Acute Pancreatitis

Overview of Acute pancreatitis

• Acute pancreatitis results from the leakage of pancreatic enzymes into pancreatic tissue, leading to auto digestion. Because acute pancreatitis is particularly, more common than chronic pancreatitis.
• Acute pancreatitis can have severe complications and high mortality despite treatment. While mild cases are often successfully treated with conservative measures.[2]

Causes of Acute Pancreatitis

Common causes such as:

• Alcohol
• Gallstones
• Idiopathic causes

Uncommon causes 

Post operative causes like:

• After endoscopic retrograde cholangiopancreatography
• Trauma
• Metabolic causes ( for instance renal failure, hyperparathyroidism, acute fatty liver of pregnancy)
• Hereditary causes
• Infections ( such as mumps, mycoplasma, echovirus)
• Vasculitis (SLE, necrotizing angilitis)
• Ampulla of vater obstruction ( for example Crohn’s disease, duodenal diverticulitis, penetrating duodenal ulcer)
• Drugs
• Hypotension may be present in as many as half of the patients; it results from vasodilatation, myocardial depressant factor, also the loss of plasma and blood in to the retro-peritoneum. [1]

Types of Pancreatitis

There are mainly two types that is;

• Acute
• Chronic

Risk Factors

• Excessive alcohol consumption. Research shows that heavy alcohol users (people who consume four to five drinks a day) are at increased risk of pancreatitis.
• Cigarette smoking. Smokers are on average three times more likely to develop chronic pancreatitis, compared with nonsmokers. The good news is quitting smoking decreases your risk by about half.
• Obesity. You’re more likely to get pancreatitis if you’re higher-weight person.
• Diabetes. Having diabetes increases your risk of pancreatitis.
• Family history of pancreatitis. The role of genetics is becoming increasingly recognized in chronic pancreatitis. If you have family members with the condition, your odds increase — especially when combined with other risk factors.[5]

Premature Activation of Trypsin:

This is a central event in acute pancreatitis. Trypsin activates other digestive enzymes, leading to autodigestion of the pancreas.

Intra-Acinar Activation of Enzymes:

This occurs due to various factors such as increased intracellular calcium, decreased ATP levels, and co-localization of lysosomal enzymes with digestive enzymes.

Microvascular Injury and Ischemia:

This can contribute to acinar cell injury and release of inflammatory mediators, exacerbating the inflammatory response.

Leukocyte Activation and Inflammation:

Activated leukocytes release cytokines and other inflammatory mediators, contributing to the systemic inflammatory response.[10]

Toxic-Metabolic Injury:

This can be caused by alcohol, drugs, or hypertriglyceridemia. These factors can induce acinar cell injury and trigger the inflammatory cascade.

Genetic Predisposition:

Certain genetic mutations can increase the risk of acute pancreatitis, such as mutations in the cationic trypsinogen gene (PRSS1).

Infectious Agents:

Certain viruses and bacteria can infect the pancreas and trigger an inflammatory response.[11]

These references provide a comprehensive overview of the complex pathogenesis of acute pancreatitis. Understanding the underlying mechanisms is crucial for developing effective diagnostic and therapeutic strategies.

Pathophysiology of Acute Pancreatitis

The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes. In biliary acute pancreatitis, outflow obstruction with pancreatic duct hypertension and a toxic effect of bile salts contribute to disruption of pancreatic ductules, with subsequent loss of extracellular compartmentation.

Alcohol induces functional alterations of plasma membranes and alters the balance between proteolytic enzymes and protease inhibitors, thus triggering enzyme activation, autodigestion and cell destruction. Once the disease has been initiated, the appearance of interstitial edema and inflammatory infiltration are the basic features of acute pancreatitis.

Accumulation of polymorphonuclear granulocytes

The accumulation of polymorphonuclear granulocytes in pancreatic and extrapancreatic tissue, and the release of leukocyte enzymes play an essential role in the further progression of the disease and in the development of systemic complications. Activation of different cascade systems by proteolytic activity, and consumption of alpha 2-macroglobulin further characterize the severe clinical course of acute pancreatitis.[6]

Sign & Symptoms

The most common symptom of acute pancreatitis is pain. Almost everybody with acute pancreatitis experiences pain.

Quality of Pain

• Pain may come on suddenly or build up gradually. If the pain begins suddenly, it is typically very severe. If the pain builds up gradually, it starts out mild but may become severe.
• The pain is usually centered in the upper middle or upper left part of the belly (abdomen). A pain is often described as if it radiates from the front of the abdomen through to the back.
• The pain often begins or worsens after eating.
• After that, Pain typically lasts a few days.
• The pain may feel worse when a person lies flat on his or her back.

People with acute pancreatitis usually feel very sick. Besides pain, people may have other symptoms and signs.

• Nausea (Some people do vomit, but vomiting does not relieve the symptoms.)
• Fever, chills, or both
• Swollen abdomen which is tender to the touch
• Rapid heartbeat (A rapid heartbeat may be due to the pain and fever, dehydration from vomiting and not eating, or it may be a compensation mechanism if a person is bleeding internally.)

In very severe cases with either infection or bleeding, a person may become dehydrated and have low blood pressure.

If the blood pressure becomes extremely low, the organs of the body do not get enough blood to carry out their normal functions. Hence, This very dangerous condition is called circulatory shock and is referred to simply as shock. [1]

Clinical Examination

The physical examination findings may be normal or reveal fever, hypotension, tachycardia, tachypnea, or diaphoresis. Abdominal examination typically reveals notable tenderness to palpation, guarding, also possible signs of peritoneal irritation, distension, or rigidity. Bowel sounds are typically decreased. Additionally, Jaundice may be present. In severe disease, patients may present with altered mental status. Overall, history also physical examination have moderate accuracy, especially when findings are abnormal (positive likelihood ratio [LR+] = 3.2; negative likelihood ratio [LR–] = 0.8).⁹ Two physical signs associated with pancreatitis are Cullen sign (ecchymosis and edema in the subcutaneous tissue around the umbilicus) and Grey Turner sign (ecchymosis of the flank).[7]

Diagnosis of Acute Pancreatitis

Once a working diagnosis of acute pancreatitis is reached, laboratory tests are obtained to support the clinical impression. In addition to confirming the diagnosis, laboratory tests are helpful in defining an etiology and looking for complications.

Serum amylase and lipase levels

They are typically elevated in persons with acute pancreatitis. Serum amylase determinations are routinely available, but they are not specific for pancreatitis.

Lipase has a slightly longer half-life and abnormalities may support the diagnosis if a delay occurs between the pain episode also the time the   patient seeks medical attention.

Elevated lipase levels are more specific to the pancreas than elevated amylase levels. The level of serum amylase or lipase does not indicate whether the disease is mild, moderate, or severe, and monitoring levels serially during the course of hospitalization does not offer insight into prognosis.

blood urea nitrogen

Obtain measurements for blood urea nitrogen (BUN), creatine, and electrolytes; a great disturbance in the electrolyte balance usually found, secondary to third spacing of fluids. Measure blood glucose level because it may be elevated from B-cell injury in the pancreas.

Measure calcium, cholesterol, and triglyceride levels to search for an etiology of pancreatitis (such as; hypercalcemia or hyperlipidemia) or complications of pancreatitis (for example, hypocalcemia resulting from saponification of fats in the retroperitoneum).

A complete blood count (CBC) demonstrates leukocytosis (white blood cell (WBC) count higher than 12,000/µL) with the differential being shifted toward the segmented polymorphonuclear (PMN) cells. Leukocytosis may represent inflammation or infection.

Abdominal radiographs have a limited role in acute pancreatitis.

Ultrasonography of the abdomen is the most useful initial test in determining the etiology of pancreatitis and is the technique of choice for detecting gallstones. Although ultrasonography can be used as a screening test, it may not be specific if overlying gas shadows secondary to bowel distention are present. Ultrasonography cannot measure the severity of disease.

CT is an important common initial assessment tool for acute pancreatitis.

Imaging is indicated during the initial presentation if i.e.:

• The diagnosis of acute pancreatitis is uncertain
• There is abdominal distension also tenderness, fever>102, or leukocytosis
• But Not improvement after 72 hours of conservative medical therapy
• There has been an acute change in status: fever, pain, or shock

While CT considered the gold standard in diagnostic imaging for acute pancreatitis, magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas, particularly of pancreatic fluid collections and necrotized debris. Additional utility of MRI includes its indication for imaging of patients with an allergy to CT’s contrast material, and an overall greater sensitivity to hemorrhage, vascular complications, pseudoaneurysms, also venous thrombosis. [1]

Differential Diagnosis

It include but is not limited to the following i.e.:

• Peptic ulcer disease
• Cholangitis
• Cholecystitis
• Bowel perforation
• Bowel obstruction
• Mesenteric ischemia
• Acute hepatitis
• Diabetic ketoacidosis
• Basilar pneumonia
• Myocardial infarction
• Renal colic
• Aortic dissection[5]

Investigation of Acute Pancreatitis

1. Firstly, Elevated serum amylase and lipase are the hallmarks of acute pancreatitis.
2. Secondly, Other findings may include leucocytosis, hypoalbuminemia, hyperglycaemia, and elevated aspartate aminotransferase (AST, serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase, and bilirubin. [2]

Treatment of Acute Pancreatitis

Often Treatment requires a stay in the hospital and may involve i.e.:

• Medicines Pain
• Fluids given through a vein (IV)
• Stopping food or fluid by mouth to limit the activity of the pancreas

Occasionally a tube will inserted through the nose or mouth to remove the contents of the stomach (nasogastric suctioning). This may  done if vomiting or severe pain do not improve, or if a paralyzed bowel (paralytic ileus) develops. The tube will stay in for 1 – 2 days to 1 – 2 weeks.

Treating the condition that caused the problem can prevent repeated attacks.

In some cases, therapy needed such as i.e.:

• Drain fluid that has either collected in or around the pancreas
• Remove gallstones
• Relieve blockages of the pancreatic duct

In the most severe cases, surgery is needed to remove either dead or infected pancreatic tissue.

Avoid smoking, alcoholic drinks, and a fatty food after the attack has improved. [1]

Prevention of Acute Pancreatitis

You can reduce your risk of developing acute pancreatitis by cutting back on drinking alcohol. This helps to prevent your pancreas being damaged.

It’s recommended that you i.e.:

• don’t drink more than 14 units a week
• spread your drinking over 3 days or more if you drink as much as 14 units a week

A unit of alcohol is equal to about half a pint of normal-strength lager or a pub measure (25ml) of spirits. A small (125ml) glass of wine (ABV 12%) or an alcopop is 1.5 units.

Remember, if you’ve had acute pancreatitis caused by drinking too much alcohol, you should avoid it completely.[8]

Homeopathic Treatment 

Homeopath treats the person as a whole. It means that homeopathic treatment focuses on the patient as a person, as well as his pathological condition. The homeopathic medicines selected after a full individualizing examination and case-analysis.

Which includes

• The medical history of the patient,
• Physical and mental constitution,
• Family history,
• Presenting symptoms,
• Underlying pathology,
• Possible causative factors etc.

A miasmatic tendency (predisposition/susceptibility) also often taken into account for the treatment of chronic conditions.

What Homoeopathic doctors do?

A homeopathy doctor tries to treat more than just the presenting symptoms. The focus is usually on what caused the disease condition? Why ‘this patient’ is sick ‘this way’?

The disease diagnosis is important but in homeopathy, the cause of disease not just probed to the level of bacteria and viruses. Other factors like mental, emotional and physical stress that could predispose a person to illness also looked for. Now a days, even modern medicine also considers a large number of diseases as psychosomatic. The correct homeopathy remedy tries to correct this disease predisposition.

The focus is not on curing the disease but to cure the person who is sick, to restore the health. If a disease pathology not very advanced, homeopathy remedies do give a hope for cure but even in incurable cases, the quality of life can greatly improve with homeopathic medicines.

Homeopathic Medicines for Acute Pancreatitis:

The homeopathic remedies (medicines) given below indicate the therapeutic affinity but this is not a complete and definite guide to the homeopathy treatment of this condition. The symptoms listed against each homeopathic remedy may not be directly related to this disease because in homeopathy general symptoms and constitutional indications also taken into account for selecting a remedy, potency and repetition of dose by Homeopathic doctor.

So, here we describe homeopathic medicine only for reference and education purpose. Do not take medicines without consulting registered homeopathic doctor (BHMS or M.D. Homeopath).

Aconite:

• When the pain has been caused by a chill.

Aloe:

• Flatulence; weak, as if diarrhoea would ensue. Soreness in sides. Over the liver, heat and pressure. Feeling of a plug in pelvis, between symphysis and coccyx, with urging. Additionally, General feeling of Fullness and heaviness.

Alumina:

• Seems to hang down, heavy, when walking (<) afternoon. Additionally, Sticking pains from below upward. Cutting pains (>) warmth. Lead colic.
• Soreness over the liver, extends to pit of stomach on stooping. Furthermore, Stitches in the region of inguinal ring (has relieved strangulated hernia); the pains extend up to the chest.

Apis:

• General soreness, aggravated by touch. Distention. Sharp, stinging pains, mostly extending upward.

Argentum nitricum:   

• Flatulent distention. Flatulent pains, often sharp, followed specifically by evacuations of gas also green, fetid mucus. Pain around hypochondria.

Arnica:

• Distention, hard. Stitches in the region of the spleen, taking away the breath. Pains (after lifting). Colic, with retention of urine. Bruised pains in the sides of the abdomen. at last, Flatulence, extremely foul [4]

Belladona:

• Nausea; vomiting after eating also drinking. Heat, with burning, cutting pain in the region of the stomach.  Extreme sensitiveness of the stomach to touch.

Mercurius:

• Flatulent distention of abdomen, with numerous pains. Intestines feel sore, (<) lying on right side. Inguinal glands swollen also inflamed, with shooting pains. Boring pains especially in the right groin.[4]

Diet & Regimen

• To best achieve those goals, it is important for pancreatitis patients to eat high protein, nutrient-dense diets that include fruits, vegetables, whole grains, low fat dairy, also other lean protein sources.
• Abstinence from alcohol and either greasy or fried foods is important in helping to prevent malnutrition and pain. [3]

References use for Acute Pancreatitis

1.  Acute and Chronic Pancreatitis
2.  Acute pancreatitis   Family Medicine Help
3. https://columbiasurgery.org/pancreas/pancreatitis-diet#:~:text=To%20best%20achieve%20those%20goals,to%20prevent%20malnutrition%20and%20pain.
4.  A Primer of Materia Medica by T. F. Allen.
5. https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227
6. https://pubmed.ncbi.nlm.nih.gov/8119636/
7. https://www.aafp.org/pubs/afp/issues/2014/1101/p632.html#:~:text=The%20physical%20examination%20findings%20may,Bowel%20sounds%20are%20typically%20decreased.
8. https://www.nhs.uk/conditions/acute-pancreatitis/prevention/#:~:text=You%20can%20reduce%20your%20risk,than%2014%20units%20a%20week
9. Robbins & Cotran Pathologic Basis of Disease, 10th Edition (Kumar, Abbas, Aster, 2021, Elsevier)
10. Harrison’s Principles of Internal Medicine, 21st Edition (Kasper, Fauci, Hauser, Longo, Jameson, Loscalzo, 2022, McGraw Hill)
11. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 11th Edition (Feldman, Friedman, Brandt, 2016, Elsevier)
12. The Washington Manual of Medical Therapeutics, 36th Edition (Sabatine, 2023, Lippincott Williams & Wilkins)
13. https://hartfordhealthcare.org/about-us/news-press/news-detail?articleId=49925&publicid=395

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