-pancreatic extension of inflammation into phrenico-colic ligament resulting in splenic flexure spasm
• D/D: IBD, Ca. colon, Mesenteric ischemia

Sentinel Loop sign

• Localized isolated ileus seen near the site of injured viscus or inflamed organ
• Body’s effort to localize traumatic or inflamed lesions
• Localized paralysis followed by gas accumulation
• Sentinel =  A soldier stationed as a guard to challenge all comers and prevent a surprise attack
• Site helpful in diagnosis

Renal Halo sign

• Peripancreatic inflammation extension into pararenal space
• Radiolucent halo of inflammation in anterior pararenal space contrasts with perirenal fat; more common on left side

Acute Pancreatitis in Ultrasonography (USG)

• Pancreatic gland (P) is edematous and there is a fluid visible in front of the pancreas (Black anechogenic strip marked by arrows).
• Other anatomical structures we see splenic vein (SV), aorta (A) and inferior vena cava (IVC).

Pancreatic Pseudocyst in USG

• Regular anechogenic mass in contact to the head of pancreas
• A pancreatic tumor may look similar but is not as anechogenic as a pseudocyst

SCORINGS FOR ACUTE PANCREATITIS

Modified ct score index (ctsi) for acute pancreatitis.

A) Pancreatic inflammation

0: normal pancreas

2: intrinsic pancreatic abnormalities with or without inflammatory changes in peripancreatic fat

4: pancreatic or peripancreatic fluid collection or peripancreatic fat necrosis

B) Pancreatic necrosis

2: 30% or less

4: more than 30%

C) Extrapancreatic complications

2: one or more of pleural effusion, ascites, vascular complications, parenchymal complications and or gastrointestinal involvement

INTERPRETATION:

Total points out of 10 to grade pancreatitis:

• 4-7: moderate
• 8-10: severe

Ranson’s score

Modified Glasgow Score

Atlanta Score for Acute Pancreatitis

BISAP score (Bedside Index for Severity in Acute Pancreatitis)

Patients with a BISAP Score >0 had an increasing risk of mortality, with mortality increasing significantly with a score of 3 or greater. A score of 5 had a mortality rate of 22%.

Findings associated with Severe course

• Platelets ≤100,000/mm3
• Fibrinogen ≤100 mg/dL
• Fibrin split products >80μg/mL
• Severe metabolic disturbance (serum calcium ≤7.5 mg/dL)
• CRP > 150 mg/L within 1st 72 hours

How BMI plays a role in severity of acute pancreatitis?

Adipose tissue or fat releases a large amount of inflammatory cytokines, what we call adipokines, 50% of the amount of TNF-a and MCP-1 is released by adipocyte tissue, but also they are fat specific cytokines such as resistant with fat and adiponectin.

Management of Acute Pancreatitis

A) initial assessment and risk stratification.

• Airway (Patency + Vomitus obstructing airway? )
• Breathing (Respiratory depth and rate + SpO2 + Wheeze/crackles?)
• Circulation (CRT + Pulse + BP + Mucous membrane)
• Disability (GCS + Glucose levels)
• Examine abdomen
• Cullen’s and Grey-Turner’s sign?
• Tenderness on palpation?
• Any signs of peritonism – rebound, guarding or percussion tenderness?
• Flank tenderness?
• Temperature measurement

B) Airway and Breathing support

• Maintatin SpO2 > 94%
• High flow oxygen with non-rebreather mask
• Pulmonary complaints necessitate supplemental oxygen
• Endotracheal intubation for ARDS or severe encephalopathy

C) Fluid resuscitation in Acute Pancreatitis

• Aggressive hydration: 250-500 ml per hour of isotonic crystalloid solution
• Early aggressive intravenous hydration is most beneficial the first 12–24 h, and may have little benefit beyond
• In severe volume depletion (hypotension and tachycardia) bolus may be needed
• RL may be the preferred isotonic crystalloid replacement fluid
• Fluid requirements should be reassessed at frequent intervals within 6 h of admission and for the next 24–48 h.
• The goal of aggressive hydration should be to decrease the BUN.

D) Blood products in Acute Pancreatitis:

• In hemorrhagic pancreatitis, transfuse to hematocrit level of 30%.
• Fresh-frozen plasma and platelets if coagulopathic and bleeding.

E) Correct Electrolyte Abnormalities if present:

• Hypocalcemia: Calcium gluconate 10%: 10 mL IV over 15–20 min
• Hypokalemia: KCl 10 mEq/h IV over 1 hr
• Hypomagnesemia (alcohol abuse): MgSO4: 2 g IV piggyback

F) Pain Management in Acute Pancreatitis

• Past – Morphine blamed to cause spasms of the sphincter of Oddi (Pethidine was the analgesic of choice)
• Recently studies showed that morphine has no proven significantly unfavorable influence on the course of AP
• Metamizole (2g/8h i.v.) vs morphine (10mg/4h s.c.): metamizole resulted in more frequent and quicker pain relief
• Buprenorphine vs Pethidine: longer-acting with similar analgesic capacity as pethidine, but a lower potential to cause physical opioid dependence
• Buprenorphine vs procaine continuous intravenous (i.v.) infusion: Patient on procaine likely to demand additional analgesics and had relatively lesser pain relief
• Procaine (2g/24hours as continuous i.v. infusion) vs pentazocine (bolus i.v. every 6 hours): Patient on procaine more likely to demand additional analgesics (98% versus 44%)

G) Antiemetics in Acute Pancreatitis

• Ondansetron 4 mg IV stat

H) Nasogastric suctioning in Acute Pancreatitis

• Not useful in cases of mild pancreatitis
• Beneficial in severe pancreatitis, intractable vomiting, severe ileus and severe abdominal distension

I) Antibiotics in Acute Pancreatitis

• Given for an extrapancreatic infection, such as cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia
• Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended
• Use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended
• Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis who deteriorate or fail to improve after 7–10 days of hospitalization. In these patients, either (i) initial CT-guided fine needle aspiration (FNA) for Gram stain and culture to guide use of appropriate antibiotics or (ii) empiric use of antibiotics without CT FNA
• In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole

J) Nutrition in Acute Pancreatitis

• In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and abdominal pain has resolved.
• In mild AP, initiation of feeding with a low-fat solid diet appears as safe as a clear liquid diet.
• In severe AP, enteral nutrition is recommended to prevent infectious complications. Parenteral nutrition should be avoided unless the enteral route is not available, not tolerated, or not meeting caloric requirements.
• Nasogastric delivery and nasojejunal delivery of enteral feeding appear comparable in efficacy and safety.
• TPN for specific indications like Paralytic ileus.

K) Specific drug therapy for Acute Pancreatitis

No proven therapy for the treatment of acute pancreatitis. All proved disappointing in large randomized studies:

• Antiproteases: Gabexate
• Antisecretory agents: Octreotide and Somatostatin
• Anti-inflammatory agents: Lexipafant

Disposition from Emergency Department

Admission Criteria

• Acute pancreatitis with significant pain, nausea, vomiting
• ICU admission for hemorrhagic/necrotizing pancreatitis

Discharge Criteria

• Mild acute pancreatitis without evidence of biliary tract disease and able to tolerate oral fluids
• Chronic pancreatitis with minimal abdominal pain and able to tolerate oral fluids

Issues for Referral

• Surgical/GI consultation for ERCP in severe pancreatitis with cholangitis or biliary obstruction
• Emergent surgical consultation mandatory in cases of suspected ruptured pseudocyst or pseudocyst hemorrhage, as definitive treatment is emergent laparotomy

ERCP in Acute Pancreatitis

• Patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP within 24 h of admission.
• ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction.
• In the absence of cholangitis and/or jaundice, MRCP or endoscopic ultrasound (EUS) rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected.
• Pancreatic duct stents and/or postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories should be utilized to prevent severe post-ERCP pancreatitis in high-risk patients.

Surgery in Acute Pancreatitis (AP)

• In patients with mild AP, found to have gallstones in the gallbladder, a cholecystectomy should be performed before discharge to prevent a recurrence of AP
• In a patient with necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize
• Asymptomatic pseudocysts and pancreatic and/or extrapancreatic necrosis do not warrant intervention regardless of size, location, and/or extension
• In stable patients with infected necrosis, surgical, radiologic, and/or endoscopic drainage should be delayed preferably for more than 4 weeks to allow liquefication of the contents and the development of a fibrous wall around the necrosis (walled-off necrosis)
• In symptomatic patients with infected necrosis, minimally invasive methods of necrosectomy are preferred to open necrosectomy.

He is the section editor of Orthopedics in Epomedicine. He searches for and share simpler ways to make complicated medical topics simple. He also loves writing poetry, listening and playing music.

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36 year old man presenting with pancreatitis and a history of recent commencement of orlistat case report

Sarah napier.

1 Bristol Royal Infirmary, Marlborough Street, Bristol, BS2 8HW, UK

Matthew Thomas

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Orlistat is an anti-obesity drug licensed in the United Kingdom for 7 years. We present a case of a patient who developed pancreatitis four days after commencing orlistat.

Case presentation

A 36 year old man presented to hospital with acute severe pancreatitis four days after starting a course of Orlistat, a lipase inhibitor used in the treatment of obesity. A diagnosis of drug related pancreatitis was made by exclusion of other causes of pancreatitis; he was a teetotaller, had a normal serum calcium, had no family history of pancreatitis or hyperlipidaemia, no history of trauma and had no evidence of gallstones on Computerised Tomography scan (CT).

Orlistat was the only drug that had been started recently and has been associated with pancreatitis previously. We found no case reports of similar cases, however 99 cases of orlistat related pancreatitis have been reported to the Food and Drug Administration (FDA), but no causative link has been found in clinical trials by the drug company. It is therefore not on the list of possible complications or side effects of the drug.

Orlistat is an anti-obesity drug licensed in the U.K. for 7 years. We present a case of a patient who developed pancreatitis four days after commencing orlistat.

A 36 year old man presented to the emergency department with a 24 hour history of central abdominal pain, two episodes of vomiting and loose stool. He had a past history of Type II Diabetes Mellitus, hypertension, asthma and obstructive sleep apnoea. He weighed 130 kg with a Body Mass Index greater than 40.

His current medications were diltiazem, lisinopril, metformin, glicazide and orlistat. The orlistat had been commenced four days previously.

He was pyrexial and on examination was tender in the epigastrium. His initial white cell count was 20 × 10 9 /L and a C reactive protein of more than 300 mg/l, an amylase of 136 iu/l, and a lactate dehydrogenase of 892 iu/l. a recent lipid profile was normal and his corrected calcium was 2.41 iu/l. The initial diagnosis was unclear and a CT scan of his abdomen was organised. This showed appearances of acute pancreatitis affecting the distal body and tail of the pancreas [figure ​ [figure1]. 1 ]. He was classified as having acute severe pancreatitis using the modified Glasgow Score 1984. Management was the standard of pancreatitis, mainly supportive. Antibiotics were not given. Common causes of pancreatitis were excluded. He was abstinent of alcohol, had a normal serum calcium, had no family history of pancreatitis or hyperlipidaemia, and had no history of trauma. His abdominal CT scan showed no evidence of gallstones. By exclusion the diagnosis of drug induced pancreatitis secondary to orlistat was made.

Computerised Tomography of abdomen on admission.

He was transferred to the intensive care and made good progress. The Medicines Control agency and Committee on Safety of Medicines were informed.

Drug induced pancreatitis accounts for 2% of all cases of pancreatitis [ 1 ]. It is a diagnosis of exclusion and should be looked for after ethanol use and cholelithiasis have been excluded. Drug induced pancreatitis usually has a milder clinical course than other causes. Over one hundred drugs have been implicated as causes of pancreatitis, the most common being azathioprine, sulphonamides, sulindac, tetracycline, valproic acid, didanosine, methyldopa, estrogens, furosemide, 6-mercaptopurine, pentamidine, 5-aminosalicylic acid compounds, corticosteroids, and octreotide. Several of these drugs are no longer in common use in the United Kingdom. The mechanisms differ according to different drugs. Some affect the biliary system; others have a direct effect on the pancreas. The diagnosis can be made by a temporal link between a drug and the development of pancreatitis in a patient who does not have other causative factors. In this patient complete abstinence from alcohol and no biliary disease make the diagnosis of drug induced pancreatitis very likely. Orlistat was the only drug that had been started recently and has been associated with pancreatitis previously although no causative link can be shown in clinical trials. The normal amylase was a feature of this case. Amylase is only elevated in 80% of cases of pancreatitis [ 2 ]. Orlistat is a pancreatic lipase inhibitor but should have no effect on pancreatic amylase production. CT has long been a well recognised diagnostic tool in pancreatitis [ 3 ]

Orlistat is a gastric and pancreatic lipase inhibitor used in obesity management, inhibiting the absorption of fat from the diet and causing a high faecal fat content. It binds to gastric and pancreatic lipase thereby inactivating them; this inhibits the hydrolysis of dietary triglycerides consequently reducing the absorption of monoglycerides and free fatty acids. This causes some unpleasant gastrointestinal side effects including oily discharge, flatulence, faecal urgency, fatty/oily stool, faecal incontinence, abdominal and rectal pain, nausea and vomiting. It is thought that these symptoms cause a behaviour modification in the patient with avoidance of fat-rich foods to avoid the adverse effects. The product information reports abdominal pain as a common and cholelithiasis as a rare complication of orlistat but not pancreatitis. Orlistat has been licensed in the UK since 1998, and gained NICE approval in 2001 [ 4 ]. It is licensed for use in the obese population with BMI ≥ 30 kg/m2 or BMI ≥ 27 kg/m2 with other risk factors e.g. hypertension, diabetes or dyslipidaemia. Our patient fitted these characteristics. A literature search found no case reports of associations between orlistat and pancreatitis. We subsequently looked at the licensing of the drug in the U.S, U.K and Canada. The Joint non-prescription drugs advisory committee and endocrinologic and metabolic drugs advisory committee meeting in Maryland in January 23 rd 2006, discussed Orlistat as a new drug application for Orlistat to become a non prescription drug, had been applied for [ 5 ]. They state that there have been 99 raw reports of pancreatitis for orlistat but say that placebo-controlled trials of orlistat in patients treated for 2 years showed no increase in incidence of pancreatitis. The Canadian Adverse Drug Reaction Newsletter reports incidences of pancreatitis secondary to orlistat [ 6 ].

Cholelithiasis would seem to be the most obvious link between orlistat and pancreatitis, but this was not present in our case. If orlistat can cause a pancreatitis with normal amylase it is possible that more cases exist but are not fully diagnosed.

We present a case of acute pancreatitis with normal amylase in a gentleman who had no evidence of biliary disease and who was abstinent of alcohol. The only recent medication change was commencing orlistat four days previously. We suggest that this is a case of orlistat induced pancreatitis. This diagnosis should be considered in patients presenting with abdominal pain, and a normal amylase would not exclude the diagnosis.

Competing interests

The author(s) declare that they have no competing interests.

Acknowledgements

Written consent was obtained from the patient, for publication of this case report.

• Wilmink T, Frick TW. Drug-induced pancreatitis. Drug Safety. 1996; 14 :406–423. [ PubMed ] [ Google Scholar ]
• Williamson RC. Early assessment of severity in acute pancreatitis. Gut. 1984; 25 :1331–9. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Dammann HG, Grabbe E, Runge M. Computed tomography and acute pancreatitis. Lancet. 1980; 2 :860. doi: 10.1016/S0140-6736(80)90204-4. [ PubMed ] [ CrossRef ] [ Google Scholar ]
• National Institute for Health and Clinical Excellence, Obesity, Orlistat, (No. 22) http://www.nice.org.uk/page.aspx?o=15712
• FDA, Joint non-prescription Drugs Advisory Committee and Endocrinologic and Metabolic Drugs Advisory Committee meeting Jan 23 rd 2006 http://www.fda.gov/ohrms/dockets/ac/06/slides/2006-4201S1_05_FDA-Golden.ppt
• Canadian Adverse Drug Reaction Newsletter. 2000. http://www.hc-sc.gc.ca/dhp-mps/alt_formats/hpfb-dgpsa/pdf/medeff/carn-bcei_v10n2_e.pdf

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A case report of acute pancreatitis with glycogen storage disease type IA in an adult patient and review of the literature

Editor(s): Saranathan., Maya

a The Department of Gastroenterology

b The Department of Radiology, The First Affiliated Hospital of Nanchang University, Jiangxi, China

c Comprehensive Cancer Center Munich, Klinikum rechts der Isar, Technical University Munich, Munich Germany.

∗Correspondence: Yin Zhu, Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, 330006 Nanchang, China (e-mail: [email protected] ).

Abbreviations: AP = acute pancreatitis, CT = computed tomography, GSD I = Glycogen storage disease type I, GSD IA = glycogen storage disease type IA, HTG = hypertriglyceridemia.

How to cite this article: Ai J, He W, Huang X, Wu Y, Lei Y, Yu C, Görgülü K, Diakopoulos KN, Lu N, Zhu Y. A case report of acute pancreatitis with glycogen storage disease type IA in an adult patient and review of the literature. Medicine . 2020;99:42(e22644).

This work was financially supported by the National Natural Science Foundation of China (81760120 and 81960128) to YZ.

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

The authors have no conflicts of interest to disclose.

All data generated or analyzed during this study are included in this published article [and its supplementary information files].

This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

Rationale: 

Glycogen storage disease type IA (GSD IA) is an inherited disorder of glycogen metabolism characterized by fasting hypoglycemia, hyperuricemia, and hyperlipidemia including hypertriglyceridemia (HTG). Patients have a higher risk of developing acute pancreatitis (AP) because of HTG. AP is a potentially life-threatening disease with a wide spectrum severity. Nevertheless, almost no reports exist on GSD IA-induced AP in adult patients.

Patient concerns: 

A 23-year-old male patient with GSD 1A is presented, who developed moderate severe AP due to HTG.

Diagnoses: 

The GSD 1A genetic background of this patient was confirmed by Sanger sequencing. Laboratory tests, along with abdominal enhanced-computed tomography, were used for the diagnosis of HTG and AP.

Interventions: 

This patient was transferred to the intensive care unit and treated by reducing HTG, suppressing gastric acid, inhibiting trypsin activity, and relieving hyperuricemia and gout.

Outcomes: 

Fifteen days after hospital admission, the patient had no complaints about abdominal pain and distention. Follow-up of laboratory tests displayed almost normal values. Reexamination by computed tomography exhibited a reduction in peripancreatic necrotic fluid collection compared with the initial stage.

Lessons: 

Fast and long-term reduction of triglycerides along with management of AP proved effective in relieving suffering of an adult GSD IA-patient and improving prognosis. Thus, therapeutic approaches have to be renewed and standardized to cope with all complications, especially AP, and enable a better outcome so that patients can master the disease.

1 Introduction

Glycogen storage disease type I (GSD I) is an extremely rare and inherited metabolic disorder occurring with an incidence of approximately 1/100,000 to 1/400,000 live births in the general Caucasian population [1,2] and induced by deficiencies of the glucose-6-phosphatase (G6Pase)/glucose-6-phosphate translocase (G6PT) complex. Specifically, glycogen storage disease type IA (GSD IA) results from mutations of the gene G6PC , located on chromosome 17q21 [3] and encoding for the G6Pase catalytic subunit, which causes loss of G6Pase function and accounts for approximately 80% of GSD I. [4] Defects in G6Pase are followed by accumulation of glycogen in the liver and other organs, and patients present with fasting hypoglycemia, hyperuricemia, lactic acidosis, and hyperlipidemia which is a secondary risk factor of acute pancreatitis (AP). [5] Hypertriglyceridemia (HTG) is the main form of hyperlipidemia, leading to AP. [6] We report an adult case of AP with GSD IA, which was induced by HTG.

2 Case report

A 23-year-old male patient presented with acute persistent pain in the upper abdomen accompanied by nausea and vomiting and was hospitalized in May 2019.

The detailed patient history is as follows. Diagnosis of GSD IA was established according to clinical features and genetic background (see below). At birth abdominal distention (frog belly) and hepatomegaly were detected. At 7 years of age the patient suffered twice from epistaxis with a much longer bleeding time than normal. Because of growth failure and obvious clinical symptoms, the patient had to frequently undergo hospital examinations and treatments. For GSD 1A therapy, medical recommendation included nutrient supplementation of cornstarch at 12 years of age. To reduce hyperlipidemia ezetimibe tablets 10 mg qd, fenofibrate 200 mg qd, and orlistat 0.12 g tid were prescribed at 13 years of age along with febuxostat tablets 40 mg qd for relieving hyperuricemia and gout. The patient is of short stature with a baby face due to beard growth defects while in puberty. In April 2016, this patient was admitted to the hospital for the first time due to HTG-AP. He was cured after treatment.

The GSD 1A genetic background of this patient was confirmed by testing performed at the Shanghai institute of pediatric medicine in August 2017. Sanger sequencing of the G6PC gene (NM_000151.3) revealed 2 distinct mutations in exon 5 of both alleles: c.648G>T (p.L216L) inherited from the father and c.986A>T (p.K329 M) inherited from the mother. Disease-associated c.648G>T mutation frequencies of G6PC are 88% in Japanese patients and 36% in Chinese patients. [7] c.986A>T has not yet been reported in the literature. Thus, it might be a novel discovery of pathogenic G6PC mutation in GSD IA.

The delivery of this patient was normal and full-term. His parents were not consanguineous. This patient has 2 healthy younger siblings. He got married 2 years ago and had a healthy child last year.

Directly after hospitalization in May 2019, laboratory tests displayed blood biochemical results as follows: amylase 209 U/L (reference values 35–135), lipase 475 U/L (reference values 0–60), triglyceride 49.64 mmol/L (reference values 0–1.7) (=4393.14 mg/dL), total cholesterol 15.51 mmol/L (reference values 0–5.7) (=599.8 mg/dL), glucose 5.82 mmol/L (reference values 3.9–6.1) as well as uric acid 662 umol/L (reference values 208–428). Urine routine examination provided a value of 1.0 g/L urinary protein (reference value 0). Arterial blood gas analysis revealed respiratory failure (PO2/FiO2 =144 mm/Hg). [8] Abdominal computed tomography (CT) exhibited:

• 1. Liver: Hepatomegaly ( Fig. 1 );
• 2. Pancreas: AP with edema in the pancreas and peripancreatic necrotic fluid collection ( Fig. 2 A);
• 3. Left renal calyces: multiple small stones.

Integrating the disease history of this patient, 3 diagnoses were established:

• 1. moderately severe HTG-AP;
• 3. hyperuricemia.

This patient was treated as follows: fasting within 24 hours and resuscitation with intravenous infusion in the initial period; pantoprazole 40 mg q12h for gastric acid suppression; somatostatin 3 mg q12h and ulinastatin 10 WU qd for inhibition of trypsin activity; combination of enoxaparin sodium 4000 IU q12 h with insulin for initial 3 days followed by fenofibrate 200 mg qd for decreasing HTG; ezetimibe 10 mg qd and orlistat 0.12 g tid for reduction of hyperlipemia; febuxostat tablets 40 mg qd and sodium bicarbonate tablets 1000 mg q8h for relieving hyperuricemia and gout; lactulose oral solution 30 ml tid, Chinese rhubarb 100 ml tid and artificially assisted purgative enema for promoting peristalsis. In the meantime, butorphanol tartrate by micro pump was used for pain relief. One day later, enteral nutrition was given by nutritional canal. After 5 days, compound Azintamide Enteric-coated tablets (2 tablets tid) were used for digestive enzyme supplementation and live triple Combined capsule of Bifidobacterium, Lactobacillus, and Enterococcus (1 tablet bid) was used to restore the intestinal flora.

Five days after hospitalization, reexamination by abdominal CT displayed an increase in peripancreatic necrotic fluid collection compared with the initial stage image ( Fig. 2 B vs Fig. 2 A). However, after an additional 10 days, the patient had no complaints about abdominal pain and distention. Follow-up of laboratory tests displayed blood biochemical result as follows: amylase 102 U/L, triglyceride 9.01 mmol/L (796.95 mg/dL), total cholesterol 6.13 mmol/L (237.2 mg/dL), glucose 2.3 mmol/L, and uric acid 232 umol/L. Arterial blood gas analysis revealed normalized oxygenation index of PO2/FiO2. Repetition of abdominal enhanced-CT exhibited a reduction in peripancreatic necrotic fluid collection compared with the previous images with a defined inflammatory wall ( Fig. 3 vs Fig. 2 B). Following recovery, this patient was discharged. Until now, around 8 months after leaving the hospital, the patient maintains normal health by means of regularly taking ezetimibe,fenofibrate, and orlistat.

3 Discussion

GSD IA is the most common of the glycogen storage diseases, [4] mainly caused by abnormal glycogen storage and hypoglycemia when fasting due to dysfunctional glycogen metabolism. Without adequate metabolic treatment, patients with GSD IA die during infancy or childhood after overwhelming hypoglycemia and acidosis. Those who survive are stunted in physical growth and delayed in puberty because of chronically low insulin levels. Therefore, the key treatment is to maintain normal blood sugar levels and inhibit various metabolic disorders secondary to hypoglycemia, thereby relieving clinical symptoms.

Up to date, specific approaches for this disease are lacking and dietary adjustment is the cornerstone of treatment. Uncooked cornstarch is a widely used treatment method for GSD IA. [9–11] After preparation, due to the large molecular weight, cornstarch is slowly digested and stays in the intestine for longer time. It gradually releases glucose to maintain blood sugar at a normal level. This patient reported here started to utilize cornstarch as dietary treatment with frequent meals (every 6 hours) when he was 12-years old, crucially enhancing his life expectancy. Cornstarch also conduces to delaying the complications fatal to GSD IA patients, as for example HTG, hyperuricemia, gout, kidney stones, liver adenoma, etc ( Table 1 ). Nonetheless, new treatments have to be established to manage GSD IA complications since dietary adjustments cannot prevent them.

The present report is the first one describing an adult patient suffering from GSD 1A-induced AP. Up to date, only few articles exist describing the cases of GSD IA-induced AP [5,12,13] ; however, not including adult patients thus highlighting the importance of this report.

HTG is a well-known cause of AP, accounting for approximately 10% to 19% of all cases. [14,15] Hyperlipidemia can be separated into hypercholesterolemia and HTG. In contrast to HTG, hypercholesterolemia does not cause AP. [6] In China, HTG-mediated AP is the second leading cause of AP accounting for around 14% of all cases but has a higher mortality rate than that of the biliary/gallstone-induced AP which is the primary leading cause of AP. [16] The most important risk factor are elevated triglycerides, reaching up to 11.3 mmol/L (1000 mg/dL). [17] Accordingly, the presented patient had a very high TG level of 49.64 mmol/L (4393.14 mg/dL). However, the pathogenesis of HTG-AP is poorly understood. Free fatty acids are reported as one of the key factors to initiate the pathogenesis of HTG-AP. [18] Hydrolysis of accumulating triglycerides by the enzyme lipase in the pancreatic capillaries triggers free fatty acids release resulting in activation of trypsinogen and damages to pancreatic capillaries by free radicals. [19,20]

The patient reported here was treated with fluid resuscitation and enteral nutrition in the early phase, as recommended by the guidelines for AP. [21] More importantly, the combination of heparin and insulin was used for the initial phase of AP to reduce serum triglycerides. Although high-volume hemofiltration was effective in rapidly reducing HTG, one randomized controlled trial from He et al compared high-volume hemofiltration with the combination of low-molecular-weight heparin and insulin, showing no difference in terms of clinical outcomes and costs. [22] For long-term management of hyperlipidemia/HTG, cholesterol absorption inhibitor and fibrates were utilized. As described previously, the present patient had AP 3 years ago and was cured. One main cause of AP-recurrence was the pausing of the cholesterol absorption inhibitor ezetimibe and fibrates fenofibrate, 20 days before recurrence. Therefore, and in line with the publication reported by Guo et al, [18] it is very important to reduce triglycerides in order to prevent AP.

The reported patient was also suffering from hyperuricemia, which is a common complication of GSD IA. Hyperuricemia occurs due to accumulation of the G6PC-substrate glucose 6-phosphate. Elevated glucose 6-phosphate is subsequently metabolized by the pentose phosphate pathway and leads to the excess production of purine. Purine catabolism then results into uric acid. Simultaneously, excretion of uric acid through renal tubules is reduced due to competitive inhibition by organic acids, [23] collectively contributing to increased levels of blood uric acid. Hyperuricemia is usually accompanied by gout during puberty. It can be improved in GSD IA-patients by controlling whole body metabolism. However, persistent hyperuricemia mostly results in gout attacks. Xanthine oxidase inhibitors (allopurinol or febuxostat) are the first-line medicine for reducing uric acid. The patient presented herein currently takes febuxostat tablets to control gout caused by hyperuricemia showing promising results. The complications of hyperuricemia commonly include renal calcification and kidney stones. [11] The CT result of this patient indicated multiple small stones in renal calyces, most probably caused by elevated uric acid.

The patient herein exhibited most of the known GSD IA-complications. GSD IA causes not only great pain and physical injury but also shortens life expectancy of patients. Hospitalization costs are high and treatments focus only on preventing GSD IA-complications. Therefore, it is urgent to find new ways for an effective cure of the disease.

Gene therapy is expected to be one possible cure for GSD IA. [7,24] Koeberl et al injected an adeno-associated viral vector (AAV2/8) carrying G6PCcDNA into 2-week old G6PC −/− mice. 14 days after injection, the liver started to shrink and fasting blood glucose level gradually increased. The median survival extended for 7 months. [25] Nevertheless, gene therapy is still in the exploratory stage. There are many problems to be solved relating to long-term safety and effectiveness. In addition, research projects focusing on GSD I are rare. However, gene therapy may show promising results in the future.

4 Conclusion

This is the first report of HTG-AP in an adult-GSD IA patient. The combination-treatment of heparin and insulin is efficient for reducing triglycerides in a short time, and the combination of cholesterol absorption inhibitor and fibrates is stably decreasing HTG / hyperlipidemia over a long term. Moreover, AP as the complication of GSD IA can be effectively managed by comprehensive treatment, thereby relieving suffering of GSD IA-patients and improving prognosis. Thus, standard therapeutic approaches have to be established to manage the complications and improve therapy of this rare genetic disease.

Acknowledgment

We would like to thank the patient's family for agreeing on publishing the data. The patient has provided informed consent for publication of this case report.

Author contributions

Jiaoyu Ai provided clinical diagnosis and care and drafted the manuscript. Wenhua He, Xin Huang, Yao Wu, Yupeng Lei provided clinical diagnosis and care. Chen Yu provided clinical diagnosis. Kivanc Görgülü and Kalliope N.Diakopoulos provided extensive discussion and edited the manuscript. Nonghua Lu and Yin Zhu provided clinical care and designed the manuscript.

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acute pancreatitis; adult patient; clinical treatment; glycogen storage disease type IA; hypertriglyceridemia

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Retinal microvascular changes in patients with pancreatitis and their clinical significance

Affiliations.

• 1 Department of Ophthalmology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
• 2 Huankui Academy, Nanchang University, Nanchang, 330006, Jiangxi, China.
• 3 Department of Ophthalmology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
• 4 Ophthalmology Department of Affiliated Hospital, Medical School of Ophthalmology and Optometry, North Sichuan Medical College, Nanchong, 637000, Sichuan, China.
• 5 Department of Ophthalmology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China. [email protected].
• 6 Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. [email protected].
• 7 National Clinical Research Center for Eye Diseases, Shanghai, 200080, China. [email protected].
• 8 Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai, 200080, China. [email protected].
• 9 Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, 200080, China. [email protected].
• 10 Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, Shanghai, 200080, China. [email protected].
• PMID: 39147923
• DOI: 10.1038/s41598-024-69493-2

Acute pancreatitis, a common exocrine inflammatory disease affecting the pancreas, is characterized by intense abdominal pain and multiple organ dysfunction. However, the alterations in retinal blood vessels among individuals with acute pancreatitis remain poorly understood. This study employed optical coherence tomography angiography (OCTA) to examine the superficial and deep retinal blood vessels in patients with pancreatitis. Sixteen patients diagnosed with pancreatitis (32 eyes) and 16 healthy controls (32 eyes) were recruited from the First Affiliated Hospital of Nanchang University for participation in the study. Various ophthalmic parameters, such as visual acuity, intraocular pressure, and OCTA image for retina consisting of the superficial retinal layer (SRL) and the deep retinal layer (DRL), were recorded for each eye. The study observed the superficial and deep retinal microvascular ring (MIR), macrovascular ring (MAR), and total microvessels (TMI) were observed. Changes in retinal vascular density in the macula through annular partitioning (C1-C6), hemispheric quadrant partitioning (SR, SL, IL, and IR), and early diabetic retinopathy treatment studies (ETDRS) partitioning methods (R, S, L, and I). Correlation analysis was employed to investigate the relationship between retinal capillary density and clinical indicators. Our study revealed that in the superficial retinal layer, the vascular density of TMI, MIR, MAR, SR, IR, S, C2, C3 regions were significantly decreased in patients group compared with the normal group. For the deep retinal layer, the vascular density of MIR, SR, S, C1, C2 regions also reduced in patient group. The ROC analysis demonstrated that OCTA possesses significant diagnostic performance for pancreatitis. In conclusion, patients with pancreatitis may have retinal microvascular dysfunction, and OCTA can be a valuable tool for detecting alterations in ocular microcirculation in pancreatitis patients in clinical practice.

Keywords: Microvascular density; Optical coherence tomography angiography; Pancreatitis.

© 2024. The Author(s).

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Sodhi M , Rezaeianzadeh R , Kezouh A , Etminan M. Risk of Gastrointestinal Adverse Events Associated With Glucagon-Like Peptide-1 Receptor Agonists for Weight Loss. JAMA. 2023;330(18):1795–1797. doi:10.1001/jama.2023.19574

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Risk of Gastrointestinal Adverse Events Associated With Glucagon-Like Peptide-1 Receptor Agonists for Weight Loss

• 1 Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
• 2 StatExpert Ltd, Laval, Quebec, Canada
• 3 Department of Ophthalmology and Visual Sciences and Medicine, University of British Columbia, Vancouver, Canada
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• Special Communication Patents and Regulatory Exclusivities on GLP-1 Receptor Agonists Rasha Alhiary, PharmD; Aaron S. Kesselheim, MD, JD, MPH; Sarah Gabriele, LLM, MBE; Reed F. Beall, PhD; S. Sean Tu, JD, PhD; William B. Feldman, MD, DPhil, MPH JAMA
• Medical News & Perspectives What to Know About Wegovy’s Rare but Serious Adverse Effects Kate Ruder, MSJ JAMA
• Comment & Response GLP-1 Receptor Agonists and Gastrointestinal Adverse Events—Reply Ramin Rezaeianzadeh, BSc; Mohit Sodhi, MSc; Mahyar Etminan, PharmD, MSc JAMA
• Comment & Response GLP-1 Receptor Agonists and Gastrointestinal Adverse Events Karine Suissa, PhD; Sara J. Cromer, MD; Elisabetta Patorno, MD, DrPH JAMA
• Research Letter GLP-1 Receptor Agonist Use and Risk of Postoperative Complications Anjali A. Dixit, MD, MPH; Brian T. Bateman, MD, MS; Mary T. Hawn, MD, MPH; Michelle C. Odden, PhD; Eric C. Sun, MD, PhD JAMA
• Original Investigation Glucagon-Like Peptide-1 Receptor Agonist Use and Risk of Gallbladder and Biliary Diseases Liyun He, MM; Jialu Wang, MM; Fan Ping, MD; Na Yang, MM; Jingyue Huang, MM; Yuxiu Li, MD; Lingling Xu, MD; Wei Li, MD; Huabing Zhang, MD JAMA Internal Medicine
• Research Letter Cholecystitis Associated With the Use of Glucagon-Like Peptide-1 Receptor Agonists Daniel Woronow, MD; Christine Chamberlain, PharmD; Ali Niak, MD; Mark Avigan, MDCM; Monika Houstoun, PharmD, MPH; Cindy Kortepeter, PharmD JAMA Internal Medicine

Glucagon-like peptide 1 (GLP-1) agonists are medications approved for treatment of diabetes that recently have also been used off label for weight loss. 1 Studies have found increased risks of gastrointestinal adverse events (biliary disease, 2 pancreatitis, 3 bowel obstruction, 4 and gastroparesis 5 ) in patients with diabetes. 2 - 5 Because such patients have higher baseline risk for gastrointestinal adverse events, risk in patients taking these drugs for other indications may differ. Randomized trials examining efficacy of GLP-1 agonists for weight loss were not designed to capture these events 2 due to small sample sizes and short follow-up. We examined gastrointestinal adverse events associated with GLP-1 agonists used for weight loss in a clinical setting.

We used a random sample of 16 million patients (2006-2020) from the PharMetrics Plus for Academics database (IQVIA), a large health claims database that captures 93% of all outpatient prescriptions and physician diagnoses in the US through the International Classification of Diseases, Ninth Revision (ICD-9) or ICD-10. In our cohort study, we included new users of semaglutide or liraglutide, 2 main GLP-1 agonists, and the active comparator bupropion-naltrexone, a weight loss agent unrelated to GLP-1 agonists. Because semaglutide was marketed for weight loss after the study period (2021), we ensured all GLP-1 agonist and bupropion-naltrexone users had an obesity code in the 90 days prior or up to 30 days after cohort entry, excluding those with a diabetes or antidiabetic drug code.

Patients were observed from first prescription of a study drug to first mutually exclusive incidence (defined as first ICD-9 or ICD-10 code) of biliary disease (including cholecystitis, cholelithiasis, and choledocholithiasis), pancreatitis (including gallstone pancreatitis), bowel obstruction, or gastroparesis (defined as use of a code or a promotility agent). They were followed up to the end of the study period (June 2020) or censored during a switch. Hazard ratios (HRs) from a Cox model were adjusted for age, sex, alcohol use, smoking, hyperlipidemia, abdominal surgery in the previous 30 days, and geographic location, which were identified as common cause variables or risk factors. 6 Two sensitivity analyses were undertaken, one excluding hyperlipidemia (because more semaglutide users had hyperlipidemia) and another including patients without diabetes regardless of having an obesity code. Due to absence of data on body mass index (BMI), the E-value was used to examine how strong unmeasured confounding would need to be to negate observed results, with E-value HRs of at least 2 indicating BMI is unlikely to change study results. Statistical significance was defined as 2-sided 95% CI that did not cross 1. Analyses were performed using SAS version 9.4. Ethics approval was obtained by the University of British Columbia’s clinical research ethics board with a waiver of informed consent.

Our cohort included 4144 liraglutide, 613 semaglutide, and 654 bupropion-naltrexone users. Incidence rates for the 4 outcomes were elevated among GLP-1 agonists compared with bupropion-naltrexone users ( Table 1 ). For example, incidence of biliary disease (per 1000 person-years) was 11.7 for semaglutide, 18.6 for liraglutide, and 12.6 for bupropion-naltrexone and 4.6, 7.9, and 1.0, respectively, for pancreatitis.

Use of GLP-1 agonists compared with bupropion-naltrexone was associated with increased risk of pancreatitis (adjusted HR, 9.09 [95% CI, 1.25-66.00]), bowel obstruction (HR, 4.22 [95% CI, 1.02-17.40]), and gastroparesis (HR, 3.67 [95% CI, 1.15-11.90) but not biliary disease (HR, 1.50 [95% CI, 0.89-2.53]). Exclusion of hyperlipidemia from the analysis did not change the results ( Table 2 ). Inclusion of GLP-1 agonists regardless of history of obesity reduced HRs and narrowed CIs but did not change the significance of the results ( Table 2 ). E-value HRs did not suggest potential confounding by BMI.

This study found that use of GLP-1 agonists for weight loss compared with use of bupropion-naltrexone was associated with increased risk of pancreatitis, gastroparesis, and bowel obstruction but not biliary disease.

Given the wide use of these drugs, these adverse events, although rare, must be considered by patients who are contemplating using the drugs for weight loss because the risk-benefit calculus for this group might differ from that of those who use them for diabetes. Limitations include that although all GLP-1 agonist users had a record for obesity without diabetes, whether GLP-1 agonists were all used for weight loss is uncertain.

Accepted for Publication: September 11, 2023.

Published Online: October 5, 2023. doi:10.1001/jama.2023.19574

Correction: This article was corrected on December 21, 2023, to update the full name of the database used.

Corresponding Author: Mahyar Etminan, PharmD, MSc, Faculty of Medicine, Departments of Ophthalmology and Visual Sciences and Medicine, The Eye Care Center, University of British Columbia, 2550 Willow St, Room 323, Vancouver, BC V5Z 3N9, Canada ( [email protected] ).

Author Contributions: Dr Etminan had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Sodhi, Rezaeianzadeh, Etminan.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Sodhi, Rezaeianzadeh, Etminan.

Critical review of the manuscript for important intellectual content: All authors.

Statistical analysis: Kezouh.

Obtained funding: Etminan.

Administrative, technical, or material support: Sodhi.

Supervision: Etminan.

Conflict of Interest Disclosures: None reported.

Funding/Support: This study was funded by internal research funds from the Department of Ophthalmology and Visual Sciences, University of British Columbia.

Role of the Funder/Sponsor: The funder had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See Supplement .

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