General Surgery 2023-2024 Full Transcript PDF

General Surgery Clinical Foundations - Harvey AY: 2023/2024 Written by: Mohammad Eisa Ali  1 General Surgery...

General Surgery Clinical Foundations - Harvey AY: 2023/2024 Written by: Mohammad Eisa Ali  1 General Surgery Clinical Foundations - Harvey 2023/2024 Table of Contents Acute Abdomen....................................................................................................................... 2 Oesophagitis............................................................................................................................ 5 Gastroesophageal Reflux Disease (GERD).................................................................................. 8 Boerhaave Syndrome............................................................................................................. 14 Gastritis................................................................................................................................. 15 Mediastinitis.......................................................................................................................... 16 Peptic Ulcer Disease............................................................................................................... 17 Acute Pancreatitis.................................................................................................................. 21 Pancreatic Carcinoma............................................................................................................. 30 Liver Tumours........................................................................................................................ 33 Portal Hypertension............................................................................................................... 39 Jaundice................................................................................................................................ 46 Disease of the Gallbladder and Bile Ducts............................................................................... 49 Cholelithiasis (Gallstones)...................................................................................................... 51 Cholecystitis.......................................................................................................................... 57 Choledocholithiasis................................................................................................................ 61 Intestinal Obstruction (Bowel Obstruction)............................................................................. 64 Appendicitis........................................................................................................................... 70 Hernia................................................................................................................................... 75 Colorectal Cancer................................................................................................................... 82 Gastrointestinal Bleeding....................................................................................................... 86 Diverticular Disease (Diverticulosis & Diverticulitis)................................................................ 95 Acute Meckel’s diverticulitis................................................................................................. 102 Peritonitis............................................................................................................................ 106  2 Acute Abdomen The term acute abdomen refers to signs and symptoms of abdominal pain and tenderness, a clinical presentation that often requires emergency surgical therapy. Because of the potential surgical nature of the acute abdomen, an expeditious workup is necessary in the usual order – history, physical examination, laboratory tests, and imaging studies. Medical History (Anamnesis): The intensity and severity of the pain are related to the underlying tissue damage. Sudden onset of excruciating pain suggests conditions such as intestinal perforation or arterial embolization with ischemia, although other conditions, such as biliary colic, can present suddenly as well. Pain that develops and worsens over several hours is typical for conditions of progressive inflammation or infection such as cholecystitis, colitis, and bowel obstruction. The history of progressive worsening versus intermittent episodes of pain can help differentiate infectious processes that worsen with time compared with the spasmodic colicky pain associated with bowel obstruction, biliary colic from cystic duct obstruction, or genitourinary obstruction. Abdominal pain is conveniently divided into visceral and parietal components. Visceral pain tends to be vague and poorly localized to the epigastrium, periumbilical region, or hypogastrium, depending on its origin from the primitive foregut, midgut, or hindgut. It is usually the result of distention of a hollow viscus. Parietal pain corresponds to the segmental nerve roots innervating the peritoneum and tends to be sharper and better localized. Referred pain is pain perceived at a site distant from the source of stimulus. For example, irritation of the diaphragm may produce pain in the shoulder. Physical Examination: The four basic methods or techniques that are used for physical assessment are: 1. Inspection 2. Auscultation 3. Percussion 4. Palpation Inspection: The physical examination should always begin with a general inspection of the patient to be followed by inspection of the abdomen itself. Abdominal inspection should address the contour of the abdomen, including whether it appears distended or scaphoid or whether a localized mass effect is observed. Special attention should be paid to all scars present and, if surgical in nature, should correlate with the surgical history provided. Fascial hernias may be suspected and be confirmed during palpation of the abdominal wall.  3 Patients with peritoneal irritation will experience worsened pain with any activity that moves or stretches the peritoneum. These patients will typically lie very still in the bed during the evaluation and often maintain flexion of their knees and hips to reduce tension on the anterior abdominal wall. Disease states that cause pain without peritoneal irritation, such as ischemic bowel or ureteral or biliary colic, typically cause patients to continually shift and fidget in bed while trying to find a position that lessens their discomfort. Other visible signs of abnormalities involve pallor (pale skin), cyanosis (bluish discoloration), and diaphoresis (excessive sweating). Auscultation: Auscultation involves listening to sounds produced by the body using a stethoscope. Bowel sounds are typically evaluated for their quantity and quality. A quiet abdomen suggests an ileus, whereas hyperactive bowel sounds are found in enteritis and early ischemic intestine. The pitch and pattern of the sounds are also considered. Mechanical bowel obstruction is characterized by high-pitched tinkling sounds that tend to come in rushes and are associated with pain. Far-away echoing sounds are often present when significant luminal distention exists. Vascular sounds, called bruits heard within the abdomen reflect turbulent blood flow within the vascular system and can suggest issues like arterial stenosis or arteriovenous fistula. Percussion: Percussion is a method of tapping the abdomen and listening to the resulting sounds to assess for gaseous distention of the bowel, free intra-abdominal air, degree of ascites, or presence of peritoneal inflammation. Hyperresonance, commonly referred to as tympany to percussion, is characteristic of underlying gas-filled loops of bowel. In the setting of bowel obstruction or ileus, this tympany is heard throughout all but the right upper quadrant where the liver lies beneath the abdominal wall. If localized dullness to percussion is identified anywhere other than the right upper quadrant, an abdominal mass displacing the bowel should be considered. When liver dullness is lost and resonance is uniform throughout, free intra-abdominal air should be suspected. This air rises and collects beneath the anterior abdominal wall when the patient is in a supine position. Ascites is detected by looking for fluctuance of the abdominal cavity. A fluid wave or ripple can be generated by a quick firm compression of the lateral abdomen. The resulting wave should then travel across the abdominal wall. Movement of adipose tissue in the obese abdomen can be mistaken for a fluid wave.  4 False-positive examinations can be reduced by first pressing the ulnar surface of the examiner’s open palm into the midline soft tissue of the abdominal wall to minimize any movement of the fatty tissue while generating the wave with the opposite hand. Palpation: Palpation typically provides more information than any other single component of the abdominal examination. In addition to revealing the severity and exact location of the abdominal pain, palpation can further confirm the presence of peritonitis as well as identify organomegaly or an abnormal mass lesion. Palpation should always begin gently and away from the reported area of pain. If considerable pain is induced at the outset of palpation, the patient is likely to voluntarily guard and continue to do so, limiting the information obtained. Involuntary guarding, or abdominal wall muscle spasm, is a sign of peritonitis and must be distinguished from voluntary guarding. To accomplish this, the examiner applies consistent pressure to the abdominal wall away from the point of maximal pain while asking the patient to take a slow, deep breath. In the setting of voluntary guarding, the abdominal muscles will relax during the act of inspiration; if guarding is involuntary, they remain spastic and tense. The principal causes of abdominal pain include inflammation/infection, perforation of the viscera, obstruction of a viscus, infarction/strangulation, intraperitoneal/retroperitoneal haemorrhage, injury, and extra-abdominal and medical causes. Upper Abdominal Pain: Upper abdominal pain refers to discomfort or pain that is experienced in the abdomen located above the navel (belly button) and below the ribcage. Upper abdominal pain can have numerous potential causes, including: 1. Gastritis 2. Peptic Ulcer Disease 3. Gallstones & Biliary Colic 4. Pancreatitis 5. Gastroesophageal Reflux Disease (GERD) 6. Esophagitis 7. Hepatitis 8. Aortic Dissection 9. Boerhaave’s Syndrome 10. Acute Cholecystitis  5 Oesophagitis Anatomy: The oesophagus, an approximately 8-inch muscular tube, facilitates peristalsis for food transport. Comprising three layers—mucosa, submucosa, and muscularis externa—it is lined with stratified squamous epithelium, lamina propria, and muscularis mucosae. At its termination lies the lower oesophageal sphincter, normally guarding against stomach acid reflux. The oesophagus begins in the neck, at the level of C6. Here, it is continuous superiorly with the laryngeal part of the pharynx (the laryngopharynx). It descends downward into the superior mediastinum of the thorax, positioned between the trachea and the vertebral bodies of T1 to T4. It then enters the abdomen via the oesophageal hiatus (an opening in the right crus of the diaphragm) at T10. The abdominal portion of the oesophagus is approximately 1.25cm long – it terminates by joining the cardiac orifice of the stomach at level of T11. There are two sphincters present in the oesophagus, known as the upper and lower oesophageal sphincters. They act to prevent the entry of air and the reflux of gastric contents respectively. Vasculature: In respect to its arterial and venous supply, the oesophagus can be divided into its thoracic and abdominal components. The thoracic part of the oesophagus receives its arterial supply from the branches of the thoracic aorta and the inferior thyroid artery (a branch of the thyrocervical trunk). The abdominal oesophagus is supplied by the left gastric artery (a branch of the coeliac trunk) and left inferior phrenic artery. This part of the oesophagus has a mixed venous drainage via two routes: - To the portal circulation via left gastric vein - To the systemic circulation via the azygous vein These two routes form a porto-systemic anastomosis, a connection between the portal and systemic venous systems. Physiology: At rest, the esophagus exhibits a virtual lumen that expands during swallowing, transforming into a real lumen. The two sphincters remain contracted at rest, preventing the aspiration of air into the esophagus (UES) on one side and averting gastroesophageal reflux (LES) on the other. Swallowing encompasses both voluntary and involuntary components.  6 The voluntary phase involves chewing, mixing food and saliva, and positioning the bolus at the back of the tongue. The involuntary phase commences with the activation of receptors, initiating the swallowing reflex. The pharyngeal phase is characterized by the closure of communication with the nose, oral cavity, and larynx, along with the opening and relaxation of the UES, pharyngeal shortening and widening, and temporary respiration suppression to prevent aspiration. The subsequent opening of the UES allows the bolus to empty from the pharynx into the esophagus. During the esophageal phase, primary peristalsis propels the bolus downward to the stomach through an open LES, which begins opening even before peristaltic activity. In the orthostatic position, bolus progression results from both gravity and peristalsis, while in the clinostatic position, peristalsis is the sole factor responsible for swallowing. Pathophysiology: Oesophagitis is the inflammation of the oesophagus that occurs when acid and pepsin reflux up from the stomach, typically due to gastro-oesophageal junction incompetence, resulting in a burning sensation in the centre of the chest, often worsening when lying flat, and accompanied by a bitter taste in the mouth, particularly at night. Gastro-oesophageal junction incompetence occurs due to the lower oesophageal sphincter decreased tone and increased transient relaxations. Sign & Symptoms: The most common symptoms and signs are retrosternal chest pain and odynophagia. Esophagitis symptoms also mainly encompass a range of discomforts, including heartburn, characterized by a burning sensation in the lower mid-chest, as well as nausea, painful swallowing (dysphagia), difficulty passing or an inability to pass food through the oesophagus, vomiting (emesis), abdominal pain, and cough. Aetiology: Inadequate sphincter function can lead to acid-induced esophagitis, while infections (bacterial, viral, fungal) and immune-related diseases may also cause it. GERD, vomiting, surgery, medications, hernias, and radiation injury can irritate the oesophagus, potentially resulting in inflammation-induced narrowing, making food ingestion challenging and causing food bolus impaction. Also, patients with large Hiatal hernias seem to have a higher incidence of reflux since they contribute to a decreased tone in the LES. In contrast, any conditions that decrease oesophageal peristalsis or affects saliva content can affect the protective mechanisms in place to prevent oesophageal injury, contributing to the development of reflux esophagitis. Infection esophagitis can be caused by bacterial, fungal, parasitic, and viral micro-organisms. Bacterial esophagitis is the least common of all. Candida albicans infection is the most common cause of infectious esophagitis. Diagnosis: The diagnosis of oesophageal conditions involves several steps. Imaging techniques such as CT scans and endoscopy are used for direct visualization of the oesophagus. A flexible tube and camera are used to look for inflammation, injury, perforation, or bleeding. Biopsy involves taking small samples of oesophageal tissue for examination under a microscope. A Barium Swallow is a special X-ray that visualizes the oesophagus while the patient swallows a contrast material. Oesophageal pH Monitoring measures acid levels in the oesophagus to assess the presence of Gastroesophageal Reflux Disease (GERD). An endoscopic biopsy of  7 oesophageal lesions can be performed, and the histology study can differentiate and confirm different esophagitis aetiology. Treatment: Treatment depends on the aetiology but core principles of treatment in addition to aetiology specific treatment include acid suppression with PPI or H2 blockers, lifestyle modification, liquid to soft or pure diet to allow adequate time for healing and dietary modification.  8 Gastroesophageal Reflux Disease (GERD) Introduction: Gastroesophageal Reflux Disease refers to reflex of gastric content out of the stomach into oesophagus. Usually, the Z line marks the transition from the stratified squamous epithelium of the oesophagus to the simple columnar epithelium of the stomach. This transition helps to protect the oesophagus from the harsh digestive juices present in the stomach. GERD occurs when gastric juice refluxes into the oesophagus excessively, leading to symptomatic presentations due to decreased tone, excessive and prolonged transient lower oesophageal sphincter relaxation. Physiologic GERD, often postprandial, is typically short-lived, asymptomatic, and lacks nocturnal symptoms. Sign & Symptom: GERD is characterized by typical and atypical symptoms: Typical Symptoms: - Heartburn - Regurgitation Atypical Symptoms: - Oesophageal Symptoms: Dysphagia, chest pain, odynophagia - Extraoesophageal Symptoms: Hoarse voice, laryngitis, globus, cough, asthma, bronchitis, pneumonia, otalgia, epigastric pain. GERD typically manifests with heartburn and acid regurgitation. Heartburn refers to a burning or hot feeling extending from the distal oesophagus upwards, generally present in the post- prandial phase. It is most common in the case of abundant, spicy, or fatty meals and is worsened by lying supine and bending forwards. On the other hand, regurgitation refers to gastric content or food spontaneously going back into the mouth without episodes of vomit or gagging. It occurs after meals, when lying supine, and when bending forward. The epigastric or retrosternal burning sensation of heartburn may persist despite treatment, evolving into non-erosive reflux disease. Acid regurgitation can lead to the aspiration of acid into the larynx and lungs, causing irritation of the upper respiratory tract. This leads to a chronic cough, especially at night, asthma, a hoarse voice, and laryngitis. Due to the Z line’s replacement of normal squamous epithelium cells with metaplastic simple columnar cells, it can lead to Barrett’s Oesophagus. Over time, this may progress to adenocarcinoma. Repeated damage to the oesophagus can cause scarring, which leads to an oesophageal stricture that can bleed (hematemesis) and cause mechanical dysphagia. Extra- oesophageal symptoms include dysphagia, dyspepsia, odynophagia, GI bleeding, anaemia, weight loss, early satiety, and vomiting. Extra-oesophageal symptoms, such as chest pain, dental erosions, chronic cough, laryngitis, or asthma, can also occur.  9 Pathophysiology: GERD occurs due to an imbalance between defensive and aggressive forces. Defensive forces involve: - Intrinsic Lower Oesophageal Sphincter Pressure - Extrinsic compression of LES by crural diaphragm - Proper gastric emptying - Integrity of epithelium - Luminal clearance Aggressive forces include: - Acidity and volume of oesophageal content - Enzymatic activity The pathophysiology of GERD involves various abnormalities contributing to uncontrolled reflux of stomach contents: A. Gastro-oesophageal junction incompetence of lower oesophageal sphincter (LES) has multiple causes. Specific foods (smoking, alcohol, high caffeine intake), medications like calcium channel blockers, and hiatal hernias can exacerbate the issue. B. Increased abdominal pressure due to conditions like obesity, pregnancy, or increased gastric volume by either high food intake and/or gastroparesis (DM). C. Hypersecretion of stomach acid production due to H2 receptor stimulation, proton pump release, or conditions like Zollinger-Ellison Syndrome can increase the volume and acidity of stomach contents. D. Decreased stomach acid clearance due to impaired peristalsis or abnormal saliva production. E. Delayed gastric emptying. F. Duodenogastric reflux of bile salts and pancreatic enzymes. Histamine-2 receptors (H2 receptors) play a vital role in increasing the production of hydrochloric acid (HCL) in the stomach. These receptors are situated on the surface of parietal cells within the stomach lining. When histamine binds to these H2 receptors, it triggers a cascade of events, prompting parietal cells to synthesize and release HCL. This increased production of HCL directly contributes to the heightened acidity within the stomach's contents. Furthermore, the proton pumps found in parietal cells are essential components in the secretion of gastric acid. These pumps release hydrogen ions (H+), which are fundamental for the formation of stomach acid (HCL). In cases of Zollinger-Ellison Syndrome, an uncommon condition characterized by gastrin-secreting tumours (gastrinomas) typically located in the pancreas or duodenum, excessive gastrin production occurs. Gastrin is a hormone responsible for stimulating stomach acid production. Consequently, in Zollinger-Ellison Syndrome, the surplus gastrin leads to an overstimulation of parietal cells, culminating in the hypersecretion of stomach acid.  10 The anti-reflux barrier serves as the initial line of defense against reflux, consisting of the lower esophageal sphincter (LES), diaphragm, the acute angle of His, the phreno-esophageal ligament, and the gastric bubble. Despite its significance, it is essential to note that this structure is imperfect. Additionally, TLESR, or transient LES release, represents the opening of the LES not associated with swallowing or esophageal peristalsis. Physiologically, TLESR occurs during meals to regulate stomach gas and is induced by gastric distension through vagal nerve signaling. In normal subjects, less than 50% of TLESR is linked to exposure to acidic fluid, while GERD patients often experience significant reflux during TLESR. Various environmental and hormonal factors can alter LES tone and motility. TLESR associated with gastric content reflux is responsible for 100% of reflux episodes in normal individuals and 70-90% in GERD patients. The remaining episodes result from sphincter incontinence, particularly in cases of distal esophagus inflammation. Hiatal hernia, while a predisposition for GERD, does not necessarily indicate its presence. A non-reducible hernia is associated with greater reflux than a reducible one due to increased TLESR and the diaphragm's facilitating effect on reflux during respiration. Gastric content contains harmful components, including HCl, pepsin and trypsin, and duodenal fluid. HCl can cause cell death by inactivating Na+/K+-ATPase, while pepsin and trypsin have a proteolytic action leading to exfoliation of epithelial cells. Duodenal fluid, in cases of trans- pyloric reflux, causes damage at lower concentrations in the esophagus compared to the stomach. The integrity and resistance of the epithelium involve pre-epithelial (mucus, bicarbonate, and the unstirred water layer), epithelial (double phospholipid layer, cell junctions), and post- epithelial factors (bloodflow, tissue acid-base equilibrium). Bloodflow is crucial for nutrient supply, removal of noxious agents, and maintaining acid-base equilibrium. Esophageal exposure to acidic contents triggers increased bloodflow through mediators like histamine, NO, and CGRP. Visceral sensitivity varies among patients, with some experiencing symptoms of gastric reflux without pathological acid exposure due to altered sensitivity to stimuli. Peripheral sensitization involves receptor up-regulation for acid stimuli, while central sensitization is mediated by pathways similar to somatic sensitivity. Other mechanisms contributing to GERD include esophageal motility disorders (e.g., in rheumatological or neurological diseases) reducing peristalsis efficiency and modifying LES basal tone. Delayed gastric emptying can lead to prolonged acid secretion and stomach distension, inducing TLESR. GERD is classified into three phenotypes: 1. Non-erosive reflux disease (NERD): Presents with typical GERD symptoms but lacks oesophageal mucosal damage upon endoscopy. It is diagnosed either by biopsy (microscopic infiltrate in the epithelium) or by measuring the pH (pH-metry). 2. Erosive esophagitis (EE): Characterized by visible erosions or mucosal damage on endoscopy. Such erosive esophagitis determines reflux esophagitis which develops upon exposure of the oesophageal mucosa to the gastric acid which may induce the appearance of inflammatory lesions.  11 3. Barrett oesophagus (BE): Involves the replacement of normal squamous epithelium with specialized intestinal-like columnar epithelium, increasing the risk of oesophageal adenocarcinoma. Examining the anatomy, key structures include the Z line (oesophagus-stomach junction), the phrenoesophageal lamina (Laimer Bertelli's membrane), and structures maintaining the Z line's alignment with the diaphragm, ensuring proper gastroesophageal junction function. In obesity, this area can become pathologic due to increased abdominal pressure. A Hiatal hernia, associated with GERD, is categorized into four types: - Type 1: Sliding type (most common) - Type 2: Rolling type. - Type 3: Mixed - Type 4: Congenital, with a shorter-than-normal oesophagus (brachyesophagus). The rolling type, or "paraesophageal hernia," involves correct Z line positioning but displacement of the stomach fundus, posing risks like strangulation and ischemia. Surgical intervention is necessary, involving stomach repositioning and addressing ischemic fundus. CT scans are useful for visualizing hiatal hernias, aiding in diagnosis, and assessing hernia size and severity. Aetiology: GERD is caused by multiple different mechanisms that can be intrinsic, structural, or both, leading to the disruption of the esophagogastric junction barrier resulting in exposure of the oesophagus to acidic gastric contents. Such risk factors for the development of GERB involve: - Obesity - Cigarette Smoke - Alcohol consumption - Meals with high fatty content - Pregnancy, both due to mechanical effects (the uterus compresses the visceral organs) and because circulating hormones alter LES motility. - Genetics  12 Diagnosis: The initial step involved performing the following laboratory examinations: 1. Positivity of Clinical Symptoms 2. Esophagogastroduodenoscopy (EGD) 3. Biopsy 4. Oesophageal Manometry 5. CT scans 6. Endoscopy 7. Barium Swallow 8. Oesophageal pH Monitoring 9. Esophageal Scintigraphy 10. Bernstein Test Carry out electrocardiogram (ECG) to rule out acute coronary syndrome, especially if the patient complained of retrosternal chest pain. Following normal ECG results, the evaluation for GERD commenced, beginning with an empiric trial of proton pump inhibitors (PPIs) when symptoms were consistent with GERD. Recognize "alarm symptoms" like dysphagia, vomiting, anaemia, and weight loss, as they could signify complications. In cases of alarm symptoms or the absence of improvement with PPI treatment, further investigation was recommended. Esophagogastroduodenoscopy (EGD) and biopsies can then be used to assess complications such as esophagitis, strictures, Barrett's oesophagus, or oesophageal cancer. Additionally, use oesophageal manometry to assess motility and lower oesophageal sphincter pressure and pH monitoring to detect acid reflux episodes, with a specific DeMeester score threshold indicative of GERD. Treatment: The treatment approach for gastroesophageal reflux disease (GERD) involves addressing several key issues: ▪ Increasing Lower Oesophageal Sphincter (LES) Tone: One of the primary problems in GERD is low LES tone. To address this, patients should avoid triggers like smoking, caffeine, and alcohol. ▪ Reducing Intra-gastric Pressure: High intra-gastric pressure can exacerbate GERD. Patients should avoid consuming very large meals and consider weight loss, especially if they are overweight or obese. Medications like metoclopramide can be considered to increase motility in patients with gastroparesis. ▪ Lowering Acid Production: Excessive hydrochloric acid production contributes to GERD. Histamine 2 receptor antagonists (H2RAs) are an option when there is no esophagitis, and the symptoms are mild (less than two episodes per week). H2RAs block H2 receptors on parietal cells, reducing acid production. For more severe cases or when esophagitis is present, proton pump inhibitors (PPIs) are recommended. PPIs block the proton pump channel, further reducing acid production. ▪ Managing Hiatal Hernia: Sliding hiatal hernias often require supportive care, but surgical intervention may be considered if severe esophagitis, strictures, or GI bleeding is present.  13 ▪ Refractory GERD: When patients do not respond to the above treatments, surgical options like Nissen fundoplication can be considered. This surgery involves wrapping the fundus around the LES to enhance tone and prevent reflux. Normal oesophageal lining composed of stratified squamous epithelium. Chronic irritation or other factors trigger metaplasia, changing cells to columnar epithelium. These columnar cells may become neoplastic, a state known as dysplasia, potentially leading to cancerous growth. When seeing a patient with GERD, doctors must recommend them a lifestyle that protects the defensive forces and impairs the aggressive forces. For example, avoid coffee, because very hot or very cold beverage will affect the integrity of the epithelium. Pregnancy and obesity will raise the stomach, and hence impair extrinsic compression. Avoiding heavy meals allows to promote proper gastric emptying: it is better to do small meals, 4 or 5 times a day. Avoiding acid food and beverages will allow to decrease acidity. Regarding oesophageal peristalsis, not much ban be done, but there is one disease (scleroderma) that can dramatically affect the oesophageal peristalsis and cause GERD.  14 Boerhaave Syndrome Introduction & Pathophysiology: Boerhaave's Syndrome (A.K.A Spontaneous Oesophageal Rupture) is a full-thickness tear occurring at the esophago-gastric junction because of forceful attempts to suppress vomiting. The act of suppressing vomiting generates a substantial pressure surge at the esophagogastric junction, ultimately leading to oesophageal rupture. This rupture induces sudden and severe pain, attributed to the stomach's contents breaching the chest cavity, inciting guarding, and abdominal and chest discomfort. This ultimately leads to inflammation, emphysema, or necrosis if left untreated. A Mallory Weiss tear will cause you to vomit blood, but it doesn't tear all the way through the oesophagus. Boerhaave's syndrome, on the other hand, ruptures the full thickness of the oesophagus wall. This is also called a transmural tear. Aetiology: What renders Boerhaave's Syndrome particularly perilous, with a mortality rate close to 80%, is its anatomical location within the mediastinum. The mediastinum is a critical anatomical region housing various vital structures, including the oesophagus, great vessels, thymus, and surrounding adipose tissue. These vital structures make oesophagus vulnerable to intra-abdominal pressure due to forceful attempts to suppress vomiting, often associated with heavy alcohol consumption, esophagitis, severe or prolonged stretching or other causes of increased intra-oesophageal pressure can lead to Boerhaave’s Syndrome. Traditional antibiotics have limited efficacy in this context due to the anatomical location within the mediastinum, which has poor circulation. This makes infections like mediastinitis highly lethal. The breach of this sterile compartment results in severe cellulitis involving poorly vascularized adipose tissue, where antibiotics struggle to penetrate. Sign & Symptoms: Ruptures most commonly occur in the left posterolateral wall of the distal third of the oesophagus, extending into the left pleural cavity. Intrathoracic oesophageal perforations can lead to mediastinal inflammation, emphysema, or necrosis due to gastric contents entering. Boerhaave's Syndrome emerges with various clinical complications such as: - Sudden and severe pain in the chest and abdomen - Tenderness - Guarding - Subcutaneous emphysema - Vomiting - Lower thoracic pain - Retrosternal chest pain - Adipose tissue, being hypovascularized, complicates infection management. Diagnosis: Treatment for Boerhaave’s Syndrome involve clinical suspicion based on history and physical examination, confirmed by imaging studies such as chest X-ray, contrast oesophagography, or computed tomography (CT) scan. Treatment: Treatment options encompass conservative, endoscopic, or surgical approaches. Critical aspects of treatment include volume replacement, broad-spectrum antibiotic coverage, and prompt surgical assessment. Surgical intervention entails primary oesophageal repair through open thoracotomy or video-assisted thoracoscopic surgery (VATS) with fundic reinforcement, with the latter being the gold standard when performed within the initial twenty- four hours.  15 Gastritis Introduction & Pathophysiology: Gastritis is a medical condition characterized by inflammation, erosion, or irritation of the gastric mucosa, the lining of the stomach. It can be acute (short-term) or chronic (long-term) and may vary in severity. Aetiology: This condition can be attributed to a variety of potential causes. The primary culprits include excessive alcohol consumption which irritates and does the stomach lining, making it more susceptible to inflammation and increase the stomach’s ability to synthesis more hydrochloric acid production. Prolonged usage of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen can also disrupt the stomach’s protective mechanisms, leading to gastritis. NSAIDs cause gastritis through the inhibition of prostaglandin synthesis. Prostaglandins are responsible for maintaining the protective mechanisms of gastric mucosa from injuries caused by hydrochloric acid. Gastritis may also develop in the aftermath of significant surgical procedures, severe injuries, burns, or infections. Individuals who have undergone weight loss surgery are also susceptible to gastritis. In the long term, bacterial infection, particularly by Helicobacter pylori, can contribute to the development of this condition. Additionally, certain medical conditions like pernicious anaemia, chronic bile reflux, high levels of stress, and specific autoimmune disorders may trigger gastritis. Sign & Symptoms: The most prevalent symptom associated with gastritis is abdominal pain, although there are other notable indicators including: - Indigestion - Abdominal bloating - Nausea - Vomiting. Some individuals may experience sensations of fullness or a burning sensation in the upper abdomen. Some cases may not exhibit noticeable symptoms. Diagnosis: To diagnose gastritis, medical professionals may employ various diagnostic methods, such as endoscopy (e.g., gastroscopy) to identify inflammation, erosion, or ulceration within the stomach. Undertaking biopsy to examine under a microscope may help identify the presence of H/pylori, or any other abnormalities. Carrying out complete blood count would help identify anaemia in the case of chronic gastritis and bleeding, high level of serum pepsinogen, a precursor to the stomach enzyme pepsin, and elevated CRP if inflamed. Treatment: Treatment strategies for gastritis encompass the use of antacids or other medications, including proton pump inhibitors, H2- blockers and antibiotics, along with dietary modifications that involve avoiding spicy or hot foods. In cases of pernicious anaemia, individuals may receive B12 injections as part of their treatment plan. Avoid aetiological causes such as alcohol intake and NSAID use. For H/pylori-associated gastritis, triple therapy should be initiated involving clarithromycin, amoxicillin, and proton-pump inhibitor.  16 Mediastinitis Pathophysiology: Mediastinitis is the inflammation or infection of the mediastinum, the central compartment of the thoracic cavity. It can affect the function and structure of the vital organs and blood vessels in this area, such as the heart, the aorta, the trachea, and the oesophagus. It can also cause complications such as sepsis, bleeding, organ failure, or superior vena cava syndrome. Aetiology: Mediastinitis can be acute or chronic, and either infectious or non-infectious. The most common causes are oesophageal perforation and chest surgery, which can introduce bacteria into the mediastinum. Other causes include dental infections, lung infections, thymus infections, tuberculosis, histoplasmosis, sarcoidosis, radiation therapy, or silicosis. These disorders can trigger an immune response and a fibrotic process that can compress the mediastinal structures. Signs and symptoms: Mediastinitis can cause severe chest pain, difficulty swallowing, high fever, rapid heart rate, difficulty breathing, swelling of the neck or upper chest, cough, guarding, and fatigue. The severity of the signs and symptoms may vary depending on the underlying cause and the extent of the inflammation or infection. Diagnosis: Mediastinitis can be diagnosed based on the clinical presentation, the history of risk factors, and the imaging findings. A chest x-ray can show air in the mediastinum, which can suggest oesophageal perforation. A computed tomography (CT) scan can confirm the diagnosis and show the extent of the disease. A needle aspiration biopsy can be done to obtain fluid samples for microbiological and histological analysis. Other tests, such as blood cultures, serology, or bronchoscopy, may be done to identify the causative agent or rule out other conditions. Treatment: Mediastinitis requires prompt and aggressive treatment to prevent fatal outcomes. The treatment may include antibiotics, surgery, supportive care, and management of the underlying causes. Antibiotics are given to treat the bacterial infection and should cover the oral and gastrointestinal flora. Surgery may be needed to drain abscesses, remove infected tissues, or repair perforations. Supportive care may include pain management, respiratory support, and nutritional support. Management of the underlying causes may involve repairing oesophageal perforations, treating dental infections, or administering antifungal or antituberculous drugs.  17 Peptic Ulcer Disease Introduction: Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower oesophagus, distal duodenum, or jejunum. An ulcer is not an erosion. An ulcer penetrates the whole thickness of the mucosa, affecting the underlying submucosal, muscular, and serosal layers. It may even cause a perforation of the entire GI wall. On the other hand, an erosion is limited to the mucosa and does not pass through the muscularis mucosa. Classification: Four different kinds of peptic ulcers can be distinguished based on their location: 1. Duodenal Ulcer 2. Gastric Ulcer 3. Oesophageal Ulcer 4. Meckel’s Diverticulum Ulcers may even form at the level of the anastomotic junction in a patient who has had a total gastrectomy. Aetiology: The two major primary cause of peptic ulcers are: 1. Helicobacter pylori (H. pylori) 2. NSAIDs e.g., low-dose aspirin Other frequent and potentially deadly aetiologies include: - Malignancy (Pancreatic tumour may penetrate the duodenal wall and ulcerate) - Haemodynamic Stress (Due to trauma or severe burn etc.) - Zollinger-Ellison Syndrome (Gastric hypersecretion) - Cocaine Consumption - Radiotherapy - Smoking cigarettes  18 Pathophysiology: Helicobacter pylori, a bacterial infection accounting for approximately 90% of gastric ulcers and 80% of duodenal ulcers. H. pylori causes the release of toxins, which lead to an inflammatory response. This response inhibits the detection of H+ in the gastric antrum, leading to an over-secretion of H+. It is not well understood why H. pylori causes duodenal ulcer in some patients and gastric ulcers in others but it’s important to remember that: - Gastric ulcers are associated with body chronic gastritis. - Duodenal ulcers are associated with antral chronic gastritis. Nonsteroidal anti-inflammatory drugs use is the second most common cause of Peptic Ulcer Disease (PUD) after H. pylori infection. The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting the COX-1 enzyme, resulting in decreased gastric mucus, prostaglandin, and bicarbonate production. This results in a decrease in mucosal blood flow and increase in H+ secretion. It’s important to take NSAIDs during the meals, as the presence of food will protect the stomach lining by buffering the acid. Smoking cigarette diminishes the production of prostaglandins (PGs), thereby impeding the generation of mucus and bicarbonates. This reduction in PGs compromises the protective mechanisms of the gastric and duodenal walls against acid-induced damage. Smoking cigarette also extends to fostering the proliferation of H. Pylori by not only facilitating the growth of this pathogen but also increases the likelihood of recurrent episodes. Sign & Symptoms: Peptic ulcer symptoms include notable epigastric abdominal pain, primarily located in the upper abdomen beneath the ribcage, often radiating to the chest. Other associated symptoms encompass: - Abdominal fullness - Nausea due to irritation of somatic innervation - Vomiting due to vasculature erosion within stomach - Hematemesis due to vasculature erosion within oesophagus - Melena due to oxidation of blood within GI by HCL & digestion - Progressive dysphagia due to irritation of somatic innervation  19 The clinical presentation of peptic ulcers exhibits slight variations depending on their location. Gastric ulcers may present with diverse symptoms ranging from iron-deficiency anaemia to an acute abdomen with bleeding and perforation. Dyspeptic symptoms such as abdominal epigastric pain, which may be dull and persistent or burning, occur, with 30% of cases experiencing night-time onset. This pain, in 20% of cases, may radiate to the back and is exacerbated by food intake. Nausea and vomiting, potentially leading to weight loss, are also common in gastric ulcers. Conversely, duodenal ulcers manifest with abdominal epigastric pain that often occurs at night, starts late after food ingestion, does not radiate, and is alleviated by food, milk, or antacids. Nausea and vomiting may also be present. Importantly, some cases, especially with duodenal ulcers, may be entirely asymptomatic. Diagnosis: The symptoms of peptic ulcers are highly non-specific, emphasizing the need for a definitive diagnosis based on esophagogastroduodenoscopy (EGDS). This procedure is coupled with a biopsy to identify potential Helicobacter pylori (H. pylori) infection or neoplastic degeneration. Therefore, when a patient presents with dyspepsia, doctors should assess for the presence of alarm symptoms. If these symptoms are identified, performing an upper gastrointestinal endoscopy is recommended. Diagnosing peptic ulcers involves three primary methods: - Esophagogastroduodenoscopy (EGD) - Biopsy - Upper GI Endoscopy - Urea Breath Test  20 Treatment: Effective peptic ulcer treatment hinges on eradicating the causative agent such as stopping or decreasing the dose of NSAIDs and treating Helicobacter pylori infection, which is typically achieved with first line triple therapy: - Proton Pump Inhibitor (PPI) - Clarithromycin - Amoxicillin First line triple therapy (Proton Pump Inhibitor, Clarithromycin, and Amoxicillin) treats and eradicate H. pylori effectively. Antibiotics are prescribed to eliminate the bacterial infection; however, success is not always guaranteed due to the bacteria's resistance. Managing excessive stomach acid production is another crucial facet of treatment, achieved through antacids categorized as: 1. PPIs (Proton Pump Inhibitors) 2. H2-Blockers (Histamine-2 receptor blockers) Both medications reduce acid production by stomach cells. However, artificially halting acid production can disrupt proper digestion. It is considered better and safer to control acid levels by staying hydrated and avoiding foods that may trigger excessive acid production. Complications of peptic ulcer disease include cancer, bleeding, perforation, penetration, and obstruction. Bleeding leads to iron deficiency anaemia with hypovolemic symptoms. Perforation leads to bacterial peritonitis.  21 Acute Pancreatitis Anatomy: The pancreas is an abdominal glandular organ with both exocrine and endocrine functions. It’s typically divided into five parts (head, uncinate process, neck, body and tail). The common bile duct is formed at the free edge of the lesser omentum by the union of the cystic and common hepatic ducts. It descends posteriorly to the superior part of the duodenum and lies in a groove on the posterior surface of the head of the pancreas before crossing the pancreatic parenchyma. It then joins the main pancreatic duct, and together they form the hepato-pancreatic ampulla (ampulla of Vater) that distally opens into the duodenum through the major duodenal papilla. Secretions into the duodenum are controlled by a muscular valve – the sphincter of Oddi. It surrounds the ampulla of Vater, acting as a valve. Vasculature: The pancreas is supplied by the pancreatic branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal (from coeliac trunk) and superior mesenteric arteries, respectively. Venous drainage of the head of the pancreas is into the superior mesenteric branches of the hepatic portal vein. The pancreatic veins draining the rest of the pancreas do so via the splenic vein. Introduction: Acute pancreatitis is characterised by reversible pancreatic parenchymal injury associated with inflammation that can be both self-limited or spread to the abdomen and give systemic complications. Pancreatitis is divided into two forms, acute and chronic, both are initiated by injuries that lead to autodigestion of the pancreas by its own enzymes.  22 Under normal circumstances, the following mechanisms protect the pancreas from self- digestion by its secreted enzymes: - Produce inactive proenzymes (zymogens), packaged within secretory granules. - Most proenzymes are activated by trypsin, which itself is activated by duodenal enteropeptidase (enterokinase) in the small intestine; thus, intrapancreatic activation of proenzymes is normally minimal. - Acinar and ductal cells secrete trypsin inhibitors, including serine protease inhibitors Kazal type 1 which further limit intrapancreatic trypsin activity. Pathophysiology: Acute pancreatitis can be subdivided into two types: - Interstitial Oedematous Pancreatitis - Necrotising Pancreatitis Acute pancreatitis is characterised by reversible pancreatic parenchymal injury associated with inflammation and diverse aetiologies, including toxic exposures (e.g., alcohol), pancreatic duct obstruction (e.g., biliary calculi), inherited genetic defects, vascular injury, and infections. Acute pancreatitis is relatively common where biliary tract disease and alcoholism account for approximately 80% of cases of acute pancreatitis. Acute pancreatitis is characterized by the inappropriate activation of pancreatic enzymes, primarily trypsinogen, within the pancreas. Normally, trypsinogen is converted into its active form, trypsin, in the duodenum to aid in protein digestion. In acute pancreatitis, trypsinogen undergoes premature activation within the pancreas, typically due to its interaction with lysosomal enzymes, especially cathepsin.  23 Early in the pathophysiological process of pancreatitis, zymogens and lysosomal enzymes co- localize. Cathepsin B, a lysosomal enzyme, activates trypsinogen within these organelles. The interaction of cathepsin B and trypsinogen, triggered by pancreatitis-inducing stimuli, can release cathepsin B into the cytosol, leading to apoptosis or necrosis and subsequent acinar cell death. Early in the pathophysiological process of pancreatitis, zymogens and lysosomal enzymes co- localize. Cathepsin B, a lysosomal enzyme, activates trypsinogen within these organelles. The interaction of cathepsin B and trypsinogen, triggered by pancreatitis-inducing stimuli, can release cathepsin B into the cytosol, leading to apoptosis or necrosis and subsequent acinar cell death. This initiation sets off a cascade of events, leading to inflammation, oedema, vascular injury, and cellular death. Cellular death in acute pancreatitis can occur through two primary mechanisms: necrosis, which is chaotic and damaging, and apoptosis, a more controlled process. The balance between these two forms of cellular death is regulated by caspases, with caspase depletion, often resulting from chronic ethanol exposure or severe insults, tipping the balance toward necrosis. The development of acute pancreatitis involves key mechanisms, including pancreatic duct obstruction, primary acinar cell injury, and defective intracellular transport. The condition triggers an extensive inflammatory response, with acinar cells releasing inflammatory mediators like TNF-alpha and IL-1, leading to neutrophil recruitment and local inflammation. Systemic complications may include hypovolemia, acute respiratory distress syndrome, disseminated intravascular coagulation, renal failure, cardiovascular failure, and gastrointestinal haemorrhage. Histologically, acute pancreatitis presents with acute inflammation and necrosis in the pancreas parenchyma, focal enzymic necrosis of pancreatic fat, and vessel necrosis (haemorrhage). These manifestations result from the intrapancreatic activation of pancreatic enzymes, particularly lipase, which induces fat tissue necrosis, vessel damage, and potential thrombosis. Inflammatory infiltrate, rich in neutrophils, may extend to adjacent fascial layers due to the pancreas's lack of a capsule.  24 Pseudocysts can develop as a complication of pancreatitis. These are the collection of fluid, tissue, and debris that form in or around the pancreas. Persistent pain or continued high amylase levels may suggest the presence of pseudocysts. These symptoms can persist for several weeks after the initial pancreatitis episode. Complications of pseudocysts may include infection, rupture, haemorrhage, or obstruction of adjacent structures. Asymptomatic, non-enlarging pseudocysts can be monitored with imaging, while symptomatic, rapidly enlarging, or complicated pseudocysts may require decompression. Aetiology: Alcohol consumption transiently increases contraction of the sphincter of Oddi (the muscle at the Papilla of Vater), and chronic alcohol ingestion results in the secretion of protein- rich pancreatic fluid that leads to the deposition of inspissated protein plugs and obstruction of small pancreatic ducts. Alcohol also has direct toxic effects on acinar cells. Alcohol-induced oxidative stress may generate free radicals in acinar cells, leading to membrane lipid oxidation and free radical production, which leads to activation of the pro- inflammatory transcription factors AP1 and NF-κB. Oxidative stress also may promote the fusion of lysosomes and zymogen granules and alter intracellular calcium levels, possibly through mitochondrial damage, promoting the intraacinar activation of trypsin and other digestive enzymes. Other proven or suspected triggers of acute pancreatitis in the remaining sporadic cases include the following: - Metabolic disorders, such as hypertriglyceridemia - Hypercalcaemic states, such as hyperparathyroidism. - Medications including furosemide, and oestrogen. - Traumatic injury of acinar cells - Ischemic injury to acinar cells, caused by shock, vascular thrombosis, embolism. - Infections - Scorpion - Hereditary (Genetic)  25 There are also potential causes of pancreatitis post-surgical in hospital setting: - Post CABG Amylase Elevation: Approximately 25% of patients who undergo Coronary Artery Bypass Grafting surgery may experience elevated amylase levels due to mechanical manipulation of the pancreas during the procedure. - Necrotizing Pancreatitis after CABG: Around 1% of CABG patients develop necrotizing pancreatitis. Typically identified on CT scan with IV contract. Obstructive factors leading to pancreatitis include pancreatis tumours (adenocarcinoma, acinar cell carcinoma), anatomical abnormalities (e.g., pancreas divisum, sphincter of Oddi dysfunction), inflammatory conditions (e.g., Crohn’s disease), and parasitic infections like ascariasis. Percutaneous Endoscopic Retrograde Cholangiopancreatography (ERCP): ERCP is a medical procedure used to diagnose and treat conditions in the bile ducts and pancreas. Necrotizing pancreatitis is a rare complication of ERCP, occurring in about 1 in 1,000 cases. Factors that can contribute to complications during ERCP include the pH and osmolarity of the contrast dye, stent displacement, mechanical issues like swelling of the papilla, use of wires in the duct, bacterial reflux, and the thermal effects of sphincterotomy. Various risk factors can increase the likelihood of complications during ERCP, such as patient-related factors, the nature of the procedure, and other specific conditions or factors. These factors include sphincter of Oddi dysfunction (SOD), dilated ducts, the absence of cancer or stones, repeated attempts at cannulation, extensive pancreatic dye injection, and more. Prophylactic measures can help reduce the risk of complications during ERCP. These measures may include the use of indomethacin (a nonsteroidal anti-inflammatory drug) per rectum (PR), the use of pancreatic duct (PD) stents, and wire- guided cannulation techniques. Drugs and Substances Associated with Acute Pancreatitis: Certain medications and substances can induce acute pancreatitis. These include various categories such as antiretroviral drugs for AIDS (didanosine, pentamidine), antimicrobial agents (e.g., metronidazole, sulfonamides), diuretics (e.g., furosemide, thiazides), immunosuppressive/antimetabolite drugs (e.g., azathioprine, L-asparaginase), neuropsychiatric drugs (e.g., valproic acid), anti-inflammatory drugs (e.g., sulindac, sulfasalazine), and others. Infections Associated with Pancreatitis: Infections, both viral and bacterial, can contribute to pancreatitis. Viruses like mumps, hepatitis B, and cytomegalovirus, as well as bacteria like Mycoplasma, Legionella, and Salmonella, are mentioned. Fungal and parasitic infections are also listed. Exotic Causes of Pancreatitis: Some exotic causes of pancreatitis, such as scorpion stings (Tityus trinitatis), bites from brown recluse spiders, and various animal-related envenomations like snake bites and encounters with African "killer" bees and Gila Monsters.  26 Trivia - Scorpion Causing Pancreatitis: The name of the scorpion as a cause of pancreatitis is Tityus trinitatis, which is found in Central and South America as well as the Caribbean. Hereditary pancreatitis is a condition characterized by recurrent episodes of severe acute pancreatitis, often beginning in childhood, and potentially progressing to chronic pancreatitis. It has a strong genetic basis, and three key genes are associated with its development: PRSS1, SPINK1, and CFTR. The PRSS1 gene mutations, known as gain-of-function mutations, render trypsin resistant to self-inactivation or more prone to proteolytic activation. Consequently, hereditary pancreatitis due to PRSS1 mutations follows an autosomal dominant mode of inheritance. Conversely, SPINK1 gene mutations, which encode a trypsin inhibitor, result in a loss of function and lead to an autosomal recessive form of hereditary pancreatitis. Furthermore, mutations in the CFTR gene, responsible for cystic fibrosis, have also been linked to pancreatitis, particularly in patients with SPINK1 mutations. Mutations in CFTR reduce bicarbonate secretion by pancreatic ductal cells, contributing to protein plugging, duct obstruction, and pancreatitis.  27 Sign & Symptoms: Abdominal pain is the cardinal manifestation of acute pancreatitis. Anorexia, nausea, and vomiting frequently accompany the pain. Other presenting features include: - Tachycardia - Tachypnoea - Fever - Abdominal guarding - Loss of bowel sounds. - Nausea & Vomiting - Jaundice - Glycosuria - Pyrexia - Hypocalcaemia - Loss of appetite - Haemodynamic instability, including shock. - Peritonitis - Hiccup - Grey Turner Sign - Cullen Sign You may also observe ‘Grey Turner Sign’ which is a rare flank discoloration due to retroperitoneal bleed in patient with pancreatic necrosis. Additionally, ‘Cullen’s sign’ may also be observed referring to periumbilical discoloration (haemorrhagic discoloration of the umbilicus). Elevated plasma level of amylase and lipase support the diagnosis of acute pancreatitis, as does the exclusion of other causes of abdominal pain. Full-brown acute pancreatitis is a medical emergency. Many of the systemic features of severe acute pancreatitis can be attributed to release of toxic enzymes, cytokines, and other mediators into the circulation and explosive activation of a systemic inflammatory response, resulting in leucocytosis, disseminated intravascular coagulation, oedema, and acute respiratory distress syndrome.  28 Diagnosis: The cornerstone of the diagnosis of AP is the clinical finding plus an elevation of pancreatic enzyme levels in the plasma. A threefold or higher elevation of amylase and lipase levels confirm the diagnosis. The serum half-life of amylase is shorter than that of lipase, hence determination of lipase levels is a more sensitive indicator to establish the diagnosis. Also, lipase is also a more specific marker of AP because serum amylase levels can be elevated in several conditions, such as peptic ulcer disease, mesenteric ischemia, salpingitis, and macroamylasemia. Patients with AP are typically hyperglycaemic; they can also have leucocytosis and abnormal elevation of liver enzyme levels in particular, the elevation of alanine aminotransferase in serum, CRP, IL-6, IL-8 and BUN. Simple abdominal radiographs such as ultrasound are not useful for diagnosis due to limitation by intra-abdominal fat and increased intestinal gas because of the ileus but done to eliminate other possibilities as differential diagnosis. Contract enhanced computed tomography show enlarged pancreas when standing. Abdominal magnetic resonance imaging (MRI) is also useful to evaluate the extent of necrosis, inflammation, and presence of free fluid. In a patient with vomiting and abdominal pain, patient must undergo hepatic markers test such as AST, ALT, GGT, ALP, Bilirubin to determine the aetiology where high AST suggests gallstones and high GGT suggest alcoholic pancreatitis. Although magnetic resonance cholangiopancreatography (MRCP) is not indicated in the acute setting of AP, it allows complete visualization of the biliary and pancreatic duct anatomy to determine the presence of gallstones. In the setting of gallstone pancreatitis, endoscopic ultrasound (EUS) is useful for evaluation of persistent choledocholithiasis and useful in obese patients. ERCP can be used selectively as a therapeutic measure.  29 General Management / Treatment: The following information outline the general management and treatment principles for pancreatitis: 1. Remove offending agent: Remove or address the agent which causes pancreatitis e.g., if gallstones are the causes, then treat or remove the gallstones may be necessary. 2. Support Care: Includes several key components such as Nil Per Os (NPO) until the patient is pain free, nasogastric suction (NG) to relieve pressure on the digestive system in case if there is ileus disruption or vomiting. 3. Aggressive Volume Repletion: Intravenous fluids (IVF) are administered to aggressively rehydrate the patient. 4. Pain Management: Narcotic analgesics are used to manage severe pain such as Meperidine and Morphine. 5. ERCP & Biliary Sphincterotomy 6. Proton Pump Inhibitors: PPI to prevent stress ulcers. Several clinical clues, such as tachycardia, hypotension, and abdominal distension, can help guide the decision to admit a patient to the ICU. Moreover, clinical indices like the Ranson score, APACHE score, and BISAP score are used to gauge the severity of pancreatitis, aiding medical professionals in determining the appropriate course of action for each patient.  30 Pancreatic Carcinoma Introduction & Pathophysiology: Ductal adenocarcinoma represents approximately 85% of all pancreatic neoplasms. Over 95% of pancreatic cancers originate from the exocrine part of the pancreas, responsible for producing digestive enzymes, with the remaining 5% or less affecting the endocrine part, specifically the neuroendocrine islet cells. The pancreas can be anatomically divided into the head, body, and tail. Notably, when imaging pancreatic cancer in the head of the pancreas, close attention must be paid to the involvement of the portal vein and superior mesenteric vein. In cases where the tumour infiltrates the duodenum but remains distant from major vessels such as the portal vein, superior mesenteric vein, and superior mesenteric artery, surgical resection is a viable option, necessitating neoadjuvant therapy. The involvement of the duodenum is not problematic because surgical intervention in cases of pancreatic head tumours involves a procedure known as pancreatoduodenectomy, also referred to as the Whipple's procedure. This operation entails the removal of both the head of the pancreas and the duodenum due to their shared blood supply. The Whipple's procedure is considered one of the most complex and challenging surgeries in the field of general surgery. Ductal adenocarcinomas, accounting for over 85% of pancreatic cancers, are exocrine in origin. They manifest most frequently in the head of the pancreas and are characterized by solid, scirrhous tumours with neoplastic tubular glands within a densely fibrous stroma. These tumours tend to infiltrate locally, often along nerve sheaths, lymphatic vessels, and blood vessels, leading to common metastases in the liver and peritoneum. Pancreatic intraepithelial neoplasia (PanIN) refers to proliferative lesions within the pancreatic ducts that can precede invasive ductal adenocarcinoma. In many cases, invasive pancreatic cancer arises from well-defined precursor lesions like PanIN. Multiple genes are somatically mutated or epigenetically silenced in each pancreatic carcinoma, consistent with their stepwise evolution from precursor lesions, and the patterns of genetic alterations in pancreatic carcinoma as a group differs from those seen in other malignancies. Such genetic mutations involve KRAS (chromosome 12p) which is the most frequently altered oncogene in pancreatic cancer, with activating point mutations being present in 90-95% of cases. Sign & Symptoms: Symptoms associated with cancer of the head of the pancreas include: 1. Jaundice: Jaundice, characterized by the yellowing of the eyes and skin, is a hallmark symptom of pancreatic head cancer. It arises from the constriction of the common bile duct, typically occurring near the ampulla of Vater. This constriction leads to the dilation of the bile duct and Wirsung duct upstream. This distinctive feature allows for the detection of the tumour in its early stages (Stage I or II) when it closely involves the biliary duct. However, if the tumour is distant from the biliary duct, jaundice may only manifest in advanced disease. 2. Back Pain and Weight Loss 3. Courvoisier’s Sign: An observable sign known as Courvoisier’s sign is the distention of the gallbladder due to obstruction of the biliary tree. It results from the compression of these structures by the tumour.  31 In cases of cancer located in the body or tail of the pancreas, symptoms are less common due to the distance from these vital structures, and they usually manifest only in the presence of a large, infiltrating tumour. Patients with body or tail pancreatic cancer are more likely to present with symptoms such as: 1. Abdominal Pain: The most common symptom in these cases is abdominal pain. 2. Weight Loss: Weight loss is another prevalent symptom. 3. Anorexia: Loss of appetite and anorexia may also be experienced. Additional symptoms that may become apparent as the tumour advances include asthenia, dark urine, nausea, diarrhoea, epigastric pain, jaundice, hepatomegaly, and a mass in the right upper quadrant of the abdomen. Signs of advanced pancreatic cancer can include ascites, which is an accumulation of fluid in the abdominal cavity. Diagnosis: The staging of pancreatic cancer is a critical step in its diagnosis and management. It involves a series of assessments and tests to determine the extent and severity of the disease. Initially, routine blood tests, including liver function tests such as bilirubin, are conducted to provide baseline information. Tumour markers like CA 19-9 and CEA are measured, although these are primarily used for follow-up rather than staging due to their variability and lack of specificity. Imaging plays a significant role in staging, with CT scans, MRI, and, on occasion, ultrasound helping to visualize the tumour and its impact. Endoscopy, specifically Endoscopic Retrograde Cholangiopancreatography (ERCP), is used to evaluate and treat tumours affecting the biliary tree, as well as to conduct biopsies. Laparoscopy is rarely used for pancreatic cancer staging. It's essential to note that tumour markers like CA 19-9 are not specific for staging and are better suited for monitoring during treatment. Ultrasound is effective for examining the pancreas, while CT scans are considered a primary imaging technique for staging. Endoscopic Ultrasound (EUS) is a specialized endoscopy that provides detailed images of the pancreatic head and allows for ultrasound-guided biopsies. PET scans are not typically used in the initial diagnosis of pancreatic cancer; instead, CT scans and, in some cases, MRI are employed for the initial assessment. These diagnostic and staging methods collectively help determine the stage and extent of pancreatic cancer, guiding subsequent treatment decisions. Classification: TNM staging is a valuable system for assessing the extent of cancer spread, incorporating T (tumour), N (nodes), and M (metastasis) factors to determine the cancer's stage. Here's an overview of the TNM stages for pancreatic cancer: 1. Stage IA (T1aN0M0): At this stage, the tumour is minimal, categorized as T1, with no involvement of nearby lymph nodes (N0) and no distant metastases (M0). It is quite uncommon to diagnose pancreatic cancer at this early stage since the tumour size must be less than 2 cm. Typically, patients with tumours of this size remain asymptomatic, showing no signs or symptoms. However, if the tumour is situated very close to the biliary tree, despite its small size, it can lead to symptoms like jaundice due to the compression of the biliary tree. In most cases, for jaundice to manifest as a symptom, the tumour needs to be at least 4 cm in size.  32 2. Stage IB (T2N0M0): This stage features larger tumours, greater than 2 cm in size, but they are still confined to the pancreas with no lymph node involvement or distant metastases. 3. Stage IIA: Tumours at this stage can extend to involve adjacent structures, such as the duodenum. 4. Stage IIB (T1-3N1M0): In this stage, tumours can vary in size (T1-3) and are associated with lymph node involvement (N1), while no distant metastases are present. 5. Stage III: This stage signifies locally advanced or unresectable tumours. The cancer has spread to major blood vessels near the pancreas, including the superior mesenteric artery, celiac axis, common hepatic artery, or portal vein. At this stage, distant metastases are not observed. 6. Stage IV: Stage IV is indicative of the most advanced stage, where cancer has metastasized to distant sites far from the pancreas. These sites can include the lung, liver, and the peritoneal cavity, among others. TNM staging offers a comprehensive framework for classifying pancreatic cancer, considering the size and extent of the tumour, lymph node involvement, and the presence or absence of distant metastases. It plays a crucial role in guiding treatment decisions and predicting the prognosis of patients with pancreatic cancer. Treatment: Treatment for pancreatic cancer is often challenging, with surgery being the only curative option. However, only a small percentage of patients, typically between 10% and 20%, are suitable candidates for surgical resection. Even among those who undergo surgery, the prognosis remains relatively poor, with a 5-year survival rate of about 20% and a median survival time ranging from 13 to 20 months. Unfortunately, up to 60% of patients are already diagnosed with metastases at the time of their diagnosis, leading to a median survival of 4 to 6 months. In recent years, new chemotherapy regimens have been introduced, such as gemcitabine and abraxane, offering additional treatment options. One of the primary surgical procedures used for resectable pancreatic cancer is the Whipple procedure which involves the removal of the affected parts of the pancreas, duodenum, biliary tree, and gallbladder. After resection, a complex reconstruction is necessary, as the remaining pancreas, biliary tree, stomach, duodenum, and jejunum need to be reconnected to maintain digestive functions. This reconstruction involves challenging anastomoses at three points: the pancreatocojejunal anastomosis, bilio-jejunal anastomosis, and duodeno-jejunal anastomosis. In cases where the tumour is in the tail of the pancreas, a pancreatosplenectomy is performed. This procedure involves the removal of both the spleen and the tail of the pancreas. The process includes creating retrogastric space, suspending the stomach, isolating, and suspending the splenic artery, and dissecting the pancreatic body after its suspension. The spleen is also isolated and removed together with the tail of the pancreas, with haemostatic material applied to the remaining pancreatic tissue.  33 Liver Tumours Liver cancer is the sixth most common cancer worldwide, and the fourth leading cause of cancer-related deaths. Liver cancer comprises a heterogenous group of malignant tumours with different histologic features and unfavourable prognosis that are divided into: - Primary Liver Neoplasm - Secondary Liver Neoplasm Primary liver cancers are further classified as: - Primary Benign Liver Neoplasm - Primary Malignant Liver Neoplasm Secondary metastatic liver cancer occurs when cancer spreads to the liver from other parts of the body through the process of metastasis. The most common types of secondary metastatic cancers are: - Breast Cancer - Colorectal Cancer - Lung Cancer - Pancreatic Cancer - Gastrointestinal Cancer - Melanoma - Neuroendocrine Cancer - Renal Cell Carcinoma - Ovarian Carcinoma Primary tumors of the liver that are of clinical significance are rare. Ninety-five percent of such lesions when encountered will be malignant and only 5% will be benign. Hepatocellular carcinoma constitutes 90% of malignant liver primaries in the adult. Seventy-five percent of cases are associated with cirrhosis of the liver and patients with hepatitis B infection have a 33- to 200-fold excess risk for this malignancy. Cholangiocarcinoma represents 5% to 10% of hepatic primary malignancies while hepatoblastoma is distinctly uncommon in adults. Primary Benign Liver Neoplasm: Due to the frequent use of medical imaging including ultrasonography, the incidence of benign liver tumours has increased, most of them being asymptomatic. The most frequent lesions of primary benign liver neoplasm are: - Hepatic Haemangioma (HH) - Focal Nodular Hyperplasia (FNH) - Hepatocellular Adenoma (HCA) 1. Hepatic Hemangioma (HH): The most common type of benign liver tumor, a hemangioma is a mass of abnormal blood vessels. They are usually small and asymptomatic, often discovered incidentally during imaging for unrelated issues.  34 2. Focal Nodular Hyperplasia (FNH): FNH is a tumor-like growth made up of several cell types, including hepatocytes, bile duct cells, and connective tissue. These tumors are usually asymptomatic and do not require treatment unless they cause symptoms. 3. Hepatic Adenoma: These are rare tumors that are more common in women. They are linked to the use of oral contraceptives and anabolic steroids. While they are typically asymptomatic, they can pose a risk of bleeding or, in rare cases, transformation into malignant tumors. In terms of further rare histological classification of benign liver lesions, Benign liver lesions can be histologically categorized into epithelial and nonepithelial types. Within the epithelial lesions, hepatocellular adenoma, focal nodular hyperplasia, nodular regenerative hyperplasia, and focal fatty change are among the conditions associated with hepatocytes. Biliary lesions include bile duct adenoma and the distinctive biliary hamartoma, known as von Meyenburg complexes. The latter presents as a collection of benign biliary ducts arranged in a hamartomatous pattern. Moving to nonepithelial lesions, the mesenchymal category encompasses hemangioma, angiomyolipoma, lipoma, and myolipoma, each with distinct compositions. Additionally, heterotopic lesions involve the presence of adrenal, pancreatic, or spleen tissue within the liver. This comprehensive classification provides a framework for understanding the diverse benign liver lesions, aiding in both diagnosis and clinical management. Primary Malignant Liver Neoplasm: The most common malignant primary liver tumor in U.S. adults is hepatocellular carcinoma (HCC) or hepatoma, which arises from hepatocytes.1 This represents ~70 to 80% of all primary liver tumors. In the western world, up to 75% of the people who develop hepatoma also have cirrhosis. Still, hepatoma is a relatively uncommon tumor in the United States, comprising only ~2% of all reported malignancies. Infection with either hepatitis B or hepatitis C is associated with an increased risk of cirrhosis and liver cancer. Chronic hepatitis B carriers have a 100-fold higher risk of developing HCC than the general population.  35 Primary malignant liver tumors are cancers that originate in the liver. The most common types include: 1. Hepatocellular Carcinoma (HCC): This is the most common type of primary liver cancer, accounting for the majority of cases. It often arises in the context of chronic liver disease, such as cirrhosis caused by hepatitis B, hepatitis C, or alcohol abuse. HCC can present as a single tumor or as multiple nodules throughout the liver. 2. Cholangiocarcinoma (Bile Duct Cancer): This cancer originates in the bile ducts of the liver. It can occur within the liver (intrahepatic cholangiocarcinoma) or outside the liver (extrahepatic cholangiocarcinoma). Risk factors include primary sclerosing cholangitis, liver fluke infection, and chronic biliary irritation. Other rare examples of primary malignant liver neoplasms include Fibrolamellar Hepatocellular Carcinoma, which typically occurs in younger individuals without pre-existing liver disease. It has distinct histological features compared to conventional HCC. Angiosarcoma and Hemangiosarcoma are other rare and aggressive cancer examples that start in the blood vessels of the liver. They are often linked to exposure to certain toxins. Another example is Hepatoblastoma, a very rare type of liver cancer that usually affects children under the age of 3. It differs from adult liver cancers in its biology and treatment. Metastatic Liver Cancer: Metastatic liver cancer refers to cancer that has spread to the liver from another part of the body. This is more common than primary liver cancer. Various types of cancers can metastasize to the liver, but the most common include: - Breast Cancer - Colorectal Cancer - Lung Cancer - Pancreatic Cancer - Gastrointestinal Cancer - Melanoma - Neuroendocrine Cancer - Renal Cell Carcinoma - Ovarian Carcinoma Colorectal cancer metastases, particularly to the liver, represent a substantial concern within the field of oncology. Colorectal cancer (CRC) is a prevalent malignancy globally, and a considerable proportion of CRC patients will experience metastases during the course of their disease. The liver stands out as the primary site for metastasis in colorectal cancer due to its pivotal role in filtering blood from the intestines, facilitating the direct spread of cancer cells through the portal venous system. Prevalence statistics highlight the impact of liver metastases in colorectal cancer, with approximately 50% to 70% of patients developing such metastases either at the time of diagnosis or later in their disease progression. Alarmingly, at the initial diagnosis, around 20% to 25% of colorectal cancer patients already present with liver metastases, emphasizing the early onset of this complication. Notably, liver metastases significantly contribute to mortality in colorectal cancer patients.  36 Sign & Symptoms: Patients typically present with HCC in one of two ways. Commonly, those with underlying cirrhosis develop a deterioration in their liver function, with worsening ascites and/or jaundice or variceal haemorrhage. Other characteristic symptoms can include weight loss, anorexia, and abdominal pain. This often-rapid deterioration can, however, be the event that leads to previously occult cirrhosis becoming clinically apparent, meaning that absence of an established diagnosis of cirrhosis does not preclude a diagnosis of HCC complicating cirrhosis. Examination may reveal hepatomegaly or a right hypochondrial mass. Tumour vascularity can lead to an abdominal bruit, and hepatic rupture with intra-abdominal bleeding may occur. Diagnosis: Diagnosing liver tumors involves a combination of clinical assessment, imaging studies, laboratory tests, and sometimes biopsy. The process is designed to determine the presence of a tumor, its type (primary or metastatic), extent of disease, and impact on liver function. Here's a step-by-step overview: - Confirmation of clinical symptoms. - Medical History: Assessment of risk factors like chronic hepatitis, alcohol use, family history of liver cancer, and history of other cancers. - Blood Tests - Liver Function Tests (LFTs) - Tumor Markers - Alpha-fetoprotein (AFP - Imaging Studies - Ultrasound - Computed Tomography (CT) Scan - Magnetic Resonance Imaging (MRI): - Positron Emission Tomography (PET) Scan - Biopsy - Percutaneous Biopsy - Laparoscopic Biopsy  37 Treatment: Treatment options for liver tumors vary based on the type of tumor (primary vs metastatic), stage of the disease, overall liver function, and the patient's general health. For Primary Liver Tumour: 1. Surgical Resection: Removal of the tumor and surrounding liver tissue. Ideal for localized tumors in patients with good liver function. 2. Liver Transplantation: Considered in cases where the tumor is unresectable but confined to the liver, especially in patients with underlying liver diseases like cirrhosis. 3. Ablation Therapies: Methods like radiofrequency ablation or microwave ablation are used to destroy tumors without removing them, suitable for small tumors. 4. Embolization Therapies: These include transarterial chemoembolization (TACE) and transarterial radioembolization (TARE), which involve blocking the blood supply to the tumor and may also deliver chemotherapy or radiation directly to the tumor. 5. Targeted Therapy: Drugs that target specific aspects of cancer cells, like sorafenib for hepatocellular carcinoma. 6. Immunotherapy: Uses the body's immune system to fight cancer. Examples include drugs like nivolumab and pembrolizumab. 7. Chemotherapy: Systemic treatment, more commonly used for cholangiocarcinoma than hepatocellular carcinoma. 8. Radiation Therapy: Can be used to control or reduce symptoms, especially in cases where surgery isn't an option. For Metastatic Liver Tumors, such as Colorectal Cancer Metastases, a range of treatment options exists. Surgical resection, involving the removal of liver metastases, stands as a potentially curative measure for select patients with limited disease. Systemic chemotherapy, often the primary treatment, proves effective, especially in cases with multiple metastases. Targeted therapy comes into play, tailored to the molecular characteristics of the primary tumor.  38 Ablation therapies, suitable for smaller tumors where surgery is not viable, include methods like Radiofrequency Ablation (RFA), Microwave Ablation (MWA), Cryoablation, Irreversible Electroporation (IRE), and Chemical Ablation using substances like alcohol. Embolization therapies, exemplified by Transarterial Chemoembolization (TACE), find application in controlling tumor growth. Immunotherapy is considered based on the specific attributes of the primary tumor, while radiation therapy, such as Stereotactic Body Radiation Therapy (SBRT), may be an option for isolated liver metastases. Liver resection techniques encompass Partial Hepatectomy, Lobectomy, Segmentectomy, and Wedge Resection, each tailored to the extent and location of the tumors. Surgical approaches include traditional open surgery, minimally invasive laparoscopic surgery, and advanced robotic surgery. Ablation therapy, performed under imaging guidance like ultrasound or CT, allows precise targeting of tumors. This procedure can be carried out percutaneously, laparoscopically, or during open surgery, with the choice of anesthesia dependent on the approach and patient's condition. In the realm of embolization, the principles of TACE combine chemotherapy with embolization to restrict the tumor's blood supply. The aim is to maximize the impact of chemotherapy on the tumor while minimizing systemic exposure and associated side effects. Procedure is performed under local anesthesia and sedation. A catheter is inserted into the femoral artery and guided through the blood vessels to the liver. Once the catheter reaches the arteries feeding the tumor, chemotherapy drugs, often mixed with a substance that embolizes the artery, are delivered directly to the tumor. The embolizing agent blocks the blood supply to the tumor, trapping the chemotherapy drugs within the tumor site. Radiotherapy employs the strategy of damaging the DNA of cancer cells, inducing cell death, and impeding the growth of tumors by affecting their blood vessels. This non-invasive approach eliminates the need for anesthesia and proves particularly valuable for targeting tumors that are either inoperable or challenging to access with other therapeutic modalities. Two advanced techniques, Stereotactic Body Radiotherapy (SBRT) and Proton Therapy, stand out for their high precision, minimizing collateral damage to surrounding healthy tissues. External Beam Radiotherapy involves delivering radiation from outside the body. This approach is widely utilized to target cancer cells with focused radiation, effectively limiting damage to adjacent healthy tissues. SBRT represents a precise form of External Beam Radiotherapy, delivering high doses of radiation over a few sessions. This focused and intense approach is especially beneficial for treating small, well-defined tumors with accuracy, reducing the overall treatment duration. Proton Therapy distinguishes itself by using protons, rather than traditional x-rays, for more precise targeting of cancer cells. This method offers the advantage of minimizing damage to surrounding tissues, making it particularly suitable for treating tumors in sensitive or critical anatomical locations. The controlled delivery of protons allows for a more targeted and localized impact on cancer cells while sparing healthy surrounding tissues from unnecessary radiation exposure.  39 Portal Hypertension Anatomy: The normal liver has a dual blood supply, deriving 70 to 80% of its blood, rich in nutrients, from the portal vein and the other 20 to 30%, rich in oxygen, from the hepatic artery. The veins that drain the gastrointestinal organs parallel the major arteries that supply the foregut, midgut, and hindgut, including the celiac, superior mesenteric, and the inferior mesenteric arteries respectively. These veins eventually convene at the portal vein, forming a single venous inflow tract into the liver. The celiac vein drains the foregut structures, including the stomach, through the second part of the duodenum. The superior mesenteric vein drains the third part of the duodenum through the initial two-thirds of the transverse colon. Finally, the inferior mesenteric vein drains the remaining one-third of the transverse colon through the rectum. These veins comprehensively drain nutrients and toxins from the digestive intake and ultimately provide approximately 75% of the liver's blood supply, the remainder coming from the hepatic artery, eventually draining into the hepatic veins and systemic circulation. The liver receives 25% of the total cardiac output during each cardiac cycle. The portal vein receives drainage from the gallbladder, spleen, pancreas, stomach, and small and large intestines. The portal vein forms from the confluence of the superior and inferior mesenteric veins, the splenic vein, gastric vein, and cystic vein. The portal vein enters the liver within the hepatoduodenal ligament, traveling posterior to the proper hepatic artery and the common bile duct.  40 When the portal vein reaches the hilum of the liver, it divides into right and left branches and feeds into the liver sinusoids. This vasculature comprises most of the blood flow to the liver, as well as draining back toxins and nutrients from the drained gastrointestinal tract. Blood then empties into the inferior vena cava (IVC). The remaining minority 25% of blood flow to the liver is supplied by the proper hepatic artery. Hepatic parenchymal cells are some of the most richly perfused cells in the entire human body due to this blood flow. They receive well-oxygenated blood from the hepatic artery and nutrient-rich blood from the splanchnic vessels via the portal venous system. This blood mixes within the hepatic sinusoids. The intrahepatic and portal venous pressures are regulated by portal venous sphincters. The portal vein branches as it enters the liver into the right and left portal veins and then further divides. The progressively smaller branches that come from the venous divisions form the portal venules. After the blood mixes within the sinusoids, it is collected within the terminal hepatic venule or central vein. These central veins then coalesce to form the hepatic vein, which drains the liver back to the IVC, allowing blood to return to the heart and systemic circulation.  41 Pathophysiology: Portal hypertension is defined by a portal pressure higher than 5 mm Hg, within the portal venous system, as determined by the portal pressure gradient. It usually occurs due to: 1. Increased intrahepatic portal venous resistance, which can be pre-hepatic, intra-hepatic, or post-hepatic in location. 2. Due to increased splanchnic blood flow secondary to vasodilation within the splanchnic vascular bed. Portal pressure gradient refers to the difference in pressure between the portal venous system and the pressure from the central venous pressure (within the inferior vena cava or the hepatic vein). Normally, this gradient is less than or equal to 5 mmHg. A pressure gradient of 6 mmHg or more suggests the presence of portal hypertension in most cases. When the pressure gradient exceeds 10 mmHg, portal hypertension becomes clinically significant. A gradient between 5 and 9 mmHg usually indicates subclinical disease. The gradient is measured by determining the hepatic venous pressure gradient (HVPG). Aetiology: Portal hypertension can have various causes, and its origins can be categorized as pre-hepatic, intra-hepatic, or post-hepatic. 1. Pre-hepatic: These are related to increased blood flow or obstruction within the portal vein or splenic vein. Increased blood flow can occur due to conditions like idiopathic tropical splenomegaly, arteriovenous malformations, or fistulas. Obstruction can result from thrombosis (e.g., portal vein obstructive thrombosis, splenic vein thrombosis, or extrahepatic portal vein obstruction) or compression by tumours or trauma. 2. Intrahepatic: These can be further classified as pre-sinusoidal, sinusoidal, or post- sinusoidal. Pre-sinusoidal causes may include conditions like schistosomiasis, congenital hepatic fibrosis, primary biliary cholangitis, and exposure to toxins. Sinusoidal causes often stem from cirrhosis, alcoholic hepatitis, vitamin A intoxication, or the use of cytotoxic drugs.  42 Post-sinusoidal causes can result from conditions like sinusoidal obstruction syndrome or veno-occlusive disease. Cirrhosis is considered a significant factor in the development of PH due to: - Alcohol-Related Cirrhosis - Toxin-Induced Cirrhosis - Viral-Induced Cirrhosis (Hepatitis) 3. Posthepatic: These causes can be related to issues at the level of the heart, hepatic vein, or inferior vena cava. Heart-related causes include elevated atrial pressure due to conditions such as constrictive pericarditis. Inferior vena cava-related causes may involve stenosis, thrombosis, webs, or tumour invasion. Other post hepatic causes include Budd-Chiari Syndrome, and tricuspid regurgitation. In all cases, the common factor is the ongoing damage to liver cells, which triggers inflammation and scar tissue formation. As scar tissue accumulates, it disrupts the liver's normal structure and impairs its vital functions, ultimately leading to cirrhosis. Early intervention and addressing the underlying causes are crucial to prevent or slow down the development of cirrhosis in at-risk individuals. Cirrhosis, characterized by the transformation of the liver into regenerative parenchymal nodules surrounded by fibrous bands and varying degrees of vascular shunting, is the most typical cause of portal hypertension. Damage to the liver parenchyma increases intrahepatic resistance, leading to portal hypertension. Consequently, portosystemic collaterals develop, and arterial vasodilation occurs. Splanchnic vasodilation results from an increase in local and systemic vasodilators and splanchnic vascular hyporesponsiveness to vasoconstrictors. Nitric oxide appears to play a crucial role in the physiopathology of this arterial vasodilation. Sign & Symptoms: The clinical consequences of portal hypertension can include ascites, portosystemic venous shunts, congestive splenomegaly, and hepatic encephalopathy. The five major clinical consequences of portal hypertension are: 1. Portosystemic Shunt (Collateral Pathways) 2. Ascites 3. Variceal Bleeding 4. Congestive splenomegaly 5. Hepatic encephalopathy Portosystemic Shunts (Collateral Pathways): With the rise in portal system pressure, the flow is reversed from portal to systemic circulation by dilation of collateral vessels and development of new vessels. Venous bypasses develop wherever the systemic and portal circulation share common capillary beds. Principal sites are veins around and within the rectum (manifest as haemorrhoids), the esophagogastric junction (producing varices), the retroperitoneum, and the falciform ligament of the liver (involving periumbilical and abdominal wall collaterals). Although hemorrhoidal bleeding may occur, it is rarely massive or life-threatening.  43 Much more important are the esophagogastric varices that appear in about 40% of individuals with advanced cirrhosis of the liver and cause massive hematemesis and death in about half of them. Each episode of bleeding is associated with a 30% mortality. In medical terms, the umbilical vein, usually inactive in healthy individuals, can dilate in portal hypertension, leading to ‘Caput medusae,’ where dilated subcutaneous veins extend from the umbilicus to the rib margins. These veins are a key sign of portal hypertension. Hemorrhoidal veins are categorized into inferior, middle, and superior types. The inferior and middle veins are associated wi