Mini-Laparoscopic Cholecystectomy with Intraoperative Cholangiogram for Symptomatic Cholelithiasis (Gallstones) - Standard
Authors: Brunt LM1, Singh R1, Yee A2
Published: September 26, 2017

AUTHOR INFORMATION
1 Department of Surgery, Washington University, St. Louis, Missouri
2 Division of Plastic and Reconstructive Surgery, Washington University, St. Louis, Missouri

DISCLOSURE
No authors have a financial interest in any of the products, devices, or drugs mentioned in this production or publication.

ABSTRACT
Minimal invasive laparoscopic cholecystectomy is the typical surgical treatment for cholelithiasis (gallstones), where patients present with a history of upper abdominal pain and episodes of biliary colic. The classic technique for minimal invasive laparoscopic cholecystectomy involves four ports: one umbilicus port, two subcostal ports, and a single epigastric port. The Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) has instituted a six-step strategy to foster a universal culture of safety for cholecystectomy and minimize risk of bile duct injury. The technical steps are documented within the context of the surgical video for (1) achieving a critical view of safety for identification of the cystic duct and artery, (2) intraoperative time-out prior to management of the ductal structures, (3) recognizing the zone of significant risk of injury, and (4) routine intraoperative cholangiography for imaging of the biliary tree. In this case, the patient presented with symptomatic biliary colic due to a gallstone seen on the ultrasound in the gallbladder. The patient was managed a mini-laparoscopic cholecystectomy using 3mm ports for the epigastric and subcostal port sites with intraoperative fluoroscopic cholangiogram. Specifically, the senior author encountered a tight cystic duct preventing the insertion of the cholangiocatheter and the surgical video describes how the author managed the cystic duct for achieving a cholangiogram, in addition to the entire technical details of laparoscopic cholecystectomy.

What could cause a blockage in the stomach? Mechanical causes of intestinal obstruction may include: Adhesions or scar tissue that forms after surgery. Foreign bodies (objects that are swallowed and block the intestines) Gallstones (rare) Hernias. Impacted stool. Intussusception (telescoping of one segment of bowel into another) Tumors blocking the intestines. Less common radiologic signs are seen in specific circumstances. Most closed-loop obstructions (75%) are caused by adhesions. A closed-loop obstruction occurs when a loop of bowel is not decompressed by the caudal passage of gas and fluid.

Diagnosis of HIV infection in infants is aided by HIV culture or DNA/RNA polymerase chain reaction (PCR); positive results are confirmed by repeating the test. In suspected cases, HIV testing should occur in the newborn period (ie, before the infant is 48 h old), at age 1-2 months, and again at age 3-6 months.

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The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions. Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation. The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia. The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis. Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites. Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.

Compartment syndrome can develop in the foot following crush injury or closed fracture. Following some critical threshold of bleeding and/or swelling into the fixed space compartments, arterial pulse pressure is insufficient to overcome the osmotic tissue pressure gradient, leading to cell death. The complicating factor is related to the magnitude of the force of the crush injury. The amount of swelling or bleeding has to be sufficient to impair arterial inflow, while not being of sufficient magnitude to produce an open injury, which decompresses the pressure within the affected compartments. When the injury is open, we then attribute the late disability primarily to the crushing injury to the involved muscles.

Arthritis occurs when the cartilage breaks down explains Dr. Derek Papp, Sports Medicine Physician with Miami Orthopedics & Sports Medicine Institute. This it’s a very common knee injury such as the damage of the cartilage and meniscus tear.
ACL tears is another common injury especially in sports like soccer or Australian football, the specialist explains.

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Osgood-Schlatter disease can cause a painful lump below the kneecap in children and adolescents experiencing growth spurts during puberty. Osgood-Schlatter disease occurs most often in children who participate in sports that involve running, jumping and swift changes of direction — such as soccer, basketball, figure skating and ballet. While Osgood-Schlatter disease is more common in boys, the gender gap is narrowing as more girls become involved with sports. Age ranges differ by sex because girls experience puberty earlier than do boys. Osgood-Schlatter disease typically occurs in boys ages 13 to 14 and girls ages 11 to 12. The condition usually resolves on its own, once the child's bones stop growing.

You're sneezing, coughing, and all stuffed up. It sounds and feels like a cold, alright. But as time goes on, you start to wonder. Is it turning into a sinus infection? They've got some things in common, but there are ways to tell them apart. The right ID lets your doctor get you the best treatment. What Is a Common Cold? It's an infection caused by a virus, a tiny living thing. You can't miss the symptoms: Nasal congestion Runny nose Post-nasal drip (drop-by-drop release of fluid from your nose into the back of the throat) Headache Fatigue You may also get a cough and a mild fever. The symptoms usually build, peak, and slowly disappear. Some medications can ease symptoms. For example, decongestants may decrease drainage and open the nasal passages. Pain relievers may help with fever and headache. Cough medicine may help, as well. Colds typically last from a few days to about a week or longer. Sometimes, a cold may cause swelling in the sinuses, hollow spaces in your skull that are connected to each other. The swelling can prevent the flow of mucus.

Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system. ... If the vessels in the liver are blocked due to liver damage, blood cannot flow properly through the liver. As a result, high pressure in the portal system develops

ACE inhibitors Email this page to a friend Print Facebook Twitter Google+ Angiotensin-converting enzyme (ACE) inhibitors are medicines. They treat heart, blood vessel, and kidney problems. How ACE inhibitors help ACE inhibitors are used to treat heart disease. These medicines make your heart work less hard by lowering your blood pressure. This keeps some kinds of heart disease from getting worse. Most people who have heart failure take these medicines. These medicines treat high blood pressure, strokes, or heart attacks. They may help lower your risk for stroke or heart attack. They are also used to treat diabetes and kidney problems. This can help keep your kidneys from getting worse. If you have these problems, ask your health care provider if you should be taking these medicines.

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Microscopic polyangiitis (MPA) is vasculitis of small vessels. It was initially considered as a microscopic form of polyarteritis nodosa (PAN). In 1990, the American College of Rheumatology developed classification criteria for several types of systemic vasculitis but did not distinguish between polyarteritis nodosa and microscopic polyarteritis nodosa. [1] In 1994, a group of experts held an international consensus conference in Chapel Hill, North Carolina, to attempt to redefine the classification of small vessel vasculitides. [2, 3]

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