​Kembara Xtra - Medicine - Acute Pancreatitis

​Kembara Xtra - Medicine - Acute Pancreatitis 
Acute pancreatic inflammation that may or may not include local tissue or distant organ systems
Complete structural and functional recovery if there is no necrosis or pancreatic ductal disruption. Symptoms are related to intrapancreatic activation of enzymes with pain, nausea, and vomiting, as well as concomitant intestinal ileus.


​Epidemiology 

No prevalent age or sex, incidence 1 to 5/10,000
19/10,000 is the prevalence. For inpatient hospitalization, the most typical gastrointestinal diagnosis is this one.

Pathophysiology and Etiology 

Alcohol is most prevalent among adults (30 to 50 years old).
Adults with gallstones (including microlithiasis) are most likely to develop them (median age: 69).
Trauma and surgery affect adults most frequently (median age: 65).
Following endoscopic retrograde cholangiopancreatography (ERCP) Acute withdrawal of drugs for diabetes or hyperlipidemia drugs (most frequent, not a comprehensive list)
- Thiazide diuretics, ACE inhibitors, angiotensin receptor blockers (ARBs), and furosemide
Mercaptopurine and azathioprine are antimetabolites.
- Mesalamine, sulfamethoxazole/trimethoprim, pentamidine, glyburide, exenatide, and corticosteroids
 Hypertriglyceridemia (typically >1,000 mg/dL); hypercalcemia; acute renal failure; even nonfasting levels as low as 177 mg/dL; metabolic reasons
- A high-glycemic-load diet
- Other vascular diseases, polyarteritis, and systemic lupus erythematosus
- Autoimmune; type I has high IgG4 levels, whereas type II has normal IgG4 levels.
- Infections Ascaris, clonorchis, cryptosporidiosis, coxsackie, CMV, and EBV
AIDS, cystic fibrosis, CFTR gene mutations, and other mutations; tumors (such as pancreatic and ampullary ones); and other obstructions, such as Celiac disease, Crohn's disease, pancreas divisum dysfunction, sphincter of Oddi dysfunction, and choledochocele.
Spirococcus venom
Idiopathic acute fatty liver of pregnancy
 Related and concurrent risk factors
- Type II diabetes, smoking, and obesity
 Enzymatic autodigestion of the pancreas with interstitial edema and third spacing of fluid is the pathophysiology.
Necrosis, pseudocyst development, pancreatic duct disruption, pancreatic ascites, multiorgan failure (early or late), walled off necrosis (late), and damage to nearby vascular systems including splenic vein thrombosis and splenic artery pseudoaneurysm are all potential sequelae.
● Cellular damage changes membrane trafficking, which changes lysosomal function and triggers the production of trypsin and the activation of the zymogen. Following a strong inflammatory reaction, there is an increase in vascular permeability, bleeding, edema, and necrosis.
● Smoking, alcohol misuse, and the severity of the initial episode of acute pancreatitis all raise the chance of developing acute recurrent pancreatitis, which raises the risk of developing chronic pancreatitis.
 Clinical traits linked to acute pancreatitis of increasing severity: age 60, obesity, and chronic, excessive alcohol usage
Genetics: Autosomal dominant; rare hereditary pancreatitis
 Multiple gene polymorphisms and mutations

Prevention 

Avoid consuming too much alcohol.
 Stopping smoking
 Treat underlying metabolic conditions (hypercalcemia or hypertriglyceridemia).
 Stop taking the problematic drugs.
Cholecystectomy (cholelithiasis symptoms)
 Diet: A diet strong in saturated fats, cholesterol, red meat, and eggs increases the risk of gallstone pancreatitis. with a diet rich in fiber and vitamin D, there is a reduced chance of gallstone pancreatitis. Diets rich in fiber, coffee, and caffeine are associated with a lower risk of non-gallstone pancreatitis.


Alcohol withdrawal, alcoholic hepatitis, diabetic ketoacidosis, and ascending cholangitis are associated conditions. Morbid obesity, an inflammatory state, worsens symptoms and has a higher fatality rate.

Symptoms of a diagnosis don't always match up with scientific findings.

Presenting History: Abdominal trauma, acute start of "boring" epigastric pain that may radiate posteriorly, nausea, and vomiting; alcohol usage; personal or family history of gallstones; drug use—look for triggering medications;

clinical assessment 

Examine vital signs for hemodynamic stability, fever, tachycardia, and hypotension. Examine abdominal organs for tenderness in the epigastrium, loss of bowel sounds, and peritoneal symptoms.
Jaundice, rales, and percussive dullness are other symptoms. Rarely, hemorrhagic pancreatitis might cause flank or umbilical discolouration (Grey Turner sign or Cullen sign).

Differential diagnoses include: Lymphoma, intestinal obstruction, perforated viscus, aortic aneurysm (dissecting or rupturing), acute cholecystitis or cholangitis, acute cholecystitis or cholangitis, macroamylasemia, macrolipasemia, mesenteric vascular occlusion, and/or infarction.

Laboratory Results 

 Consider laboratory and radiographic results in light of the patient's clinical history; false-positive and false-negative results are frequent.
BISAP score, or Bedside Index for Severity in Acute Pancreatitis In the first 24 hours, patients receive one point for each component: BUN >25 mg/dL, diminished mental status, and SIRS—a score of 0 indicates a low death rate of 1%, and a score of 5 indicates a high mortality rate of 22%.
● An older method of estimating pancreatitis severity is the Ranson criteria. It has 11 criteria, five of which are evaluated at admission and six more in the 48 hours that follow. Mild pancreatitis is defined as a score of 3 or less, and as the score rises, mortality increases significantly.
According to the American College of Gastroenterology, acute pancreatitis must have two out of the three of the following characteristics: distinctive abdominal pain, particular radiographic abnormalities, and a lipase level three times the upper limit of normal (ULN).
 Serum amylase elevation >3 times ULN (Severity is unrelated to elevation level. Amylase does not just cause pancreatitis.)
 Serum lipase elevation >3 times ULN (may last longer than amylase in mild instances). Compared to amylase, lipase is more specialized for the pancreas.)
Increased total bilirubin level. Consider common bile duct obstruction if >3 mg/dL.
With acute pancreatitis present, a 3-fold increase in alanine aminotransferase (ALT) provides a 95% positive predictive value for gallstone pancreatitis. Triglyceride values over 1,000 mg/dL point to hypertriglycemia as the underlying condition.
In severe illness, glucose and calcium levels increased.
 A WBC rise of 10,000 to 25,000/L is feasible but not necessarily a sign of an infection in progress.
A severe third spacing with accompanying hemoconcentration and an elevated baseline hematocrit >44 or growing hematocrit are unfavorable prognostic indicators.
Rising BUN and creatinine levels are indicative of acute renal failure or volume depletion.
Organ failure is predicted by elevated D-dimer levels.


Initial examinations (lab, imaging)
Utilize follow-up labs to evaluate tissue oxygenation, sepsis, biliary obstruction, sepsis, and renal function.
A chest x-ray (CXR) can rule out subdiaphragmatic air (a perforated viscus) and assess for early acute respiratory distress syndrome (ARDS) and pleural effusion.
 Using ultrasound to check for biliary/gallbladder stones
The CT scan validates the diagnosis, evaluates the severity, creates a baseline, offers prognostic data, and excludes the majority of other illnesses (with the exception of noncalcified cholelithiasis).
- IV contrast is not required for the initial CT scan; individuals who are volume-depleted should not receive contrast.
- If necrotizing pancreatitis is suspected, a CT scan with IV contrast on day 3 can evaluate the extent of necrosis if it is not contraindicated.
- Although the absence of gas in the peripancreatic collection does not rule out infection, the presence of gas is strong evidence for infection.
The assessment of choledocholithiasis, pancreas divisum, dilated pancreatic ducts, and ductal alterations is assisted by magnetic resonance cholangiopancreatography (MRCP).
Esophagogastroduodenoscopy (EGD) may be required to rule out an ampullary tumor or piercing duodenal ulcer.
To relieve pressure on the common bile duct caused by an impacted stone, ERCP may be required.
Endoscopic ultrasonography (EUS) is helpful if individuals have "idiopathic pancreatitis."
if there is a suspicion of autoimmune pancreatitis, EUS-guided fine needle aspiration

Tests in the Future & Special Considerations

a contrast-enhanced CT scan on day 3 to check for necrosis if renal function is steady. Aspiration and drainage of abscesses are aided by CT guidance, which is mostly advised if a fungal infection or infection that is resistant to treatment is suspected.

Management Acute pancreatitis management is constantly changing. The medical treatment of acute pancreatitis has evolved as a result of early feeding, cautious antibiotic use, and less treatments.
15-20% of acute pancreatitis cases evolve from mild to severe, including persistent organ failure; many instances of acute pancreatitis necessitate hospitalization; ICU if multiorgan dysfunction or hypotension/respiratory failure.
Rehydratation with fluids
Significant volume loss as a result of the third spacing
 Infuse a 500 mL/hr bolus over the course of 4 hours (lactated Ringer may be preferable to normal saline, unless the patient is hypercalcemic); the follow-up rate should be modified based on the patient's age, weight, hemodynamic response, and concomitant conditions (2)[A].
○ The desired urine output should be between 0.5 and 1 mL/kg/hr.
When this objective is met or when the BUN drops, the infusion rate should be reduced; the maximum total fluid intake on day 1 should be 4 L.
After 24 hours, fluid resuscitation is of limited use, and fluid overload causes serious consequences (3)[A].
- Discontinue all unneeded drugs, particularly those linked to pancreatitis.
Follow renal function, fluid status, calcium, and oxygenation via a nasogastric (NG) tube in cases of uncontrollable emesis. Pancreatic necrosis is a less significant prognostic indication than organ failure.
Start eating tiny amounts of high-carbohydrate, low-fat, and low-protein foods orally when the discomfort, soreness, and ileus have subsided. If the vomiting doesn't stop, use a NPO or NG tube. A soft low-fat diet may be started in mild pancreatitis instances even before the pain and elevated enzyme levels have entirely subsided.
- Enteral nutrition at the Treitz ligament level in the absence of oral feeding within 5–7 days (preferable to total parenteral nutrition [TPN] due to lower infection rates and death). Stop if pain intensity, amylase/lipase levels, or fluid retention rise.
If oral or nasoenteric feedings are not tolerated, TPN (without lipids if triglycerides are excessive) may be used.

First Line of Medicine
Hydromorphone (Dilaudid) 0.5 to 1.0 mg IV q1-2h PRN - AVOID meperidine (Demerol) due to the possibility of an accumulation of a toxic metabolite. Analgesia: there is no consensus; recommendations vary.
Antibiotics - The use of preventive antibiotics is no longer advised, even in cases with necrotizing pancreatitis, where there is a definite lack of infection.
- Consider using an empiric imipenem class or beta-lactam/ beta-lactamase inhibitor (e.g., piperacillin/tazobactam 4.5 g IV q8h) for first treatment in patients with ascending cholangitis or necrotizing pancreatitis if there is a high suspicion of an active infection before cultures (particularly aspirates) are returned.
- Levofloxacin 500 mg QD IV if there is cholangitis and a penicillin allergy
- When using preventive antibiotics, keep an eye out for fungal superinfections.

Referral 

If pancreatitis is severe or actively progressing, or when advanced imaging or endoscopic therapy is being considered, consult a tertiary center.

Surgery To lower the risk of recurrence in patients with cholelithiasis and nonnecrotizing pancreatitis, consider cholecystectomy before discharge.
Both diseased and noninfected necrosis should be treated nonsurgically by necrosectomy. After four weeks of observation (and, if necessary, antimicrobial treatment), walled-off necrosis should be treated by percutaneous or dualmodality drainage, if available. If there are no indications of infection, drainage may not be necessary. If an infection is suspected and the patient is responding well to the recommended antibiotic therapy, aspiration and culture are not necessary.
ERCP should be performed as soon as there is evidence of acute cholangitis or at 72 hours if there is evidence of persistent biliary obstruction; if ductal disruption lasts longer than 1 to 2 weeks, ERCP should also include the implantation of a pancreatic ductal stent. Bleeding pseudoaneurysms should be resected or embolized.
If you have severe necrotizing pancreatitis brought on by hypertriglyceridemia, you should exchange your plasma with insulin within 24 hours of your diagnosis.


Admission 

Low-grade fever and mild leukocytosis do not always indicate infection and may take weeks to resolve. Pain controlled. Tolerating oral diet. Alcohol rehabilitation and smoke abstinence.
Due to secondary infection of necrotic material, infections may still develop after 10 days in 33% of patients with necrotizing pancreatitis, necessitating surgical debridement.


Follow-Up If the initial CT scan revealed a fluid collection or necrosis or if the amylase/lipase level remains elevated, follow-up imaging should be performed in a few weeks. Follow-up findings could show:
- A symptomless pseudocyst with a diameter of up to 6 cm can be treated conservatively if it is a pseudocyst (occurs in 10% of cases) or an abscess (sudden onset of fever).
- 16–18% of people with necrotizing pancreatitis have splenic vein thrombosis.
- Splenic, gastroduodenal, and intrapancreatic pseudoaneurysm bleeding can be fatal.
Subclinical exocrine and endocrine disorders is common. However, patients with ductal blockage, steatorrhea, or necrotizing pancreatitis should be given enzyme supplements.
Diabetes risk doubles following the first episode of acute pancreatitis.
The likelihood of experiencing acute recurrent pancreatitis is 17% after experiencing acute pancreatitis for the first time. 8% of people are at risk of getting chronic pancreatitis.

Diet 
Advance diet as tolerated; cut back on alcohol, added sugars, and fat.


Prognosis 

85–90% of acute pancreatitis episodes spontaneously resolve; 3-5% of cases result in death (17% in necrotizing pancreatitis).

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