11/15/08

*** Final will not be cumulative…It is the last material of the trimester, after test #4 ***

PERITONITISDiagnosis of Peritonitis -- History and EtiologyThe most characteristic symptom of an acute abdominal problem is complaints of abdominal pain. Pain is reported of sudden or insidious onset.. Pain becomes constant and severe. Pain worsens with movement. Pain is initially localized and later generalizes as inflammation spreads.

Causes of PeritonitisA. Conditions that Can Perforate & Lead to Peritonitis

Peptic UlcerColonic DiverticulumAppendicitisTrauma

B. Causes of Intra-abdominal BleedingRuptured Abdominal Aortic AneurysmRuptured ectopic pregnancyRuptured aneurysm (non-aortic ruptured aneurysm)Ruptured retroperitoneal vessel

C. Severe PancreatitisD. Rupture of a Solid Organ

Causes of peritonitis, key word = RUPTURE…ANYTHNG IN THE ABDOMINAL CAVITY THAT CAN RUPTURE CAN BE A SOURCE OF PERITONITIS. Peritonitis is a complication that results from other problems (typically rupture).

Physical ExamPatients rarely have normal abdominal physical examination findings. Observation is an important initial step. The patient with peritonitis lies still to less the pain, usually either supine or curled up.

AuscultationThe abdomen is usually quiet.

*** Note (Ruptured Sigmoid Diverticulum VS Ruptured Appendix ***Ruptured sigmoid diverticulum = Associated with local inhibition and local

peritonitisVS.Appendix Rupture = Huge puss pocket develops with 4 quadrants of peritonitis (puss and bacteria are triggers)

PalpationVery gentle palpation allows estimation of both voluntary and involuntary guarding. Signs of direct and rebound tenderness can be elicited by gentlest pressure.

PercussionGentle percussion over the RUQ helps to ascertain whether the normal area of liver dullness is present. KUB X-ray can help show organ location, size, and #. Ascites may be present if the liver purcusses differently and is located in the correct position. Fluid in the abdominal cavity (ascites) presents as an “increased liver size” with percussion, but palpation and KUB show the size to be normal.

Rectal ExamA rectal exam should always be done and the stool checked for gross or occult blood.

X-RayUpright Chest X-ray: Helps to detect pneumo-peritoneum (free air). Free air is best sought under the right diaphragm where it outlines the liver.

Upright KUBThis study also helps detect free air in the R hemi diaphragm. Normally the liver is below the R hemi diaphragm. When free air is present, we can’t tell where the diaphragm ends and liver begins. A black stripe is the + ID of free air & indicates rupture.

1. The most common cause of rupture and free air in the abdomen = RUPTURED DIVERTICULUM 2. The most common cause of RLQ pain due to rupture= APPENDICITIS3. The most common cause of LLQ pain & rupture = SIGMOID DIVERTICULUM

Abdominal RadiographMickey Mouse Sign = Fluid pooling in the pelvic bowl that looks like Mickey’s Face.

Upright Abdominal X-rayWe look for 3 or more air fluid levels to indicate rupture.

Hemogram With Differential Leukocyte UrinalysisThe hemogram typically shows leukocytosis with left shift

PancreatitisEffusion occurs from pancreatic enzymatic release. Pancreatic enzymes digest and irritate, creating pleural effusion. Pleural effusion blunts the borders of the abdomen on film.

Contrast X-Ray StudiesStudies of the esophagus, stomach, and duodenum with water-soluble contrast material may help differentiate between a perforated ulcer and pancreatitis. Absence of dye migration does not rule out earlier perforation. Presence of dye migration proves perforation.

In some cases, you don’t want to do barium studies. Barium can leak is progressive situations.

CT ScanHelical CT produces fast results. Helical CT is the diagnostic tool of choice to assess severe pancreatitis, free abdominal air/rupture, and to confirm appendicitis, diverticulum or abscess. The use of CT is reserved for delineating specific underlying clinical entities.

DX UltrasoundA cheap &quick tool that can be used in identification of the problem.

ParacentesisCan be used for the initial diagnosis of non-specific, generalized peritonitis.. Paracentesis is quick, effective and has a high degree of reliability in this role.

Procedure1. Doctors cut the linea alba and insert a catheter with saline solution. 2. Doctors then drain the abdomen and remove fluid. 3.

a. In normal patients = Fluid goes in and fluid comes out easily (FUID WILL MOSTLY BE SALINE)b. In rupture patients = BLOOD, FECAL MATERIAL, BILE can all be removed. A vessel can

rupture and lead to blood removed via paracentesis. The colon can rupture leading to fecal content removed via paracentesis. The gallbladder may rupture leading to bile removed via paracentesis. A combination of material may also be removed.

Paracentesis is a quick tool that guides the doctor where direct further investigation.

ManagementAs chiropractors:

1. We can take history2. Provide physical exam3. Recommend X-ray or Dx. Ultrasound to discover the site of the lesion.

The goal is to identify if the most common complication of peritonitis is present (ABDOMINAL ABSCESS).

If the patient doesn’t feel a little better, start thinking about abscess formation. Increased residual pain and tenderness that is not normal are signs.

Identification of AbscessUltrasound: Sensitivity is about 60%CT: Very good (higher sensitivity). Non-contrast CT’s are preferred. MRI: Can be used to identify abscess. MRI’s are not widely used and very expensive. Plain Film: Don’t waste your time (won’t help us)Radioactively tagged WBC’s: Patients own blood is used. WBC’s are tagged and put back into the blood stream. A radionucleotide scan is performed about 2 hours after the WBC’s are put back into the system. The location of the WBC’s may give an indication of active infection/abscess. In abscess patients, the white cells go to the periphery of the abscess, giving us a hot spot.

Treatment of AbscessLaparoscopy is performed teasing the abscess out and flooding the area with antibiotics. This is often an outpatient procedure that is tolerated well by the patient. Flooding the area with antibiotics gives better results than IV antibiotics because more antibiotic can be administered to a specific location.

ECTOPIC PANCREATIC TISSUEEctopic Pancreas/Ectopic TissueEctopic tissue can be located in Meckel’s Diverticulum, small intestine or stomach. Ectopic tissues are locally irritating. We may need to find the ectopic tissue and surgically remove it. The tissue can release enzymes that destroy tissue.

ACUTRE PANCREATITISInflammation of the pancreas due to escape of enzymes. The pancreatic duct is very different than the pancreas itself. Obstruction of the pancreatic duct can lead to duct not holding product and leakage back into the parenchyma. Leakage back into the parenchyma causing digestion of the pancreatic tissue.

3 Differentials That Lead to Acute Pancreatitis1). Biliary Obstruction = Gallstone that escapes gallbladder and can be stuck in the opening of the pancreatic duct (about 50%) 2). Alcohol Induced = Alcohol abuse (about 20%) 3). Idiopathic (about 30%) = We don’t have an identifiable reason

Pancreatic Products that Cause Pathology2 pancreatic products produce pathology:

1. Plasmokinin: Plasmokinin breaks the bonds of vascular tissue. The enzyme causes weeping of blood within the pancreas. The damage can be seen on MRI.

2. Elastase: Elastase breaks connective tissue. Elastase destruction can lead to pseudocyst formation with pancreatic product within the pseudocyst. Pseudocyct is a consequence of a pancreas trying to digest itself. The finding is often found on diagnostic ultrasound.

Presentation of Acute PancreatitisAcute pancreatitis comes on hard and strong with SEVERE ABDOMINAL PAIN. They need to go to the hospital as they have great pain. Patients are not comfortable lying down supine. They roll onto their side or sit up and tip forward. SITTING UP AND LEANING FORWARD is suggestive of acute pancreatitis. Patients assume this position to lessen discomfort.

Pulsations of the abdominal aorta trigger annoying sensations and pain.. Patients tend to have nausea and vomiting. They don’t get relief from vomiting. Patients present as diaphoretic, weak, lethargic, and run a low grade fever. Pulse and heart rate are rapid. Shallow respiration is present.

Gallbladder & Biliary Obstruction Induced Acute Pancreatitis1. You may be able to find a palpable gallbladder with acute pancreatitis. The MOST COMMON REASON FOR A PALPABLE GALLBLADDER IS GALLSTONE/OBSTRUCTION. Cholecystitis leads to obstruction. Obstruction leads to acute pancreatitis. Tenderness will be present.

2. You may find an enlarged non-tender gallbladder. ABOUT 1/3 OF THE TIME AN ENLARGED NON-TENDER GALLBLADDER IS PANCREATIC CANCER. Tumor induces obstruction. The gallbladder will enlarge in size creating greater mechanical room for product. Tenderness will not be present.

Lab DiagnosisSerum Amylase = First and best check for acute pancreatitis.Serum Lipase = If you see amylase and lipase increases, think chronic pancreatitis not acute pancreatitis.

Imaging of Acute PancreatitisPlain Film – KUB: D ystrophic calcification must be present to visualize the pancreas on plain film. Dystrophic calcification indicates a long standing condition. MRI = May show pseudocyst. . Ultrasound: Gas in the area may obstruct the view. Air in the GI tract breaks the signal. Helical CT: Better quality and quick results. CT’s can show pseudocysts.

Prognosis with Acute PancreatitisThe prognosis is pretty good overall for the known causes of acute pancreatitis. Idiopathic pancreatitis is more difficult to manage. In all cases, patients should go directly to the hospital.

CHRONIC PANCREATITIS Patient presentation:

1. Mild Discomfort2. Repeat Episodes of biliary disease3. Patient denies past medical management

At Risk Patients1. Alcoholics = At greater risk for chronic pancreatitis (they are often 1/3 of the patients)2. Hyperlipidemia (lipids) = Occlude the vasculature of the pancreas leading to chronic pancreatitis.3. Hereditary Pancreatitis = Genetic Predisposition. 4. Idiopathic = About 40% of chronic pancreatitis is idiopathic. Idiopathic is diagnosis by exclusion.

Signs and Symptoms1. Modest elevation of amylase and lipase…The mild elevation helps differentiate chronic from acute. 2. No pain to mild pain is present. 3. Dystrophic calcification pattern develops…The pattern presents as white polka dots that cross midline. 4. Imaging =

a. Early in the disease = The pancreas is bigger than usual. b. Mid-late disease = Pancreas shrinks. We see irregularly contoured and irregularly shaped pancreas.

5. Chronic pancreatitis comes and goes6. An attack, shows midline RUQ and LUQ pain with adynamic ileus.

a. Crampy pain . b. More gassy. c. Diarrhea d. .Fecal composition changes as food is not completely digested

ManagementConservative management is the best choice. Dietary change is important:

1. Reduce fat intake2. Reduce protein intake3. Eat leaner meats4. Pancreatic enzyme supplements can help.5. Manage diabetes appropriately…This patient becomes a diabetic due to loss of insulin. Chronic pancreatitis is a

cause of diabetes, rather than a complication of diabetes. 6. Drainage of Pseudocysts…Chronic pancreatitis patients can acquire pseudocysts as pancreatic function is lost. CT

guided drainage can help in management.

PANCREATIC CANCER1. Very quick & very destructive2. Painful3. TERMINAL DIAGNOSIS4. No Safe Location = ¾ in the head and ¼ in the tail5. Universal weight loss with no good reason occurs6. Obstructive Jaundice7. Hepatitis8. Anorexia = True suppression of appetite

Common Bile Duct and Clinical Triad 30% with pancreatic cancer have a palpable non-tender gallbladder because pancreatic cancer obstructs the common bile duct. A CLINICAL TRIAD DEVELOPS = JAUNDICE, PAIN, ANOREXIA. Blockage of the common bile duct impacts 3 organs: pancreas, liver, gallbladder.

Seated PositionThey sit up and lean forwards to relieve pain

Serum Amylase ElevationThis patient may/may not have serum amylase elevation (depending on if obstruction is present or not).

ImagingCT, MRI, Diagnostic Ultrasound….X-ray is not a good choice

12/1/08

GENERAL OVERVIEW OF BILIARY DISEASELiver, pancreas and gallbladder can all be involved in biliary disease. BILIARY DISEASE IS THE #2 CAUSE OF ABDOMINAL PAIN AND #2 REASON FOR ABDOMINAL SURGERY.

Definitions1. Cholecystitis = Inflammation of the gallbladder…Stone disease is the most common cause of cholecystitis.2. Cholelithiasis = Gallstones…You can have stones and no pain and pain and no stones.3. Chodocholithiasis = Obstruction of the common bile duct…Stones (gallstone) that makes it out of the gallbladder,

beyond the pancreatic duct and obstructs the common bile duct. The stone can be in the common bile duct or the ampulla of Vater. There can be hepatitis, cholecystitis and pancreatitis. This person is very uncomfortable. This may be the worst biliary presentation (hepatitis, cholecystitis & pancreatitis).

4. Cholangitis = Inflammation of the bile ducts of the liver itself due to backup. Cholangitis can lead to hepatitis. This can be a product of backup. It can lead to hepatitis.

5. Hydrops = Distention of the gallbladder (with clear fluid). 6. Biliary Colic = Cramping pain from unsatisfied contraction. Sensory and motor systems are intact but cannot express

work due to obstruction. Work is resisted leading to discomfort. The patient will have quiet periods followed by periods of cramping pain.

______________________________________________________________________________________________________CHOLELITHIASISStone disease can occur independent of symptoms. Cholesterol is the most frequent component of stones. Pure cholesterol stones may not be visualized easily on plain film. Fatty meals trigger stone formation. Cramping pain ensues. Most stones are cholesterol based (either 100% cholesterol or cholesterol mixed with calcium).

Dx. UltrasoundDx. Ultrasound has been used to great affect to find stones. The more superior the location of the gallbladder (especially in younger people), the easier it is to find a stone. The liver acts as an acoustic window aiding in visualization.

Patients in pain can gulp air. Gulped air obstructs the views of diagnostic ultrasound.

The gallbladder mostly lies on the R side we can find it in the upper or lower quadrant (patient dependent). R upper or lower quadrant pain is about 95% of gallbladder pain .

Stone FormationStasis is a big reason for stone formation. The longer a fluid is held in place the more concentrated it is. Supersaturation ensues from stasis and leads to stone formation.. Dehydration does not play a big role in GI stone formation. Dehydration plays a bigger role in stone formation in the GU system. Emphasize stasis as the mechanism.

Gender BiasWomen suffer slightly more than men from GI stones. Upper R quadrant pain is classic. The differential list is the same for both men and women.

Types of Stones The #1 stone = Cholesterol Stones Secondarily, some stones have calcium (10-20%).

CALCIUM BILLIRUBINATE PIGMENTED STONES ARE CLINICALLY SIGNIFICANT BECAUSE THEY ARE SIGNS OF OTHER DISEASE.

Causes of Calcium Billirubinate Pigmented StonesHemolytic AnemiaBiliary InfectionBleeding into the biliary treeCirrhosis of the LiverAlcoholism

Pigmented stones indicate other problems expressing themselves. We have to deal with both the gallstone and the disease ( anemia, infection, etc.) to help the patient out.

Predisposing Factors to Stone FormationStasis is the most common reason for stone formationFatty Diets: Simple things like decreasing fat in the diet, but not eliminating fats in the diet can help.

Nutrisystems Diet: The diet advocates elimination of fats. Decreasing the fat, decreases the amount of bile salts needed. At the end of the diet, patients binged on fatty foods. The body adapted to lack of fat in the diet and stones were formed. Biliary obstruction occurred. 5/6 of the patients had cholecystitis and 2/3 had cholecystectomy.

ManagementChanging eating habits is imperative: A healthy mindset is to “be good to yourself.” Diets are temporary, but changing habits can be lifelong. Have the patients bring a copy of the diet to you…Watch out for fat elimination diets. Occasional amounts of fat that stress the system is actually good for the gallbladder and internal organs. Cholecystectomy: When clinically necessary

GallstonesSome stones are very large with flat spots. Gallstones are pearl shaped, concentric around a central nidus.

CholecystectomyThe best predictor for cholecystectomy was the areas with the greatest amount of physicians, meaning that the procedure is performed when not clinically necessary. Unnecessary surgery leads to greater risk. Most patients with cholecystitis (85-95%) only get it once, yet surgery is still performed way too often.

Prophylactic CholecystectomyProphylactic cholecystectomy may be beneficial in patients with:

Hemolytic anemias: Hemolytic anemia patients can show red cell ruptureMorbidly obese: The obese cannot reduce their weight and reduce risk factors, so they may benefit from surgery.Military (Submarine): Submariners may need prophylactic surgery because the submarine may not be able to surface to get the patient to an emergency center. The surgery allows them to remain a submariner. If the patient does not get prophylactic surgery, they will need to change jobs within the Navy. The Navy doesn’t want the patient with gallstone formation getting on board. Diabetics

Inflammatory Bowel Disease Patients: If they are doing abdominal surgery in the area, they may also choose to remove the gallbladder. Patients with IBD are statistically more likely to form gallstones.

Stone Formation RisksAbnormal Composition of Bile: Too much bile salts and cholesterol that overwhelm the system and lead to aggregationInfection: Leads to AggregationAge: Leads to increased stone formationGender: 2:1 women over menFamily History: Genetic component can affect the type of material stored in the gallbladderRapid Weight Loss: How is the weight lost? Unexplained loss is a red flag. A yellow flag is a strict elimination diets and negative calorie diets. You may want them to take good fats (omega fatty acid) to keep good gallbladder function via stressing the system with a “healthy” fat load.Fasting: Biliary stasis is the consequence leading to stone formationDiabetesCrohn’s Disease & IBD’sObesity: Strongly linked to stone formationCeliac Disease: Body has decreased cholecystokininEstrogen Therapy Pregnant Women: Kinks in the cystic duct can lead to delayed emptying and stonesFertility Drugs & Oral Contraceptives

Prevalence of Gallstones10%-20% of the population may have gallstones. 10-20% is a significant # of the population to get stones. In the elderly, the risk rate is higher. Surgery is required about 7% of the time according to the medical literature (JAMA); however, surgery is actually performed more than that (unnecessary surgery).

Chiropractor’s RoleChiropractors need to be part of the educational process. We need to be in a teaching/counseling mode.

Abdominal Exam and Plain FilmMost times we won’t see the cholesterol stone on plain film, so other radiographic studies and physical exam is necessary.

Radiographic StudiesDx Ultrasound = Ultrasound is a pretty good diagnostic tool (highly sensitive and specific) in young people and people without bowel gas. It is often the best choice early (Good, safe and cheap). If bowel gas breaks up the sound source, we won’t be able to image. If we don’t find it with diagnostic ultrasound, go to CT. Ultrasound has become the ideal test for demonstrating calculi and gallbladder morphology without X-ray exposure. Ultrasonography can image intraluminal particles less than 1 mm in size.Spiral CT: Reformatted images show good detail. Spiral CT is very fast and accurate in diagnosis.MRI: A good exam, but the expense is an issue. Plain Film: Most stones will not appear, because they are cholesterol based. The stone must have calcification to be present on plain film X-ray. Supine/recumbent and upright abdominal X-rays provide objective evidence of radio-opaque stones, gallbladder wall calcification or gallbladder perforation. Perforation is indicated by free intra-abdominal air. Think cholesterol stone when not visible on X-ray with physical presentation that matches stone formation. ERC (Endoscopic Retrograde Cholangeopancreatography): We see the gallbladder, pancreatic tree and biliary tree with this contrast exam. Contrast is forced against the stone aiding in visualization. We can find even a small stone. ERC can be used with both X-ray and CT.THC (Trans-Hepatic Cholangeopancreatography): Done under ultrasound or CT guidance. The goal is to force contract into the area around the biliary tree. *** Iodine based contrast is used. We should be concerned about allergic reaction to iodine *** Biliary Scintography: Biliary scintography fails to visualize the gallbladder in cases of cystic duct obstruction. It fails to visualize during chronic cholecystitis and acute gallstone pancreatitis. The imaging tool is not used as much as before.

*** Contrast Studies: The above 3 studies (ERC, THC and Biliary Scintography) are contrast based exams. There is no agreed upon method of which is better to use. Oral cholecystography may prove superior to biliary scintography in cases of cystic duct obstruction, chronic cholecystitis, and acute gallstone pancreatitis. Ductal gallstones can be pinpointed and potentially treated via techniques that instill radio-contrast directly into the biliary tree – either retrograde cholangiopancreatography or percutaenous transhepatic cholangiography ***

Pre-Test Protocol For Contrast ExamsA fatty meal is given to the patient to stimulate gallbladder reaction. A normal gallbladder will empty without stone formation. If the patient has stones, contrast is absorbed making the rim of the stone evident. We stopped performing contrast exams because we don’t want to create an acute cholecystitis event that generates pain. Now we just use diagnostic ultrasound because it is a better, more efficient tool.

Physical ExamRight upper quadrant tendernessGuardingAdynamic Ileus (very likely)

Lab AbnormalitiesMild LeukocytosisModerate Elevations in serum bilirubinModerate Elevations in alkaline phosphataseModerate Elevations in Aspartate aminotransferase (an enzyme that is a sign of liver injury)*** Generally speaking: Liver enzymes will be elevated ***

Symptoms of CholelithiasisFeverNauseaVomitingPostprandial biliary colic: 60-70% of people with symptomatic cholelithiasis experience episodes of biliary colic, typically described as postprandial epigastric or right upper quadrant pain, sometimes radiating to the back or up to the right shoulder. Pain is from unsatisfied contraction of the gallbladder (the gallbladder cannot fully empty due to blockage of the cystic duct). The gallbladder is stimulated to contract primarily by cholecystokinin which is released from the small bowel mucosa.Severe R Upper quadrant painBelchingBloatingDyspepsiaFlatulence

Liver Flush/Gallstone Elimination ProtocolsVery strict fat elimination diets are done by patients for days to fill the gallbladder with bile Doctors then stimulate the gallbladder with oil triggering a response. There is a risk of acute episode by doing this protocol. Keep this patient in the office to monitor them and be prepared to move them to the hospital.

CHOLECYSTITIS Complications of CholecystolithiasisCholangitisCholecystitisEmpyema of the gallbladderCommon bile duct stricturePerforationPancreatitis: The most severe/significant damage is done by pancreatitis due to local damage and release of destructive enzymes . Fistula formation

Acute Cholecystitis Work Up Vs. Chronic Cholecystitis Work UpChronic = Milder, with the patient seeking diagnostic work up between boutsVSAcute = Guarding, rebound tenderness, severe pain that persists in the RUQ, palpable mass, peritonitis, fever, + Murphy’s Sign (pain that stops a patient from inspiration) and vomiting are present…Patient will need to be hospitalized. Persistent blockage of the cystic duct leads to the clinical signs.

12/2/08

Signs/Symptoms of CholecystitisBiliary colic: RUQ Pain (General/Vague Pain that localizes to the RUQ) NauseaVomitingFatty Meal Provocation: Fatty meals will trigger an episode within 15-20 min. The body cannot pass the fat leading to colic. The episode can last several hoursPalpation/Poking Causes PainDilated Area (may be palpable)

Cholecystitis = Inflammation of gall bladderMost cases of gallbladder inflammation are due to stone obstruction. The duct is acutely blocked, leading to general pain that eventually localizes to the RUQ. Poking the area causes pain. Dilation occurs that leads to palpable areas of obstruction.

Timing of fatty meals and onset of symptoms are key as fatty meals are a trigger. Most symptoms present within 15-20 minutes of fatty meals. Nausea & Vomiting occur in about 75% of people.

Abdominal exam- KUB Most of the time you won’t see a stone & if you do see a stone, it has calcium in it, or it will be a pigmented stone. Pigmented stones cause us to look for other things.

CHOLDOCHOLITHIASISThe LIVER, PANCREAS AND GALLBLADDER are all involved via blockage of the common bile duct. STONE IS THE MOST COMMON REASON FOR BLOCKAGE OF THE COMMON BILDE DUCT.

The stone can even be lodged in the ampulla of Vater, common bile duct, or pancreatic duct. Supersaturation is the mechanism by which the stone enlarges.

Pancreatic tube/duct obstruction occurs due to high pressure. Active contraction by the pancreas pushes the stone into the opening of the duct. The edge of the stone is caught in the tube/duct leading obstruction and inflammation of 3 organs.

Patient presentationPancreatitisCholecystitisHepatitis (all 3 of the above occur due to location of the obstruction)Prominent R Upper Quadrant PainJaundiceMurphy’s Punch +Meals/Eating aggravates

Stone Vs. TumorClassically = Stone is the cause, but tumor can also lead to obstruction. Tumor shows prodrome symptoms initially, as the tumor is not big enough for complete obstruction. Later, tumor growth can trigger full choldocholithiasis as enlargement leads to full obstruction.

Acute Stone PresentationPatients will go to the hospitalA lot of pain and discomfortImaging for source of pain occurs:

Plain film = Doctors will start with plain film.Dx. Ultrasound = Doctors will use Dx Ultrasound if nothing is found on the plain film Contrast studies = Also available (ERTC – flexible Fiber optics & other contrast options)

Management Options LaserLithotripsy/UltrasoundBasket Retrieval *** Stone location is important as management is slightly different based on location ****** The less significant the stone, the more likely they’ll use ultrasound/lithotripsy to shake it lose ****** Cholesterol stones are soft and tend to absorb energy, so ultrasound/lithotripsy may not be a good option. Calcium stones are easier to fracture with sound waves and easier to remove. ***

SurgeryOpen: More recovery time, easier to do due to incision, greater complication rateLaparoscopic: Smaller surgery sites, quicker return home, lower cost, lower complication rate. The procedure is technically more difficult to perform than open surgery.

*** Overhead Pictures – Mercedes Benz Sign ***There is an Y Shape stone on the film. This is called the MERCEDES BENZ SIGN. It is linked with a cholesterol based stone. Overtime, cholesterol stones dehydrate and form the Y shape of Mercedes Benz Sign. A white ringed-cholesterol structure in RUQ with partial lucency and patient stone history are keys to diagnosis. These stones are not completely round. They can have flat edges, called faceting. Faceted gallstones are there for a long time (often years). They acquire flat sides over time.

*** Overhead Pictures – Gallstone Under the Ribs***The stone is too large to appear to move through a tight area. In some cases, unnecessary surgery is done because of the “apparent” fear of migration.

*** AP Lumbar Spine Study – Porcelain Gallbladder ***The gallbladder is evident and it shouldn’t be. This is called Porcelain Gallbladder. PORCELAIN GALLBLADDER IS A REASON FOR SURGERY AND IS CONSIDERED PRE-MALIGNANT. The gallbladder may not be cancerous at the time of removal, but statistics strongly support later malignancy. Prophylactic cholecystectomy should be done.

*** Abdominal Spot Shot -- Close Up of Porcelain Gallbladder ***Calcium is deposited in the wall of the gallbladder. The gallbladder is enlarged in size and is pre-malignant.

*** Abdominal Spot Shot -- Porcelain Gallbladder & TB***Speckled white area next to the spine is the cold abscess of the psoas muscle associated with TB. The patient in this film has TB (cold abscess), porcelain gallbladder, and pathologic compression fracture.

*** Oral Cholecystogram – Before and After Images After Fat Administration***No evidence of stone is present after fat is given.

*** THC Contrast Exam ***A stone is present near the ampulla of Vater. This is choldocholithiasis. Retrograde endoscopic exam may help to further visualize the stone and assist with removal.

Predisposing Conditions for Cholesterol Based GallstonesIncreasing AgeFemale GenderRacial/Ethnic predilection+ Family HistoryObesity/body fat distributionVery rapid weight lossFasting/total parenteral hyper-eliminationHyper estrogen states Medication (oral contraceptives, colfibrate, thiazide diuretics)Small Intestine diseasesHypertriglyceridemiaDyslipoproteinemiasPrimary sclerosing cholangitis

Pathophysiologic Factors in Cholesterol Gallstone FormationSupersaturation of bile with cholesterolImpaired Gallbladder emptyingIncreased nucleating and decreased anti-nucleating proteinsGallbladder mucin

*** DEHYDRATION IS NOT A VALID REASON FOR STONES IN THE GI SYSTEM…Hydration is a reason for stones in the GU system ***

Complications of CholdocholithiasisEmphysematous cholecystitisGallbladder cancerPorcelain GallbladderCholecystolithiasis: This is the most common complication (stones)Calculous Cholecystitis

Surgical RemovalOpen Cholecystectomy: Conventional open cholecsytectomy entails a subcostal midline or transverse abdominal incisionLaparoscopic: More difficult for the surgeon but a number or reports proves much easier for the patient. Minimal post-op pain and decreased chances for adynamic ileus. The patient will also have smaller scars and shorter hospital stay. It is essential that the surgeon be properly trained and experienced in the procedure.Ureteroscope: Endoscopic insertion of a camera with removal tools can help mechanically retrieve the stone, or provide the chance for ultrasound or laser loosening of the stone.

Contraindications for Laparoscopic SurgeryScar tissueEndometriosisPeritonitis

Size of Gallstones(All locations)Variable: Very small (mm or less wide) to centimeters wide (width of a cell phone)

What is our role in cases like this (cholecystitis, cholelithiasis and choldocholithiasis?1. Patient education

a. Predictive variables: What factors influence success…consider the fact that # of surgeons in an area dictates the likelihood for surgery more than clinical need

b. Patient presentation (acute vs. chronic): Should it say or should it go?c. Surgical Choices: Open cholecystectomy versus laparoscopic removald. Chemicals/Drugs can loosen/remove stones but be dangerous to the internal environment of the body

2. Prevention a. Prevention of Further Stones in the patientb. Family/Genetic Susceptibility: Family members of patients with stone disease should know risk factors and

changeable habits to prevent stones in themselves and further stones in the involved family memberc. Prophylactic Removal: . Who benefits from prophylactic removal (Submariners, Morbidly Obese, etc.)d. Liver Flush

HEPATITIS (General Information)*** 2 Papers to read for the exams ***

DefinitionHepatitis is inflammation of the liver.

Causes for Hepatitis There are many causes & reasons for liver inflammation:

A. Viral Hepatitis = Most common reason for inflamed liver (86%).B. Non –Viral Hepatitis = 14% is non-viral hepatitis and is divided amongst bacterial & drug causes (hepatotoxic

drugs).

*** HIV, Cytomegalovirus, Epstein Barr Virus are other viral causes (other than Hepatitis A-E). ***

Silent CarriersThese are silent hepatitis cases or “healthy carriers” that can transfer the disease.

Reportable IllnessHepatitis is a reported illness (to the county and/or state). The reporting is anonymous for the patient. The sole purpose is to identify the source of the illness and people in contact with the source of the illness decreasing the spread of the disease.

Clinical pictureIs essentially the same for all types. All types have a prodromal phase:

Prodromal Phase = Mild, non specific signs and symptoms (malaise, discomfort in the RUQ, pressure over the liver, uneasiness to liver palpation, dull ache, and variable fever).

Lab Tests Lab findings help to identify hepatitis in the prodromal phase. Signs of liver damage can be found with serum transaminase. Late in the prodromal phase viral testing can occur, identifying the specific viral pathogen..

JaundiceJaundice is inclusion criteria as it can be found in about 40% of people. Jaundice does not change your differential list because it is only present 40% of time.

HEPATITIS AThe first form of hepatitis virus found. This form is testable. This form is also famous for ORAL FECAL SPREAD . People who don’t wash their hands after defecation may get hepatitis A. Hepatitis A is a SELF-LIMITING DISEASE that DOES NOT HAVE A CHRONIC STATE. Transplant is not required.

*** Pneumonic: A = Anus (Oral Fecal Spread) ***

We find the body responding with IgM to assist the liver. Clumping occurs when antigen-antibody is present during tests. The faster and greater the clumping occurs, the greater the immune response. We can get immunity from hepatitis A (a patient may get the disease and never contract the disease again based on immunity).

Hepatitis A GROWS ONLY IN LIVER TISSUES. We can’t grow it in Petri dishes unless liver tissue is present. We often find this by STOOL SAMPLE ANALYSIS. We can find it in stool before antigen-antibody clumping in blood.

HEPATITIS BPARENTERALLY SPREAD BY BLOOD. Spread by needles, broken skin, broken glass via breach of the skin. B is considered to be occupational hazard for medical professionals. Hepatitis B vaccine should be taken when there is risk for occupational exposure.

*** Pneumonic: B = Blood ***

Hepatitis B HAS BEEN FOUND OUTSIDE THE LIVER AND IN EVERY BODILY FLUID (tears, sweat, saliva, urine, etc.). Hepatitis B has a CHRONIC FORM and can require patient need for liver transplant.

There is a very strong viral envelope. The envelope takes the bug into cell and allows for replication. Hepatitis B viral envelope introduces hepatitis B virus and hepatitis D into a cell (UNIQUE).

Hepatitis B also has a CARRIER STATE. Carriers continue to produce new generations of viable viruses that spread disease. We need to search these patients out. Presentation can be from mild to very sick. We mostly look for populations exposed by parenteral methods (needle sticks).

HEPATITIS CWas called Non A, Non B hepatitis. We now know that BLOOD TRANSFUSIONS TRANSER HEPATITIS C as WELL AS PARENTERAL MEANS. ½ of C patients get chronic disease. Hepatitis C killed Mickey Mantle (chronic disease).

When we found the disease, we started testing blood banks. These people were treated with gamma globulin booster shots to help them. IN the UK, when they discovered the disease they did nothing. 7 years after the discovery, UK citizens sued their own government (successfully).

Liver transplants are very difficult to spare and to perform. There have to be many matches between donor an recipient for the procedure to even be considered. Not even some fraternal twins meet the criteria to be suitable donors. Hepatitis C is almost a death sentence (due to problems finding a suitable match for liver transplant).

Drug addicts, needle users (shared needles) are now the primary method how C is spread. We don’t’ see much transfusion spread of disease because we test for it. Most + tests of transfusion blood is actually a faulty test rather than actual infection of blood with hepatitis C.

½ of these patients lose their liver. The condition is SLOWLY PROGRESSIVE. They can be asymptomatic for a long time. We need to go searching for these patients (tracking the trail of blood). Hemophiliacs are at risk. Snorting (cocaine, methamphetamine) as well as IV drug use are ways it can be spread. Perirectal veins stretch and can pass the organism through the wall of the anus (homosexuals).

3 Methods of Spread = 1). HOMOSEXUAL MALE SEX 2). IV DRUG USE/NEEDLES 3). SNORTING

HEPATITIS DDOESN’T HAVE A VIRAL ENVELOPE AND CANNOT UNDERGO AN ANTIGEN-ANTIBODY CLUMPING TEST (due to lack of envelope). D is not very invasive by itself and requires co-infection with hepatitis B.

D has a target population different than B. B affects health care employees exposed to blood. D is linked DRUG ADDICTS providing susceptibility to opportunistic infections. Anal intercourse (male homosexual sex) can pass the organism into the bloodstream.

HEPATITIS ETransmitted by ORAL-FECAL ROUTE. The condition is SELF-LIMITTING. Hepatitis E is a world-wide problem. THE MOST FREQUENT FORM OF HEPATITIS WORLD-WIDE IS HEPATITIS E. When we see it in the US, it comes in from other countries (ex. Nepal, India, etc.). Hepatitis E is classically oral fecal, but can be water borne and endemic. Tainted water supply from animal or human waste is the source.

*** Pneumonic: E = Enema ***.

ALCOHOLISM14% of people have alcohol abuse. A good percentage of this show genetic alcoholism expression. The second most common cause of acute pancreatitis is alcoholism and the first most common cause of chronic pancreatitis is alcoholism.

12/8/08

NCADD Fact Sheet: Alcoholism

*** Handout given…Most of the information below is directly from the handout ***They once treated alcoholism with religious and psychological interventions. They thought the dieses was mental/psychological more so than physiological (dependency). We now recognize that the disease is multi-factorial.

Genetics appears to predispose the disease. We once had a 5% success rate, and now we have seen the rate of success increase past 15-20% because of recognition of multi-factorial concerns.

Environment plays a role in alcoholism. It an put off or accelerate the process. It is not causative.Psychosocial: Complex interaction…This is a brain disease

Alcoholism can be progressive and fatal, but doesn’t have to be. WE should be motivated by the fact that it can be fatal. Interventions can be life saving. Continuous or impaired control over drinking is an important part of the puzzle. Most people can have 1 drink and not have a second. These people have 1 drink and then binge. They can’t control the amount consumed.

CostAlcohol costs the nation a lot of money in health care expenses. We have a war on drugs, yet we don’t have a war on alcoholism.

Family ProblemsAlcohol related family problems strike one in every four American homes.

Twin Studies – Genetic LinkTwin Studies provide evidence for genetic transmission of vulnerability to alcoholism

Hospitalized PatientsAbout ¼ of all hospitalized patients have alcoholismSuicideAlcohol is linked to suicide

Population2/3 of the population drinks

Alcohol and Accidents

*** Have a feel for the points made, not the numbers specifically ***

DefinitionNo agreed definition1976 AMA Reference: Chronic progressive and potential fatal disease, characterized by tolerance, physical dependence and/or pathological organ changes as a consequence of alcoholSpectrum of disease20% of patients seeing primary physicians suffer from alcohol abuse and dependenceBest treated as a disease, not a moral issue

At times alcoholics, when approached about their drinking in a stressful situation causes them to drink more. 30/30..For the next 30 days you only get 1 shot of your favorite drink (no more and no less)…The test is to see if they can finish the 30 days with the instructions given. In some cases, they can’t because the first drink will lead to more drinks. They can’t follow the instruction of 1 drink per day.

Example of Comment That an Alcoholic Made“2 things a patient reported they can’t do: Swim and Drink.” – The patient can’t swim and has no urge to get in a pool. The patient can’t drink because of prior alcoholism, yet wants to drink every day.

Risk FactorsIrish, English, French are 4-7 time more likely than Mediterranean descent, Italian, Jewish, Lebanese and TurkishNative Americans have high rate of alcoholism and high rate of abstention alsoAsian American and Pacific Islanders exhibit lower rates versus the United States

African Americans and Hispanics have specific patterns of abuse, but overall rates are in line with US population at largeAlcoholism cuts through all races, ages, genders, classes and occupation. There is no immunity.

Family HistoryVery strong predictor…There is an inherited predisposition

Twin studies support genetic influenceEnvironment: Does play a role (exposure to alcohol sooner can lead to sooner destruction from alcohol)

Sons of alcoholic persons raised by non-drinking adoptive parents have 4x greater risk

The twin in the drinking home discovered alcohol first and had a profile drinking. Genetics trumps environment. Environment does have a role; its role is acceleration of the problem. Whether they express the gene or not, and first contact of alcohol is important.

Antisocial PersonalityAntisocial personality disorder patients are frequent alcoholics (many alcoholics are people pleasers as a rule)Boys with behavioral problems in school are 3 xs more likelyPsychiatric instability, unhappy childhood, depression and anxiety may increase severity of alcoholism, but are not independent risk factors

AgeAs the population ages, we see higher rates of alcoholics and alcoholism in the elderly

OccupationUnemployedAccess at workCoworker pressureMinimal SupervisionHigh Stress Job (Professionals)Lack of routine (writing)Ca be found in any occupation

Telescoping of DiseaseWomen start smoking and drinking later than males; yet demonstrate the disease and symptoms (“catch up”) at the same age as males that start much earlier.

Symptoms Heartburn or GI upsetMorning Cough or headache, with or without nausea and vomitingAnxiety, Tension, and StressInsomniaConcentration of memory deficit

SingsTachycardiaHypertensionTremorPurpura or ecchymosisPalmar ErythemaScars from TraumaGynecomastiaHepatic Enlargement or Abdominal tendernessSpider NeviSensitivity regarding the topic of alcohol

Positive Lab FindingsHyperglycemiaHyperuricemiaMacrocytosisElevated AST level (AST = aspartate aminotransferease)

Elevated HDL-cholesterol level

The body attacks endogenous sources. Uric acid and urea will increase. We take overwhelm the kidneys and produce azotemia.

Quantity and Frequency of DrinkingMost patients accurately reportPeople who abuse under report…They are often not inclined to answer. Sometimes, they’ll get frankly angry or refuse the question altogether.Neither quantity nor frequency is sensitive or specific initiators for alcoholism

Primary Care provider’s Role in Managing Patients with Alcoholism (table in packet)Identify and treat alcoholism as early as possibleIncrease patient motivation with specific feedback about the problems, clear advice to abstain, and persistent follow-up, and an empathic attitudeAdvise alcohol-abusing patients unwilling to abstain to at least reduce their alcohol intake: The alcoholic cannot do this…Abstinence (total abstinence) is the best policy. Match patients to appropriate treatment programs, often in consultation with specialists: This is important to what we can do as chiropractorsIdentify and manage coexistent psychosocial problems: We should be able to find a good person to help them psychosociallyAdvise patients to participate in AA or other relapse prevention programs following treatmentEncourage patients to restructure their lives by developing new habits, new social supports and new community involvementsEnsure continuity of care by scheduling regular follow-up visits, contacting patients after missed appointments, and being receptive and supportive toward relapse patients.

Acting sooner will produce better results. The safe level for alcohol for an alcoholic is zero. Sometimes, these patients are minute to minute, struggling to fight addiction to alcohol.

We now know that there are specific genes that encode for alcoholism. We need to learn more, but we have identified that specific locations on the DNA strings encode for this problem. The condition is similar to other disease (like hemophilia). The genetic predisposition is there, with the DNA creating the predisposition for addiction. We know that treating alcoholism as a disease is much better than treating is as a religious/psychological based problem.

“The only thing you have to change with alcoholism is everything.” – Life changes need to be made.

Criteria for Alcohol Abuse and DependenceAlcohol often taken in larger amounts or over longer period than the person intendedPersistent desire or one or more unsuccessful efforts, to cut down or control alcohol useA great deal of time spent in activities necessary to get alcohol taking the substance or recovering from its effectsFrequent intoxication or withdrawal symptoms when expected to fulfill major role obligations at work, school, or home or when alcohol is physically hazardousImportant social, occupational, or recreational activities given up or reduced because of alcoholContinues alcohol use despite the knowledge of having a persistent or recurrent social, psychological, or physical problem that is caused or exacerbated by the use of the substanceMarked tolerance: Need for markedly increased amounts of the substance in order to achieve intoxication or the desired effect, or markedly diminished effect with continued use of the same amount: Characteristic withdrawal symptomsAlcohol often taken to relieve or avoid withdrawal symptoms

An alcoholic’s liver can handle process and metabolize alcohol very quickly. This is a tolerance issue. Over time, the liver gets burned out. You go from efficiency, to loss of functional capacity. So the tolerance will decrease over time. 5 drinks --- 15 drinks ---- 5 drinks.

Testing involves liver function. Loss of liver function will show quicker effects of alcohol impacting the patient. Sometimes liver function will decline in years (probably within 10-15 years). Liver disease dictates when tolerance is exhausted. It is dependent on the amount of dose given to the liver and in what time frame.

Skinner’s Trauma Scale for AlcoholismSensitivity Specificity

Have you had fractures or dislocation? 88 59Have you ever been injured in a MVA? 59 74Have you injured your head? 85 76Have you been injured in an assault or fight?69 91Have you been injured after drinking 88 93

***Both Skinner’s and Cage questionnaires are non-threatening ways to get information. We can good sensitivity and specificity with the questions ***

Cage QuestionsHave you ever felt you ought to cut down on your drinking?Have people annoyed you by criticizing your drinking?Have you ever felt bad or guilty about your drinking?Have you ever had a drink in the morning (eye opener) to steady your nerves or get rid or a hangover?