Anatomy clinical correlates: Other abdominal organs

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Anatomy clinical correlates: Other abdominal organs

Surgery

Surgery

Preoperative evaluation: Clinical
Postoperative evaluation: Clinical
General anesthetics
Local anesthetics
Neuromuscular blockers
Protein synthesis inhibitors: Aminoglycosides
Miscellaneous cell wall synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
Laxatives and cathartics
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Insulins
Abdominal pain: Clinical
Esophageal surgical conditions: Clinical
Gastrointestinal bleeding: Clinical
Peptic ulcers and stomach cancer: Clinical
Inflammatory bowel disease: Clinical
Appendicitis: Clinical
Diverticular disease: Clinical
Hernias: Clinical
Bowel obstruction: Clinical
Colorectal cancer: Clinical
Abdominal trauma: Clinical
Anal conditions: Clinical
Gallbladder disorders: Clinical
Pancreatitis: Clinical
Adrenal masses and tumors: Clinical
Breast cancer: Clinical
Benign breast conditions: Pathology review
Anatomy clinical correlates: Anterior and posterior abdominal wall
Anatomy clinical correlates: Breast
Anatomy clinical correlates: Viscera of the gastrointestinal tract
Coronary artery disease: Clinical
Valvular heart disease: Clinical
Pericardial disease: Clinical
Aortic aneurysms and dissections: Clinical
Chest trauma: Clinical
Pleural effusion: Clinical
Pneumothorax: Clinical
Lung cancer: Clinical
Anatomy clinical correlates: Thoracic wall
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Pleura and lungs
Anatomy clinical correlates: Mediastinum
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
cGMP mediated smooth muscle vasodilators
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Benign hyperpigmented skin lesions: Clinical
Skin cancer: Clinical
Blistering skin disorders: Clinical
Bites and stings: Clinical
Burns: Clinical
Dizziness and vertigo: Clinical
Thyroid nodules and thyroid cancer: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Neck trauma: Clinical
Nasal, oral and pharyngeal diseases: Pathology review
Antihistamines for allergies
Stroke: Clinical
Seizures: Clinical
Headaches: Clinical
Traumatic brain injury: Clinical
Brain tumors: Clinical
Lower back pain: Clinical
Anatomy clinical correlates: Vertebral canal
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Thrombolytics
Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review
Eye conditions: Retinal disorders: Pathology review
Eye conditions: Inflammation, infections and trauma: Pathology review
Joint pain: Clinical
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Prostate disorders and cancer: Pathology review
Testicular tumors: Pathology review
Kidney stones: Clinical
Renal cysts and cancer: Clinical
Urinary incontinence: Pathology review
Anatomy clinical correlates: Male pelvis and perineum
Androgens and antiandrogens
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Peripheral vascular disease: Clinical
Leg ulcers: Clinical
Anatomy clinical correlates: Peritoneum and diaphragm
Anatomy clinical correlates: Other abdominal organs
Anatomy clinical correlates: Inguinal region
Anatomy clinical correlates: Bones, fascia and muscles of the neck
Anatomy clinical correlates: Skull, face and scalp
Anatomy clinical correlates: Trigeminal nerve (CN V)
Anatomy clinical correlates: Facial (CN VII) and vestibulocochlear (CN VIII) nerves
Anatomy clinical correlates: Glossopharyngeal (CN IX), vagus (X), spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy clinical correlates: Ear
Anatomy clinical correlates: Temporal regions, oral cavity and nose
Anatomy clinical correlates: Vessels, nerves and lymphatics of the neck
Anatomy clinical correlates: Viscera of the neck
Anatomy clinical correlates: Spinal cord pathways
Anatomy clinical correlates: Cerebral hemispheres
Anatomy clinical correlates: Anterior blood supply to the brain
Anatomy clinical correlates: Cerebellum and brainstem
Anatomy clinical correlates: Olfactory (CN I) and optic (CN II) nerves
Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy clinical correlates: Eye
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Testicular and scrotal conditions: Pathology review
Skin and soft tissue infections: Clinical
Anatomy clinical correlates: Posterior blood supply to the brain
Anatomy clinical correlates: Female pelvis and perineum

Transcript

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The abdominal cavity is home to plenty of organs. Some of them, like the stomach and intestines, are part of the gastrointestinal tract. Other organs, like the liver, gallbladder and pancreas, help with digestion, even though they’re not part of the GI tract itself. And then there are also organs like the spleen, kidneys and ureters, which are part of other important, non gastrointestinal systems. So let’s take a look at the injuries and diseases that can affect these abdominal organs.

First off, we have portal hypertension, which basically means increased pressure in the portal venous system. This is most commonly caused by liver cirrhosis, but can also be caused by vascular obstruction. Some causes of vascular obstruction include portal vein thrombosis, Budd-Chiari syndrome which is thrombosis or compression of the hepatic veins, as well as the parasitic flatworm infection known as schistosomiasis.

Okay, now, when fibrosis in the liver from cirrhosis obstructs the portal vein, the pressure rises in the portal vein and into its tributaries. This large volume of congested blood flows out from the portal system into the systemic system at the sites of portosystemic anastomoses, also called portocaval anastomoses.

The first site of portosystemic anastomosis is at the lower esophagus. At this point, the high pressure in the portal system can reach the anastomosis between the left gastric veins and the esophageal veins in the lower esophagus, causing engorged varicose veins which may then go on to rupture and lead to upper gastrointestinal bleeding.

In more severe cases of portal hypertension, the veins of the anterior abdominal wall, called the epigastric veins, which anastomose with the paraumbilical veins become varicose and look like small snakes radiating from the umbilicus under the skin. This clinical sign is called caput medusae.

There is another portosystemic anastomosis in the rectum, which in the case of portal hypertension, can lead to anorectal varices. Some other signs and symptoms of liver cirrhosis include palmar erythema, petechiae, ascites, and jaundice. These might be present in addition to the signs of portal hypertension as we discussed: anorectal varices, caput medusae and esophageal varices.

Now let’s talk about the gallbladder, which is often affected by gallstones. Gallstones are tiny stones that form in the gallbladder, and the technical term for these gallstones in the gallbladder is “cholelithiasis”.

To understand the clinical repercussions of gallstones, let’s review the anatomy of the hepatobiliary tree and the pancreatic ducts. So the liver cells, called hepatocytes, secrete bile, and the bile drains from the hepatocytes through bile canaliculi, to the interlobular biliary ducts, then the collecting bile ducts, and finally into the right and left hepatic ducts. The right and left hepatic ducts then join to form the common hepatic duct. Also, the gallbladder has its own duct, called the cystic duct. The common hepatic duct meets the cystic duct, and they join together to form the common bile duct.

The common bile duct then descends and passes posterior to the first part of the duodenum and the head of pancreas. At this point, it converges with the main pancreatic duct and together they form the hepatopancreatic ampulla, or Ampulla of Vater, which empties into the duodenum.

Now, gallstones are mainly made of cholesterol crystals and they arise more commonly in biological females (n). Even though they usually form and stay in the gallbladder, sometimes they can migrate and obstruct different parts of the hepatobiliary tree. When a gallstone blocks the cystic duct, it obstructs the passage of bile from exiting the gallbladder. In this case, contraction of the gallbladder, like after a fatty meal, can lead to biliary colic, which is an intense, spasmodic pain located in the right hypochondrium or right upper quadrant. When the gallbladder relaxes, the stone might move back into the gallbladder relieving symptoms.

Alternatively, it can remain lodged in the cystic duct, and this causes inflammation and enlargement of the gallbladder, known as cholecystitis. Symptoms of cholecystitis include right upper quadrant pain or epigastric pain, along with anorexia, nausea, vomiting and fever. Since the stone is only obstructing the gallbladder from emptying via its cystic duct, while the common bile duct remains open, patients with cholecystitis do not often present with jaundice.

On clinical examination, there’s a positive Murphy sign. This is when the individual is asked to take a deep breath while the doctor palpates the area of the gallbladder, just beneath the edge of the liver. Deep breaths cause the gallbladder to descend and press against the examining fingers, which in individuals with acute cholecystitis leads to pain and discomfort. A positive Murphy sign is when the patient catches their breath and ceases to inspire due to the pain of the inflamed gallbladder descending against the examiner’s hand.

Gallstones can also migrate and obstruct the common bile duct, which is known as choledocholithiasis. Obstruction at this level leads to inflammation of the common bile duct and bile stasis which can then allow bacteria from the small intestine to multiply within the common bile duct. This situation is called ascending cholangitis, a fancy term for “the common bile duct is obstructed, inflamed, and bacteria are wreaking havoc inside”. Symptoms of ascending cholangitis include fever, abdominal pain and jaundice, also known as Charcot triad. Jaundice occurs due to the obstruction of the common bile duct and subsequent build-up of bilirubin in the liver and then in the blood.

Interestingly, gallstones can also migrate to where the common bile duct meets the pancreatic duct at the ampulla of Vater and obstruct both the common bile duct and the main pancreatic duct. This obstruction of the pancreatic ducts leads to pancreatitis, which is the inflammation of the pancreas. Symptoms of pancreatitis include anorexia, malaise and epigastric pain which often radiates to the back. With the gallstone obstructing the common bile duct at the same time, patients often appear jaundiced as well.

Finally, an enlarged and inflamed gallbladder can attach itself to and form communications with adjacent viscera, and these are called fistulae. For example, a cholecystoenteric fistula is when a communication between the gallbladder and the intestine forms. The location of the gallbladder affects which organs are most likely to develop a fistula with it. These organs are the superior part of the duodenum and the transverse colon. A large enough gallstone won't be able to enter and pass through the cystic duct, but it could pass through a cholecystoenteric fistula and enter the gastrointestinal tract. Such a stone can then travel distally and become trapped at the ileocecal valve, causing small bowel obstruction.

This particular type of bowel obstruction is called a gallstone ileus. Symptoms include recurring diffuse abdominal pain and vomiting. Air from the intestinal tract may also enter the biliary tree through this fistula leading to pneumobilia which can be detected on imaging.

Luckily, a cholecystectomy, which is when the gallbladder is surgically removed, can be done to manage several gallbladder issues, some of which we’ve just discussed. Surgery ultimately depends on the patients clinical symptoms and surgeon preference, but reasons for cholecystectomy include choledocholithiasis, gallstone pancreatitis, uncomplicated cholecystitis, acalculous cholecystitis, porcelain gallbladder, gallbladder polyps larger than 0.5 centimeters, as well as asymptomatic cholelithiasis in individuals at increased risk for developing gallbladder cancer.

During surgery, it’s important to identify Calot triangle or the cystohepatic triangle in order to ensure safe ligation of the cystic duct and cystic artery. The triangle is bounded inferiorly by the cystic duct, medially by the common hepatic duct and superiorly by the inferior surface of the liver. The cystic artery is located within the triangle and is identified during a laparoscopic procedure and then ligated or clipped off. The triangle also contains the right hepatic artery, and might contain anomalous bile ducts. Because of this, ligation of the cystic artery should only happen once the boundaries of Calot triangle have been identified and the structures passing through it have been dissected and identified.

During cholecystectomy, the common bile duct can be damaged, which can lead to leakage of bile into the abdomen and consequent peritonitis. The surgical instruments used to remove the gallbladder can also injure other structures, like the intestine and surrounding blood vessels.

Before moving on, a quick quiz: what can happen when a gallstone migrates to the common bile duct? Now, let’s have a quick chat about the spleen and the pancreas. The spleen is an intraperitoneal organ that lies in the left hypochondrium close to other intraperitoneal organs, like the stomach, the transverse colon and the descending colon. It’s also close to the left kidney and the pancreas, both of which are retroperitoneal organs. In most individuals, the spleen doesn’t extend inferiorly past the rib cage, unless it’s enlarged.

The spleen is the most commonly injured organ during blunt trauma, for example by car crashes, sports injuries and fist fights. Splenic injuries can occur due to fracture of the overlying ribs or impact to the spleen itself and can range from a simple contusion or subcapsular hematoma, to splenic laceration and subsequent internal bleeding. Individuals with a ruptured spleen can present with nausea, abdominal pain, abdominal guarding, tenderness in the epigastrium and pain in the left flank as well as hypotension or shock due to profound intra abdominal bleeding from this highly vascular organ.

Moreover, a ruptured spleen can present with a positive Kehr sign, which is when there’s referred pain typically to the upper left shoulder due to irritation of the phrenic nerve in the diaphragm.

Sources

  1. "Spontaneous Bacterial Peritonitis" Digestive Diseases (2005)
  2. "Normal main portal vein diameter measured on CT is larger than the widely referenced upper limit of 13 mm" NY (2016)
  3. "2016 WSES guidelines on acute calculous cholecystitis" World Journal of Emergency Surgery (2016)
  4. "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013" The Lancet (2015)
  5. "Postcholecystectomy syndrome (PCS)" International Journal of Surgery (2010)
  6. "Structure and function of the spleen" Nature Reviews Immunology (2005)
  7. "Gallstone Disease: Diagnosis and Management of Cholelithiasis, Cholecystitis and Choledocholithiasis" UK (2014)