Surgery 66-111

66.Gastric and duodenal ulcers. Zollinger–Ellison syndrome.

67.Stomach and duodenal ulcers: complications.
68.Upper gastrointestinal bleeding (UGI hemorrhage).
69.Benign tumors of the stomach. Precanceroses.
70.Malignant tumors of the stomach.
71.Duodenostasis.
72.Diseases of the small intestine. Benign and malignant tumors. Meckel's diverticulum.
73.Cholecystitis: definition, types, causes, diagnosis, complications and treatment. Cholelithiasis
(gallstones)
74.Choledocholitiasis.
75.Cholangitis.
76.Mechanical jaundice (Icterus mechanicus).
77.Gallbladder mucocele (hydrops). Gallbladder empyema. Biliary peritonitis.
78.Cancer of the gallbladder and the biliary ducts.
79.Hydatid cyst (echinococcosis) of the liver.
80.Abscesses of the liver.
81.Benign tumors of the liver.
82.Liver cancer.
83.Cirrhosis of the liver: definition, stages, causes, symptoms, diagnosis, and treatment.
84.Liver transplantation.
85.Portal hypertension.
86.Acute pancreatitis.
87.Chronic pancreatitis. Pseudocysts of the pancreas. Pancreatic fistulas. 88.Cancer of the pancreas.
89.Endocrine tumors of the pancreas.
90.Spleen: surgical diseases and injuries. Blood disorders and diseases of surgical importance.
91.Abscess of the spleen. Echinococcosis of the spleen. 92.Acute appendicitis and Meckel's diverticulum.
93.Infection Bowel Disease.
94.Megacolon.
95.Diverticulosis of the colon.
96.Benign diseases of the colon: polyps and polyposis syndromes.
97.Colon cancer.
98.Injuries of the abdomen: types.
99.Obstruction syndrome - Ileus: definition, causes, diagnosis, classification, compications and treatment.
Paralytic and spastic ileus.
100.Acute abdomen .
101.Mesenteric ischemia (acute mesenteric arterial occlusion; mesenteric venous occlusion )
102. Peritonitis: definition, causes, classification, symptoms, diagnosis and treatment.
103.Hematogenic peritonitis.
104.Congenital diseases of the colon. Hirschsprung's disease.
105.Congenital diseases of the rectum and anus.
106.Rectal haemorrhage.
107.Rectal cancer.
108.Prolapse of the rectum and anus.
109.Acute and chronical paraproctitis. Dermoid cyst (pilonidal cyst).
110.Perianal fistulas.
111.Hemorrhoids.
Endocrine tumors of pancreas

-Endocrine Tumors of the Pancreas (Pancreatic Neuroendocrine Tumors, pNETs) are a

diverse group of neoplasms arising from the islet cells of the pancreas.

-They can be either functioning (hormone-secreting, causing clinical syndromes) or

non-functioning (silent). Though rarer than pancreatic adenocarcinomas, their clinical
significance is high due to hormone hypersecretion syndromes and potential malignancy.

Classification:

-Functioning pNETs (secrete hormones causing clinical syndromes):

● Insulinoma (secretes insulin)

● Gastrinoma (secretes gastrin)
● Glucagonoma (secretes glucagon)
● VIPoma (secretes vasoactive intestinal peptide)
● Somatostatinoma (secretes somatostatin)
● ACTH-secreting tumors (rare)

-Non-functioning pNETs (do not secrete active hormones or secrete insufficient quantities to
cause symptoms). These tumors often present later, with symptoms due to mass effect or
metastasis.

Insulinoma:

-Pathophysiology: These tumors secrete excessive amounts of insulin, leading to

hypoglycemia.

-Clinical Features: Symptoms of hypoglycemia include sweating, tremors, confusion,

palpitations, and, in severe cases, seizures or coma. Symptoms typically occur after fasting
or exertion.

-Whipple’s triad: hypoglycemia symptoms, low blood glucose levels, and relief upon
glucose administration

-Diagnosis: Elevated insulin and C-peptide levels during hypoglycemia.

-Treatment: Surgical resection. Diazoxide and somatostatin analogs can control symptoms
preoperatively.

Gastrinoma (Zollinger-Ellison Syndrome):

-Pathophysiology: Gastrin-secreting tumors result in excessive gastric acid secretion,

leading to recurrent peptic ulcers, gastroesophageal reflux disease (GERD), and diarrhea.
-Clinical Features: Multiple or refractory ulcers, diarrhea (due to malabsorption), abdominal
pain, and heartburn.

-Diagnosis: Elevated fasting serum gastrin levels (>1000 pg/mL) with a positive secretin
stimulation test (gastrin levels increase after secretin administration).

-Treatment: Proton pump inhibitors (PPIs) to reduce acid secretion. Surgical removal of the
tumor is the definitive treatment if localized.

Glucagonoma:

-Pathophysiology: Overproduction of glucagon, leading to hyperglycemia and catabolic

symptoms.

-Classic presentation includes the “4 Ds”: Dermatitis (necrolytic migratory erythema),

Diabetes mellitus, Deep vein thrombosis, and Depression.

-Diagnosis: Elevated plasma glucagon levels (>1000 pg/mL).

-Treatment: Surgical resection is the preferred treatment. Octreotide (a somatostatin analog)

can be used to control symptoms.

VIPoma (Verner-Morrison Syndrome):

-Pathophysiology: These tumors secrete vasoactive intestinal peptide (VIP), leading to

massive watery diarrhea, dehydration, and electrolyte imbalances.

-Clinical Features: Watery diarrhea, hypokalemia and achlorhydria (WDHA syndrome).

-Diagnosis: Elevated VIP levels in plasma.

-Treatment: Fluid and electrolyte replacement, octreotide to control diarrhea, and surgical
resection.

Somatostatinoma:

-Pathophysiology: Excessive somatostatin inhibits multiple hormones, including insulin,

gastrin, and secretin, leading to various metabolic dysfunctions.

-Clinical Features: Diabetes mellitus, cholelithiasis (due to decreased gallbladder motility),

diarrhea/steatorrhea, and hypochlorhydria.

-Diagnosis: Elevated somatostatin levels.

-Treatment: Surgery is the mainstay. Symptomatic treatment with somatostatin analogs

(paradoxically).

Non-functioning pNETs:
Clinical Features: These tumors often present with mass effect symptoms such as
abdominal pain, jaundice (if the bile ducts are compressed), or weight loss. They may also
be discovered incidentally on imaging.

-Diagnosis: Typically diagnosed with imaging studies (CT, MRI) and confirmed by biopsy.

Treatment: Surgical resection is the treatment of choice if localized. Chemotherapy and

targeted therapies (e.g., everolimus, sunitinib) are options for advanced disease.

Diagnosis of pNETs:

-Hormonal assays: Depending on the type of pNET, specific hormone levels (insulin, gastrin,
glucagon, VIP, somatostatin) should be measured.

-Chromogranin A: A general marker for neuroendocrine tumors, though it lacks specificity.

-24-hour urinary 5-HIAA (hydroxyindoleacetic acid): Elevated in some neuroendocrine

tumors that secrete serotonin.

-CT Scan/MRI: Used for localization and staging of pNETs.

-Endoscopic Ultrasound (EUS): Useful for small lesions and facilitates fine-needle aspiration
(FNA) biopsy.

-Somatostatin Receptor Scintigraphy (Octreoscan): Highly sensitive for detecting

somatostatin receptor-expressing tumors.

-Ki-67 Index and Mitotic Rate: Used to classify pNETs into grades, which influence
prognosis:

● Grade 1 (G1): Low-grade tumors, slow-growing.

● Grade 2 (G2): Intermediate-grade tumors.
● Grade 3 (G3): High-grade tumors, more aggressive, with worse prognosis.

Treatment:

-Surgical Resection: The mainstay of treatment for localized pNETs. Complete resection
offers the best chance for cure.

-Enucleation: For small, benign tumors.

-Pancreaticoduodenectomy (Whipple procedure): For larger tumors or those located in the

head of the pancreas.

-Distal Pancreatectomy: For tumors in the body or tail of the pancreas.

Pancreatic pseudocysts
-Pancreatic pseudocysts are fluid-filled collections that develop as a complication of acute or
chronic pancreatitis, or after pancreatic trauma.

-Unlike true cysts, pseudocysts lack an epithelial lining and are instead surrounded by a
wall of fibrous or granulation tissue.

Pathophysiology:

-Pseudocysts result from pancreatic ductal disruption or leakage of pancreatic

secretions (including enzymes) into surrounding tissues. This occurs in response to
inflammation, often seen in pancreatitis, where the enzyme-rich pancreatic fluid causes
tissue damage, leading to a local collection of fluid.

-Over time, a fibrous wall forms around the fluid collection, resulting in a pseudocyst. Unlike
true cysts, which are lined with epithelial cells, pseudocysts have no epithelial lining but are
surrounded by granulation tissue or fibrosis.

Etiology:

-Acute Pancreatitis: Pseudocysts develop in about 10-20% of cases of acute pancreatitis,

typically 3-4 weeks after the initial inflammatory episode. They form when pancreatic
enzymes and fluid leak into surrounding tissue.

-Chronic Pancreatitis: Pseudocysts are also seen in 20-40% of cases of chronic

pancreatitis, especially in patients with a history of alcohol use, where repeated injury to the
pancreatic ducts leads to fluid collections. Gallstone-related pancreatitis is the second
leading cause.

-Trauma: Blunt or penetrating trauma to the pancreas can cause ductal injury and leakage of
pancreatic fluid, leading to pseudocyst formation.

Signs and symptoms:

-Abdominal Pain: The most common symptom, usually localized to the upper abdomen,
often with a dull, persistent character. Pain may radiate to the back.

-Palpable Mass: In some cases, a large pseudocyst may present as an abdominal mass.

-Nausea, Vomiting, and Early Satiety: Due to pressure on adjacent organs (stomach,
intestines).

-Jaundice: If the pseudocyst compresses the bile duct, it can lead to obstructive jaundice.

-Fever and Chills: These may indicate infection of the pseudocyst, leading to an abscess.

Complications:

-Infection: An infected pseudocyst can lead to the formation of a pancreatic abscess,

requiring urgent intervention.
-Rupture: Rare but potentially life-threatening if the pseudocyst ruptures into the peritoneal
cavity, leading to peritonitis, or into the gastrointestinal tract.

-Hemorrhage: Pseudocysts can erode into nearby blood vessels, causing gastrointestinal
bleeding or hemorrhagic shock.

-Obstruction: Large pseudocysts can compress adjacent structures, leading to gastric

outlet obstruction (vomiting, early satiety) or biliary obstruction (jaundice).

Diagnosis:

-Abdominal Ultrasound (US): A useful initial imaging modality that can visualize fluid
collections. It is non-invasive and can detect the presence and size of the pseudocyst.

-CT Scan: The preferred imaging technique for diagnosing pseudocysts. It provides
detailed information about the size, location, and relationship of the pseudocyst to
surrounding structures. It is also useful for detecting complications such as infection, rupture,
or hemorrhage.

-MRI/MRCP (Magnetic Resonance Cholangiopancreatography): Useful in evaluating the

pancreatic duct and its relation to the pseudocyst, helping to identify ductal disruptions.

-Endoscopic Ultrasound (EUS): Provides high-resolution imaging and allows for fine-needle
aspiration (FNA) of the pseudocyst fluid for diagnostic purposes (e.g., to exclude malignancy
or infection).

-Cyst Fluid Analysis: If aspiration is performed, fluid analysis can help differentiate
pseudocysts from other types of cysts. Elevated amylase levels and the absence of mucin or
carcinoembryonic antigen (CEA) favor pseudocysts.

Treatment:

-Observation: Asymptomatic pseudocysts or small (<6 cm) pseudocysts can be monitored

with serial imaging, as many will resolve on their own over time (4-6 weeks).

-Endoscopic Drainage:The most common and least invasive approach, using either
endoscopic retrograde cholangiopancreatography (ERCP) or endoscopic ultrasound (EUS).

-Trans-gastric or trans-duodenal drainage: Involves creating a fistula between the

pseudocyst and the stomach or duodenum, allowing the pseudocyst contents to drain
internally.

-Trans-papillary drainage: Performed during ERCP, useful for pseudocysts that

communicate with the pancreatic duct.

-Percutaneous Drainage:

● Performed under radiological guidance (usually CT or ultrasound), involves inserting

a catheter into the pseudocyst through the skin.
 ● Used for large, infected pseudocysts or in patients not suitable for surgery or
endoscopy. It may require long-term catheter placement and follow-up imaging.

-Cystogastrostomy: Creating a direct communication between the pseudocyst and the

stomach.

-Cystojejunostomy: Creating a drainage route between the pseudocyst and the jejunum.

-Cystoduodenostomy: Creating a drainage route between the pseudocyst and the

duodenum.

-Resection: In rare cases, if the pseudocyst is causing significant complications or has an

uncertain diagnosis, surgical resection of the pseudocyst or part of the pancreas may be
necessary.

-Infected Pseudocysts: Require drainage (typically percutaneous) and antibiotics targeting

common pancreatic pathogens (Gram-negative bacteria, anaerobes).

Pancreatic fistulas
-Pancreatic fistulas are abnormal connections between the pancreas and other nearby
structures or surfaces, resulting from the leakage of pancreatic secretions.

Types of Pancreatic Fistulas:

-External Pancreatic Fistula:

● Occurs when pancreatic secretions leak externally, through the skin. This can
happen following pancreatic surgery, trauma, or drainage of a pseudocyst or
abscess.
● Clinical Presentation: Pancreatic fluid drains externally from a wound or a surgical
drain, often containing high levels of pancreatic enzymes (amylase and lipase).

-Internal Pancreatic Fistula:

● Pancreatic secretions leak into nearby structures within the abdomen.

● Pancreaticopleural Fistula: An abnormal communication between the pancreas and
the pleural cavity. Pancreatic enzymes leak into the pleural space, leading to
recurrent pleural effusions (fluid collection in the lungs).
● Pancreaticoperitoneal Fistula: Leakage of pancreatic fluid into the peritoneal cavity,
which may cause ascites (pancreatic ascites) or chemical peritonitis.
● Pancreaticocolonic Fistula: Leakage of pancreatic fluid into the colon, leading to
diarrhea and possibly gastrointestinal bleeding.
● Pancreaticoduodenal or Pancreaticoenteric Fistula: Communication between the
pancreas and the duodenum or other parts of the intestine, leading to abnormal
digestive symptoms.

Etiology:
-Acute Pancreatitis: In severe acute pancreatitis, especially necrotizing pancreatitis,
pancreatic enzymes can erode through the pancreatic ducts and surrounding tissues,
leading to fistula formation.

-Chronic pancreatitis: Ductal strictures or obstruction may result in pancreatic fluid

leakage, forming a fistula.

-Pancreatic Surgery: One of the most common causes of pancreatic fistula is surgical
procedures involving the pancreas, particularly distal pancreatectomy or Whipple procedure
(pancreaticoduodenectomy). The leakage occurs when surgical anastomoses (connections)
between the pancreas and other organs fail to heal properly, or there is incomplete closure
of the pancreatic duct.

-Pancreatic Trauma: Blunt or penetrating trauma to the pancreas can cause ductal injury,
leading to a fistula. Trauma may occur during accidents, invasive procedures, or after
pancreatic biopsies.

-Drainage of Pancreatic Pseudocysts or Abscesses: Pseudocyst or abscess drainage

procedures, particularly if poorly controlled, may result in leakage of pancreatic secretions
and fistula formation.

Signs and symptoms external pancreatic fistulas:

-Persistent drainage from surgical sites, wounds or drains, often with fluid rich in pancreatic
enzymes.

-Local skin irritation due to the corrosive nature of pancreatic fluid.

Signs and symptoms pancreaticopleural fistulas:

-Recurrent pleural effusions, often left-sided, causing symptoms like shortness of breath,
cough, and chest pain. These effusions are rich in amylase.

-Refractory pleural effusions that fail to respond to conventional treatments (thoracentesis).

Signs and symptoms pancreaticoperitoneal fistulas (Pancreatic Ascites):

-Ascites that recurs after paracentesis, with high levels of amylase in the ascitic fluid.

-Abdominal pain and distension.

-Peritonitis may occur in severe cases.

Signs and symptoms pancreaticocolonic fistulas:

-Diarrhea and steatorrhea due to pancreatic secretions entering the colon.

-Potential for gastrointestinal bleeding if there is significant tissue erosion.

Signs and symptoms pancreaticoduodenal or pancreaticoenteric fistulas:

-Nausea, vomiting, diarrhea, and abdominal pain.

-Malabsorption of nutrients if significant amounts of pancreatic enzymes are lost through the
fistula.

Diagnosis:

-Fluid Analysis: High levels of amylase in drained fluid (e.g., pleural effusion, ascitic fluid, or
external fistula drainage) suggest a pancreatic origin. Serum Amylase and Lipase may be
elevated, particularly in cases of acute pancreatitis or during acute exacerbations of chronic
pancreatitis.

-CT Scan: Useful for visualizing the pancreas and detecting fluid collections or abscesses. It
may help identify the site of leakage or fistula.

-MRI/MRCP (Magnetic Resonance Cholangiopancreatography): Offers a non-invasive way

to visualize the pancreatic ducts and surrounding structures, providing detailed information
on ductal disruptions and fistula tracts.

-Endoscopic Retrograde Cholangiopancreatography (ERCP): Allows direct visualization of

the pancreatic duct and can help identify the site of leakage or ductal obstruction. It is also
therapeutic, as stenting the pancreatic duct may help close the fistula.

-Thoracentesis (for pleural effusions) or paracentesis (for ascites) can provide fluid for
analysis. A diagnosis of pancreatic fistula is supported by finding high amylase levels in the
fluid (>1000 IU/L).

Treatment:

-Somatostatin Analogs (Octreotide): These medications reduce pancreatic enzyme secretion

and may help reduce fistula output, promoting closure. They are particularly useful in
high-output external fistulas.

-Drainage: External fistulas may require external drainage to prevent fluid accumulation and
infection.

-Pancreatic Duct Stenting (ERCP): In cases of ductal disruption, an endoscopic stent may be
placed across the site of the ductal injury to reduce pressure and promote fistula healing.
This is commonly used for internal fistulas, particularly after pancreatic surgery.

-Endoscopic Drainage: In the case of pseudocysts or fluid collections causing fistula

formation, endoscopic drainage may be required.

-Percutaneous Drainage: Used for abscesses or large collections of fluid associated with the
fistula. It can help prevent infection and promote healing.

-Fistula Excision: The fistula tract may be excised, or surgical reanastomosis

(reconnection) of pancreatic ducts may be performed.
-Resection: In some cases, part of the pancreas may need to be resected, particularly if
there is a persistent ductal leak or if a pseudocyst is causing the fistula.

Liver transplantation
-Liver transplantation (LT) is a surgical procedure where a diseased liver is replaced with a
healthy liver from a donor.

-It is often the treatment of choice for patients with end-stage liver disease (ESLD) or acute
liver failure when other medical and surgical treatments have failed. Liver transplantation
has significantly improved survival rates and quality of life for patients with irreversible liver
damage.

Indications for Liver Transplantation:

-Chronic Liver Diseases:

● Cirrhosis: The most common indication for liver transplantation. Causes of cirrhosis
include:
● Chronic viral hepatitis (Hepatitis B and C)
● Alcoholic liver disease
● Non-alcoholic steatohepatitis (NASH)
● Autoimmune hepatitis
● Primary biliary cholangitis (PBC)
● Primary sclerosing cholangitis (PSC)
● Genetic disorders: hemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency
● Hepatocellular Carcinoma (HCC): Patients with small, unresectable liver tumors
confined to the liver may be eligible for liver transplantation. Criteria such as the
Milan criteria are used to select patients with HCC for transplantation, typically
requiring:
● A single tumor ≤5 cm or up to 3 tumors, each ≤3 cm, with no extrahepatic disease or
vascular invasion.

-Acute Liver Failure (ALF) causes fulminant hepatic failure due to:

● Acute viral hepatitis: Hepatitis B, C

● Drug-induced liver injury: acetaminophen overdose
● Autoimmune hepatitis
● Wilson’s disease
● Toxin exposure: Amanita phalloides mushrooms

-Metabolic Diseases affecting the liver, such as:

● Wilson’s disease
● Crigler-Najjar syndrome
 ● Glycogen storage diseases
● Primary hyperoxaluria

-Biliary atresia: The most common cause of liver transplantation in children.

-Polycystic liver disease when it causes severe symptoms or complications.

Contraindications for Liver Transplantation:

-Active alcohol or substance abuse (unless documented abstinence and rehabilitation)

-Uncontrolled infections

-Severe cardiovascular or pulmonary disease

-Metastatic malignancy

-Severe extrahepatic disease that would limit survival after transplantation

-Non-compliance with medical treatment or inability to follow up post-transplant care

Types of Liver Transplants:

-Orthotopic Liver Transplantation (OLT): The most common type, where the diseased liver
is removed and replaced by a donor liver in the same anatomic location (orthotopic). This
can be from a deceased donor or a living donor.

-Deceased Donor Liver Transplant (DDLT): In this case, the entire liver from a deceased
donor is transplanted into the recipient. Deceased donors are often individuals who have
suffered brain death but have healthy organs suitable for transplantation.

-Living Donor Liver Transplant (LDLT): A portion of the liver (typically the right or left lobe)
is taken from a living donor, often a family member or close friend, and transplanted into the
recipient. Both the donor’s remaining liver and the recipient’s transplanted liver can
regenerate to full size within a few months. LDLT offers benefits such as reduced waiting
time and improved planning of the surgery. However, it carries risks for the donor, including
surgical complications.

Surgical Procedure:

-Orthotopic Liver Transplantation: The patient’s native liver is removed, and the donor liver is
anastomosed to the recipient’s blood vessels (hepatic artery, portal vein, inferior vena cava)
and bile ducts. Meticulous care is taken to restore proper blood flow and biliary drainage.

Complications:

-Graft Rejection: It occurs when the immune system recognizes the transplanted liver as
foreign. It can be acute or chronic.
-Acute Rejection: Usually occurs within the first few weeks post-transplant and is treated
with high-dose steroids or adjustment of immunosuppressants.

-Chronic Rejection: Less common but leads to gradual liver dysfunction and can ultimately
require re-transplantation.

-Infections:

● Opportunistic infections: CMV, Epstein-Barr virus (EBV), fungal infections (e.g.,

Candida, Aspergillus), and bacterial infections.
● Prophylactic antibiotics and antiviral medications are administered to reduce this risk.

-Hepatic Artery Thrombosis (HAT): A severe complication that can lead to graft failure.
Prompt recognition and intervention, often with surgery or anticoagulation, are required.

-Biliary Complications: Strictures, leaks, or infections (cholangitis) can occur, often

necessitating endoscopic or surgical interventions.

-Recurrence of Original Disease: Diseases like hepatitis B, hepatitis C, and primary

sclerosing cholangitis may recur in the transplanted liver.

-Post-Transplant Lymphoproliferative Disorder (PTLD): A type of lymphoma associated

with EBV infection due to long-term immunosuppression. It requires a reduction in
immunosuppression and, in some cases, chemotherapy.

Abscess of liver
-A liver abscess is a collection of pus in the liver due to infection or injury. It can be classified
into two main types: pyogenic (bacterial) and amoebic (parasitic), though fungal liver
abscesses can also occur but are less common.

Types of Liver Abscess:

-Pyogenic Liver Abscess:

● Caused by bacterial infection, commonly by Escherichia coli, Klebsiella pneumoniae,

and Staphylococcus aureus.
● Infection may originate from the biliary tract (cholangitis), portal vein (from
appendicitis, diverticulitis), or direct extension from adjacent infections.

-Amoebic Liver Abscess:

● Caused by Entamoeba histolytica, a protozoan parasite.

● Common in tropical and subtropical regions, transmitted via the fecal-oral route,
typically following ingestion of contaminated food or water.
Pathophysiology:

-Pyogenic abscesses result from bacterial invasion of the liver parenchyma either via
hematogenous spread, biliary infection, or direct extension.

-Amoebic abscesses occur when E. histolytica invades the intestinal wall and reaches the
liver via the portal circulation.

Symptoms:

-Fever (usually with chills)

-Right upper quadrant (RUQ) abdominal pain

-Hepatomegaly

-Jaundice (sometimes)

-Malaise, anorexia, and weight loss

-Tender hepatomegaly

-RUQ guarding or rebound tenderness

-Fever spikes (may be accompanied by sweating)

-In amoebic abscesses, diarrhea may also be present.

Complications:

-Pyogenic Abscess:

● Septicemia
● Rupture into the peritoneum, pleura, or pericardium
● Chronic abscess formation
● Liver failure in severe cases

-Amoebic Abscess:

● Abscess rupture (can lead to peritonitis or pleuro-pericardial rupture)

● Empyema
● Secondary bacterial infection of the abscess

Diagnosis:

-Blood Tests:

● Leukocytosis with neutrophilia.

● Elevated liver enzymes (AST, ALT, ALP).
● Positive blood cultures (in pyogenic abscess).
● Serology for Entamoeba histolytica antibodies (in amoebic abscess)
-Ultrasound: Often the first imaging modality, showing a hypoechoic or anechoic area in the
liver.

-CT Scan: More detailed, shows the extent of abscess, typically a low-density lesion with
peripheral enhancement.

-MRI: Useful for further detailing, especially when CT is contraindicated.

-Aspiration:

● Ultrasound or CT-guided aspiration can help in both diagnosing and treating the
abscess.
● The aspirated fluid is sent for Gram stain, culture, and microscopy (in amoebic
abscesses, the pus is typically “anchovy paste” in appearance).

Treatment:

-Pyogenic Abscess:

● Antibiotics: Empirical broad-spectrum antibiotics covering Gram-negative and

anaerobic organisms. Typically, a combination of cephalosporins, metronidazole, or
carbapenems is used.
● Percutaneous drainage: Recommended if the abscess is large or unresponsive to
antibiotics alone. This is usually ultrasound or CT-guided.
● Surgical drainage: Reserved for abscesses that are inaccessible or fail to resolve
with percutaneous drainage.

-Amoebic Abscess:

● Metronidazole is the first-line treatment for amoebic liver abscess, usually given for
7-10 days.
● Aspirin or drainage is rarely required unless there is a high risk of rupture or the
abscess is unusually large.
● Follow-up with luminal agents like paromomycin to eradicate intestinal amoebas and
prevent recurrence.

Cancer of biliary ducts

-Cancer of the biliary ducts (biliary tract cancer or cholangiocarcinoma) refers to
malignancies originating from the epithelial cells of the bile ducts, which transport bile from
the liver to the small intestine.

-These cancers can arise from any part of the biliary tree, including the intrahepatic (inside
the liver), perihilar (junction of right and left hepatic ducts), and distal (outside the liver, closer
to the pancreas) bile ducts.

Classification:
-Intrahepatic Cholangiocarcinoma (iCCA): Arises from the bile ducts within the liver

-Perihilar Cholangiocarcinoma (pCCA): Also known as Klatskin tumors, arises at the hilum
of the liver where the right and left hepatic ducts join.

-Distal Cholangiocarcinoma (dCCA): Occurs in the bile ducts outside the liver, often near
the pancreas.

Risk Factors:

-Primary Sclerosing Cholangitis (PSC): Chronic inflammation of the bile ducts increases the
risk of cholangiocarcinoma, especially in people with ulcerative colitis.

-Congenital Biliary Abnormalities: Conditions such as choledochal cysts or Caroli disease

predispose to cancer due to chronic bile stasis and recurrent infections.

-Liver Flukes: Infections with Opisthorchis viverrini or Clonorchis sinensis (common in

Southeast Asia) significantly increase the risk.

-Chronic Biliary Inflammation: Long-standing biliary diseases like chronic cholecystitis,

hepatolithiasis, or biliary cirrhosis.

-Hepatitis B, C, and cirrhosis are also linked to an increased risk, particularly for intrahepatic
cholangiocarcinoma.

-Obesity, smoking, and exposure to thorotrast (a radiographic contrast agent no longer in

use) are additional risk factors.

Pathophysiology:

-Bile duct cancers originate from the bile duct epithelial cells, which undergo mutations,
leading to uncontrolled growth and invasion of surrounding tissues.

-Chronic inflammation, bile stasis, and exposure to carcinogens from bile or infections
increase the likelihood of DNA damage, promoting malignant transformation.

Symptoms:

-Obstructive Jaundice: The most common symptom, due to bile duct obstruction.

● Yellowing of the skin and sclera

● Dark urine and pale stools
● Pruritus (itching)

-Right Upper Quadrant (RUQ) Pain: May present as a dull ache or discomfort in the liver
area.

-Systemic Symptoms:

● Unexplained weight loss

● Fever
 ● Fatigue and malaise

-Cholangitis: In some cases, fever with chills, rigors, and abdominal pain (Charcot’s triad)
may occur if secondary infection develops.

-Palpable Gallbladder (Courvoisier’s Sign): In distal cholangiocarcinoma, a palpable,

non-tender gallbladder may indicate malignancy.

Diagnosis:

-Liver Function Tests (LFTs): Elevated bilirubin (conjugated), alkaline phosphatase (ALP),
and gamma-glutamyl transferase (GGT).

-Tumor Markers: CA 19-9 and CEA may be elevated, though these markers are nonspecific.

-Ultrasound: Often the first imaging modality, shows dilated bile ducts.

-CT Scan/MRI: Helps in staging the tumor, identifying its extent, and detecting metastasis.
MRI with MRCP (Magnetic Resonance Cholangiopancreatography) provides detailed
images of the biliary tree.

-ERCP (Endoscopic Retrograde Cholangiopancreatography): Diagnostic and therapeutic

tool. Can help visualize strictures, take brush cytology or biopsy, and place stents to relieve
obstruction.

-Histopathology: Confirmation through biopsy, often obtained via ERCP or percutaneous

approaches, is essential for definitive diagnosis.

Treatment:

-Surgery:

● The only curative treatment is complete surgical resection.

● Liver resection for intrahepatic cholangiocarcinoma.
● Whipple procedure (pancreaticoduodenectomy) for distal cholangiocarcinoma.
● Liver transplantation may be an option for small, early-stage perihilar tumors.
● Surgery is often challenging due to the late presentation of the disease and
involvement of vital structures.

-Adjuvant Therapy:

● Chemotherapy: Commonly used agents include gemcitabine and cisplatin. Used in

both adjuvant settings (after surgery) and palliative care for unresectable disease.
● Radiotherapy: May be considered in some cases, either as adjuvant therapy or
palliatively to control symptoms in advanced disease.

-Palliative Treatments:

● Biliary Drainage: Placement of stents (via ERCP or percutaneous) to relieve

jaundice.
 ● Radiofrequency ablation (RFA) or photodynamic therapy (PDT) may be used to
manage biliary obstruction or control local tumor growth.

Gallbladder mucocele
-Gallbladder mucocele is a condition in which the gallbladder becomes distended and filled
with mucus, rather than bile, due to an obstruction of the cystic duct.

-It differs from a typical gallbladder distension caused by bile stasis, as the mucin-secreting
cells of the gallbladder lining produce excess mucus in response to inflammation or other
stimuli.

Pathophysiology:

-Cystic duct obstruction (due to stones, sludge, or external compression by a mass) prevents
the normal flow of bile from the gallbladder into the common bile duct.

-The mucus, produced by goblet cells in the gallbladder lining, accumulates within the
gallbladder, gradually replacing bile.

-Over time, this results in a distended, enlarged gallbladder filled with thick, clear, or white
mucus (as opposed to purulent material seen in empyema).

-The gallbladder wall may thicken and become fibrotic due to chronic inflammation, and in
severe cases, ischemia or necrosis can develop due to increased intraluminal pressure.

Etiology and Risk Factors:

-Gallstones: The most common cause of cystic duct obstruction, leading to mucocele
formation.

-Chronic cholecystitis: Chronic inflammation of the gallbladder, often due to gallstones,

can predispose to mucus overproduction.

-Tumors: Rarely, tumors in the gallbladder or surrounding areas can compress the cystic
duct.

-Biliary Sludge: A mixture of bile pigments, cholesterol, and calcium salts, can block the
cystic duct and lead to a mucocele.

-Postoperative or post-traumatic biliary changes: Surgical interventions or trauma

affecting the biliary system may also obstruct the cystic duct.

Signs and symptoms:

-Asymptomatic: In many cases, a mucocele is discovered incidentally during imaging for

other reasons. Small mucoceles may not cause noticeable symptoms.
-Right upper quadrant (RUQ) pain: If symptoms are present, the most common is dull,
aching pain in the RUQ or epigastrium, which may be intermittent.

-Palpable Gallbladder (Courvoisier’s Sign): In large mucoceles, the distended gallbladder

may be palpable as a non-tender, smooth mass in the RUQ.

-Nausea and Vomiting: Non-specific gastrointestinal symptoms may be present.

Complications:

-If a mucocele becomes infected, it can progress to empyema (gallbladder filled with pus),
or if the pressure increases significantly, it can cause gallbladder necrosis or perforation,
leading to peritonitis or bile peritonitis.

Diagnosis:

-Ultrasound:

● The preferred imaging modality for diagnosis.

● Shows an enlarged, distended gallbladder filled with anechoic or echogenic material
(mucus).
● The absence of gallstones (or their presence) can be noted, along with any
thickening of the gallbladder wall.

-CT Scan or MRI:

● May be used if the ultrasound findings are inconclusive or if complications like

perforation or abscess are suspected.
● A distended gallbladder with low-attenuation content (mucus) and possible cystic
duct obstruction can be visualized.

-Endoscopic Retrograde Cholangiopancreatography (ERCP): Rarely used for diagnosis but

can be useful for therapeutic decompression of the biliary system or in cases of coexisting
choledocholithiasis (bile duct stones).

-Cholescintigraphy (HIDA Scan): Can help demonstrate cystic duct obstruction and lack of
bile flow from the gallbladder, but is rarely needed unless the diagnosis is unclear.

Treatment:

-Cholecystectomy (gallbladder removal) is the definitive treatment for symptomatic

gallbladder mucocele. Laparoscopic cholecystectomy is the preferred approach and is
usually safe and effective.

-If the mucocele is large or there is concern for necrosis or perforation, an open
cholecystectomy may be necessary.

-Percutaneous Cholecystostomy: In high-risk patients who are poor surgical candidates, a

percutaneous cholecystostomy (drainage of the gallbladder through a catheter inserted
under ultrasound guidance) can provide temporary relief until the patient is stable enough for
surgery.

Gallbladder empyema
-Gallbladder empyema is a serious condition in which the gallbladder becomes filled with
pus due to a bacterial infection.

-It is often a complication of acute cholecystitis (inflammation of the gallbladder) and can be
life-threatening if not treated promptly.

Pathophysiology:

-Gallbladder empyema typically occurs as a result of:

● Acute cholecystitis: Biliary obstruction (commonly from gallstones) leads to

inflammation
● Cystic duct obstruction: This blocks the outflow of bile, creating a favorable
environment for bacterial overgrowth, which turns the bile into purulent material
(pus).
● Secondary bacterial infection: Bacteria such as Escherichia coli, Klebsiella
pneumoniae, Streptococcus faecalis, and Enterobacter species often invade the
stagnant bile, leading to pus formation.

-As the infection progresses, the intraluminal pressure within the gallbladder rises, which can
lead to ischemia of the gallbladder wall, necrosis, and, in severe cases, perforation, resulting
in bile peritonitis.

Risk Factors:

-Gallstones: The most common cause of cystic duct obstruction.

-Diabetes mellitus: Diabetic patients have an increased risk of severe infections, including
gallbladder empyema.

-Immunocompromised status: Patients on immunosuppressive drugs or with underlying

conditions like HIV are at higher risk.

-Severe acute cholecystitis: Progression of untreated or poorly managed acute cholecystitis.

Signs and symptoms:

-Severe Right Upper Quadrant (RUQ) Pain: Typically sharp, constant pain that worsens
with deep breaths or movement.

-High-grade fever and chills: The infection is often associated with systemic signs of
sepsis.
-Tachycardia and hypotension: Signs of systemic infection or sepsis.

-Leukocytosis: Often marked and higher than in uncomplicated cholecystitis.

-Murphy’s sign: A physical exam finding where palpation of the RUQ during inspiration
causes the patient to suddenly stop inhaling due to pain.

-In advanced or complicated cases:

● Jaundice: Indicates either common bile duct involvement or significant biliary

obstruction.
● Signs of Sepsis: Confusion, hypotension, and multi-organ dysfunction may be
present.

Complications:

-Perforation: Rupture of the gallbladder, leading to bile peritonitis and abscess formation,
requiring emergency surgical intervention.

-Gangrenous cholecystitis: Ischemia of the gallbladder wall due to increased pressure and
inflammation, which can lead to tissue necrosis.

-Sepsis and Septic Shock: Systemic spread of the infection, causing life-threatening organ
dysfunction.

-Abscess formation: The infection may spread to the surrounding tissues, leading to
localized abscesses around the liver or peritoneum.

-Fistula formation: Rarely, the inflamed gallbladder can form abnormal connections
(fistulas) with adjacent organs such as the intestines.

Diagnosis:

-Blood Tests:

● Complete blood count (CBC): Shows leukocytosis with a left shift (increased
neutrophils).
● Liver function tests (LFTs): May show elevated bilirubin, alkaline phosphatase (ALP),
and gamma-glutamyl transferase (GGT) if there is biliary obstruction.
● Blood cultures: Should be obtained to identify the causative organism in septic
patients.

-Ultrasound: The first imaging modality used. It may reveal:

● Distended gallbladder.
● Internal echoes or debris within the gallbladder, indicating pus.
● Pericholecystic fluid, indicating inflammation or impending perforation.

-CT Scan: More sensitive in detecting complications like gangrene or perforation and in
identifying the extent of the infection. It shows a distended gallbladder with fluid collections,
gas within the gallbladder (suggesting gangrenous cholecystitis), or pericholecystic
abscesses.

-ERCP (Endoscopic Retrograde Cholangiopancreatography): Rarely used primarily for

diagnosis in empyema but may be used if there is suspicion of choledocholithiasis (bile duct
stones).

Treatment:

-Broad-spectrum IV antibiotics: Empirical coverage against Gram-negative and anaerobic

organisms. Common choices include piperacillin-tazobactam, ceftriaxone with
metronidazole, or carbapenems.

-Cholecystectomy (gallbladder removal) is the definitive treatment:

● Laparoscopic cholecystectomy is the preferred approach in stable patients without

complications.
● Open cholecystectomy is required for patients with severe inflammation, perforation,
or in cases where laparoscopic surgery is not feasible.

-Percutaneous cholecystostomy: In critically ill or high-risk surgical patients who are not
stable enough for immediate surgery, a drainage catheter is placed under ultrasound or CT
guidance to drain the pus from the gallbladder. This can stabilize the patient until they are fit
for surgery.

Bile peritonitis
-Bile peritonitis is a serious and potentially life-threatening condition characterized by the
inflammation of the peritoneum (the lining of the abdominal cavity) due to the presence of
bile.

-It typically occurs when bile leaks into the peritoneal cavity, leading to chemical irritation and
secondary bacterial infection.

Etiology:

-Perforated Gallbladder: Often as a complication of acute cholecystitis or empyema of the

gallbladder. The ruptured gallbladder releases bile into the peritoneal cavity.

-Biliary Obstruction: Conditions such as choledocholithiasis (bile duct stones) can cause
bile to back up and subsequently leak into the peritoneum, especially if there is secondary
infection.

-Trauma: Penetrating abdominal injuries or blunt trauma can cause bile duct injury, leading
to leakage.

-Iatrogenic Causes: Surgical complications during procedures such as cholecystectomy or

ERCP may inadvertently cause bile leakage.
-Chronic Liver Disease: Conditions leading to bile stasis and subsequent rupture of bile
ducts may result in bile leakage into the peritoneum.

Pathophysiology:

-When bile enters the peritoneal cavity, the bile causes chemical irritation of the peritoneum,
leading to inflammation. The presence of bile can also lead to bacterial contamination from
the gastrointestinal tract, resulting in secondary bacterial peritonitis.

-The body’s immune response can further contribute to the inflammatory process, leading to
symptoms of peritonitis, which may rapidly progress to sepsis.

Signs and symptoms:

-Abdominal Pain: Severe, diffuse abdominal pain, often described as sharp or constant.
Pain may worsen with movement or palpation.

-Rebound Tenderness: Increased pain upon releasing pressure during palpation, indicating
irritation of the peritoneum.

-Guarding: Involuntary tensing of the abdominal wall muscles due to pain.

-Nausea and Vomiting: Patients may experience persistent nausea, vomiting, and loss of
appetite.

-Fever and Chills: Signs of systemic infection, often indicating the development of sepsis.

-Tachycardia and Hypotension: Signs of shock due to severe infection or fluid loss.

-Signs of Sepsis: Confusion, altered mental status, and evidence of multi-organ dysfunction
may occur in severe cases.

Diagnosis:

-Complete Blood Count (CBC): Often shows leukocytosis indicating infection.

-Liver Function Tests (LFTs): May show elevated bilirubin, alkaline phosphatase, and liver
enzymes depending on the underlying cause.

-Blood Cultures: Should be obtained to identify any bacterial pathogens.

-Ultrasound: Can detect free fluid in the abdominal cavity and identify gallbladder or bile
duct pathology.

-CT Scan: Provides detailed imaging to assess for bile leakage, abscess formation, and
other complications.

-HIDA Scan: May be used to visualize bile leaks if the diagnosis is unclear.

-Paracentesis: If free fluid is present in the peritoneal cavity, a paracentesis may be

performed to obtain fluid for analysis. Bile-stained fluid is indicative of bile peritonitis.
Treatment:

-Exploratory Laparotomy: Necessary to identify the source of bile leakage and to perform
any necessary repairs.

-Cholecystectomy: If the gallbladder is the source of the leakage, it is often removed.

-Repair of Bile Duct Injuries: If identified, any injuries to the bile duct must be surgically
repaired.

-Broad-Spectrum Antibiotics: Initiated early to cover for polymicrobial infections. Coverage

typically includes Gram-negative bacteria, anaerobes, and potential enteric pathogens.

Cholangitis
-Cholangitis is an infection of the bile ducts, typically caused by the obstruction of the bile
duct system, often due to gallstones, strictures, or malignancies.

-It is characterized by a triad of symptoms known as Charcot’s triad, which includes fever,
jaundice, and right upper quadrant pain.

-When severe, it can progress to Reynolds’ pentad, which includes confusion and
hypotension in addition to the triad.

Etiology:

-Choledocholithiasis: The presence of stones in the common bile duct, leading to blockage
and infection.

-Biliary Strictures: Narrowing of the bile duct due to injury, surgery, or conditions like
primary sclerosing cholangitis (PSC) or cholangiocarcinoma (bile duct cancer).

-Biliary Obstruction: External compression from tumors or lymphadenopathy.

-Post-surgical Complications: Following procedures like cholecystectomy or ERCP,

leading to infection or inflammation.

-Infections: Some cases may be caused by bacterial infections in the absence of

mechanical obstruction, particularly in patients with immunocompromised states.

Pathophysiology:

-The infection usually occurs when there is an obstruction in the bile duct that leads to bile
stasis due to blockage allowing bacteria to multiply in the stagnant bile. Enteric bacteria
(e.g., Escherichia coli, Klebsiella pneumoniae, Enterobacter, and Bacteroides) ascend from
the intestine into the bile ducts, causing infection.
-The body’s immune response leads to inflammation of the bile duct walls, which can further
worsen obstruction and promote infection.

Signs and symptoms:

-Fever and Chills: Due to the systemic infection.

-Jaundice: Caused by bile duct obstruction and subsequent elevation of bilirubin levels.

-Right Upper Quadrant Pain: Often severe and may be accompanied by tenderness on
physical examination.

-Nausea and Vomiting: Common gastrointestinal symptoms associated with cholangitis.

-Reynolds’ Pentad: In severe cases, patients may exhibit:

● Confusion or Altered Mental Status: Indicating possible sepsis or advanced infection.

● Hypotension: A sign of septic shock, often due to severe infection.

Diagnosis:

-Complete Blood Count (CBC): May show leukocytosis.

-Liver Function Tests (LFTs): Elevated bilirubin, alkaline phosphatase, and transaminases
(AST, ALT) indicating cholestasis.

-Blood Cultures: Should be obtained to identify causative organisms, especially in severe

cases.

-Ultrasound: First-line imaging modality to detect bile duct dilatation and potential stones in
the bile duct.

-CT Scan: Provides detailed information about the biliary tree, identifying stones, strictures,
or masses.

-MRCP (Magnetic Resonance Cholangiopancreatography): Non-invasive imaging technique

useful for visualizing the biliary tree and detecting strictures or stones.

-ERCP (Endoscopic Retrograde Cholangiopancreatography): May be both diagnostic and

therapeutic, allowing for direct visualization of the bile duct and potential removal of stones.

Treatment:

-Antibiotic Therapy: Broad-spectrum IV antibiotics should be started promptly to cover for

common bacteria associated with cholangitis, such as E. coli and Klebsiella species.
Common regimens may include piperacillin-tazobactam or Ceftriaxone plus metronidazole.

-ERCP with Stone Extraction: Often performed for choledocholithiasis and is both
diagnostic and therapeutic.
-Percutaneous Drainage: For patients who are not surgical candidates or in cases of biliary
obstruction where ERCP is not possible.

-Surgical Exploration: May be necessary if there are complications or if endoscopic

approaches fail.

Choledolithiasis
-Choledolithiasis is the condition characterized by the presence of gallstones in the common
bile duct (CBD). These stones can obstruct the flow of bile, leading to a variety of
complications, including cholangitis, pancreatitis, and biliary colic. The management of
choledolithiasis often requires both medical and surgical interventions.

Types of gallstones:

-Cholesterol: The most common type, usually formed from supersaturation of bile with
cholesterol.

-Pigment Stones: Made primarily of bilirubin, these stones are more common in conditions
that cause hemolysis (such as sickle cell disease) or biliary tract infections.

Etiology:

-Obesity: Increases cholesterol saturation in bile.

-Rapid Weight Loss: Can alter bile composition and promote stone formation.

-Diet: High-fat, high-cholesterol diets are risk factors.

-Age: Increased incidence with age.

-Gender: Females are at higher risk, particularly during reproductive years due to hormonal
influences.

-Pregnancy: Hormonal changes can promote gallstone formation.

-Genetic Predisposition: Family history of gallstones may increase risk.

Pathophysiology:

-When gallstones form in the gallbladder, they can migrate into the CBD, causing
obstruction. The obstruction can lead to:

● Bile Stasis: Increased pressure in the bile duct.

● Bacterial Overgrowth: If bile is stagnant, it can lead to infection (cholangitis).
● Inflammation: Increased pressure can irritate the bile duct walls.
Signs and symptoms:

-Biliary Colic:

● Pain: Sudden onset of severe, intermittent right upper quadrant pain, often radiating
to the back or right shoulder. The pain typically occurs after meals (especially fatty
meals) and lasts for several hours.
● Nausea and Vomiting: May accompany the pain.

-Jaundice: If the bile duct is obstructed, the accumulation of bilirubin can lead to yellowing of
the skin and eyes.

-Cholangitis Symptoms: If an infection occurs, the patient may exhibit Charcot’s triad
(fever, jaundice, and right upper quadrant pain) or Reynolds’ pentad (adding confusion and
hypotension).

-Pancreatitis Symptoms: If the stone obstructs the pancreatic duct, it can lead to acute
pancreatitis, presenting with severe abdominal pain, vomiting, and elevated serum
amylase/lipase levels.

Diagnosis:

-Complete Blood Count (CBC): May show leukocytosis if there is an infection.

-Liver Function Tests (LFTs): Typically reveal elevated alkaline phosphatase and bilirubin
levels due to bile duct obstruction.

-Ultrasound: The first-line imaging modality, it can identify dilated bile ducts and the
presence of stones.

-CT Scan: Useful for detecting complications, such as pancreatitis or biliary obstruction.

-MRCP (Magnetic Resonance Cholangiopancreatography): Non-invasive imaging that

provides detailed visualization of the biliary tree, particularly useful for detecting stones and
strictures.

-ERCP (Endoscopic Retrograde Cholangiopancreatography): Both diagnostic and

therapeutic, allowing for the visualization of the bile ducts and possible removal of stones.

Treatment:

-Antibiotics: If cholangitis is suspected, broad-spectrum IV antibiotics should be initiated.

-ERCP: The first-line therapeutic intervention for removing stones from the CBD. It can
decompress the bile duct and resolve obstruction.

-Cholecystectomy: Surgical removal of the gallbladder is often indicated after ERCP to

prevent recurrence. Laparoscopic cholecystectomy is the preferred approach unless
contraindicated. If the patient has severe acute cholangitis or pancreatitis, the timing of
surgery may vary, urgent intervention may be necessary.
-Open Cholecystectomy: May be required in complicated cases or when laparoscopic
methods are not feasible.

-Biliary Drainage Procedures: In cases where ERCP is unsuccessful or when the patient is
not a candidate for surgery.

Duodenostasis
-Duodenostasis refers to the condition of impaired motility or obstruction in the
duodenum, the first part of the small intestine.

-This results in the accumulation of intestinal contents, leading to various gastrointestinal

symptoms and complications. Understanding the causes, pathophysiology, clinical features,
diagnosis, and treatment of duodenostasis is crucial for managing affected patients.

Etiology:

-Intramural Lesions: Tumors (benign or malignant), strictures, or inflammatory masses.

-Extrinsic Compression: Surrounding structures such as pancreatic tumors,

lymphadenopathy, or adhesions from previous surgeries.

-Intestinal Hernias: Can obstruct the duodenum if the herniated tissue is trapped.

-Neuromuscular Disorders: Conditions like diabetes mellitus (autonomic neuropathy) can

impair intestinal motility.

-Post-Surgical Changes: Adhesions or altered motility patterns after abdominal surgery.

-Duodenitis: Inflammation of the duodenum due to infections, autoimmune disorders, or

medications (e.g., NSAIDs).

-Pancreatitis: Inflammation of the pancreas can lead to peritoneal irritation and obstruction.

-Duodenal Atresia: A congenital blockage of the duodenum that is usually diagnosed in

infancy.

Pathophysiology:

-The pathophysiology of duodenostasis involves the disruption of normal peristalsis and

movement of chyme through the duodenum. Obstruction leads to the buildup of
accumulation of Fluid and Gas, resulting in distension and increased intraluminal pressure.

-Stagnation of intestinal contents can promote bacterial overgrowth, leading to

malabsorption and potential sepsis.

-Electrolyte Imbalance: Fluid accumulation may cause dehydration and electrolyte

disturbances, particularly affecting sodium, potassium, and chloride levels.
Symptoms:

-Abdominal Pain: Cramping or colicky pain, often localized in the upper abdomen.

-Nausea and Vomiting: May include bilious vomiting, particularly if the obstruction is
proximal.

-Abdominal Distension: Visible swelling and tympany on palpation due to gas and fluid
accumulation.

-Changes in Bowel Habits: Constipation or reduced bowel movements may occur due to
impaired motility.

-Malabsorption Symptoms: Weight loss, steatorrhea (fatty stools), and nutritional

deficiencies may develop over time, particularly if the condition is chronic.

Diagnosis:

-Complete Blood Count (CBC): May show signs of infection or dehydration.

-Abdominal X-ray: Can reveal signs of obstruction, such as air-fluid levels and distended
loops of bowel.

-Ultrasound: Useful for assessing the presence of masses, organ enlargement, or fluid
collections.

-CT Scan: Provides detailed images of the abdomen and pelvis, helpful in identifying
obstructive lesions, masses, or inflammatory processes.

-Upper Endoscopy (EGD): Can directly visualize the duodenum and may be used for both
diagnosis and therapeutic interventions (e.g., dilating strictures).

Treatment:

-Electrolyte Replacement: Particularly for sodium, potassium, and chloride.

-Nasogastric Tube: May be placed for decompression to relieve abdominal distension and
prevent aspiration.

-Surgical Intervention: Necessary for mechanical obstructions, such as:

● Resection: Removal of obstructive tumors or strictures.

● Bypass Surgery: If the obstruction is non-resectable, bypassing the obstructed
segment may be indicated.

Benign and malignant tumors of small intestine

-Benign and malignant tumors of the small intestine are relatively rare compared to tumors of
other parts of the gastrointestinal (GI) tract.

-Benign tumors of the small intestine include adenomas, leiomyomas, lipomas, and
hamartomas. These tumors are generally asymptomatic but may cause complications such
as obstruction or bleeding. The risk of malignancy is typically low but varies depending on
the specific tumor type.

-Malignant tumors of the small intestine include adenocarcinoma, neuroendocrine tumors,

lymphoma, and leiomyosarcoma. These tumors are more aggressive, presenting with
symptoms like obstruction, bleeding, and weight loss, and often require surgical and
systemic treatment.

Benign Tumors of the Small Intestine

Adenomas:

-Origin: Glandular epithelial cells.

-Location: Most commonly found in the duodenum, particularly near the ampulla of Vater.

-Histology: Tubular, villous, or tubulovillous adenomas.

-Clinical Features: They are often asymptomatic but can cause bleeding, especially if large.
They may rarely lead to obstruction.

-Risk of Malignancy: Adenomas can transform into adenocarcinomas, particularly if

dysplastic.

-Increased risk of malignant transformation (especially villous adenomas).

-Diagnosis:

● Endoscopy: For direct visualization and biopsy.

● Imaging: CT or MRI if large or causing obstruction.

-Treatment:

● Endoscopic removal: For smaller adenomas.

● Surgical resection: If larger or located in a difficult-to-access area.

Leiomyomas:

-Origin: Smooth muscle cells of the intestinal wall.

-Location: Often found in the jejunum or ileum.

-Clinical Features: Usually asymptomatic but can cause bleeding or obstruction if they grow
large.

-Risk of Malignancy: Low, but can transform into malignant leiomyosarcoma in rare cases.
-Diagnosis:

● CT or MRI: Used to identify and characterize the tumor.

● Endoscopy: May show submucosal masses.

-Treatment: Surgical excision, If symptomatic or large.

Lipomas:

-Origin: Adipose tissue in the submucosa.

-Location: Jejunum and ileum.

-Clinical Features:Usually asymptomatic, but they can cause intussusception or bowel

obstruction if large.

-Risk of Malignancy: No malignant potential.

-Diagnosis: CT scan, which typically shows a well-defined, homogeneous, low-density mass.

-Treatment: Surgical removal, If large or symptomatic.

Hamartomas:

-Origin: Disorganized growth of normal tissue.

-Associated Syndromes: Seen in Peutz-Jeghers syndrome, which is characterized by

multiple hamartomas in the GI tract.

-Risk of Malignancy: Hamartomas themselves are benign, but Peutz-Jeghers syndrome is

associated with an increased risk of GI malignancies.

-Clinical Features: Bleeding, obstruction, or intussusception.

Diagnosis: Endoscopy, shows multiple polyps.

Treatment: Polypectomy, in order to remove symptomatic or large polyps.

Malignant Tumors of the Small Intestine

Adenocarcinoma:

-Origin: Glandular epithelial cells.

-Location: Most commonly in the duodenum, particularly near the ampulla of Vater.

-Risk Factors:

● Hereditary Conditions: Familial adenomatous polyposis (FAP), Lynch syndrome.

● Chronic Inflammation: Crohn’s disease, celiac disease.
 ● Dietary Factors: High intake of animal fat and low fiber.

-Clinical Features:

● Obstruction: Due to tumor growth.

● Bleeding: Occult or overt GI bleeding.
● Weight loss and anemia.
● Jaundice: If located near the ampulla of Vater, causing bile duct obstruction.

-Diagnosis:

● Endoscopy with Biopsy: Diagnostic gold standard.

● CT or MRI: For staging and assessing tumor spread.

-Treatment:

● Surgical Resection: Primary treatment for localized adenocarcinoma.

● Chemotherapy: For advanced disease.

Neuroendocrine Tumors (Carcinoid Tumors):

-Origin: Neuroendocrine cells, often producing serotonin and other hormones.

-Location: Most commonly in the ileum.

-Clinical Features:

● Often asymptomatic.
● Carcinoid Syndrome: Flushing, diarrhea, wheezing, and right-sided heart failure,
particularly in metastatic cases.
● Obstruction: Due to the tumor mass or desmoplastic reaction.

-Diagnosis:

● Urinary 5-HIAA levels: Increased in carcinoid syndrome.

● Somatostatin receptor scintigraphy: To locate tumors.
● CT/MRI: For tumor staging.

-Treatment:

● Surgical Resection: If localized.

● Somatostatin Analogues (e.g., octreotide) for symptom control in carcinoid syndrome.

Lymphoma:

-Origin: Lymphoid tissue in the wall of the small intestine.

-Types:

● Non-Hodgkin’s Lymphoma: The most common type.

● MALT (Mucosa-Associated Lymphoid Tissue) Lymphoma.
-Location: Ileum is the most common site due to the abundance of lymphoid tissue.

-Risk Factors:

● Immunosuppression: HIV, post-organ transplant.

● Celiac Disease: Associated with an increased risk of enteropathy-associated T-cell
lymphoma.

-Clinical Features: Abdominal Pain, weight loss and anemia, obstruction or perforation due
to tumor mass.

-Diagnosis:

● Endoscopy with Biopsy: For tissue diagnosis.

● CT or PET Scan: For staging.

-Treatment:

● Chemotherapy: Mainstay of treatment.

● Surgical Resection: For localized disease or to manage complications like
perforation.

Leiomyosarcoma:

-Origin: Malignant smooth muscle cells.

-Location: Jejunum and ileum.

-Clinical Features:

● Abdominal Mass: Often palpable on examination.

● Pain and Bleeding: Due to tumor growth.

-Diagnosis:

● CT or MRI: To evaluate the tumor and surrounding structures.

● Biopsy: For histological confirmation.

-Treatment:

● Surgical Resection: Primary treatment.

● Chemotherapy or Radiotherapy: For metastatic or recurrent disease.

Benign tumors of stomach

-Benign tumors of the stomach are non-cancerous growths that generally have a favorable
prognosis and a lower potential for malignancy compared to malignant gastric tumors.

-While most benign gastric tumors remain asymptomatic and are incidental findings, some
may present with clinical symptoms, particularly if they grow large or cause bleeding.

Gastric Polyps:

-Definition: Small, often asymptomatic mucosal growths protruding into the gastric lumen.

-Types:

● Hyperplastic Polyps: The most common type, usually associated with chronic
gastritis or Helicobacter pylori infection. These rarely become malignant.
● Fundic Gland Polyps: Occur in the fundus of the stomach, often associated with
proton pump inhibitor (PPI) use or familial adenomatous polyposis (FAP). They have
a low risk of malignancy, except in FAP.
● Adenomatous Polyps: Premalignant lesions, accounting for about 10% of gastric
polyps. These have a significant risk of progressing to adenocarcinoma, especially if
they are large (>2 cm).

-Clinical Features:

● Usually asymptomatic.
● May cause upper GI bleeding, iron deficiency anemia, or epigastric pain if large.

-Diagnosis: Endoscopy, which allows direct visualization and biopsy are required to classify
the polyp type.

-Treatment: Endoscopic Polypectomy, which is recommended for adenomatous polyps

and large or symptomatic hyperplastic polyps.

Leiomyoma:

-Origin: Smooth muscle cells in the muscularis propria of the stomach.

-Location: Typically found in the gastric antrum or body.

-Clinical Features:

● Often asymptomatic.
● Can cause bleeding, ulceration, or gastric outlet obstruction if large.

-Diagnosis:

● Endoscopy: Often appears as a submucosal mass.

● Endoscopic Ultrasound (EUS): Helps to determine the depth and origin of the tumor,
differentiating it from malignant counterparts like gastrointestinal stromal tumors
(GIST).
● CT Scan: Can be used for larger tumors to assess their characteristics.
-Treatment:

● Observation: For small, asymptomatic leiomyomas.

● Surgical Excision: Indicated if the tumor is symptomatic or if there is suspicion of
malignancy.

Gastric Lipoma:

-Origin: Adipose tissue in the submucosa of the stomach.

-Location: Typically found in the antrum.

-Clinical Features:

● Mostly asymptomatic.
● Can present with dyspepsia, nausea, or obstruction if large.

-Diagnosis:

● Endoscopy: Shows a submucosal lesion, often with a characteristic yellowish color.

● CT Scan: Typically shows a well-circumscribed, low-density mass (fat).
● EUS: Can confirm the submucosal origin.

Treatment: Surgical or Endoscopic Resection, used for large or symptomatic tumors.

Adenomyoma:

-Origin: A rare benign tumor composed of both glandular and smooth muscle components.

-Location: Usually found in the gastric antrum or pylorus.

-Clinical Features:

● Asymptomatic in most cases.

● Can cause obstruction or bleeding if large.

-Diagnosis:

● Endoscopy: Submucosal mass often found incidentally.

● Histopathology: Required to confirm the diagnosis.

-Treatment: Surgical Resection, which is recommended for symptomatic cases.

Gastric Schwannoma:

-Origin: A rare benign tumor arising from Schwann cells (nerve sheath cells) in the stomach
wall.
-Location: Typically found in the gastric body or fundus.

-Clinical Features: Often asymptomatic but can cause bleeding or mass effect.

-Diagnosis:

● Endoscopic Ultrasound (EUS): A useful tool for visualizing the tumor’s submucosal
origin.
● CT or MRI: For further evaluation of large tumors.

Treatment: Surgical Resection, if symptomatic or to confirm diagnosis.

Pancreatic Heterotopia (Ectopic Pancreas):

-Definition: The presence of pancreatic tissue in the stomach that is not connected to the
normal pancreas.

-Location: Most commonly in the gastric antrum.

-Clinical Features: Usually asymptomatic, but it can cause bleeding, ulceration, or

obstruction in rare cases.

-Diagnosis:

● Endoscopy: May reveal a submucosal lesion, often with a central umbilication.

● Biopsy: Required for definitive diagnosis.

-Treatment: Surgical or Endoscopic Resection, for symptomatic lesions.

Upper gastrointestinal bleeding

-Upper gastrointestinal (UGI) bleeding refers to hemorrhage originating from the
gastrointestinal tract above the ligament of Treitz, which includes the esophagus, stomach,
and duodenum.

-It is a medical emergency that requires prompt diagnosis and intervention. UGI bleeding is
typically classified as either acute (sudden and severe) or chronic (slow, leading to anemia).

Etiology:

-Peptic Ulcer Disease (PUD): Duodenal or gastric ulcers are the most common cause.

● Pathophysiology: Ulcers erode into blood vessels, causing hemorrhage.

● Risk factors: Helicobacter pylori infection, Nonsteroidal anti-inflammatory drugs
(NSAIDs), excessive alcohol use and smoking
● Clinical features: Epigastric pain, hematemesis, melena. But If bleeding is
severe,there are signs of hypovolemic shock (tachycardia, hypotension).
-Esophageal Varices: Dilated submucosal veins in the lower esophagus due to portal
hypertension, commonly in cirrhotic patients.

● Pathophysiology: High portal vein pressure causes veins to dilate and rupture.
● Clinical features: massive hematemesis.
● History of chronic liver disease (e.g., jaundice, ascites).
● Can cause shock in severe cases.
● Complications: Life-threatening due to rapid blood loss.

-Mallory-Weiss Tear: A linear tear in the mucosa at the gastroesophageal junction, caused
by forceful vomiting, retching, or coughing.

● Risk factors: Alcoholism, vigorous retching, bulimia.

● Clinical features: Sudden hematemesis after an episode of vomiting, bleeding is
self-limiting typically

-Gastritis and Gastropathy: Acute or erosive gastritis due to NSAIDs, alcohol, stress (e.g.,
trauma, sepsis), or H. pylori.

● Clinical features: Vague epigastric pain or discomfort.

● May lead to mild to moderate bleeding, presenting as coffee-ground emesis or
melena.

-Esophagitis:

● Causes: GERD, infections (e.g., Candida, HSV in immunocompromised patients), or

radiation.
● Clinical features: Heartburn, dysphagia (difficulty swallowing).
● Occult blood loss, typically leading to iron deficiency anemia in chronic cases.

-Dieulafoy’s Lesion: A large, tortuous arteriole in the stomach that can erode and cause
severe bleeding.

● Clinical features: Sudden, massive bleeding without prior warning.

-Gastrointestinal Stromal Tumor (GIST) or Other Tumors

● Cause: Benign or malignant tumors of the stomach or duodenum can erode into
blood vessels, leading to bleeding.
● Clinical features: occult bleeding or acute hemorrhage, unexplained weight loss and
other systemic symptoms if malignant.

-Vascular Malformations (Angiodysplasia): Abnormal blood vessels in the GI tract, often

in elderly patients.

● Clinical features: Painless bleeding, which may be occult or manifest as melena.

Signs and symptoms:

-Hematemesis: Vomiting of bright red blood or coffee-ground material (indicating bleeding
from the stomach or esophagus).

-Melena: Black, tarry stools, usually indicating bleeding from the upper GI tract.

-Hematochezia: Bright red blood per rectum (more typical of lower GI bleeding but can
occur in massive UGI bleeding).

-Symptoms of Anemia: Fatigue, pallor, dizziness, and weakness due to chronic blood loss.

-Signs of Hypovolemic Shock: tachycardia, hypotension, cold and clammy skin, altered
mental status in severe cases.

Diagnosis of Upper GI Bleeding:

-Laboratory Tests:

● Complete blood count (CBC): To assess for anemia (low hemoglobin/hematocrit).

● Liver function tests (LFTs): Especially in patients with suspected liver disease.
● Coagulation profile: Prothrombin time (PT), INR, especially in patients on
anticoagulants.
● Blood urea nitrogen (BUN): Elevated in UGI bleeding due to increased absorption of
blood proteins.

-Endoscopy (Esophagogastroduodenoscopy - EGD):

● Diagnostic and therapeutic tool.

● Performed within 24 hours of presentation to identify the source of bleeding.
● Can also be used for therapeutic interventions, such as coagulation or banding of
varices, clipping or injecting bleeding ulcers.

-Imaging:

● CT angiography: Useful in cases where endoscopy fails to localize the bleeding

source, especially in severe or ongoing bleeding.
● Tagged red blood cell scan: Can detect ongoing bleeding by tracking radiolabeled red
blood cells.

Management of Upper GI Bleeding:

-Intravenous Fluids: Isotonic saline or lactated Ringer’s to restore circulating volume.

-Blood Transfusions: For patients with significant blood loss (hemoglobin <7-8 g/dL).

-Proton Pump Inhibitors (PPIs): Given intravenously to patients with suspected peptic ulcer
disease or after endoscopic treatment to reduce gastric acid and promote clot formation.

-Octreotide: Used for variceal bleeding to reduce portal venous pressure, administered as a
continuous IV infusion.
-Antibiotics:Given to patients with liver cirrhosis and variceal bleeding to prevent infections
(e.g., ceftriaxone).

-Endoscopic Therapy: Performed to control the source of bleeding

● Injection Therapy: Injection of epinephrine into bleeding ulcers.

● Thermal Coagulation: Using heat to coagulate and seal bleeding vessels.
● Endoscopic Band Ligation: Used for variceal bleeding.
● Clipping: Mechanical application of clips to close bleeding vessels or tears.

-Surgical and Radiologic Interventions:

● Transjugular Intrahepatic Portosystemic Shunt (TIPS): Used for patients with

variceal bleeding unresponsive to medical and endoscopic therapy.
● Angiographic Embolization: Used in cases where endoscopy fails to control the
bleeding.

-Surgery: Indicated for patients with persistent or recurrent bleeding not controlled by
endoscopic or radiologic means.

Abscess of spleen

-A splenic abscess is a rare but serious infection characterized by a collection of pus within
the spleen, resulting from bacterial, fungal, or parasitic infection. It is a life-threatening
condition that requires prompt diagnosis and treatment to prevent complications such as
sepsis and rupture.
-Splenic abscesses are uncommon due to the spleen’s rich blood supply, phagocytic
activity, and immune function.

Etiology:

-Bacterial Infection:

● Common pathogens include Staphylococcus aureus, Streptococcus species, and

Escherichia coli.
● In immunocompromised individuals, organisms like Salmonella or Klebsiella

-Endocarditis: Septic emboli from bacterial endocarditis may lodge in the spleen, leading to
abscess formation.

-Fungal Infections:Typically seen in immunocompromised patients, such as those with

HIV/AIDS or undergoing chemotherapy. Candida and Aspergillus are common fungal
organisms.

-Parasitic Infections: Rare in developed countries, but parasitic organisms like

Echinococcus or Entamoeba histolytica may cause abscesses, especially in endemic
regions.
-Trauma: Direct trauma to the spleen can result in subcapsular hematomas, which may
become infected and evolve into abscesses.

-Hematogenous Spread: Bacteria or fungi can spread to the spleen via the bloodstream
(hematogenous seeding), especially in cases of bacteremia or fungemia.

-Sickle Cell Disease: Patients with sickle cell disease have an increased risk due to
infarction of splenic tissue, which may serve as a nidus for infection.

-Immunosuppression: Individuals with weakened immune systems, including those with

HIV, diabetes mellitus, or undergoing immunosuppressive therapy (e.g., chemotherapy,
corticosteroids), are at higher risk of splenic abscess formation.

-Intravenous Drug Use: IV drug users may introduce bacteria directly into the bloodstream,
increasing the risk of septic emboli and splenic abscesses.

Pathophysiology:

-The formation of a splenic abscess typically follows an initial infection in another part of the
body. Bacteria or fungi enter the bloodstream and are filtered by the spleen.

-In the spleen, pathogens can become trapped in microabscesses, which coalesce into a
larger abscess. In patients with predisposing conditions, such as trauma or splenic infarction,
damaged splenic tissue is more susceptible to infection.

-Over time, the abscess enlarges, causing localized inflammation and destruction of splenic
tissue.

Signs and symptoms:

-Fever and Chills: Persistent high-grade fever is the most common symptom, often
accompanied by rigors.

-Left Upper Quadrant Abdominal Pain: Pain is localized to the left upper quadrant,
sometimes radiating to the left shoulder (referred pain via the phrenic nerve).

-Splenomegaly: The spleen may be enlarged and tender on palpation.

-Leukocytosis: Elevated white blood cell count is usually present, reflecting the body’s
response to infection.

-Malaise and Fatigue: Patients may experience general weakness and fatigue due to
systemic infection.

-Pleural Effusion: In some cases, particularly with larger abscesses, patients may develop a
reactive left-sided pleural effusion.

-Sepsis: If untreated, a splenic abscess can lead to septic shock, characterized by

hypotension, tachycardia, altered mental status, and multi-organ failure.

Complications:
-Rupture of the Abscess: Splenic abscess rupture can lead to peritonitis, sepsis, and shock.
It is a life-threatening emergency that requires immediate surgical intervention.

-Sepsis: The most serious complication, which can result in multi-organ failure and death if
untreated.

-Pleural Effusion or Empyema: Abscesses near the diaphragm can cause inflammation
and infection of the pleural cavity.

Diagnosis:

-Ultrasound: Initial imaging modality often used, especially in patients with suspected splenic
pathology. Ultrasound may reveal a hypoechoic or complex mass in the spleen.

-CT Scan: The gold standard for diagnosing splenic abscesses. CT typically shows a
low-density lesion within the spleen, with possible fluid levels, gas formation, or surrounding
inflammation. CT can also assess for complications like splenic rupture or abscess spread.

-MRI: Occasionally used for better soft tissue contrast, particularly in cases of fungal
abscesses or when radiation exposure is a concern.

-Laboratory Tests:

● Complete Blood Count (CBC): Shows leukocytosis with a left shift (increased
immature neutrophils).
● C-Reactive Protein (CRP): Elevated levels, reflecting the acute phase of
inflammation.
● Liver Function Tests: May be elevated if there is associated hepatic involvement or
septicemia.

Treatment:

-Antibiotic Therapy

-Percutaneous Drainage: Image-guided percutaneous drainage is often the first-line

treatment for large or multiloculated abscesses. It is minimally invasive and allows for direct
evacuation of the pus and culture of the fluid, guiding further antibiotic therapy. This
approach is particularly beneficial in patients who are poor surgical candidates.

-Splenectomy: Reserved for patients with:

● Large or multiple abscesses that are not amenable to percutaneous drainage.

● Ruptured abscesses.
● Persistent or worsening infection despite adequate drainage and antibiotics.

-Partial Splenectomy: May be considered in select cases to preserve some splenic function,
particularly in immunocompromised patients.

-Laparotomy: Performed in emergent situations, such as splenic rupture or generalized

peritonitis.
Indications for splenectomy

-A splenectomy is the surgical removal of the spleen.

Trauma:

-Splenic Rupture: One of the most common indications for an emergency splenectomy is
traumatic rupture of the spleen, often resulting from blunt abdominal trauma, such as motor
vehicle accidents or falls. The spleen’s fragile structure and rich blood supply make it
susceptible to rupture, leading to life-threatening internal bleeding (hemoperitoneum).

-Subcapsular Hematoma: A collection of blood under the splenic capsule that may lead to
splenic rupture if it enlarges or the capsule tears.

Hematologic Disorders:

-Splenectomy is often indicated in hematologic conditions, especially those that result in

excessive destruction of blood cells or splenomegaly (enlargement of the spleen).

-Idiopathic Thrombocytopenic Purpura (ITP)

-Hereditary Spherocytosis

-Thalassemia: In patients with beta-thalassemia major

-Sickle Cell Disease

-Autoimmune Hemolytic Anemia

Splenomegaly:

-Hypersplenism: A condition where an enlarged spleen leads to excessive destruction of

blood cells (red blood cells, white blood cells, and platelets), causing pancytopenia.
Splenectomy is indicated when hypersplenism causes significant cytopenias or symptoms
that are not controlled by medical management.

-Myeloproliferative Disorders: Conditions such as myelofibrosis or chronic myeloid

leukemia can cause massive splenomegaly, leading to discomfort, pain, and severe
cytopenias. Splenectomy can relieve symptoms and reduce blood cell destruction.

Infections and Abscesses:

-Splenic Abscess: If a splenic abscess is large, multiloculated, or unresponsive to

percutaneous drainage, splenectomy is indicated to prevent rupture and sepsis.

-Splenic Tuberculosis: Rare in developed countries, but in regions where tuberculosis is

endemic, splenic involvement may require splenectomy if medical treatment is ineffective.
-Fungal Abscesses: Immunocompromised individuals, especially those with HIV or
undergoing chemotherapy, may develop fungal infections of the spleen. Splenectomy may
be required if antifungal treatment fails.

Malignancy:

-Primary or Metastatic Tumors: Although primary splenic tumors (e.g., splenic lymphoma)
are rare, splenectomy may be indicated for diagnostic purposes or to treat localized
malignancy.

-Splenic Marginal Zone Lymphoma: A type of low-grade lymphoma involving the spleen,
where splenectomy can help reduce tumor burden and alleviate cytopenias.

-Hodgkin’s and Non-Hodgkin’s Lymphoma: In some cases, splenectomy is performed for

diagnostic staging or to treat splenic involvement in these malignancies.

Cysts and Benign Tumors:

-Splenic Cysts: Large or symptomatic splenic cysts, whether congenital or acquired, may
require splenectomy, especially if they are at risk of rupture.

-Hemangiomas and Lymphangiomas: Benign vascular tumors of the spleen that may
cause pain, splenomegaly, or spontaneous rupture. Splenectomy is indicated if the lesion is
large or symptomatic.

Splenic Vein Thrombosis:

-Portal Hypertension: Thrombosis of the splenic vein can cause increased pressure in the
splenic circulation, leading to splenomegaly and hypersplenism. Splenectomy may be
considered to alleviate these complications, particularly in the context of cirrhosis or
pancreatitis.

Congenital Anomalies:

-Polysplenia Syndrome: A rare congenital disorder in which multiple small spleens

(polysplenia) are present. If these accessory spleens cause symptoms, surgical intervention
may be necessary.

-Accessory Spleens: Occasionally, small accessory spleens can be problematic after

primary splenectomy, particularly in cases of hematologic disorders. These may need to be
removed to fully resolve the underlying condition.

Splenic Artery Aneurysm:

-Aneurysms of the Splenic Artery: These are rare but can rupture, causing life-threatening
hemorrhage. Splenectomy is sometimes performed along with repair or ligation of the
aneurysm.

Therapeutic Splenectomy for Immune Modulation:

-Felty’s Syndrome: This is a rare complication of rheumatoid arthritis characterized by
neutropenia, splenomegaly, and recurrent infections. Splenectomy is considered when
medical treatment fails to correct the neutropenia or reduce infection risk.

-Gaucher Disease: A lysosomal storage disorder that can lead to splenomegaly and
hypersplenism. Splenectomy may be considered when there is significant cytopenia or
splenic discomfort despite enzyme replacement therapy.

Infection of echinococcus
-Echinococcosis (Hydatid Disease) is a parasitic infection caused by the tapeworms of the
Echinococcus genus.

-The two most common species responsible for human infections are Echinococcus
granulosus (causing cystic echinococcosis) and Echinococcus multilocularis (causing
alveolar echinococcosis). These infections are zoonotic, with humans acting as accidental
intermediate hosts.

Epidemiology:

-Echinococcus granulosus is more prevalent worldwide, especially in regions with extensive

livestock farming (such as sheep and cattle), including South America, Central Asia, the
Mediterranean, and parts of Africa.

-Echinococcus multilocularis is found mainly in the northern hemisphere, particularly in

central Europe, North America, and parts of Asia.

Lifecycle:

-Definitive Hosts: Primarily dogs for E. granulosus and foxes for E. multilocularis. These
hosts harbor adult tapeworms in their intestines.

-Intermediate Hosts: Herbivores like sheep (E. granulosus) or rodents (E. multilocularis).
Humans act as accidental intermediate hosts.

-Transmission: Humans are infected by ingesting eggs of Echinococcus species, usually

through contaminated food, water, or contact with infected animals. The eggs hatch in the
intestine, and the larvae penetrate the intestinal wall, entering the bloodstream and migrating
to various organs, where they form cysts.

Pathophysiology of Cystic Echinococcosis (CE):

-Caused by Echinococcus granulosus.

-The larval form (oncosphere) travels through the bloodstream, commonly affecting the liver
and the lungs. Less frequently, it can involve the brain, bones, and other organs.
-Cysts are typically slow-growing, spherical, and filled with fluid. Over time, they can grow
and compress surrounding tissues, causing symptoms. The cyst wall consists of two layers:
an inner germinal layer and an outer laminated layer.

Pathophysiology of Alveolar Echinococcosis (AE):

-Caused by Echinococcus multilocularis.

-This form behaves more like a malignant neoplasm, with aggressive growth and potential
for local invasion and metastasis, especially to the liver. Unlike the cysts in E. granulosus,
those of E. multilocularis are small, multiloculated, and lack a distinct boundary, infiltrating
tissues.

Signs and symptoms of Cystic Echinococcosis (CE):

-Symptoms depend on the cyst’s size and location. The majority of patients are
asymptomatic for years until the cyst becomes large enough to cause symptoms due to
pressure effects.

-Liver involvement: Hepatomegaly, abdominal pain, and jaundice (if bile ducts are
compressed).

-Lung involvement: Chronic cough, chest pain, and dyspnea. In severe cases, cyst rupture
can lead to hemoptysis or anaphylaxis.

-Complications: Rupture of the cyst can cause secondary infection, anaphylactic shock, and
dissemination of the infection.

Signs and symptoms of Alveolar Echinococcosis (AE):

-Often presents as chronic liver disease with hepatomegaly, jaundice, and right upper
quadrant pain.

-Complications: Metastasis to other organs (lungs, brain), secondary biliary cirrhosis,

portal hypertension, and liver failure.

Diagnosis:

-Ultrasound (US): The primary diagnostic tool for liver involvement, showing cystic lesions.

-CT and MRI: Useful in assessing organ involvement, cyst structure, and complications. For
E. multilocularis, CT can reveal a “honeycomb” appearance.

-ELISA and indirect hemagglutination test (IHA) can detect antibodies against Echinococcus
antigens, though the sensitivity varies with the type of echinococcosis and cyst location.

-Western blot is more specific and can help differentiate between E. granulosus and E.
multilocularis.

-Biopsy/Fine Needle Aspiration: Rarely performed due to the risk of cyst rupture and
anaphylaxis.
Treatment:

-Cystic Echinococcosis:

● Surgery: The primary treatment for accessible cysts, aiming to remove the entire cyst
without rupture. Surgical techniques vary depending on cyst location, size, and
complications.
● Percutaneous Aspiration (PAIR): A minimally invasive alternative involving
puncture of the cyst, aspiration of the fluid, injection of a scolicidal agent, and
re-aspiration.
● Antiparasitic Therapy: Albendazole is commonly used pre- and post-operatively or
when surgery is contraindicated. It inhibits the parasite’s glucose uptake, eventually
leading to its death. Mebendazole is an alternative but less effective.

-Alveolar Echinococcosis:

● Surgery: Radical resection of the affected tissue is the preferred treatment when
possible, although complete removal is often challenging due to the infiltrative nature
of the disease.
● Long-term Antiparasitic Therapy: Albendazole is typically required for extended
periods (years or lifelong), as relapse rates are high.

Spleen disorders
- A ruptured spleen can occur when there’s damage to the spleen’s surface.

- The spleen is an organ located in the upper left side of the abdominal cavity, underneath
the rib cage. It plays an important role in filtering blood by removing old or damaged cells
and debris, as well as in helping the body fight infections.

-Splenic rupture may result in internal bleeding that can be life threatening if not treated
promptly.

Etiology:

-Splenic rupture is most commonly caused by an injury to the spleen. Penetrating

abdominal trauma, such as a stab wound or gunshot, can cause acute ruptures. Blunt
trauma to the left upper abdomen can either cause acute splenic injury upon contact, or a
delayed rupture that develops days or weeks after the initial injury. Such injuries most often
occur in contact sports and motor-vehicle crashes.

-Spontaneous splenic rupture can happen as a result of an enlarged spleen

(splenomegaly), which occurs when blood cells accumulate in the spleen. The most common
cause of spontaneous rupture due to an enlarged spleen is infectious mononucleosis, a viral
infection that is spread through saliva. Additional infections include bacterial infections such
as syphilis and parasitic infections such as malaria. Splenomegaly can also be a sign of
several underlying conditions including liver disease, metabolic disorders, or some types of
blood cancer.

Signs and symptoms:

-Symptoms of a ruptured spleen can vary depending on the associated injury, however, the
most common symptom is pain and tenderness in the left upper abdomen.

-The pain may be referred to the left shoulder, which is known as Kehr’s sign, and typically
feels worse when breathing.

-Individuals may also develop low blood pressure from the blood loss, which may cause
additional symptoms such as lightheadedness, confusion, dizziness, and blurred vision.

-In some cases, massive blood loss can evolve into hemorrhagic shock, causing a rapid
heart rate, pale skin, shallow breathing, and restlessness or anxiety.

Management;

-A ruptured spleen is a medical emergency and can be life-threatening. Management for a

ruptured spleen typically depends on the underlying conditions and the severity of the injury.

-Physicians will first diagnose the condition based on symptoms and a physical exam. Blood
tests may also be performed. To check for blood in the abdomen, they may administer an
ultrasound. A computed tomography (CT) scan can also be performed to determine the
severity of the injury.

-In mild splenic ruptures, the spleen can heal itself with rest and time. Physicians may
recommend hospitalization during recovery to monitor the condition and provide supportive
care. Follow-up CT scans can show progress and determine whether any additional
measures are needed.

-In more severe cases, a ruptured spleen may require surgery to repair or remove the
spleen. If the bleeding is controllable, surgeons may be able to fix the spleen by repairing the
tear with stitches or other methods. In some cases, it may be possible to remove part of the
spleen to repair the rupture. If the bleeding is more serious, it may require the full removal of
the spleen (splenectomy).

-Although one can survive without a spleen, it does increase the risk of infection and sepsis.
Individuals without a spleen are at an increased risk of infections from encapsulated
bacteria, thus vaccination against pneumococcus, meningococcus, and Haemophilus
influenzae is advised after splenectomy.

-Generally, recovery from a ruptured spleen can take anywhere from 3 to 12 weeks,
depending on the severity and treatment. To promote healing, rest is encouraged, along with
refraining from high-impact exercise, strenuous activities, and heavy lifting until physician
approval. Alternatively, low-impact exercise and activity, such as walking, may help recovery
if suggested by a physician.
Splenomegaly
-Splenomegaly refers to an enlarged spleen.

-The spleen is located in the left upper quadrant of the abdomen, under the rib cage. It plays
an important role in filtering blood by removing old or damaged cells and debris, as well as
helping the body fight infections. The spleen also stores white blood cells and platelets.

-An enlarged spleen is characterized as one that is larger than 12 cm in length or over 400
grams in weight. Splenomegaly usually occurs as a result of secondary causes rather than
primary diseases of the spleen and is considered a rare condition, but can affect anyone.

Etiology:

-Splenomegaly can be caused by a wide range of disorders. It is most commonly caused by

infections, certain cancers, and portal hypertension. However, several other conditions may
also lead to splenomegaly.

-Infections associated with splenomegaly include viral infections, such as infectious

mononucleosis, parasitic infections, such as malaria and leishmania, and bacterial
infections, such as bacterial endocarditis. When the body is fighting these infections, the
spleen works hard to produce antibodies against the infectious agent, leading to an increase
in the number of splenic cells. This can ultimately cause enlargement of the spleen.

-Splenomegaly can also occur as a result of certain blood cancers, such as leukemias and
lymphomas. In these diseases, cancer cells can infiltrate the spleen and lead to
enlargement.

-Additionally, splenomegaly can result from portal hypertension which refers to increased
blood pressure in the portal vein. Liver disease such as cirrhosis, or liver scarring, can cause
the blockage of blood flow through the liver, thus causing blood to back up in the portal vein
resulting in increased pressure or portal hypertension. As a result, the spleen becomes
engorged with blood, leading to splenomegaly.

-Several less common conditions can also lead to splenomegaly. Hemolytic anemias, for
example, occur when defective red blood cells are rapidly destroyed in the spleen causing
the spleen to work harder than usual and potentially enlarge. Sickle cell disease, in which
red blood cells can take the shape of a crescent, or a sickle, due to defective hemoglobin,
can also cause splenomegaly. In sickled form, red blood cells can stick together and block
the splenic capillaries, preventing blood flow out of the spleen and causing its enlargement.
Additionally, chronic inflammatory diseases like systemic lupus erythematosus and
rheumatoid arthritis can also cause splenomegaly. While the mechanism is not clear, the
increased demand for white blood cells can cause the spleen to overwork, which in turn,
may cause enlargement.

-Other rare conditions which lead to splenomegaly include metabolic diseases, such as
Gaucher disease and Niemann–Pick disease. In Gaucher disease, low levels of a particular
enzyme cause fatty substances to accumulate in various organs and tissues, including the
bone marrow, liver, and spleen. This build-up can also cause the spleen to enlarge. Similarly,
people with Niemann-Pick disease cannot break down a fat called sphingomyelin due to
another enzyme deficiency, resulting in fat build-up in cells which can accumulate in various
organs, including the spleen.

Signs and symptoms:

-Individuals with splenomegaly most commonly experience vague abdominal discomfort,

which might also be accompanied by localized pain near the spleen.

-Abdominal bloating and decreased appetite due to stomach compression by the enlarged
spleen may also occur. Some individuals may experience symptoms of cytopenias
(decreased circulation of blood cells), such as fatigue due to anemia, susceptibility to
infections, or episodes of bleeding.

-Furthermore, affected individuals also typically have the signs and symptoms of the
underlying condition that is causing the enlarged spleen. For example, individuals with
splenomegaly caused by an infection may present with fever or chills, while individuals with
splenomegaly caused by cancer may experience night sweats and weight loss. Similarly,
individuals who suffer from liver disease can present with a wide variety of signs and
symptoms that accompany the condition.

Complications:

-Splenomegaly is a serious condition and it is recommended to seek out immediate medical

attention if spleen enlargement is suspected. An enlarged spleen can rupture easily upon
trauma and, in some cases, can rupture spontaneously.

-Splenic rupture can lead to a life-threatening loss of blood. In these cases, splenectomy, or
removal of the spleen, may be required. Moreover, an enlarged spleen can cause the
destruction of circulating blood cells, such as white blood cells, red blood cells , and
platelets. The consequent low counts of white blood cells can result in an increased
susceptibility to infections. Similarly, the lowered counts of red blood cells may result in
anemia, and lowered counts of platelets may increase the risk of bleeding.

Massive splenomegaly:

-Massive splenomegaly refers to significant enlargement of the spleen, usually larger than
20 cm in length or over 1 kg in weight.

- In such cases, the spleen may cross the midline of the body and extend toward the right
lower quadrant of the abdomen. Diseases that can cause massive splenomegaly include
various cancers, such as chronic myelogenous leukemia, myelofibrosis and splenic marginal
zone lymphoma, as well as certain infections, such as malaria.

Diagnosis:

-Splenomegaly can usually be diagnosed through palpation during a physical exam. On rare
occasions a normal-sized, healthy spleen can also be felt during a physical exam. In
massive splenomegaly, the spleen might be palpated across the midline of the abdomen and
also extend to the right lower quadrant of the abdomen and in the pelvis.
-Additionally, blood tests can be administered to check the number of red blood cells, white
blood cells, and platelets, as well as the shape of red blood cells.

-CT scans may be used to determine the size of the enlarged spleen. An ultrasound can also
be helpful in diagnosing splenomegaly. Finally, magnetic resonance imaging (MRI) can be
used to examine blood flowthrough the spleen.

Treatment:

-Treatment of splenomegaly primarily focuses on treating the underlying cause. In general,

however, all individuals with splenomegaly are recommended to avoid contact sports and
other potential sources of abdominal injuries in an effort to prevent the occurrence of a
ruptured spleen.

-In certain cases, such as with massive splenomegaly caused by cancer, splenectomy, or
the removal of the spleen, may be required. In cases that require a splenectomy, vaccination
against certain bacteria is highly recommended. Although one can survive without a spleen,
it does increase the risk of infection and sepsis. Individuals without a spleen are at an
increased risk of infections from encapsulated bacteria, thus vaccination

against Pneumococcus, Meningococcus, and Haemophilus influenzae is advised after

splenectomy.

Diverticular disease
-Diverticula are small outpouchings that form along the walls of a hollow structure, most
commonly, the large intestine.

-According to their pathogenesis, diverticula can be broadly grouped into traction and pulsion
diverticula.

Traction diverticula:

-Traction diverticula occur due to the pulling forces of an adjacent inflammatory site, resulting
in scarring and outpouching of all layers of the intestinal wall.

-These are also known as true diverticula.

Pulsion diverticula:

-Pulsion diverticula are a result of high pressures created during a strained bowel
movement. The pressure pushes on the mucosa and submucosa until they bubble out
through weak spots along the wall, like where a blood vessel penetrates the muscle layer of
the intestine.

-These are also known as false or pseudodiverticula since they don’t involve all layers of
the intestinal wall.
-For your exams, it’s important to know that, most of the time, diverticula in the large
intestine, and particularly, the left and sigmoid colon, are pulsion or false diverticula.

Diverticulosis:

-Having diverticula in the colon is called diverticulosis, and it’s more common in individuals
older than 60 years old, consuming a diet low in fiber and high in fatty foods, like red meat.
Fiber helps stool move more easily through the colon, so diets low in fiber can lead to
constipation which means more force is required to move bulky, hard stool.

-Most of the time, people won’t even know they have diverticulosis because they don’t have
any symptoms besides constipation and mild or vague abdominal discomfort after meals.

-Diagnosis is typically made incidentally during a colonoscopy or CT scan that might be done
for another reason entirely.

-Okay, so even though diverticulosis doesn’t cause major distress in the person, they can
still cause serious complications. One complication is bleeding due to weakening and
breaking of blood vessels near a diverticula. It’s important to know that diverticulosis is the
most common cause of acute lower gastrointestinal bleeding. This will typically appear in
your exam as an elderly patient with a history of chronic constipation and painless
hematochezia, which means bright red or maroon blood passing from the rectum.

-Remember, bright red blood usually means lower GI bleed, and painful hematochezia
usually indicates hemorrhoids.

Acute diverticulitis:

-A complication of diverticulosis is acute diverticulitis, which is an infection of the diverticula.

-Typically it starts when there’s increased pressure in the lumen of the intestines or food
impaction in the diverticulum that leads to micro-perforations in the diverticula. The bacteria
in the lumen of the gut dive into these microperforations, and cause infection within the
intestinal wall.

-Symptoms include left lower quadrant abdominal pain and low- grade fever, along with a
change in bowel habits, like alternating constipation and diarrhea.

-Treatment is with antibiotics.

Diverticular abscess:

-Acute diverticulitis can also lead to the formation of an abscess within the inflamed
diverticula.

-The symptoms of a diverticular abscess are about the same as the symptoms of acute
diverticulitis, the clue for abscess is that the oral antibiotics are ineffective so the
symptoms persist.
-In some cases, inflammation leads to a partial obstruction of the colon, and that can
cause abdominal distention, nausea, and vomiting.

-In other cases, if the diverticula become distended enough, it may rupture and cause
peritonitis, resulting in a tender, distended abdomen with guarding and rigidity. Alternatively,
it can create a fistula, which is a connection with an adjacent organ or structure.

-Since it sits pretty close to the bladder, a fistula connecting the large intestine to the bladder
may form, called a colovesicular fistula, and this might result in dysuria, pneumaturia, or
passage of gas in the urine, as well as fecaluria, or stool in the urine.

-Diagnosis of acute diverticulitis and its complications is usually made with a CT scan with
contrast of the abdomen and pelvis.

-A key concept that is frequently tested is that colonoscopy is contraindicated in acute

diverticulitis, because it increases the risk for perforation and subsequent peritonitis.

Meckel’s diverticulum
-Meckel’s diverticulum is a common and often harmless birth defect that can occur in your
baby’s small intestine. It affects 2% to 3% of all babies.

-Meckel’s diverticulum occurs during fetal development and it can contain leftover tissue
from development that wouldn’t ordinarily be there. Normal body tissue that grows in an
abnormal place is called ectopic tissue.This tissue can occasionally cause complications.

Rule of 2:

-Meckel’s diverticulum occurs in 2% of the population.

-Only 2% of people who have it develop complications or symptoms.

-Symptoms usually appear in children under 2.

-Symptoms occur twice as often in those assigned male at birth (AMAB).

-It’s usually located about 2 feet from the lower end of the small intestine.

-It may have either of two types of ectopic tissue in it (stomach tissue or pancreatic tissue).

Etiology:

-Meckel’s diverticulum occurs early in fetal development, when the yolk sac that fed the
embryo during its first weeks is replaced by the placenta. The duct that once connected the
yolk sac to the embryo (the vitelline duct or omphalomesenteric duct) detaches at this point,
and the developing fetus is supposed to reabsorb it. But sometimes, it doesn’t detach or
reabsorb completely, and a remnant is left over.
-This remnant becomes Meckel’s diverticulum. The duct that once fed into the embryo’s
small intestine remains as a small indentation in the baby’s small intestine. It can have
different variations, too. Sometimes, a fibrous band of tissue remains attached to the
diverticulum, which can cause an obstruction later. About 25% of the time, it has ectopic
tissue in it, though scientists aren’t sure why.

-Meckel’s diverticulum appears to affect anyone. But you might be more likely to have it or to
have complications from it if you also had another common congenital disorder, like
esophageal atresia or anorectal malformation. Other risk factors include assigned male sex
and age under 50 years.

Signs and symptoms:

-Meckel’s diverticulum by itself isn’t something you’d notice, and people can live their whole
lives without knowing they have it. If complications do develop, they’re likely to do so in early
childhood. But sometimes, they don’t show up until adulthood. The symptoms can be vague,
and tracing them back to the cause can be a process.

-Gastrointestinal bleeding: The most common complication is ectopic tissue secreting

digestive juices that don’t belong in this part of the small intestine. This can lead to ulcers in
your intestinal wall — open sores that bleed. Bleeding from your small intestine is often
painless, but it’ll come out in your poop (stool). In children, it usually shows up as dark red
blood in their stool. In adults, it may be tarry, black stool. If bleeding continues, you might
develop anemia symptoms.

-Diverticulitis: Less commonly, you might develop inflammation and pain inside your
Meckel’s diverticulum if it gets a bacterial infection. This might happen if passing stool gets
stuck in the pouch. This can cause abdominal swelling and tenderness to the touch,
especially near your belly button. If you or your child has ever had appendicitis, it might feel
similar to that.

-Intestinal obstruction: Rarely, Meckel’s diverticulum may cause a bowel obstruction,

partially or completely blocking the passage of solids through your small intestine. It can
cause this in a few different ways. Sometimes, it has extra tissue attached to it that clogs the
passageway. The pouch can also fold in on itself, causing another segment of the bowel to
collapse into it. This is called intussusception. Bowel obstructions may cause bloating,
cramping, nausea and vomiting.

-Complications of Meckel’s diverticulum could become life-threatening in severe cases.

You’d probably notice symptoms before this stage. But if you didn’t, and they went untreated,
they could escalate. For example, constant bleeding from an ulcer could lead to significant
blood loss and shock. An ulcer that erodes through your intestinal wall could leak bacteria,
causing an infection that could become septic.

Diagnosis:

-Some people discover they have Meckel’s diverticulum by accident when they have an
imaging test for some other reason. Other people discover it when they begin to have
symptoms due to complications.
-Pediatricians are more likely to suspect Meckel’s diverticulum in young children who
develop unexplained abdominal pain or painless rectal bleeding. Meckel’s diverticulum
accounts for about half of all lower gastrointestinal bleeds in children under 2.

-Meckel’s scan: This nuclear medicine imaging scan is usually the first choice for
diagnosing Meckel’s diverticulum, especially when rectal bleeding is the primary symptom. It
can detect ectopic stomach tissue in the diverticulum.

-Mesenteric arteriography (angiogram):An imaging study of the blood flow through your
mesenteric arteries can reveal the blood supply to Meckel’s diverticulum. If there’s an
abnormal branch from your superior mesenteric artery to your lower small intestine, it can
show where the diverticulum is located and reveal any active bleeding from the site. The
blood supply doesn’t always look abnormal in everyone, though, so this doesn’t work every
time.

Endoscopy: If the above tests don’t reveal the diverticulum, a gastroenterologist may pass a
tiny camera on a long tube into your small intestine (enteroscopy). Alternatively, you can
swallow a tiny, pill-sized camera (capsule endoscopy).

Treatment:

-If Meckel’s diverticulum causes complications, surgery can fix it. The procedure is called a
small bowel resection. It just means cutting out the small piece of the bowel with the
diverticulum in it.

-Also, surgeons can treat Meckel’s diverticulum with laparoscopic surgery, which uses small
incisions that heal quickly.

Megacolon
-Megacolon is an abnormal dilation of the colon that is not caused by mechanical
obstruction. It is usually accompanied by symptoms such as abdominal discomfort, but may
result in serious complications (colonic perforation, peritonitis, and/or sepsis) if left untreated.

Types of megacolon:

-Megacolon can be classified as acute or chronic depending on whether the dilation is

temporary or ongoing.

-All cases of acute megacolon are acquired, whereas chronic megacolon can be both
acquired or congenital.

-Acute megacolon can be further categorized depending on whether there is inflammation of

the colon. If inflammation is present, this usually results in systemic toxicity, so the resulting
condition is referred to as toxic megacolon. If no inflammation is present, the resulting
condition is referred to as Ogilvie syndrome, or just acute megacolon.

Etiology:
-Megacolon has a wide range of causes, including infection, disease, medication, and
various congenital disorders. It may also occur following a major surgery; however, the
condition is often idiopathic, which means the exact cause is not known.

-Infection: One of the most common causes of megacolon is infection. This includes
bacterial infections such as Clostridium difficile, Salmonella, Shigella, and Campylobacter,
as well as parasitic infections such as Trypanosoma cruzi (commonly known as Chagas
disease) and Entamoeba histolytica.

-Disease: Megacolon can also be caused by a variety of neurological and systemic

diseases. Common neurological causes are diabetic neuropathy and Parkinson's disease,
while systemic causes include some muscular dystrophies, scleroderma, and systemic lupus
erythematosus.

-Medication: In rare cases, megacolon may be the adverse effect of a medication. Most
notably, drugs such as risperidone, clozapine, and loperamide are associated with increased
risk of megacolon.

-Congenital disorders: Megacolon can also be caused by some congenital disorders, as is

true in the case of Hirschsprung’s disease, where functional obstruction of the intestines is
often observed.

-Other: Other possible causes of megacolon include electrolyte imbalances (e.g.

hypokalemia) and hypothyroidism.

Pathophysiology:

-The exact mechanism by which megacolon develops is not known. However, the end result
is the same: severely decreased intestinal motility causes a buildup of feces, air, and
intestinal secretions in the colon, which presents as dilation of the colon.

-In acute, non-toxic megacolon, there is damage to the autonomic nervous system

-In chronic megacolon, there is inherent neurological and/or muscular dysfunction in the
bowels

-In toxic megacolon, there is reduced smooth muscle activity, likely as the result of
inflammation. This may be related to increased nitric oxide synthesis.

Signs and symptoms:

-Common symptoms of megacolon include constipation, bloating, and abdominal pain or

tenderness. In more severe cases, hard fecal masses called fecalomas may also be present.

-Depending on the cause, megacolon may have additional symptoms. In toxic megacolon,
usually caused by infection, additional symptoms include fever, tachycardia, and shock. In
disease-related cases of megacolon, additional symptoms are those of the disease itself.

Diagnosis:
-Megacolon can be diagnosed by observing the size of the colon on an abdominal x-ray
scan. Most physicians agree that a colon diameter greater than 12 centimeters at the cecum
should be classified as megacolon.

-A contrast enhanced CT scan is used to confirm these findings, additionally showing the
colon is free of mechanical obstruction.If a CT scan is not possible, colonoscopy can be
performed to verify the colon is free of mechanical obstruction. However, in toxic megacolon,
colonoscopy should not be performed due to high risk of perforating the colon.

Treatment:

-Treatment for megacolon starts by addressing the underlying cause (such as the offending
medication or disease), if known.

-In acute megacolon, all food and drink should be withheld and a nasogastric tube placed.

-If non-toxic, neostigmine should be administered, and if necessary, the colon itself should
be decompressed by means of a colonoscopy.

-If toxic, steroids and broad spectrum antibiotics should be given.

-In chronic megacolon, both dietary and pharmacological methods should be used to
increase intestinal motility. Laxatives and enemas may also be used to prevent fecal
impaction.

-If the patient does not respond to these treatments within one to three days, it may be
necessary to use surgery to remove all or part of the colon. Following colectomy, options
include ileorectal anastomosis and ileostomy.

Colorectal polyps
-Colorectal polyps are overgrowths of epithelial cells in the colon or rectum. They are
subdivided into non-neoplastic polyps, such as hamartomatous polyps, hyperplastic
polyps, inflammatory pseudopolyps, mucosal, and submucosal polyps and neoplastic
polyps, which include adenomatous and serrated polyps.

Non-neoplastic polyps:

-Hamartomatous polyps are solitary, disorganized masses that contain normal tissue found
at the site of the polyp. These polyps can occur sporadically, or in genetically inherited
conditions, such as juvenile polyposis syndrome or Peutz-Jeghers syndrome; and they have
mild malignant potential.

-Hyperplastic polyps are the most common polyps and they are small and typically located
in the rectosigmoid region. Usually, these polyps are benign lesions, but in rare cases, they
can evolve into serrated polyps, which have malignant potential.
-Inflammatory pseudopolyps are multiple benign pseudopolyps that occur during
regenerative and healing phases in chronic inflammation, and they are most commonly seen
in inflammatory bowel disease.

-Mucosal polyps, which are clinically insignificant, are usually small, less than 5mm, and
they look similar to surrounding normal mucosa. On the flip side, submucosal polyps can
include lipomas, leiomyomas, fibromas, or other lesions.

Neoplastic polyps:

-Adenomatous polyps are caused by a mutation in the tumor suppressor gene called
adenomatous polyposis coli or APC for short, which is located on chromosome 5 and is
responsible for the regulation of cell growth and cell adhesion. Moreover, the mutation of the
APC gene is present in all familial polyposis syndromes and most cases of sporadic colon
cancer.

-Based on histological appearance, there are three types of adenomatous polyps: villous,
which are cauliflower-like polyps that have the highest malignant potential, tubular, which
are pedunculated polyps that protrude out in the lumen of the intestine, they have the lowest
malignant potential and tubulovillous, which have characteristics of both, tubular and villous
polyps, and they have an intermediate malignant potential. Usually, adenomatous polyps are
asymptomatic, but in some cases, villous polyps can cause bleeding, secretory diarrhea, and
partial intestinal obstruction.

-The adenoma-carcinoma sequence includes three steps. The first step is the mutation of
one allele of the APC gene, which leads to the formation of a small polyp, also called early
adenoma. The second step occurs when the small polyp acquires a mutation of
protooncogene called KRAS, which is further followed by an increase in the size of adenoma
and formation of the late adenoma. Finally, the third step requires mutation of tumor
suppressor genes p53 and DCC. Now, adenomatous polyps less than 1cm, are less likely to
acquire these mutations and undergo malignant transformation, in contrast to adenomatous
polyps greater than 4cm which are more likely to progress to adenocarcinoma.

-Serrated polyps are often flat or sessile and are characterized by saw-tooth appearance
under the microscope. They contain methylated CpG islands in their genes. DNA
methylation regulates gene expression, which can cause silencing of DNA-repair genes,
eventually leading to more mutations and malignancy.

Lynch syndrome:

-Lynch syndrome is also known as hereditary nonpolyposis colorectal cancer.

-It’s caused by an autosomal dominant mutation in one of four DNA mismatch repair genes,
MLH1, MSH2, MSH6, or PMS2, with subsequent microsatellite instability. Individuals with
Lynch syndrome have inherited a mutation in one allele of the gene, while mutation of the
second allele occurs during adult life. Mutation of both alleles leads to colonic
adenocarcinoma.
-In contrast to sporadic colonic adenocarcinoma, which is usually left-sided and occurs in
individuals older than 50 years of age, in Lynch syndrome colon cancer is usually right-sided
and it occurs in adults under 50 years of age.

-Lynch syndrome is also associated with extraintestinal malignancies, such as endometrial,

ovarian, stomach, and skin cancers.

Familial adenomatous polyposis (FAP):

-This is a pancolonic condition involving hundreds to thousands of polyps and it always

affects the rectum.

-It is an autosomal dominant inherited condition caused by a mutation in the tumor

suppressor gene on chromosome 5q22 called APC gene.

-Polyps usually begin to develop during puberty and initially, they are asymptomatic, but as
they grow they can present with colonic manifestations such as palpable abdominal mass,
abdominal pain, diarrhea, and hematochezia.

-Moreover, chronic gastrointestinal bleeding from many polyps can lead to iron-deficiency
anemia, even in children.

-Familial adenomatous polyposis can be also associated with extracolonic manifestations,

such as congenital hypertrophy of retinal pigment epithelium, sessile polyps in the stomach
called fundic gland polyps, and duodenal adenomas.

Attenuated familial adenomatous polyposis (AFAP):

-They include fewer than 100 polyps, typically in the ascending colon.

-If left untreated polyps from FAP and AFAP can progress to colorectal cancer via two-hit
hypothesis. The first step is the inherited APC mutation, while the second step is the
mutation of the second allele which occurs as the polyps grow.

-The favored diagnostic method for diagnosing familial adenomatous polyposis is a

colonoscopy, followed by genetic testing. For your tests, remember that individuals with a
positive family history should start regular screening at 10 years of age. Screening includes
colonoscopy once a year, and if polyps are found, treatment includes prophylactic
colectomy.

Gardner syndrome:

-It is a subtype of familial adenomatous polyposis characterized by prominent extracolonic

bone and soft tissue tumors, such as osteomas, fibromas, lipomas, desmoid tumors, and
epidermoid cysts.

-These individuals can have congenital hypertrophy of retinal pigment epithelium,

supernumerary impacted teeth, and multiple jaw osteomas and odontomas.

Turcot syndrome:
-It ia described as the association of familial adenomatous polyposis syndrome, or Lynch
syndrome, with malignant brain tumors, like medulloblastomas or gliomas.

Peutz-Jeghers syndrome:

-It is an autosomal dominant condition caused by a mutation of the tumor suppressor STK11
gene.

-Peutz-Jeghers Syndrome is characterized by multiple hamartomatous polyps

throughout the gastrointestinal tract. These can develop into colorectal, stomach, and
small bowel cancer.

-Outside of the GI tract, there’s also an increased risk of developing breast cancer. It can
also present with mucocutaneous hyperpigmentation macules, which are usually located on
the lips, buccal mucosa, palms, soles, or genitalia.

Juvenile polyposis syndrome:

-There are mutations in BMPR1A and SMAD4 genes, which can be inherited in an
autosomal dominant manner with incomplete penetrance or they can be de novo mutations.

-Typically, juvenile polyposis syndrome affects children younger than 5 years old and these
polyps can arise in any part of the gastrointestinal tract, but the majority of is found in the
colon and rectum.

-Children with juvenile polyposis syndrome can present with hematochezia and
iron-deficiency anemia, but more importantly, they are at risk for developing colorectal
cancer.

-Diagnosis is made by endoscopic studies, such as endoscopy, colonoscopy, or

sigmoidoscopy, and the criteria for diagnosis is more than five juvenile polyps in the colon
and rectum or multiple juvenile polyps throughout the gastrointestinal tract or any number of
juvenile polyps in a person with a family history of juvenile polyposis syndrome. Diagnosis is
confirmed with a biopsy.

Colorectal cancer
-Most commonly it affects people older than 50 years old, and in 25% of the cases, there's a
positive family history.

Risk factors:

-Risk factors for colorectal cancer include hereditary factors, such as familial adenomatous
polyposis, adenomatous and serrated polyps, inflammatory bowel disease, such as
ulcerative colitis, lifestyle factors, such as obesity, smoking, alcohol, and physical inactivity
and finally, dietary factors, which include high consumption of processed red meat and low
consumption of fruits and vegetables.
-Individuals with acromegaly, a condition where the pituitary gland produces too much
growth hormone, are at higher risk of developing colorectal cancer.

-Increased cyclooxygenase-2 activity is linked to some forms of colon adenocarcinoma, so

frequent use of inhibitors of this enzyme like aspirin can lower risks.

Adenocarcinoma:

-The most common form of colorectal cancer is adenocarcinoma and it’s most commonly
located in the rectosigmoid, then ascending colon, and rarely in descending colon.

-Initially, adenocarcinoma can be asymptomatic but as they grow, their location determines
their manifestations.

Left-sided colon tumors:

-Left-sided colon tumors are usually smaller, but as they infiltrate the wall of the colon, they
encircle the lumen, eventually narrowing the lumen and causing obstruction.

-A frequently tested concept is what is the presentation of an individual with left-sided

colorectal cancer, therefore it’s important to know that these individuals present with
obstruction and altered bowel habits, such as narrowing of stool, colicky pains,
constipation, abdominal distension, but also hematochezia, nausea, and vomiting.

Right-sided colon tumors:

-Right-sided colon cancers grow as exophytic masses but they don’t tend to cause colon
obstruction, because the right-sided colon has a larger diameter than the left. Instead,
right-sided tumors tend to cause chronic bleeding, eventually causing iron-deficiency
anemia. Colorectal cancer is the most common cause of iron-deficiency anemia in
postmenopausal women or men aged 50 or older.

-Other manifestations of right-sided colon cancers include progressive fatigue, malaise, and
weight loss.

-Common complications of colorectal cancer include local and distant metastasis, but also
bowel perforation and peritonitis. Non-enterococcal group D streptococci, Streptococcus
bovis, can also cause bacteremia and subacute endocarditis.

Screening:

-Now as far as screening goes, you should screen average-risk individuals at the age of 45,
while individuals with a first-degree relative who has colon cancer, at the age of 40 or 10
years prior to their relative’s diagnosis. Screening includes visualization methods, such as
colonoscopy and flexible sigmoidoscopy, and laboratory findings, such as fecal occult blood
test, which is further subdivided into guaiac fecal occult blood test, or FOBT, and fecal
immunochemical test, or short FIT. On the other hand, individuals with hereditary polyposis
syndromes or inflammatory bowel disease have different guidelines for screening like earlier
and more frequent colonoscopies.
Diagnosis:

-Diagnosis of colorectal cancer, just like screening of colorectal cancer, includes visualization
methods, such as colonoscopy and flexible sigmoidoscopy, but it also includes imaging
methods, such as CT colonography and barium enema x-ray, which might show “apple
core” lesions. Diagnosis is confirmed with biopsy!

Treatment:

-Colorectal cancer can be treated with surgical resection of the colon, colectomy, and
chemotherapy.

-Serum carcinoembryonic antigen levels, or CEA levels are increased in 60-90% of

individuals with colon cancer. But, the CEA level is not specific for colon cancer only, it’s also
increased in pancreatic, gastric, breast malignancies, as well as in inflammatory bowel
disease, cirrhosis, and pancreatitis. Therefore it can be only used to monitor the recurrence
of colorectal cancer. Moreover, if a routine check shows that CEA level is rising again after
surgery, these individuals should undergo additional diagnostic methods, such as X-ray, CT,
colonoscopy, to search for possible cancer recurrence or metastases.

-Finally, you should remember that aspirin and other NSAIDs can be chemopreventive in
colonic adenocarcinoma because colonic adenocarcinoma is associated with increased
activity of an enzyme called cyclooxygenase-2.

Differences between rectal and colon cancer

Differences in symptoms:

-Colon cancer patients most often have other clinical symptoms than RC patients. CC may
be detected due to anemia, abdominal pain, meteorism, paradoxical diarrhea, and fatigue.

-Rectal cancer may become clinically evident by overt blood admixtures to the stool,
pencil-stools, incontinence and pain while sitting.

Differences in surgery:

-The management of rectal cancer is slightly different to that of colonic cancer. This reflects
the rectum's anatomical location and the challenges posed as a result.

-Tumors located in the rectum can be surgically resected with either an anterior resection
or an abdomino-perineal excision of rectum(APER).

-The technical aspects governing the choice between these two procedures can be complex
to appreciate and the main point to appreciate for the exam is that involvement of the
sphincter complex or very low tumours require APER. In the rectum a 2cm distal clearance
margin is required and this may also impact on the procedure chosen.

-In addition to excision of the rectal tube an integral part of the procedure is a meticulous
dissection of the mesorectal fat and lymph nodes (total mesorectal excision/ TME).
-In rectal cancer surgery involvement of the circumferential resection margin carries a high
risk of disease recurrence. Because the rectum is an extraperitoneal structure, it is possible
to irradiate it, something which cannot be offered for colonic tumours. This has a major
impact in rectal cancer treatment and many patients will be offered neoadjuvant radiotherapy
(both long and short course) prior to resectional surgery.

-Patients with T1 and T2,N0 disease on imaging do not rquire irradiation and should proceed
straight to surgery. Patients with T4 disease will typically have long course chemotherapy.
Those with T3 , N0 tumours may be offered short course radiotherapy

prior to surgery. Patients presenting with large bowel obstruction from rectal cancer should
not undergo resectional surgery without staging as primary treatment (very different from
colonic cancer). This is because rectal surgery is more technically demanding, the
anastomotic leak rate is higher and the danger of a positive resection margin in an unstaged
patient is high. Therefore patients with obstructing rectal cancer should have a defunctioning
loop colostomy.

Obstruction syndrome
-Bowel obstruction is when the normal flow of contents moving through the intestines is
interrupted.

-The causes of bowel obstruction can be either mechanical or functional, also called ileus.

-Mechanical obstruction is caused by actual blockages in the large or small intestine, and it
can be defined as partial or complete. Partial obstruction is when gas or liquid stool can pass
through the point of narrowing, while complete obstruction is when nothing can pass.

-Functional causes disrupt peristalsis, which are the waves of contraction that move through
the smooth muscles of the bowel wall that pushes food through the intestines

Physiology:

-The small and large intestines are tube-shaped structures through which chyme, or food
that has been partly digested by the stomach, and stools pass until they’re excreted.

-Now if we zoom into a cross-section of the intestinal wall, it’s lined by four layers of tissue:
First, there’s the adventitia, or serosa,which is the outermost layer that faces the abdominal
or peritoneal cavity. This is the space between the abdominal wall and the abdominal
organs, and it’s lined by peritoneal membranes that contains a thin film of serous fluid.
-Moving on, there’s the muscularis externa, which is smooth muscle that contract to move
food through the bowel.

-Deep beneath this layer is the submucosa, which has connective tissue as well as glands,
blood and lymph vessels that supply the intestinal wall.

-The innermost layer is the mucosa and it’s composed of a few of its own layers: the
muscularis mucosae, which has smooth muscle, the lamina propria, which is rich with blood
and lymph vessels, and the innermost layer which is the epithelial lining that faces the
lumen.

Mechanical causes for bowel obstruction:

-The most common cause in the small intestine is postoperative adhesions. After a
surgery, the scar tissue that forms during the healing process can form fibrous bands that
cause organs to attach to the surgical site or to other organs, causing the lumen of the bowel
to get kinked or pinched tight in certain spots. Another cause of small intestinal obstruction is
hernias and they can occur when a portion of the bowel protrudes out of the abdominal
cavity and can get trapped or tightly pinched at the point where it pokes out.

-Mechanical causes for large bowel obstructions, on the other hand, are most often due to a
volvulus, which is when a loop of intestine twists upon itself, kinking off the lumen.
Sometimes the volvulus can occur around a mass like in colorectal cancer.

-Some mechanical causes of both small and large bowel obstruction include inflammatory
bowel disease which can cause strictures and adhesions, ingestion of a foreign body,
which can get lodged along the gastrointestinal tract, and intussusception, which is where
a part of the intestine folds into the lumen of an adjacent section of bowel, kind of like
retracting a telescope. This is the most common cause of bowel obstruction in children under
the age of 2.

Functional causes for bowel obstruction:

-Functional obstruction causes include anything that decreases smooth muscle contractility.

-The most common one is postoperative ileus, which is transient paralysis of the smooth
muscles in the intestinal wall, and it’s usually caused by trauma during surgery.

-Other causes include infection or inflammation, such as appendicitis or peritonitis,

hypothyroidism, meaning the thyroid gland does not produce enough thyroid hormones,
and electrolyte abnormalities like hypokalemia, meaning low potassium in the blood, or
hypercalcemia which is high calcium in the blood, or various medications such as opioids.

Signs and symptoms:

-When there's a bowel obstruction, whatever the cause, the bowel contents distal to the
obstruction get passed, but after that happens, proximal to the obstruction, gas and stool
start to accumulate, causing the bowel to dilate, and therefore, the overall abdominal cavity
to distend.
-Over time, all this gas and stool causes pressure inside the bowel lumen to increase, so the
intestinal contents push towards the intestinal wall, compressing the mucosal blood and
lymphatic vessels. Since the walls of veins and lymphatics are weaker and easier to
compress compared to arteries, venous and lymphatic drainage are the first ones to get
blocked. The pressure pushes the water in these vessels into the surrounding tissue, leading
to mucosal edema.

-If pressure inside the lumen gets even higher, it also compresses mucosal arteries, leading
to ischemia or reduced blood flow to the intestinal wall.

-In turn, ischemia causes hypoxia, or low oxygen supply.

-At the cellular level, this is accompanied by the production of reactive oxygen species;
which can damage DNA, RNA, and proteins of the cells in the epithelial layer and lamina
propria of the mucosa, leading to cell death, or mucosal infarction.

-So, when the mucosa becomes damaged and capillary blood vessels in the lamina propria
rupture, blood enters the bowel lumen. All this stool and blood in the lumen becomes a
nutritious feast for bacteria that normally reside in the intestines, and they start growing out
of control. These bacteria can then get into the intestinal wall, where they get attacked by
macrophages rushing into the mucosa. These macrophages then release inflammatory
cytokines like tumor necrosis factor-alpha, which cause blood vessels to become more
permeable to fluid and to more immune cells, further increasing mucosal edema,
inflammation, and damage.

-The overall result is the compromised ability of the mucosa to absorb food and water, which
may lead to dehydration and loss of electrolytes, like sodium, potassium and chloride.

-Now, as all these lumen contents continues to build up, intraluminal pressure rises even
higher, making the problem even worse if not corrected

Complications:

-The complications of a bowel obstruction are life-threatening without emergency care.

-Perforation and infection: The fluids, gases and digestive juices that build up behind the
obstruction can create ballooning pressure that causes your intestine to tear (perforation).
The contents can leak out, putting you at risk of an abdominal infection called peritonitis and
a life-threatening system-wide infection called sepsis.

-Strangulation (tissue death): With strangulation, an obstruction prevents parts of your

intestine from getting enough blood. Eventually, gangrene sets in as the tissue dies, putting
you at risk of serious infection and even death.

Diagnosis:

-Medical history: Your healthcare provider will ask about your medical history, including
whether you’ve had any previous abdominal surgeries.
-Physical examination: Your provider will perform a physical exam to check for a swollen
abdomen or masses. They may use a stethoscope to listen for bowel sounds that signal an
obstruction.

-Blood tests: You may need a complete blood count and electrolyte analysis. A blood test
checks for signs of infection. Electrolyte levels can show if you have severe dehydration. If
so, you’ll need fluids immediately.

-Abdominal X-rays: Abdominal X-rays can show a blockage’s location. These images can
also show air around your intestines or diaphragm (the muscle that separates your stomach
and chest). Air in these places can indicate a dead section of intestine or a rupture.

-Computed tomography (CT) scan: A CT scan provides more detailed photos than X-rays.
You may need one to confirm your diagnosis and give more accurate information about
where the bowel obstruction is and what’s caused it.

-Barium enema X-ray: A barium enema X-ray is an X-ray of your colon. While you’re
sedated with anesthesia, a provider inserts a catheter (thin tube) into your rectum. The
catheter fills your intestine with a safe liquid that travels through your colon while a machine
takes X-rays. The liquid makes your intestine stand out more clearly on the X-rays.

Treatment:

-Intravenous (IV) fluids: You may need IV fluids and electrolytes to treat dehydration.

-Nasogastric tube: You may need a nasogastric tube to suction out fluids and air backed up
from the blockage. A nasogastric tube is a long, thin tube that goes in through your nose but
reaches down into your stomach or intestines.

-Medications: You may need anti-emetics to prevent nausea and vomiting and pain
relievers to keep you more comfortable.

-Bowel rest: You may need to refrain from eating or drinking to give your intestine time to
clear the obstruction or shrink to its normal size. Or you may only be allowed to drink a
special liquid containing the nutrients you’d otherwise get from food.

-Surgery: You’ll likely need surgery if your intestine is completely blocked. Your healthcare
provider may remove adhesions or tumors that are causing a blockage. Rarely, they may
need to remove diseased segments of tissue. Sometimes, your provider can place a stent (a
mesh tube) to keep your intestine open and resolve the obstruction without additional
surgery. Or you may need a stent as a temporary solution until you’re healthy enough for
surgery to repair the obstruction.

Ileus
-An ileus is the temporary slowing of digestive tract mobility which can lead to a buildup and
blockage in the digestive tract.

-The smooth muscle of the digestive tract moves in a series of waves called peristalsis,
pushing the contents of food or drink from the esophagus through the large intestine.
Disruptions in peristalsis can occur anywhere throughout the digestive tract and can range
from acute to chronic. Severe acute peristaltic disruptions, also known as paralytic ileus, can
lead to a functional intestinal obstruction in which the muscles fail to contract and can cause
a buildup of gasand other liquid or solid contents. Chronic severe peristaltic disruptions are
known as a pseudo-obstruction and result from chronic neuromuscular problems.

Paralytic ileus:

-Paralytic ileus is a severe form of ileus that occurs when peristalsis has been significantly
reduced or stopped, leading to a buildup of stomach contents in part of the intestine.

-Risk factors for paralytic ileus include abdominal surgery, infection or inflammation of
various parts of the digestive tract, such as the stomach or intestines (e.g. gastroenteritis)
and pouches in the intestines (e.g. diverticulitis) or the pancreas (e.g. pancreatitis).

Gallstone ileus:

-More accurately referred to as a mechanical intestinal obstruction, gallstone ileus occurs

due to the physical blockage of the small intestine by a gallstone.

-Large gallstones can enter the small intestine through an opening that forms between the
gallbladder and intestinal wall, known as a cholecystoduodenal fistula. Gallstone ileus is a
rare complication of cholelithiasis (the formation of gallstones) and those at higher risk
include older adults with comorbid conditions like diabetes, chronic lung disease, or heart
failure.

Meconium ileus:

-Meconium ileus is a severe form of ileus that occurs in infants and may be a sign of cystic
fibrosis, which is a genetic condition affecting the lungs and digestive systems.

-Meconium refers to a dark green stool passed within the first 24 hours of life by a newborn.
It can become abnormally thick and sticky, especially in those with cystic fibrosis. The thick
meconium can then cling to the intestinal wall, impeding its movement through the digestive
tract, and eventually causing meconium to build up and block the last part of the small
intestine.

Etiology:

-Conditions that impair digestive peristalsis can lead to an ileus.

-The digestive tract consists of many nerve cells and smooth muscle fibers that control
peristalsis; damage to these components can occur under various conditions. The most
common cause of an ileus is abdominal or pelvic surgery which activates a stress
response that immobilizes the digestive tract. Typically, it takes about 24 to 72 hours for the
digestive tract to resume normal function, though certain factors—such as longer surgical
operation time and open surgical procedures—can increase the duration of the ileus.

-Certain medications can also slow peristalsis, such as anesthetics, opioids, chemotherapy
agents, psychotropic agents (such as those used for depression and anxiety), and
anticholinergic agents (used for urinary incontinence and Parkinson’s disease). Systemic
inflammation and severe pain requiring prolonged opioid use can often lead to an ileus.

-Other causes include infections within the abdomen like gastroenteritis, systemic
infections such as sepsis, and metabolic abnormalities such as hypothyroidism and
electrolyte imbalances.

-Risk factors for an ileus include increased age, severe infection, severe electrolyte
disturbances, and comorbidity of certain medical conditions such as diabetes or digestive
disorders like diverticulitis and irritable bowel syndrome.

Signs and symptoms:

-The severity of signs and symptoms often depends on the presence of intestinal obstruction
and may include abdominal pain, bloating, loss of appetite, feeling of fullness, nausea,
vomiting, and inability to pass gas or stool.

Diagnosis:

-During an abdominal assessment, healthcare providers may hear reduced bowel sounds.

-Diagnostic imaging tests may begin with an abdominal X-ray to detect areas of possible
obstruction. In mild to moderate cases, an X-ray is sufficient to confirm an ileus. However, in
severe obstruction cases, a computed tomography (CT) scan may provide more detailed
information about the location and type of obstruction, and may be combined with IV or oral
contrasts. Other diagnostic imaging tests may include magnetic resonance imaging (MRI),
ultrasound imaging, or barium enema (a special X-ray examination of the large intestine).

Treatment:

-An ileus can lead to potentially life threatening complications and should be addressed
immediately.

-Treatment for an ileus focuses on bowel rest by limiting oral intake and discontinuing
medications that may be causing the ileus.

-In cases where oral fluids are not tolerated, rehydration with IV fluids may be necessary.

-If severe nausea and vomiting is present, nasogastric tube decompression can be
performed by inserting a tube from the nose to the stomach, in order to relieve pressure
caused by bloating and buildup of stomach contents.

Acute abdomen
-Acute abdomen refers to sudden, severe abdominal pain. Many times, it’s a sign of a
medical emergency that requires immediate surgery.

Etiology:
-Surgical acute abdomen causes include blood loss, infections, blood flow blockages,
obstructions and perforations.

-Blood loss (hemorrhage): mallory-Weiss tear, ruptured ectopic pregnancy, trauma,

ruptured spleen, ruptured abdominal aortic aneurysm

-Infections: appendicitis, cholecystitis, peptic ulcer disease, acute pancreatitis, diverticulitis

-Blood flow blockage (ischemia) :buerger’s disease, colitis, mesenteric ischemia,

strangulated hernia, testicular torsion

-Obstructions: inflammatory bowel disease (IBD), intussusception, small bowel obstruction,

large bowel obstruction

-Perforations: boerhaave’s syndrome, gastrointestinal perforation, perforated stomach

ulcer, malrotation

-Nonsurgical causes most likely don’t require surgery. Nonsurgical causes of acute abdomen
include endocrine and metabolic disorders, hematologic disorders, and toxins or drugs

-Endocrine and metabolic disorders: uremia, diabetes-related ketoacidosis (DKA),

addison’s disease, acute intermittent porphyria

-Hematologic disorders: sickle cell disease, acute leukemia, certain genetic disorders,
anemia

-Toxins: lead poisoning, other heavy metal intoxications, nicotine withdrawal, black widow
spider bite poisoning, some scorpion stings

Signs and symptoms:

-The most common acute abdomen symptom is sudden, severe pain in your abdominal
region.

-Distended abdomen: Abdominal distention means your abdomen is extensively swollen

beyond its normal size.

-Symptoms of shock: Shock may cause rapid heart rate, low blood pressure, sweating and
confusion.

-Symptoms of peritonitis: Inflammation of the inside of your abdomen (peritonitis) may

cause constant pain or pain that gets worse when you gently touch the area or bump into it.

Diagnosis:

-Physical examination: Examination of the skin of the abdominal region and look for any
external abnormalities, use of stethoscope to listen to your bowel sounds (auscultate),
palpitation of the entire abdominal area looking for any tender areas or masses, location of
the pain is very important
-Laboratory tests: complete blood count (CBC), comprehensive metabolic panel (CMP),
arterial blood gas (ABG), amylase test, liver function tests, kidney function tests, urinalysis

-Imaging tests: abdominal ultrasound, abdominal computed tomography (CT) scan,

endoscopic ultrasound

Treatment:

-Treatment will vary based on the cause of your acute abdomen. No matter the cause, rapid
diagnosis and treatment are vital.

-Acute abdomen may need emergency surgery.

-Replenishment of fluids and electrolytes

-Broad-spectrum antibiotics

-Pain relievers

-Anti-emetics

Mesenteric ischemia
-Mesenteric ischemia is an uncommon and serious medical condition that happens when
parts of your digestive system don’t get enough blood flow and oxygen.

-This usually happens because of a blockage in your blood vessels that provide blood to
those areas. This condition is more common in people who are older, especially those with
cardiovascular disease or blood clotting disorders.

-Without enough blood flow, the affected organs and tissues don’t have enough oxygen and
can’t function correctly. If the blockage is severe enough, the affected organs and tissues
may start to die. This condition is often deadly, so a quick diagnosis and treatment are very
important.

Classification of mesenteric ischemia:

-Acute mesenteric ischemia: Heart attacks and strokes often happen because of
blockages in critical arteries, and acute mesenteric ischemia can happen in a similar way.
This usually happens because of blood clots, which cause sudden and very severe
symptoms. This condition is a medical emergency that needs immediate care.

-Chronic mesenteric ischemia: Chronic mesenteric ischemia happens more gradually,

usually because your mesenteric arteries start to narrow. This condition takes longer to
develop, and the symptoms usually worsen over time.
Acute mesenteric ischemia:
- A waxy substance called plaque can build up inside of your arteries, causing them to
harden. This condition, atherosclerosis, happens commonly with cardiovascular disease. If
an area of plaque breaks open, blood clots can form there.

-A clot forming in your mesenteric artery: Certain conditions make it easier for clots to
form in your blood vessels. If one forms in your mesenteric arteries, it can cause acute
mesenteric ischemia.

-A clot getting stuck in your mesenteric artery: This happens when a clot forms
somewhere else in your body, breaks free and gets stuck in a mesenteric artery. Blood can’t
get past the clot, causing acute mesenteric ischemia.

-A clot forming in nearby veins of your mesentery: This often happens with disorders
that make your blood clot too easily (including conditions you inherit from your parents).
Clots in your mesenteric veins slow down blood flow overall, causing blood to back up
behind the clot. This is more common in people who are younger.

-Non-occlusive mesenteric ischemia (NOMI) happens without a blockage. Acute NOMI

happens when blood vessels constrict or there are spasms in the muscles lining those
vessels. This can be caused by drugs, such as heart medications or cocaine, medical
procedures, such as dialysis or surgery or Health conditions, such as sepsis, heart attack,
dehydration, allergic reactions and low blood pressure. Acute NOMI usually takes longer to
become severe but is still dangerous.

Chronic mesenteric ischemia:

-Chronic mesenteric ischemia often happens because of circulatory diseases that cause
blood vessels to narrow. This narrowing, known as stenosis, means that blood flow to your
mesentery drops over time.

-This condition can also happen because a blood clot forms in a mesenteric blood vessel.
When this happens, the clot can grow over several days or even weeks, with symptoms
getting worse as it gets larger.

-While this condition isn’t usually life-threatening right away, about 40% of acute mesenteric
ischemia cases happen after a person has chronic symptoms. That’s because early
symptoms from narrow blood vessels suddenly become severe when a new clot blocks the
narrowed blood vessels.

Signs and symptoms of acute mesenteric ischemia:

-Abdominal pain: This symptom is the most common. This usually happens after eating,
isn’t in a specific place in your belly and can be very severe. In many cases, the pain is
much worse than your healthcare provider might expect based on their examination. In
cases of acute NOMI, this may be the only symptom.

-Bloating, nausea and vomiting: These usually happen along with abdominal pain.
Vomiting is especially common.
-Changes in bathroom habits: These changes affect how frequently you need to poop.
One of these changes is constipation, which can make you poop less often.

-Diarrhea: It may happen off and on rather than consistently. Diarrhea may also be very
intense, and severe pain can follow. In the late stages of this condition, bloody diarrhea is
more common.

-Weight loss: This symptom happens often, even in acute cases. It can indicate avoiding
food because of pain or other symptoms that happen before this condition reaches a severe
level.

-Fever: This can be a sign of a dangerous infection.

-It’s very common for this condition to happen after you have chronic mesenteric ischemia
symptoms.

Signs and symptoms of chronic mesenteric ischemia:

-Symptoms of this condition can happen slowly and usually worsen over time.

-Abdominal pain: This pain is most noticeable for about one or two hours after a meal. The
pain often feels similar to cramps and usually happens in the upper belly area or around your
navel (belly button).

-Food fear and weight loss: As this condition gets worse, the pain becomes more intense.
That can cause “food fear,” which is when you want to avoid food because you anticipate
pain after eating. This usually leads to unintentional weight loss.

-Changes in bathroom habits: This includes needing to poop more or less often than you
did before.

-Diarrhea: This happens in about one-third of people with this condition, and is usually
chronic (meaning it happens over a long period of time).

Diagnosis:

-Physical examination: looking for bloating, tenderness, guardness, borborygmi

-Lab tests: looking for changes in blood, amount of oxygen, clotting ability and infection

-Imaging tests: ultrasound, angiography, endoscopy

Treatment:

-Acute mesenteric ischemia: Surgery is the solution. The purpose is to directly access and
remove any existing clots and widen some narrow blood vessels. A stent can be
placed,which is a support frame device that holds a section of blood vessel wide open.

-Non- occlusive acute mesenteric ischemia: Vasodilators are used in order to prevent the
constriction of blood vessels and expand them. There is a surgery solution for the most
severe cases. A catheter-based procedure known as balloon angioplasty is used. This
procedure involves inserting a catheter into a major blood vessel and steering that device to
the affected area.

-Chronic mesenteric ischemia: Surgery for this issue is common, especially when it involves
a slow-growing clot or blood vessels that have become too narrow. It’s also more likely to
happen when a person has internal bleeding, infections or sepsis, or other dangerous
complications. Bypass surgery is also possible when other options can’t restore blood flow.
Balloon angioplasty and other catheter-based procedures are often considered with this
condition. Vasodilators and clot-busting medications can be used.

Peritonitis
-Peritonitis refers to the inflammation of the peritoneum, which is the inner membrane that
lines the abdominal cavity and abdominal organs. Peritonitis is typically caused by an
infection involving gastrointestinal or pelvic organs, and it can be life threatening if left
untreated.

Etiology:

-Depending on its cause, peritonitis can be classified into two main types of peritonitis:
spontaneous bacterial peritonitis and secondary peritonitis.

-Spontaneous bacterial peritonitis is usually a complication of liver or kidney failure, resulting

in fluid buildup in the abdominal cavity, also known as, ascites. Spontaneous bacterial
peritonitis is the development of an infection of the ascitic fluid in the peritoneum, with no
identifiable source of the infection.

-Secondary peritonitis, on the other hand, has a clear source. It is typically the result of a
ruptured organ in the abdomen, which can allow bacteria to enter the peritoneal cavity.
Secondary peritonitis most often occurs as a complication of gastrointestinal disorders,
such as appendicitis, pancreatitis, a ruptured stomach ulcer, or a perforated colon.
Additionally, diverticulitis may cause peritonitis if one of the diverticula (infected pouches in
the digestive tract) rupture and spill waste into the abdominal cavity. Secondary peritonitis
may also result from abdominal trauma or injury. Finally, secondary peritonitis can also
occur as a complication of certain medical procedures, such as gastrointestinal surgery,
the use of feeding tubes, or peritoneal dialysis.

-Other not often causes include tuberculosis, which causes tuberculous peritonitis, and
lupus.

Peritoneal dialysis:

Dialysis is used to clean an individual’s blood when their kidneys can no longer do so,
typically due to kidney failure. In peritoneal dialysis, the peritoneum is used as a natural filter
for the blood by inserting a catheter into the individual’s abdomen. The dialysis fluid is then
introduced into the abdomen through the catheter, where it absorbs wastes and excess
fluids from the blood. This fluid is then drained and discarded. The catheter should be
cleaned properly before each infusion. Poor hygiene or contaminated equipment may result
in infection and peritonitis.

Signs and symptoms:

-Signs and symptoms of peritonitis may vary depending on the underlying cause.

-Common symptoms of peritonitis include abdominal discomfort, nausea and vomiting, loss
of appetite, diarrhea, constipation, fever, fatigue, and confusion.

-Early stage peritonitis will often present as dull, generalized pain in the abdomen,
whereas later stage peritonitis may cause more severe, localized abdominal pain. If
undergoing peritoneal dialysis, cloudy dialysis fluid can also be a sign of peritonitis.

-Peritonitis is a medical emergency that requires prompt medical attention, as it develops

very rapidly. Upon rupture of the abdominal wall or abdominal organs, the peritoneum can
become infected within 24 to 48 hours.

Diagnosis:

-Physical examination and review of medical history can reveal underlying conditions or
medical procedures that may have caused peritonitis.

-A blood test may be taken to check for high white blood cell counts or the presence of
bacteria.

-A peritoneal fluid analysis can also be performed to determine if there is infection or

inflammation.

-Imaging studies, such as X-rays or CT scans, can show perforation or other trauma in the
gastrointestinal tract.

-If peritonitis is associated with peritoneal dialysis, a physical exam assessing signs and
symptoms may be enough to diagnose the condition. In particular, cloudy dialysis fluid is
highly indicative of peritonitis.

Treatment:

-Treatment for peritonitis depends on the underlying cause of the condition. Antibiotics will
often be prescribed to fight infection and control the potential spread of infection. The type
and duration of antibiotics are determined by the severity and cause of the peritonitis.

-In some cases, surgery may also be required to remove the source of infection and control
its spread. Surgery may also be performed to treat underlying conditions, such as a burst
appendix or colon.

-Peritonitis may also require additional supportive care including pain management,
intravenous fluids, and oxygen.
-If the peritonitis is associated with peritoneal dialysis, physicians may recommend switching
to another form of dialysis until the infection has healed.

Congenital peritonitis
-Congenital peritonitis occurs when inflammation of the peritoneum develops in utero.

-It is typically a sterile inflammation, but can sometimes be associated with infection. This
condition can be detected either during pregnancy via prenatal imaging or immediately after
birth.

Etiology:

-Bowel perforation: Intrauterine bowel perforation is one of the leading causes of congenital
peritonitis. This may occur due to:

● Meconium ileus: commonly associated with cystic fibrosis

● Intestinal atresia or stenosis: congenital narrowing or absence of parts of the bowel
● Volvulus: twisting of the bowel leading to ischemia and perforation
● Congenital diaphragmatic hernia: intestinal herniation through the diaphragm
● Intrauterine infection: chorioamnionitis, funisitis

-Meconium peritonitis: This specific form of congenital peritonitis occurs when bowel
perforation allows meconium to leak into the peritoneal cavity. It leads to inflammation and
calcification in the peritoneum. The meconium can also induce a chemical peritonitis, which
is generally sterile but may lead to adhesions and fibrosis.

-Infectious causes: Although congenital peritonitis is usually sterile, it can be caused by

intrauterine infections, particularly those related to chorioamnionitis, when pathogens invade
the fetus’ peritoneal cavity either through transplacental transfer or ascending infection from
the birth canal.

Clinical Presentation:

-Prenatal: abdominal calcifications (due to meconium peritonitis), free fluid in the abdomen,
fetal bowel dilatation, polyhydramnios (excess amniotic fluid, often seen in cases of bowel
obstruction)

-Postnatal: abdominal distension, respiratory distress due to diaphragm elevation caused by

abdominal distension

-In cases of bowel perforation: symptoms of peritonitis, such as poor feeding, vomiting,
irritability, signs of sepsis, develop shortly after birth.

-The presence of calcifications and ascites may be noted on postnatal imaging.

Diagnosis:

-Prenatal ultrasound: The key tool for diagnosing congenital peritonitis before birth. Findings
such as echogenic areas in the peritoneum and ascites suggest intra-abdominal pathology.

-Abdominal X-rays: Postnatal imaging can show calcifications, bowel obstruction, or free air
in the peritoneal cavity.

-CT/MRI: More detailed imaging to assess the extent of inflammation or bowel abnormalities.

-Blood tests: In suspected infectious cases, markers of infection (C-reactive protein, elevated
white blood cells) or blood cultures may be used to diagnose sepsis.

Treatment:

-Conservative management: In the absence of signs of bowel obstruction or sepsis, the

inflammation may resolve spontaneously. Meconium peritonitis that causes calcifications
may be treated conservatively unless there is ongoing obstruction.

-Surgery: Required in cases of bowel obstruction, ischemia, or persistent peritonitis. The

surgical approach depends on the underlying cause (e.g., resection of atretic bowel
segments, correction of volvulus, or repair of bowel perforation).

-Antibiotics: If infection is suspected or confirmed, broad-spectrum antibiotics are initiated to

treat potential sepsis.

Hematogenic peritonitis
-Hematogenic peritonitis refers to peritoneal inflammation caused by blood-borne pathogens,
where the infection reaches the peritoneum via the bloodstream rather than through direct
contamination from the GI tract or trauma. This form of peritonitis is relatively uncommon
and is often associated with bacteremia or systemic infections, especially in neonates or
immunocompromised patients.

Etiology:

-Bacterial infections: Hematogenic peritonitis most commonly occurs when bacteria or

other pathogens enter the bloodstream and colonize the peritoneal cavity. Common
pathogens include:

● Gram-negative bacteria: Escherichia coli, Klebsiella pneumoniae, and Pseudomonas

aeruginosa
● Gram-positive bacteria: Staphylococcus aureus, Streptococcus species
● Fungal infections: Candida species
-Neonatal sepsis: In neonates, hematogenic peritonitis can arise from systemic infections,
such as neonatal sepsis. The pathogens may reach the peritoneum from the bloodstream,
particularly if there are predisposing factors such as prematurity, low birth weight, or
immunodeficiency.

-Peritoneal dialysis: Patients undergoing peritoneal dialysis are at risk of hematogenic

peritonitis if pathogens enter the bloodstream or the peritoneal cavity through contaminated
equipment.

Clinical Presentation:

-Systemic symptoms: Patients may present with signs of sepsis, including fever, tachycardia,
hypotension, and altered mental status. The peritoneal involvement manifests as abdominal
pain, tenderness, distension, and signs of peritoneal irritation (rebound tenderness,
guarding).

-Neonates: Hematogenic peritonitis in neonates may present as nonspecific symptoms of

sepsis: lethargy, poor feeding, temperature instability, respiratory distress, and abdominal
distension.

-Chronic renal failure patients: In patients on peritoneal dialysis, hematogenic peritonitis may
present with cloudy dialysate fluid, abdominal pain, and fever.

Diagnosis:

-Blood cultures: Essential for identifying the causative pathogen, especially in cases of
systemic infection. Cultures from the peritoneal fluid (paracentesis) may also be performed.

-Peritoneal fluid analysis: If ascites or peritoneal fluid is present, a diagnostic paracentesis is

performed to analyze the fluid for white blood cell count, protein levels, glucose levels, and
to obtain cultures.

-High neutrophil count: Suggests bacterial peritonitis.

-Gram stain and culture: Helps identify the pathogen responsible.

-Imaging: Ultrasound or CT scan can help detect fluid collections or abscesses in the
abdomen and confirm the diagnosis of peritonitis.

Treatment:

-Antibiotics: The cornerstone of treatment for hematogenic peritonitis. Empiric

broad-spectrum antibiotics should be initiated while awaiting culture results. Once the
pathogen is identified, therapy should be tailored to the specific organism.In neonates,
common choices include antibiotics covering E. coli, Group B streptococcus, and
Staphylococcus species.

-Supportive care: Intravenous fluids, electrolyte management, and in some cases,

vasopressors for septic shock are necessary.
-Surgery: Surgical intervention is rarely needed unless there is an underlying source such as
abscess formation or bowel perforation that requires drainage or repair.

Congenital anomalies of colon

-Congenital anomalies of the colon refer to structural abnormalities present at birth that
affect the normal development of the colon. These anomalies can lead to various
complications ranging from obstruction, infection, to issues with waste elimination.

Colonic Atresia:

-Colonic atresia results from a failure of the normal recanalization of the colonic lumen
during embryonic development. It may also be due to vascular insults or ischemia during
intrauterine life. This leads to a complete blockage of the colon.

-Newborns present with failure to pass meconium, abdominal distension, and vomiting, often
bilious if the obstruction is proximal.

-Diagnosis is made by Abdominal X-ray, which shows signs of intestinal obstruction with
dilated bowel loops and absence of air in the distal colon, and contrast enema, which can
help in identifying the level of atresia.

-Treatment includes surgical correction by anastomosis after excision of the atretic segment.

Malrotation with Volvulus:

-During embryonic development, the midgut undergoes a complex process of rotation

around the superior mesenteric artery. Failure of this rotation results in abnormal positioning
of the colon (and other bowel segments), with a predisposition for volvulus (twisting of the
bowel around the mesentery), leading to bowel ischemia.

-Clinical Presentation includes sudden onset of bilious vomiting, abdominal distension, and
signs of shock in severe cases. Older children may present with chronic abdominal pain and
malabsorption.

-Diagnosis includes upper GI Series(X-rays, fluoroscopy and barium) looking for the
“corkscrew” sign, which suggests volvulus.Also, an abnormal location of the duodenojejunal
junction is indicative of malrotation.

-Treatment: Surgical intervention, which is called Ladd’s procedure, to correct the

malrotation and prevent volvulus.

Congenital Redundant Colon:

-This condition involves excessive length or coiling of the colon, particularly in the sigmoid
area. It may cause constipation or colonic volvulus.
-Patients may have chronic constipation, bloating, and abdominal pain. In severe cases,
colonic volvulus can occur, leading to obstruction.

-Diagnosis includes Barium Enema,which shows elongated and coiled segments of the
colon.

-Treatment includes conservative management for mild cases. Surgery is indicated for
volvulus or refractory symptoms. Surgery includes resection of the redundant segment.

Hirschsprung disease
-Hirschsprung disease is also known as congenital aganglionic megacolon, so
Hirschsprung’s is a disease that’s present since birth, in which a ganglion, or cluster of
nerves is missing, which ultimately leads to a blocked colon, causing it to enlarge.

Pathophysiology:

-The intestines move waste through the bowels via peristalsis, which is this series of
coordinated wave-like muscle contractions that helps move feces in one direction, and this is
essentially automatic, happening without you even having to think about it. The type of
muscle that causes these contractions is smooth muscle, as opposed to skeletal muscle or
cardiac muscle.

-In the gut, there’s a layer of smooth muscle just under the submucosa, which sits under the
mucosa, which is the innermost layer of the gut nearest to the lumen. On the other side of
the smooth muscle layer is the serosa. Now if we look closer at the smooth muscle layer, it’s
actually composed of the circular muscle layer, arranged in circular rings which contract and
constrict the gut behind the feces, which keeps it from moving backward, while the
longitudinal muscle layer, arranged along the length of the gut, relaxes which lengthens and
therefore pulls things forward.

-Also though, within these layers are two plexuses, or networks of nerves, which are made
up of ganglia—which are clusters of individual nerves, which help coordinate muscle
contraction and relaxation. First there’s the myenteric plexus, also known as Auerbach’s
plexus, which when activated, primarily causes smooth muscle relaxation. The myenteric
plexus connects with the second plexus—the submucous plexus, or also known as
Meissner’s plexus, which is buried in the submucosa and is responsible for helping to
control blood flow and epithelial cell absorption and secretion. These groups of nerves are
clearly super important for normal bowel function.

-For people with Hirschsprung’s disease, both these plexuses are gone—they’re completely
absent in some parts of the gut.

-Well during fetal development, there are cells called neural crest cells, which are basically a
group of fetal cells that migrate away and differentiate into a variety of different cell types. In
this case, some of them become neuroblasts, and eventually the nerve fibers of the plexuses
in the gut. Starting from the mouth, the neuroblasts start migrating toward the anus. Around
week 8 of development the neuroblasts get to the proximal colon of the gut, and pass
through the distal colon, and around week 12 they finally reach the rectum. A disruption of
that neuroblast journey in that time window, means that nerve fibers don’t develop in the
rectum and parts of the colon.

Etiology:

-Two specific genes that are thought to be important for migration and development of these
nerve fibers are RET and EDNRB, so mutations in either could lead to an absence of the
plexuses.

-Also, mutations in the RET gene have also been linked to Down syndrome, which might
help explain why Down’s syndrome is associated with Hirschsprung disease.

Signs and symptoms:

-So without these nerves, peristalsis in the gut is seriously impaired, because those muscles
tend to lose the ability to relax, and they stay in their default contracted position, which
essentially blocks the movement of feces.

-Babies that are born with Hirschsprung therefore fail to pass the meconium, their first stool,
a process that usually happens within the first 2 days after birth.

-The rectum and the distal sigmoid colon, which are the areas closest to the anus are usually
affected, so feces builds up before the obstruction, which causes serious constipation as
well as colon dilation, or megacolon, which is a risk for rupture.

Diagnosis:

-An abdominal X Ray with contrast dye might shows an enormous megacolon full of stool
that can’t be easily pushed out, but a definitive diagnosis is by rectal suction biopsy of the
narrowed area in the colon, where both the mucosa and submucosa are extracted, as
opposed to a normal biopsy where just the mucosa is taken.

-Remember that those plexuses are in the muscle layer or submucosal layer, so a normal
biopsy with just the mucosa wouldn’t cut it, you need a sample of submucosa to see if the
submucosal plexus is there or not.

Treatment:

-Treatment is typically surgical resection of the area that’s lacking the nerve fibers, and then
the healthy end is connected to the anus.

Congenital disease of the rectum and anus

-An anorectal malformation is a condition in which the rectum and anus of the developing
fetus don’t form properly before birth.
Etiology:

-Experts don’t know exactly what causes anorectal malformation. Some think gene changes
(mutations) that develop before birth may play a role

Signs and symptoms:

-Inability to pass stool (constipation)

-Stool that leaks from their vagina or is visible in their urine

-Urine that comes from their anus

Types of anorectal malformations:

-Cloaca: The urinary tract and rectum share a single opening.

-Fistulas: The rectum connects to other parts of your baby’s body, such as their urethra,
bladder, vagina or perineum (skin between the anus and genitals), through an irregular
passage.

-Imperforate anus: The rectum and anus aren’t connected.

Association with other health problems:

-Down syndrome

-Gastrointestinal (GI) diseases

-Spinal conditions

-Townes-Brocks syndrome: a genetic condition causing the anus to be missing or completely

blocked (imperforate) and irregularly shaped hands and ears

-Urinary tract problems

-VATER syndrome (VACTERL association): a disorder that affects multiple body systems,
including the spine, heart, digestive system, kidneys and limbs

Diagnosis:

-Barium enema tests: inserting a fluid through their rectum that coats the inside of their
digestive organs so they show up more clearly on an X-ray.

-Barium swallow tests (esophagram): swallowing a fluid that coats the inside of their
digestive organs so they show up more clearly on an X-ray.

-CT scans: using computers and X-rays to take pictures of the inside of their body.

-MRIs: using magnets and radio waves to see inside their body.
-Ultrasounds: using high-frequency sound waves to look at internal organs.

-X-rays: using low doses of radiation to take pictures of the inside of their body.

Treatment:

-Surgery: a single procedure to open a narrowed passageway or remove tissue that covers
your child’s anus

-Anoplasty: to reconstruct their anus

-Colostomy: The surgeon divides the large intestine and brings the two ends through
openings in their stomach. Babies wear collection bags outside their body where stool and
mucus pass through.

-Anorectal repair: Surgeons typically connect the rectum and anus when your baby is a few
months old. Stool continues to leave their body through the colostomy bag while they heal
from surgery.

-Colostomy closure: Babies have a procedure to remove the colostomy bags about two to
three months after the second surgery. Children begin passing stool through their rectum
within a few days.

Rectal hemorrhage
-Rectal hemorrhage refers to the passage of blood from the rectum, which can manifest as
bright red blood on toilet paper, in the stool, or as a separate discharge.

-It is an important clinical symptom that may indicate various gastrointestinal disorders,
some of which require urgent evaluation and management.

Etiology and symptoms based on cause:

-Anorectal Causes:

● Hemorrhoids: Swollen blood vessels in the rectum or anus. They can be internal
(above the anal canal) or external (around the anus). Symptoms include bright red
blood on stool or toilet paper, often associated with pain during defecation.
● Anal Fissures: Small tears in the lining of the anus, often due to passage of hard
stools. These typically present with sharp pain during and after bowel movements,
and bright red blood on the surface of the stool.
● Anorectal Abscess: Localized collection of pus in the anal region, which can lead to
inflammation and bleeding. Symptoms include pain, swelling, fever, and sometimes
rectal bleeding.
● Fistulas: Abnormal connections between the rectum and the skin or other structures.
Fistulas can cause recurrent infections and may bleed intermittently.
-Colonic Causes:

● Diverticular Disease: Diverticulosis can lead to diverticulitis or diverticular bleeding.

Diverticular bleeding is usually painless and results in bright red blood in the stool.
● Colorectal Polyps: Benign growths in the colon that can lead to bleeding, especially
if they are large or ulcerated. Polyps can also be precursors to colorectal cancer.
● Colorectal Cancer: Malignancies can present with rectal bleeding, often
accompanied by changes in bowel habits, weight loss, or anemia.
● Inflammatory Bowel Disease (IBD): Both Crohn’s disease and ulcerative colitis can
cause rectal bleeding. The blood may be mixed with stool, and symptoms may
include abdominal pain and diarrhea.
● Ischemic Colitis: Reduced blood flow to the colon can cause pain and bleeding. It is
often seen in older patients or those with vascular diseases.

-Systemic Causes:

● Coagulation Disorders: Conditions affecting blood clotting, such as hemophilia or

the use of anticoagulants, can result in rectal bleeding.
● Vascular Malformations: Angiodysplasia or arteriovenous malformations can lead to
chronic bleeding in older adults.

-General associated symptoms include pain, diarrhea, constipation, weight loss, or changes
in bowel habits.

Diagnosis:

-Colour of bleeding: Bright red suggests distal source, while dark suggests upper GI source.

-Physical Examination: Inspection of the anal region for external hemorrhoids, fissures, or
abscesses and digital rectal examination (DRE) can assess for internal hemorrhoids, anal
fissures, and occult blood.

-Abdominal examination may reveal tenderness, masses, or signs of peritonitis.

-Laboratory Tests: Complete Blood Count (CBC), Coagulation Studies (in patients with a
history of bleeding disorders)

-Colonoscopy: Gold standard for visualizing the colon and rectum, it can diagnose and treat
polyps or tumors directly.

-Sigmoidoscopy: Useful for evaluating the lower part of the colon and can be performed
quickly.

-CT Scan: Especially in cases of suspected diverticulitis, bowel obstruction, or cancer. It can
also help identify sources of bleeding.

-Angiography: If there is significant bleeding and a vascular source is suspected.

Treatment:
-Initial stabilization: IV fluids for significant blood loss and monitoring of vital signs.

-Blood transfusions: if hemoglobin is critically low.

-Treatment depends on each cause.

Rectal prolapse
-Rectal prolapse is a condition in which the rectum protrudes through the anus, resulting in
the rectal wall being visible externally.

-This condition can vary in severity, from a partial prolapse where only the rectal mucosa
protrudes, to a complete prolapse involving the full thickness of the rectal wall.

Etiology:

-Anatomical Factors:

● Weakness of Pelvic Support Structures: The pelvic floor, composed of muscles

and connective tissue, supports the rectum. Weakness in these structures can lead
to prolapse.
● Age: Advanced age is a significant risk factor due to degeneration of pelvic support
tissues.

-Functional Factors:

● Chronic Straining: Conditions that lead to chronic straining during defecation, such
as constipation or diarrhea, can increase intra-abdominal pressure and contribute to
prolapse.
● Neurological Disorders: Conditions like spinal cord injuries or multiple sclerosis can
impair the neural control of bowel function and contribute to prolapse.
● Chronic coughing or sneezing

-Acquired Factors:

● Obesity: Increased abdominal pressure associated with obesity can exacerbate or

lead to the development of rectal prolapse.
● Childbirth: Vaginal delivery, especially in cases of prolonged labor or traumatic
delivery, can weaken pelvic support structures.
● Surgery: Previous pelvic or abdominal surgeries can alter anatomical support and
lead to prolapse.

Classification:
-Partial Prolapse: Only the mucosal layer of the rectum descends through the anus, which
may not be visible at rest but can be observed during straining or bowel movements.

-Complete Prolapse: The entire rectal wall protrudes through the anus, typically appearing
as a cylindrical mass. This type is more prominent during activities like straining or walking.

Signs and symptoms:

-Visible protrusion of rectal tissue through the anus

-Mucous discharge, fecal incontinence, or constipation

-Sensation of incomplete bowel evacuation

-Pain or discomfort during bowel movements

-A reddish, tubular protrusion from the anus

-Symptoms of urinary incontinence may also be present due to associated pelvic floor
dysfunction.

Complications:

-Fecal incontinence: As your anal muscles continue to stretch, you may have increased
difficulty holding in gas and poop. Of those with rectal prolapse, 50% to 75% of people report
this complication.

-Constipation: Bunching of the rectum and muscle coordination problems may cause you
difficulty evacuating your stool. Some people have alternating constipation with incontinence.

-Rectal ulcers: Friction and exposure of the mucous lining of your rectum may cause rectal
ulcers and painful sores which can bleed. Uncontrolled bleeding could lead to anemia.

-Incarceration: An “incarcerated” rectum gets stuck hanging out of your anus and can’t be
pushed back in. The danger of this is that it could become cut off from blood supply
(“strangulation”). This could lead to tissue death and decay of the rectum (gangrene).

Diagnosis:

-Digital rectal examination (DRE) can assess the degree of prolapse, surrounding tissue
integrity, and check for rectal masses or strictures.

-Assessment of pelvic floor function may be indicated if associated pelvic organ prolapse is
suspected.

-Imaging Studies: While not routinely required, imaging studies such as defecography (to
assess rectal function and dynamics) or MRI may be used to evaluate associated pelvic floor
disorders.
-Anorectal Manometry: It can assess anal sphincter function and rectal sensation, useful in
understanding the dynamics of the pelvic floor.

Treatment:

-Dietary Modifications: High-fiber diet and adequate hydration to prevent constipation and
reduce straining.

-Pelvic Floor Exercises: Kegel exercises to strengthen the pelvic floor muscles.

-Rectopexy: This procedure restores your rectum to its original position in your pelvis. Your
surgeon will attach your rectum to the back wall of your pelvis (your sacrum) with permanent
stitches or reinforce it with mesh. These will hold your rectum in place long enough for scar
tissue to develop, which will hold it in place after that. Rectopexy can be done by either open
abdominal surgery or minimally invasive (laparoscopic) surgery.

-Altemeier procedure: In this procedure, the surgeon pulls the prolapsed rectum out
through your anus and removes it. He may also remove the lower part of the colon (sigmoid
colon) if it is involved in the prolapse (proctosigmoidectomy). Then he sews the two ends of
your large intestine (your remaining colon and your anus) back together. The new end of
your colon now becomes your new rectum. This procedure is less invasive than open
abdominal surgery and easier to recover from, but its disadvantage is that prolapse may
recur afterward. One reason is that the new rectum made from your colon is not as strong as
your original rectum was. Because of this, some surgeons combine the altemeier procedure
with a “levatorplasty” — tightening the pelvic floor muscles by sewing them closer together.

-Delorme procedure: If you only have a mucosal prolapse, or a small external prolapse,
your surgeon may choose a more minor procedure. The Delorme procedure only removes
the prolapsed mucosal lining of your rectum. Your surgeon then folds back the muscle wall of
the rectum onto itself and stitches it together inside your anal canal. The double muscle wall
helps to reinforce the rectum.

Anal prolapse
-Anal prolapse, often referred to as rectal mucosal prolapse, occurs when a portion of the
anal or rectal mucosa protrudes through the anus.

-It is different from rectal prolapse, which involves the entire rectum. Anal prolapse primarily
affects the anal canal’s mucosa and can occur in both adults and children.

Etiology:

-Anatomical Factors:

● Weakness of Supportive Structures: The pelvic floor and anal sphincter support
structures may weaken due to aging or congenital factors, leading to anal prolapse.
● Anatomic Variations: Conditions such as anal stenosis or abnormal muscle tone
can predispose individuals to anal prolapse.
-Functional Factors:

● Chronic Straining: Persistent straining due to constipation or other gastrointestinal

conditions can increase pressure on the anal canal and contribute to prolapse.
● Neuromuscular Disorders: Conditions affecting the nervous system, such as spinal
cord injuries or neurological diseases, can impair the control of the anal sphincters
and lead to prolapse.

-Acquired Factors:

● Obesity: Increased intra-abdominal pressure from obesity can exacerbate pelvic

floor dysfunction.
● Pregnancy and Childbirth: The physical stress and hormonal changes during
pregnancy can weaken pelvic support, leading to prolapse, especially in women who
have experienced multiple pregnancies or traumatic deliveries.
● Surgery or Trauma: Prior surgical procedures or trauma to the pelvic region may
predispose individuals to anal prolapse.

Signs and symptoms:

-Visible protrusion of anal mucosa during defecation or straining.

-Mucous discharge, often associated with irritation or itching.

-Sensation of incomplete bowel evacuation.

-Pain or discomfort during bowel movements.

-Bleeding, though this is less common compared to rectal prolapse.

-Presence of the prolapsed mucosa, which often appears as a red, moist mass.

Diagnosis:

-Digital rectal examination (DRE) can help assess the extent of prolapse, sphincter tone, and
other associated anal or rectal pathologies.

-Anorectal manometry may be performed to evaluate anal sphincter function and rectal
sensation.

-Imaging Studies: While not routinely necessary, imaging studies such as defecography may
be utilized to evaluate anal function and dynamics, especially in complex cases or when
associated pelvic floor disorders are suspected.

-Endoscopy: In some cases, flexible sigmoidoscopy or colonoscopy may be performed to

rule out other conditions such as anal tumors or inflammatory bowel disease.

Treatment:

-Dietary Modifications: A high-fiber diet and adequate hydration to prevent constipation and
reduce straining during bowel movements.
-Pelvic Floor Rehabilitation: Exercises to strengthen pelvic floor muscles, including
biofeedback therapy, can be beneficial.

-Mucosal Resection: Resection of the prolapsed mucosa may be performed to relieve

symptoms and prevent recurrence.

-Surgical Repair: Procedures to restore the anatomy of the anal canal and improve support
to the anal sphincter.

-Sphincteroplasty: This may be indicated in cases where anal sphincter weakness is

contributing to prolapse.

Key differences between rectal and anal prolapse

Anatomical Structure:

-Rectal Prolapse involves the rectum, specifically the portion that connects the colon to the
anus. It can manifest as partial (mucosal prolapse) or complete (full-thickness rectal
prolapse) where the entire rectal wall descends.

-Anal Prolapse, on the other hand, primarily affects the anal canal, specifically the anal
mucosa, resulting in protrusion without the involvement of the full rectal wall.

Clinical Presentation:

-In rectal prolapse, the individual may experience a visible protrusion of rectal tissue, often
accompanied by symptoms such as fecal incontinence, mucus discharge, and a sensation of
incomplete bowel evacuation. The rectal tissue may appear as a reddish mass during bowel
movements or straining.

-In anal prolapse, the presentation is usually localized to the anal verge with a protrusion of
anal mucosa. Patients typically report mucous discharge and irritation but do not usually
experience fecal incontinence, and the protrusion is often more of a “tag” or “bulge” during
defecation.

Etiology:

-Rectal prolapse is often associated with factors such as weakened pelvic support
structures due to aging, chronic straining from constipation or diarrhea, neurological
disorders, and trauma from childbirth.

-Anal prolapse is frequently linked to chronic straining, particularly in patients with

constipation, as well as conditions such as anal stenosis or other functional disorders
affecting anal sphincter function.
Acute paraproctitis
-Paraproctitis is an inflammatory condition of the perianal tissues and may involve the
formation of abscesses.

Etiology:

-Bacterial infection, typically stemming from anal glands or perianal skin, caused by:

● Staphylococcus aureus
● Escherichia coli
● Bacteroides species

-Predisposing factors may include:

● Anal fissures
● Hemorrhoids
● Poor hygiene
● Immunosuppression

Signs and symptoms:

-Sudden onset of severe perianal pain, often exacerbated by sitting or defecation.

-Swelling and redness in the perianal region

-Fever and systemic signs of infection may be present

-Possible drainage of purulent material if an abscess forms

Diagnosis:

-Inspection may reveal erythema, swelling, or a visible abscess.

-Digital rectal examination may be limited due to pain.

-Imaging (e.g., ultrasound or MRI) may be used to assess the extent of the abscess or to
identify deep tissue involvement.

Treatment:

-Antibiotic therapy to cover common pathogens (e.g., broad-spectrum antibiotics).

-Incision and drainage (I&D) are typically performed to relieve pressure and allow for
proper drainage of purulent material.

Chronic paraproctitis
-Paraproctitis is an inflammatory condition of the perianal tissues and may involve the
formation of abscesses

Etiology:

-Chronic paraproctitis can occur following an episode of acute paraproctitis or may arise
from persistent irritation or infection.

-Residual infection after an acute episode

-Persistent drainage from a chronic anal fistula

-Conditions such as Crohn’s disease, which can cause perianal inflammation.

Symptoms:

-Persistent perianal discomfort or pain.

-Intermittent drainage of mucus or purulent material from the anal area.

-Swelling may be less prominent than in acute cases.

-Possible pruritus or irritation around the anus.

Diagnosis:

-Chronic changes may be evident, including skin irritation or the presence of a fistula.

-Tenderness may be present, but fluctuating masses are less common compared to acute
paraproctitis.

-Imaging Studies: Ultrasound, MRI, or fistulography may be utilized to assess for associated
fistulas or abscesses.

Treatment:

-Antibiotics if an infection is suspected.

-Fistulotomy may be performed to excise the fistula tract and promote healing.

-If associated with Crohn’s disease, medical management of the underlying inflammatory
condition is critical.

Pilonidal cyst
-A pilonidal cyst, also known as pilonidal disease or pilonidal sinus, is a skin condition
characterized by the presence of an abnormal sac-like structure in the skin filled with hair,
fluid, and skin debris.
-A pilonidal cyst typically appears in the tailbone area, usually in the crease of the buttocks
or in the cleft on top of the buttocks.

Etiology:

-The exact cause behind the formation of a pilonidal cyst is not completely understood and is
likely multifactorial. Pilonidal cysts are commonly caused by ingrown hairs, which result
when hairs grow in the crease of the buttocks and burrow under the skin. Formation of an
ingrown hair may lead to an immune response, thereby resulting in cyst formation. Loose
hairs may also become trapped in the crease of the buttocks, which occurs more commonly
in individuals who have coarse or stiff body hair that is likely to puncture the skin. Certain
factors that can stimulate the formation of ingrown hairs include sitting or exercising for
prolonged periods of time, wearing tight clothing, obesity, and anything that may increase
friction, sweat, and heat in the buttocks area. These situations may also irritate hair follicles,
which can become blocked with dead skin cells and bacteria, leading to cyst formation.

-Young males are at higher risk of developing a pilonidal cyst. They typically develop after
puberty due to changes in hormones and increased hair growth during this period, but they
may develop until the age of 40.

-Pilonidal cysts may also be congenital and appear at birth.

- Other risk factors for developing a pilonidal cyst include an inactive lifestyle, previous
occurence of pilonidal cysts, or having a family history of pilonidal cysts.

Signs and symptoms:

-The most common signs and symptoms of a pilonidal cyst include the presence of a small
dimple or irritated mass in the buttock area, typically characterized by inflammation,
redness, swelling,tenderness , and pain that worsens when walking or sitting.

-An infected pilonidal cyst may drain pus or blood and can be foul smelling.

- Some individuals with an infected pilonidal cyst may experience nausea, fever, or extreme
fatigue, but these symptoms are less common.

-If a pilonidal cyst becomes infected due to lack of treatment, painful skin abscess or sinus
tracts, which are empty spaces underneath the skin, may develop. If a chronically infected
pilonidal cyst is not treated appropriately, the individual may be at a higher risk of developing
a skin cancer known as squamous cell carcinoma.

Diagnosis:

-A pilonidal cyst is most commonly diagnosed upon visual inspection of the buttock area by
a medical professional.

-In rare cases where infection is suspected, blood tests, urine samples and fluid samples
from the pilonidal cyst may be assessed.
-In certain cases, imaging in the form of an X-ray, CT, or MRI may be ordered to explore
sinus cavities, infection spread, or the depth of the cyst.

-If any type of skin cancer is suspected, biopsies of the skin may be taken as well.

Treatment:

-The most common treatment for a pilonidal cyst is incision and drainage of the cyst in
which a small incision is made in the cyst, which releases any fluid, hair, and debris in the
cyst and prevents infection.

-If infection has already occurred or is suspected, incision and drainage is useful in draining
pus and may be followed by a course of oral and/or topical antibiotics.

-Incision and drainage of a pilonidal cyst may result in chronic pilonidal cysts, which are
prone to repeated infections.

-In severe cases with high recurrence of infection, limited healing, or the presence of multiple
openings in the cyst, surgery may be required to fully remove it. This may decrease the rate
of recurrence. After surgery, the wound may be left open and packed with dressing or may
be closed with stitches. It must remain clean, dry, and free of hair until fully healed.

-In very mild cases, oral antibiotics such as cephalexin or sulfamethoxazole-trimethoprim

and/or topical antibiotics, such as fucithalmic acid, may be prescribed with close monitoring
of the cyst. However, while antibiotics may aid in relieving inflammation, they may not
completely treat pilonidal cysts. Less common treatments include the use of localized
injections of acidic chemical compounds, such as phenol, to treat and prevent
mild-to-moderate pilonidal cysts. This method, however, is associated with a high recurrence
rate and is not commonly used.

-During treatment, hot water soaks or sitz baths may be used to provide symptomatic relief.
Non-prescription pain relieving medications, such as acetaminophen or ibuprofen, may also
be used. It is important to keep the affected area clean, dry, and free of hair if possible.

-Formation of a pilonidal cyst can be prevented through hair removal in the tailbone area and
crease of the buttocks by shaving, using hair removal cream, or undergoing laser hair
removal. Additional prevention methods include avoiding tight clothes, sitting and exercising
for shorter periods of time, sitting on soft surfaces, practicing good posture and hygiene, and
regularly exfoliating the area.

Perianal fistulas
-A perianal fistula is an abnormal, tube-like connection between the anal canal or rectum and
the perianal skin.

Classification of Perianal Fistulas based on anatomical location:

-Intersphincteric Fistula: It is the most common type.The fistula tract runs between the
internal and external sphincter muscles, exiting the skin near the anus.

-Trans-sphincteric Fistula: The tract crosses the external sphincter muscle and exits at the
skin. It is more complex and can involve more sphincter muscle, increasing the risk of
incontinence if not treated carefully.

-Suprasphincteric Fistula: The tract originates above the internal sphincter, curves over the
top of the puborectalis muscle, and exits at the skin.

-Extrasphincteric Fistula: It originates from the rectum or sigmoid colon and extends
through the levator ani muscle to the skin, bypassing the sphincter complex. It is often
associated with other conditions like Crohn’s disease or diverticulitis.

Classification of Perianal Fistulas based on complexity:

-Simple Fistula: It is a single, straightforward tract and often involves the intersphincteric or
low trans-sphincteric tract.

-Complex Fistula: It involves multiple tracts and is often associated with conditions like
Crohn’s disease, radiation therapy, or previous surgeries. It can involve high
trans-sphincteric, suprasphincteric, or extrasphincteric types.

Etiology:

-Perianal fistulas most commonly arise from an anorectal abscess that fails to heal
completely, leaving behind a persistent abnormal tract.

-Infection: Abscess formation due to blocked anal glands, leading to infection and eventual
fistula formation.

-Inflammatory Conditions: Crohn’s disease and ulcerative colitis are major contributors to
complex fistula formation.

-Trauma: Post-surgical trauma or perianal trauma can result in fistula formation.

-Radiation Therapy: Radiation for pelvic cancers can damage tissues and lead to fistulas.

-Tuberculosis: In certain parts of the world, tuberculous fistulas are a recognized cause.

Symptoms:

-Pain: Localized pain around the anus, particularly during defecation.

-Discharge: Persistent drainage of purulent or serous material from the fistula opening.

-Swelling: Recurrent swelling or lump near the anal opening.

-Pruritus: Chronic irritation and itching due to constant discharge.

-Recurrent Abscess: Fistulas may lead to repeated formation of perianal abscesses.

Diagnosis:

-Inspection often reveals an external opening near the anus, which may discharge pus or
mucus.

-Gentle palpation may identify the fistulous tract and its relationship to the sphincter
muscles.

-A digital rectal examination (DRE) may help locate the internal opening of the fistula, though
this is often painful.

-Endoanal Ultrasound: Useful for delineating the course of the fistula in relation to the
sphincter muscles.

-Magnetic Resonance Imaging (MRI): Gold standard for assessing complex fistulas,
especially those involving deep or multiple tracts. MRI provides detailed images of the
fistula, abscesses, and surrounding tissues.

-Fistulography: Involves injecting contrast into the fistula tract and taking X-rays to trace its
path, though it is less commonly used now due to advancements in MRI.

-Anoscopy or Sigmoidoscopy: These may be performed to visualize the internal opening of

the fistula and assess any involvement of the rectum or anal canal.

-Examination Under Anesthesia (EUA): In difficult cases, the patient may be examined under
anesthesia, allowing a more thorough assessment of the fistula without causing discomfort.

Treatment:

-Antibiotics: May be used for treating infections or for patients with inflammatory bowel
disease, but antibiotics alone rarely resolve the fistula.

-Seton Placement: A seton is a surgical thread placed through the fistula tract to allow for
continuous drainage while avoiding cutting the sphincter muscles. It helps in maintaining the
fistula open to prevent abscess formation and may be used for prolonged periods to
encourage healing.

-Fistulotomy: The most common procedure for simple, low fistulas. It involves laying
open the fistula tract to allow it to heal from the inside out. It is used for low intersphincteric
or low trans-sphincteric fistulas with minimal risk to continence.

-Fistulectomy: It involves complete excision of the fistulous tract. This may be reserved for
complex cases where a simple fistulotomy is not feasible.

-LIFT Procedure (Ligation of Intersphincteric Fistula Tract): A relatively newer technique

for treating trans-sphincteric fistulas. The fistula tract is ligated and excised through a small
incision in the intersphincteric plane, which preserves the anal sphincter muscles and
reduces the risk of incontinence.
-Advancement Flap: It is used for complex fistulas where there is significant risk to
continence. A flap of healthy rectal or anal mucosa is used to cover the internal opening of
the fistula, promoting healing while minimizing sphincter damage.

-Fibrin Glue or Collagen Plug: These techniques involve filling the fistula tract with a
biocompatible material (fibrin glue or collagen) to seal the tract and promote healing. These
are less invasive options but have variable success rates, particularly in complex fistulas.

Hemorrhoids
-Hemorrhoids are swollen veins in the lower rectum or anus, similar to varicose veins, which
result from increased pressure in the pelvic and rectal regions. They are classified as
internal or external depending on their location relative to the dentate line (a
mucocutaneous junction in the anal canal).

Internal Hemorrhoids:

-They are located above the dentate line and covered by columnar epithelium, which lacks
pain receptors.

-They are usually painless but may cause rectal bleeding, especially during bowel
movements.

-Classified into four degrees based on the extent of prolapse:

● Grade I: Bulging into the anal canal without prolapsing.

● Grade II: Prolapse during defecation but spontaneously reduce.
● Grade III: Prolapse during defecation and require manual reduction.
● Grade IV: Permanently prolapsed and irreducible.

External Hemorrhoids:

-They are located below the dentate line and covered by skin (anoderm), which contains
pain receptors.

-They are painful, especially when thrombosed (clot formation within the hemorrhoid),
leading to significant swelling and discomfort.

Etiology and Risk Factors:

-Hemorrhoids develop due to increased pressure in the rectal and anal veins, which
causes them to enlarge and weaken.

-Chronic constipation: Straining during bowel movements increases pressure on

hemorrhoidal veins.

-Chronic diarrhea: Frequent bowel movements irritate the anal region.

-Prolonged sitting: Sitting for long periods, especially on the toilet, increases pressure on the
rectal veins.

-Pregnancy: Increased pressure from the enlarging uterus and hormonal changes can lead
to hemorrhoid formation.

-Obesity: Excess body weight puts pressure on the pelvic veins.

-Low-fiber diet: Leads to harder stools and increased straining.

-Aging: Weakening of supporting tissues with age increases the risk of hemorrhoid
development.

Signs and symptoms of internal hemorrhoids:

-Painless rectal bleeding: Bright red blood seen on toilet paper or in the toilet bowl.

-Prolapse: Feeling of a lump protruding from the anus during bowel movements, especially
in more advanced cases (Grades III-IV).

-Mucus discharge: Irritation and itching due to mucus secretion from prolapsed
hemorrhoids.

Signs and symptoms of external hemorrhoids:

-Pain: Particularly severe if thrombosed, causing sharp, continuous pain.

-Swelling: A tender lump around the anus.

-Itching and irritation: Due to friction or hygiene issues from the swollen external
hemorrhoid.

Diagnosis:

-Physical Examination: Inspecting the perianal area to identify external hemorrhoids or

prolapsed internal hemorrhoids.

-Digital Rectal Examination (DRE): To assess for internal hemorrhoids or other anorectal
conditions.

-Anoscopy: Used to visualize internal hemorrhoids and assess their degree of prolapse.

-Proctoscopy or Sigmoidoscopy: To rule out other causes of rectal bleeding, especially in

older adults.

Treatment:

-Dietary Modifications: A high-fiber diet (20-30g/day) and increased fluid intake to soften
stools and reduce straining.
-Lifestyle Changes: Regular exercise, avoiding prolonged sitting, and practicing good bowel
habits.

-Sitz Baths: Soaking in warm water several times a day to relieve discomfort.

-Topical Treatments: Over-the-counter creams, ointments, or suppositories containing

hydrocortisone, witch hazel, or local anesthetics to reduce inflammation and relieve
itching.

-Stool Softeners: Medications like docusate to soften stools and prevent straining during
bowel movements.

-Rubber Band Ligation: A rubber band is placed around the base of the hemorrhoid to cut
off its blood supply, causing it to shrink and fall off.

-Sclerotherapy: A chemical solution is injected into the hemorrhoid to shrink it.

-Infrared Coagulation: Heat is applied to the hemorrhoid, causing it to harden and shrink.

-Laser Therapy: Laser energy is used to vaporize hemorrhoidal tissue.

-Hemorrhoidectomy: Surgical removal of hemorrhoids, considered the most effective

treatment for large or prolapsed hemorrhoids, but with a longer recovery period.

-Stapled Hemorrhoidopexy: A circular stapling device is used to reposition prolapsed

hemorrhoids and reduce blood flow to them, causing them to shrink.

-Thrombectomy: For acutely thrombosed external hemorrhoids, a small incision is made to

remove the clot and relieve pain.