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11/10/08

MECKEL’S DIVERTICULUM

Meckel’s vs. Appendictis

Meckel’ s diverticulum involves the small intestine and ileum. The diverticulum is similar functionally to the appendix, which is attached to the cecum. Both Meckel’s Diverticulum and the appendix end in a blind sac. Appendicitis is usually the result of obstruction. IN appendicitis, bacteria reproduce exponentially leading to septicemia and peritonitis. Meckel’s Diverticulum can also hold bacteria, potentially more bacteria can exist and leave Meckel’s Diverticulum than in appendicitis. Meckel’s can have more serious complications.

Rule of 2’s: A). Location is in the last 2 feet of the ileum B). 2% of population has it (whether known or unkown) C). Symptomatic Meckel’s is diagnosed in people over the age of 2

Embryological Development

Meckel’s is a congenital remnant that was once the omphalo-mesenteric duct. It is also called the vitalline duct. It communicates between fetal gut and yolk sac. As the fetus matures, it becomes a cord/ligamentous attachment. The collapse of the ligament may not be complete and can store product. If a patient makes it to adulthood without diagnosis, the sac isn’t a problem. The sac can store secretory by-products in it and is called a “blind sac.”

Meckel’s Signs and Symptoms

Rectal bleeding is the most common sign and symptom. If they make to adult hood the condition is mostly silent. .

Pain can be lower R or L quadrant as the last 2 feet of ileum can be variable (based on malrotation or referred pain).

Radiographic Studies

Angiogram is a good tool to help identify the condition

Dx. Ultrasound can aid our diagnosis

Barium studies show a contrast column/”finger” projection of contrast in the area of the diverticulum.

Surgical vs. Non-SurgicalManagement

Surgical removal is favored in children…Young Children, Obstructed and Bleeding requires removal

VS.

Incidental identification in the adult does not favor surgery.

Surgery can be done laproscopically. Laproscopic removal takes out tissue and stitches the intestine back together. Surgery is often associated with good outcome in children. In adults, they usually leave it alone. Harm can occur with performing surgery in the elderly. The odds are that the diverticulum will be OK in geriatrics throughout the rest of their life (risk to benefit ratio does not favor surgery in geriatrics).

*** Picture on Overhead of Meckel’s ***

Ectopic tissue may cause symptoms. Bleeding is the most significant sign (particularly in pediatrics). Meckel’s may be confused with appendicitis or colonic diverticulitis. IT IS IMPORTANT TO ALWAYS CHECK FOR MECKEL’S DIVERTICULITIS DURING APPENDECTOMY WHEN THE APPENDIX IS FOUND TO BE NORMAL (because of similar presentation). The similar presentation between appendicitis and Meckel’s is periumbilical general pain that localizes. Surgery is scheduled to check the appendix and doctors find nothing wrong with the appendix. Doctors should then check Meckel’s. Aberrant gastric or pancreatic tissue may cause ulceration, leading to either bleeding or a chronic daze due to anemia.

Meckel’s and Rectal Bleedingg

MECKEL’S IS THE #1 CAUSE OF RECTAL BLEEDING IN CHILDREN.

Impact of Meckel’s

Meckel’s is essentially a FAMOUS, FREQUENT CONGENITAL ANOMALY. The condition occurs in about 2% of the population. It is the most common cause of rectal bleeding under 2 years of age. Bleeding is due to ectopic tissue in the diverticulum (gastric or pancreatic tissue). The tissue can produce gastrin and HCl.

CHRONIC MESENTERIC OCCLUSION vs. ACUTE MESENTERIC OCCLUSION

Acute Mesenteric Occlusion

Typically as chiropractors, we won’t run into the acute presentation. The pain is so great that they will go direct to the hospital. These patients need a vascular and GI surgeon. This is usually an atheromatous, embolic event of large vessels. Acute lesions involve large caliber vessels that impact feet of bowel leading to gangrene. Surgery is done to remove and reconnect (anastomose) the segments. The only thing we can do as chiropractors, is to recommend dietary changes to reduce the risk of atheroma formation following patient recovery from surgery.

Chronic Mesenteric Occlusion

We do see the chronic mesenteric population as chiropractors as these patients do not call 911. The typical complaint of chronic presentation is pain. POST PRANDICAL PAIN IS TYPICAL (pain after meals). Post prandial pain is key to making the diagnosis. The timing is predictable with pain within ½ hour after meals. The atheroma produces meaningful occlusion of multiple vessels. Atheroma forms in area of turbulence into smaller tributaries. There can be multiple sites of mild-moderate occlusion.

Great variability in blood flow requirements is present depending on rest vs. digestive states. Most work in the gut and arterial blood flow is done when passing a meal through. Blood supply takes away product from small intestine. At rest (non-digestive states), work load is sufficient and can keep up. Mechanical work increases during meals. Chronic mesenteric occlusion presents when patients do not meet the workload requirements with blood flow. These patients cannot get enough nutrients to the area. Hypoxia develops.

The chief complaint is frequency of problems more so than the intensity. Chronic occlusion is not an embolic event. The diameter is limited and blood flow cannot match demand leading to symptoms.

Complications of Chronic Mesenteric Occlusion

The chronic patient is offered drugs by MD’s (Lipitor and Statins). There is not much scientific support. Additionally, the drugs have complications. There is not much else from a medical standpoint.

As chiropractors, we can offer dietary change and behavior modification. Long standing changes (eating good for life) can be beneficial. There is no downside to conservative care(no complications) vs. medical-drug management (complications). The patient may choose to do both medical and conservative management. Eating better/dietary management is comparable to statin drugs with regards to the outcome

Smaller more frequent meals may also be advised. Some named diets may benefit (South Beach, Mediterranean) chronic mesenteric occlusive patients.

OBSTRUCTIVE LESIONS

High Grade vs. Low Grade

HIGH GRADE OBSTRUCTION ---- CLASSIC SIGNS

1. GRABBING AT THE TRANSVERSE COLON

2. DECREASED BULK of stools

3. INCREASED INTERVAL BETWEEN BOWEL MOVEMENTS

4. Upstream = Fecal material doesn’t move vs. Downstream = Fecal material moves out of the colon

5. CRAMPY, COLICKY PAIN OF UNSATISFIED CONTRACTION (area of obstruction)

6. LACK OF BWEL SOUNDS IN THE AREA OF OBSTRUCTION (does not auscultate in area of obstruction) Vs. Very noisy in area above obstruction (due to stretch stimulation)

7. PALPITORY PAIN IN AREA OF OBSTRUCTION

The bowel dilates and mechanoreceptors (stretch receptors) are stimulated in the area of the obstruction. The signal goes to the cord and reflexive activity occurs. Large stretch simulation ascends to the brain (motor center). The motor center increases parasympathetic tone and peristalsis. (Sphincters are driven by sympathetics). Increased tone, increased frequency of contractions occurs leading to pushing of fecal content into the pile of obstruction. No more fecal content passes the areas of obstruction and we accumulate a lot of material beyond the area of obstruction. We increase peristaltic activity with waves of dilation that packs the fecal content right by the area of obstruction.

The bowel is dilated near physiologic limit at the point of obstruction. We don’t feel or hear bowel sounds. Contraction power is due to cross sectional area. We don’t have motor force and contraction power, so no sounds occur in the area. The abdominal exam shows an overly full area in the area of obstruction (increased in size), that is uncomfortable to probing. Auscultation is quiet in the area. Auscultation above the area is very noisy. Colicky patients show fatigue due to repetitive motions. Once smooth muscle recovers it can recover and continue. The cramping pain gets worse, tails off and later continues.

Worst Case Scenario = High Grade Obstruction

The greatest risk is to the pre-obstructive segment at the point of obstruction, where maximal dilation occurs. Venous engorgement occurs with pressure as veins are subject to the greatest stretch. Venous pressure increases causing no net flow, bowel ischemia, bowel death, and rupture of bowel. Refer them for medical management.

Jejunal Obstruction

In jejunal obstruction, more bowel movements occur as everything below the jejunum clears. We get more nausea and vomiting with jejunal obstruction. The location of obstruction shifts things.

Importance of KUB Exam in Obstruction

We can do an upright KUB exam to get obstruction information. WE can alter compare an upright KUB study to a supine KUB study. We check for multiple air fluid levels to indicate obstruction at multiple levels. Air fluid levels increase during times of static stool. There are 4 common locations for gas to collect:

1). Stomach (Fundal gas bubble is the #1 spot - Meganblaz)

2) Cecum (pooling of product in R lower quadrant – no significance)

3). R Hepatic Flexure on Ascending Colon (gas collects above the flexure)

4). Transverse Colon Side of Splenic Flexure

3 OR MORE AIR FLUID LEVELS IS CONSIDERED ABNORMAL. 3 OR MORE AIR FLUID LEVELS INDICATES HIGH GRADE OBSTRUCTION.

Management of High Grade Obstruction

Get the patient to the hospital.

a). Dx. Ultrasound can be done (safe, quick, in-expensive). Gas disrupts the sound signal. It is also important to remember that 3 or more gas densities may be present. The transverse colon may be palpable and maybe imaged by ultrasound

b). Non-Contrast KUB may be repeated.

c). Spiral CT is very common today and it may take 7 minutes for the exam (we can localize the soft tissue density).

Barium Upper GI is not done (high grade obstruction and you add a non-water soluble product to the system that can really plug the system).

LOW GRADE OBSTRUCTION

Fibrous bands and small tumors constitute low grade obstruction. We have a fixed diameter section. We get narrower diameter stools. The more distal, the more likely the stool is narrow. We can get content through the hole, but it takes longer. We don’ see a big change in fecal bulk, unless there is discomfort (discomfort causes anorexia – loss of apetite). The timing changes. It takes longer to get fecal material past the section. Sigmoid filling is lengthened or offset. Change in bowel habits has occurred.

High grade obstruction shows diminished bulk and increased interval VS. Low grade obstruction shows ALTERED TIMING WITH THE SAME VOLUME. Low grade obstruction shows dilation and discomfort. Waves of peristalsis are driven by stimulation. The peristalsis becomes normal dilation pat the point of obstruction. They are OK till the next meal as the condition starts again. This is a post-prandial problem based on diameter of the intestine. This condition does not show static stool, so air fluid levels do not increase as much as they do in high grade obstructive conditions.

Management

1. Cancer = Treat Cancer

2. Fibrous Bands = Balloon Dilation or Laproscopic management

3. Poop Plug (Big blockage)e = Endoscopic Removal (the endoscope shakes it lose)

4. High fiber diets = Help with Obstruction VS Low Fiber, Highly Refined Diets = Cause Obstruction

List of Obstructive Lesion Causes

1. Functional/Adynamic Ileus (can’t clear a loop of bowel)

2. Sigmoid Cancer

3. Adhesive Peritonitis

4. Volvulus (twisting of an organ)

5. Intususception (bowel telescoping)

6. Tumor from Within (GI cancer)

7. Hernias

HERNIA AND ADHESIONS CONSTITUTE ABOUT 90% OF OBSTRUCTIVE LESIONS. 10% is the remaining categories (cancer, functional adynamic ileus, volvulus, intususception).

A). Adhesion/Adhesive Peritonitis

THE #1 REASON FOR OBSTRUCTION IS ADHESION. We are doing more abdominal surgery today and that is the reason for adhesion in the GI tract. Laproscopic surgery and other minimally invasive techniques have decreased abdominal surgery complication rates and allowed the procedure to be performed with greater frequency. Prescription of early antiobiotics have also helped decrease the complication rates.

Reasons for adhesions can be post-srugical peritnoiits and drug complications. Migraine medication can lead to retroperitoneal fibrosis. A common area for fibrosis is the posterior loop of the GI tract.

B). Hernias

Hernias used to be the #1 reason, but has succumbed to adhesions. We don’t want hernias to migrate or re-migrate. Inguinal, Femoral, Umbilical and prior surgery sites are areas of hernias.

C). Intususception

Intususception in Children

Intususception is more common in kids, particularly newborns. Uncoordinated, hyperdynamic bowels occurs in children. Auerbach’s and Meisner’s function does not develop properly. Watchful waiting occurs in children, waiting for coordination to occur with time. As coordination occurs, the condition doesn’t return.

Intususception in Adults

In adults, we think intususception is DUE TO CANCER FIRST. A pedunculated adenoma or polyp is propulsed forward like fecal material. The tumor is anchored to the wall and drags the wall of the bowel with it, leading to intususception.

We can also have a lyomyoma that thickens the wall, creating a propusible stiffness. Peristaltic waves force the lyomyoma forward through the system leading to intususception.

D). Volvulus

Volvulus occurs due to hyperdynamic contractions with the bowel twisting on itself. Pivot points exist where the twisting occurs. The vitalline duct can be a pivot point for ileal rotation that can lead to both volvulus and fibrous, adhesion formation. Surgery can be done to cut the attachment site, but it can also lead to fibrosus.

In older people (60+), volvulus is an acquired problem (gravity). Gravity causes transverse colon sag. Drooping can lead to bowel twisting on itself (volvulus).

Sigmoid Colon Vs. Cecum

The sigmoid colon is the storage organ for the large intestine. It is the :bladder” of the GI system. Sigmoid colon has the thickest muscular wall and highest pressure in the GI system. Evacuation of the sigmoid requires significant contraction.

The cecum is easy to stretch and has the thinnest wall. The last fluid from the system is removed via the large intestine. The large intestine also removes a lot of fluid from the system.

E). Functional Obstruction/Adynamic Ileus or Bowel/Paralytic Ileus

Motor function is inhibited due to lack of neurological stimulation (reflexive inhibition).

Causes

1. Surgery 2. Perforated Bowel 3. Anesthesia 4. Renal Colic 5. Hepatitius 6. Pancreatitis 7. Diverticulitis 8. Severe Back Pain (back pain leads to avoidance of defecation creating functional obstruction)

People that claim the worst back pain of their life, usually claim poor bowel movements.

Classic Cauda Equina Syndrome

1. Forces them to pee

2. Forces them to hold poop

The classic is opposites: Incontinence (urine) with constipation (fecal over-continence – due to adynamic ileum)

Abdominal Exam with Functional Obstruction

They get normal to modest dilation. The whole length of the intestine is impaired with general anesthesia. In most cases the condition has quiet zones (non-anesthesia cases). The next section after the quiet section is hyperactive as it tries to force more content through. The upstream or downstream segments works more to compensate.

Imaging of Functional Obstruction

1. Working section = no air fluid levels

2. Non-working section = Static Stool with air fluid levels.

Presentation of Functional Obstruction

1. Resolution of Functional Obstruction = Ruptured Viscous (serious condition)

2. Back Pain = Most typical presentation that chiropractors see

3. Cord Injury and Cauda Equina = Contained or not-contained is important to determine. The condition is an emergency situation. Doctors may try steroids first and surgery second

OVERVIEW OF INFLAMMATORY BOWEL DISEASE

1. Ulcerative colitis

2. Crohn’s

3. Whipple’s

CROHN’S

We used to think Crohn’s and Ulcerative colitis was the same thing but different locations. The two are related but not the same. They are both inflammatory conditions that have differences.

CLASSICALLY, CROHN’S IS A MOUTH TO ANUS INFLAMMATORY BOWEL DISEASE. Pharyngeal lesions down to rectal lesions can be present (not typical). CLASSIC CROHN’S AFFECTS THE DISTAL ILEUM (#1) OR CECUM (#2). About 40-45% of the patients also have cecal involvement. The condition is noted as full thickness going deep into tissue with possible perforation of the tissue vs. ulcerative colitis which is affects more shallow tissue and is less destructive.

Crohn’s AKA

1. Crohn’s

2. Regional Iliaitis (Distal Ileum – mostly)

3. Granulomatous Ileocolitis (granulation induced tissue in distal segments ileum and colon).

*** Know all three names for the exam and national boards ***

Diagnosis of Crohn’s

Crohn’s occurs in the 2nd or 3rd decade (peak diagnosis is 2nd and 3rd decades) and without gender bias. The condition is 2-3x more frequent genetically. Young and old can be diagnosed. In the elderly, the condition was mild disease that was unrecognized (missed for numerous years). The complaints are altered bowel habits. Diarrhea and constipation both occur and can alternate. Most transition from normal (periods of remission) to periods of either constipation or diarrhea.

THE CONDITION IS IDIOPATHIC. MILK IS A TRIGGER OF CROHN’S, BUT NOT A CAUSE. Milk and dairy avoidance can help treat the condition. The condition has been described as autoimmune with milk/dairy products as an irritant.

11/11/08

*** Review of Test 3 ***

*** Common Questions Wrong (If you got the 4 Commonly Missed Questions on the past exam you got credit ***

Skip Lesion

Crohn’s classically shows skip lesions. The lesions can skip from one location to another, bypassing a region of the GI tract.

Viral Theory

A current theory notes a genetic predisposition with a viral trigger. The theory is hard to prove or disprove.

Patient Presentation

Most patients have a mild course of disease that is explained away as “GI Flu.” Mis-diagnosis as a common feature. The duration shows periods of time where the condition is normal, periods of times with constipation, and periods with diarrhea. The more serious the condition, the greater the time periods of altered bowel movements (altered bowel movements = periods of time between diarrhea and consitpation). The condition can go to remission for months to years (up to 2 years). There is NO CURE FOR THIS CONDITION.

IBS VS. Crohn’s

IBS is 2x more likely than Crohn’s. IBS is way more manageable than Crohn’s. We can test them as chiropractors to differentiate between the two. We can give them a chance to succeed via some common sense advice.

Management Advice

We can immediately offer dietary advice. We don’t understand what causes Crohn’s, but we do know triggers. A TRIGGER IS DAIRY PRODUCTS/MILK. Suggest don’t drink milk. Have them try soy milk.

Contrast Exam

There is normal tissue ---- narrowing and stricture ----- normal tissue ------ narrowing and stricture…This presentation indicates skip lesions that literally skip over areas of the GI tract.

Weight Loss and Surface Area

Surface loss by small intestine induces weight loss. Crohn’s mostly targets small intestine, our best source of caloric uptake. We need to recommend MORE FREQUENT MEALS WITH DENSER FOODS (TO GET MORE CALORIES).

Retrograde Endoscopic Exam

Retrograde endoscopic exam can sow ulceration of the cecum (40% of patients with Crohn’s) and check the ileocecal vavle. Retrograde is easier to perform than Anterograde exam.

Endoscopic Exam and Contrast Exam

It is not uncommon to have both contrast exam and endoscopic exam. Contrast is quick, cheap and easy to perform. It has lots of pros. It can show evidence of skip lesions. We can check for abnormal communication. Crohn’s shows fistula formation. The fistulas are abnormal channels that fill with contrast. These channels can be missed with endoscope because they are too small.

Physical Signs of Fistulas

Fecal smelling vaginal or urinal discharge may indicate fistula formation. Contrast study should be ordered if fistula formation is suspected. Fistulas happen due to full thickness damage induced by Crohn’s. Contrast exam is the best way to check for fistulas. Surgical management is required for fitstulas.

Treatment for Crohn’s

Treatment for Crohn’s is drug management (corticosteroids) to suppress the immune response. Surgery for fistulas is not done unless necessary. Years ago, they snipped the damaged bowel out and found it became a new source of Crohn’s lesions. We don’t take out bowel unless gangrenous or fistulas form. Drug management is about 40% successful in managing the condition (2x what the placebo is).

In chiropractic, we claim 40% to 50% success rate with acupuncture and SMT as our chief treatment. There is no one good therapy. You can treat them between bouts of steroid therapy with conservative care. he literature is inconclusive regarding auriculotherapy to treat Crohn’s. It may not harm the patient, but may not help them. If you do get close to 40% success, you are doing as good as medial therapy without side effects.

LAY OFF THE HIGH FIBER DIETS. Raw fruits, vegetables, and wheat products are insolubles that block the absorption site. Bulking agents increase stimulation setting up rapid export out of the system. Waves of peristalsis occur and speeds up removal leading to greater malabsorption

Significant absorptive problems occur with loss of greater than 25% of the small intestine. We need to up the intake of vitamins (particularly the fat soluble) and minerals. We offer them smaller more frequent meals and supplementation. Frequent small-moderate doses of supplements can help them gain nutrients. Vit B12 can be very beneficial.

These patients are notorious stone formers. The composition is often calcium oxalate. Inflammatory bowel diseases often show calcium oxalate stones forming in either or both GI and GU. We try to reduce oxalate foods by diet (rhubarb, Swiss chard, green leafy vegetables, etc.). Have them take Calcium Gluconate (OScal) which binds dietary oxalates to be pooped away, rather than excreted through the urinary system.)

*** Crohn’s (Pictures on Overhead) ***

a). Perforation can causes abscess due to leaky content.

b). Peritonitis can be a consequence of rupture.

c). Fistula = Can link any hollow organ

d). Perianal Abscess: The abscess can grow and cause discomfort

e). Cobblestoning is present and occurs in Crohn’s

ULCERATIVE COLITIS

Clinical Features of Ulcerative Colitis

Most prominent feature = BLOOD IN STOOL AND DIARRHEA

Mild Disease

More than half of patients have mild disease. The chief symptom is rectal bleeding. Diarrhea may or may not be present. Systemic Symptoms are usually absent. The patent does not have to have systemic symptoms when they transition to moderate disease

The condition is usually written off as a hemorrhoid. The condition is explained away, improperly. True hemorrhoid diagnosis requires palpation.

Moderate Diseae

This is characterized by significant diarrhea. Usually four to six loose bloody bowel movements per day. Abdominal cramps may occur and often relieved by defecation.

Severe or Fulminant Disease

1. High Fever (101-103)

2. Dehydration

3. Pallor

4. LBP (due to frequent blood loss)….These patients may need transfusions due to blood loss.

5. Tachycardia

6. Ten or more bowel movements (often markedly bloody) per day (often 30-40 bloody loose stools)

Lab Findings: Leukocytosis, Anemia, Hypoalbuminemia

We try to improve quality of life for Ulcerative Colitis patients. Have them use a bede. The bede can be used during exacerbation periods. Warm water and Cetaphil (soap) or tearless shampoo (Baby Shampoo) can be used to keep good hygiene. THERE IS NO CURE, JUST MANAGEMENT ADVICE.

Involvement of Other Areas (a feature of Ulcerative Colitis)

Eyes: Iritis, Episcleritis,

Liver: Percholangitis, Sclerosing Cholangitis, Fatty infiltration, Chronic Active Hepatitis, Bile Duct Carcinoma, Pyogenic Liver Abscess

Blood: Iron deficiency anemia

Joints: Peripheral arthropathy acro-ilitis, Ankylosing Spondylitis , Enteropathic Arthritis (due to Crohn’s, UC or Whipple’s)

Skin: Erythema Nodosum, Pyoderma Gangrenosum, Necrotizing Cutaneous Vasculitis

Other

Major Complications of Ulcerative Colitis

Toxic Megacolon = The colon is enlarged. Dilation of the colon, thins the vein and causes chance of migration of pathogen leading to septicemia. There is a 40% mortality rate with toxic megacolon.

Stricture: 5% have stricture. It starts as low grade obstruction and progresses to stricture.

Massive Hemorrhage: About 4%. They bleed profusely from rectum. They may need blood transfusion.

Perforation: Colonic perforation can occur with or without megacolon. It is usually associated with colitis and is more common during first attacks (15%).

Carcinoma: Risk increases with duration of illness. Less than 10 years shows negligible risk vs. over 20 years shows increased risk for adenocarcinoma.

Endoscopic Studies Contrasting Crohns and UC

Characteristics UC Crohns

Distribution Symmetric Asymmetric

Continuous Involvement Always Exceptional

Rectal Involvmente Always Usually Absent

Vessel Appearance Blunted Freqenty Normal

Magins Absent

Friability Often Present Infrequent

Erythema Often Present less Frequent

Spontanoues Petechiae Often Present Infrequent

Profuse Bleeding Common Infrequent

Apthous Ulcers Rare Freqnet

Linear Ulcers Rare Frequent

Serpingous Ulcers Rare Frequent

Deep Long. Ulcers Rare Frequent

Cobblestoning Rare Frequent

Mucosa Surrounding Ulcers Abnormal Frequent Normal

Pseudopolyps Frequent Frequent

Briding Occasional Occasional

Pain Occasional Frequent

Vomiting Rare Often

Diarrhea Frequent Frequent

Bloody Common Uncommon

Tenesmus Common Uncommon

Weight Loss Minimal Frequent

Anal Fissures Occasional Frequent

Perianal Fistuals Rare Frequent

Palpable Adbominal Mass Rare Frequent

Clubbing Rare Frequent

Hemorrhage Frequent Occasional

Sclerosing Cholangitis Increased Rare

Cholelithiasis No Increase Increased

Nephrolithiasis No Increase Increased

*** ULCERATIVE COLIITS DOES NOT CAUSE MANY ULCERS VS. CROHN’S WICH CAUSES MANY TYPES OF ULCERS ***

*** UC on Overhead Pictures***

Contrast study shows flat and shallow craters

Complicaitons of UC

Bleeding, carcinoma, adhesions, diarrhea & Systemic complications (Polyarticular arthropathy that doesn’t go away)

APPENDICITIS

Periumbilical pain is the chief complaint with the patient circling the belly button with their hand. The vermiform appendix is the source of the problem. Obstruction causes increased bacteria produced. Transient R Lower Quadrant pain may resolve. The stone may be force back into the lumen or may rupture the appendix. There is no reliable way to predict which of the two will happen, so they need diagnostic workup.

*** Lateral Lumbar Film ***

Free communication with cecum exchanges material and limits bacteria proliferation. If the appendix is plugged, bacteria overgrowth occurs.

*** AP Pelvis X-ray ***

There is a stone in the pelvic bowl (RLQ). The patient reports pain in RLQ that eventually localizes, increased temperature, sweating, diarrhea or constipation and rebound tenderness. They don’t poop. Hard, dried stool forced into the opening of the appendix (appendicolith). The condition is called fecalith in the small intestine. History, plain film study, Dx. Ultrasound and Helical CT can help make the diagnosis.

Ruptured Appendix

Even if the patient feels better (pain goes away) they should go to emergency room (the appendix could have ruptured). If we wait, lethal choices could present. They should go to emergency room for Dx. Ultrasound. You must tell them you can’t wait at home! Document the conversation with the patient.

IBS

Chronic or recurrent GI symptoms (attributed to pharynx, esophagus, stomach, biliary tree, small or large intestine or anorectum) not explained by structural or biochemical abnormalities.

IBS was often the dumping ground and a dismissive diagnosis. We later set more rigid standards for IBS diagnosis. Examination and testing must be done with diagnosis now made by exclusion of other disease. The nervous system can be implicated leading to IBS.

IBS Slides

Chronic or recurrent

Lower abdominal pain

Disturbed Defecation

Bloating: Tissue is thickened when compared to normal people

Not explained by structural or known biochemical abnormalities

Prevalence

12% of Primary Care Practice (IBS)

28% of GI Specialist (IBS)…(IBS is different from IBD)

IBD is 14% (Inflammatory bowel disease is worse than IBS)

Peptic Ulcer 21% and declining

Liver 10%

Other Functional problem 13%

Effects of Stress

Abdominal Pain: Over 60% of IBS patients report GI pain….Over 40% of patients report pain as normals

Bowel Dysfunction: Over 80% of IBS report dysfunction…Over 60% of normals report dysfunction

Pain Tolerance

Colonic Distention: Greater pain reported with IBS than normals

Ice Water Immersion: NO statistically different response to painful stimulus (between normals and IBS)

Integration

Pathophysiology is recognized and explainable. There is a definitive neurophysiological process associated. This is a parasympathetically driven process during diarrhea. Diarrhea with mucus/sputum causes us to consider IBS over IBD. IBD shows destruction of the wall and reduction of mucus secretion on the membrane.

11/17/08

Paris-Rome Criteria of 1990

Led to categorization of IBS.

IBS Conceptual Model

Early Life: Genetics and Environment

Psychosocial Factors: Life Stress, Psychologic state, Coping, Social Support

Physiology: Motility

IBS Psychosocial

Stress exacerbates symptoms: No biochemical abnormality and no structural abnormality are present. We can have a significant role in diagnosis and management of the condition. Medial therapies may not be effective and if so come with complications. Behavioral management is something we can do as chiropractors to help these patients.

Known stress triggers for IBS are loss of loved ones and severe physical and psychological stress. Managing stress becomes important in treating the condition. People diagnosed with IBS have greater linkages between life events and stressors affirming the connection between stress and IBS.

Psychosocial factors affect outcome = If things get better, they’ll get better and if worse, they’ll get worse

IBS Treatment Approach

Education/Reassurance

Identify and adjust subluxations

Body Wall Reflex work

Treatment List

#9. Referral for Pain Management: There can be significant pain, so much so that you may think organic disease. We should be doing enough testing to check for anatomic defect and/or biochemical abnormality. We can help manage pain very simplify. A simple tool to help pain management is exercise. There has been great success with just simple exercise like walking around the local park.

#8 Antidepressants: Physical activity may be a better option.

#7 Focus on health, not illness: We are better equipped to do this than other practitioners

#6 Set realistic goals: Realistic goals particularly with lifestyle changes, weight loss and exercise is important to keep the patient motivated.

#5 Psychological Treatments: One of the most effective treatments for IBS

#4 Pharmacotherapy: Very high on the hierarchy (fast and convenient) for primary care MD’s and gastroenterologists…It should be lower on the list

#3 Monitoring and modification

#2 Dietary Modifications: In IBD we focus on milk elimination, enzyme deficiency, sensitivity and dietary modifications are important. IN IBS, dietary modifications can help, but there is not overwhelming evidence that food is a trigger. In fact, food may create psychosocial problems more than actual physiological problems. If so, eliminate the food to see if the condition decreases.

#1 Education/Reassurance: We should be suspicious if a patient is diagnosed with IBS or IBD upon the first visit. A single visit cannot separate IBS from IBD as testing must be done. IBS is very manageable (no disease of bowel and no change in biochemistry = it is good news!)….IBD may not be such a good thing for the patient. Many – tests can lead to the diagnosis of IBS. (Ex. Colonoscoopy will be – and not find polyps, tumors…leading to IBS diagnosis).

IBS Psychotherapy – Interpersonal Treatment

Interpersonal treatment superior to medical treatment for reducing:

Diarrhea

Abdominal Pain

MD visits

Anxiety/Depression

Bowel Symptom Improvement parallels psychological improvement

We think patients can literally talk themselves into an IBS state.

MALABSOPRTION/MAL-ABSORPTIVE STATES

General Information

There are many conditions leading to malabsorption. Global or local based problems can lead to mal-absorptive states. Disturbance in digestion, proper uptake, loss of surface area of the SI can all lead to the problem.

Causes of Malabsorption

1. IntraluminalHydrolysis = Seen in patients that lack bile. Cholecystectomy patients that eat fatty meals lack bile salts. Lack of bile salts impacts fat digestion. They shoow steatorheaa (diarrhea due to lack of lipid breakdown)

2. Disease of Gallbladder= Gallbladder is present but the salts are not normal or not capable of emulsifying. There is lack of bio-availability.

3.Pancreas Problems = Disease of the pancreas leads to histological change. Alcoholics are at greater risk for this.

4. Alcoholics= Alcoholism can lead to mal-absorption problems.

5.Bacteria = Decreased bacterial numbers may lead to lack of available nutrients. Balance is important (proper amount of bacteria in the correct location)…There are people that eat anything they want and don’t gain weight. The person that eats a lot may be in a mal-absorptive state because of lack of normal colonies and lack of bioavailability requiring them to consume more calories to get the proper amount of nutrients.

6. Mucosal Cell Abnormalities = Can lead to mal-absorption. This type typically misses an enzyme (like dissacharidase in lactose intolerance.) There are strong genetic linkages.

7.Inflammatory Bowel Disease = Whipple’s, Crohn’s, Celiac are examples. Inflammatory conditions can also lead to enteropathic arthritis (multi-joint arthritis that doesn’t go away)

8. Lymphatic Obstruction = Can lead to mal-absorption. The abdomen is a rich, lymph area. Leaky vessels lead to proteins not returning to the lymph system. Proteins stay in the wall in the small intestine. Edema forms forms in the wall of the small intestine due to attractions with proteins. We see decreased absorption in sections of the bowel. Edema prevents the uptake of calories and nutrients.

9. Short Bowel Syndrome = Acquired conditions. Loss of surface area for uptake occurs. The person must eat several small meals a day with higher caloric intake and less complex meals to get calories and nutrients

10. Tropic Sprue= Recent infection in a tropical area is the history.

11. Colonics = High colonics (forcing content back across the IC valve) can lead to mal-absorptive issues.

12. Abuse of Home Remedies and Over the Counter Products = Stringent diets as well as abuse of home remedies/over the counter products can lead to mal-absorption issues. Laxatives and colonics can make the patient ill.

Mal-absorptive States & Fecal Content

Abnormality in fecal make-up occurs. Check fecal content/use fecal analysis to identify the cause of the mal-absorptive states. Examples:

1. Lactose intolerant = May show abnormal test of high twin sugars in fecal matter.

2. Post-cholecystectomy = Patients show overwhelming of the liver during high fat meals. You’ll see high fecal content of lipids (steatorhea). Normal fecal material is denser than water. Normal feces sinks quickly vs. steatorhea, which actually floats in the toilet and does not sink. This is a cheap quick way to look for steatorheaa.

3. Iron deficiency anemia = High iron count in feces.

Supplementation

The story is to supplement what you lack to help with the mal-absorptive state.

3 M/C Causes of Mal-Absorptive States

1. Crohn’s

2. Chronic Pancreatitis

3. Celiac Sprue/Non-Tropical Sprue/Celiac Disease

Less Common Causes

Whipple’s, Diverticulitis, Dissacharidase Deficiency, Tropical Sprue

CELIAC DISEASE/CELIAC SPRUE/NON-TROPICAL SPRUE

Celiac disease is a digestive disease that damages the small intestine and interferes with absorption of nutrients from food. People who have celiac disease cannot tolerate a protein called gluten. Gluten is found in wheat, rye, barley, and possibly oats. When people with celiac disease eat foods containing gluten, their immune system responds damaging the small intestine. Specifically, tiny fingerlike protrusions, called villi, on the lining of the small intestine are lost during the disease. Nutrients from food are absorbed into the bloodstream through villi. Without villi, a person becomes malnourished – regardless of the quantity of food eaten.

Symptoms

Recurring abdominal bloating and pain

Chronic Diarrhea

Weight Loss

Pale, Foul-Smelling Stool

Unexplained Anemia (lack of absorption)

Bone pain

Behavior changes

Muscle Cramps

Fatigue

Delayed Growth: Can be lethal when younger

Failure to Thrive

Pain in joints

Seizures,

Tingling numbness in legs (nerve damage)

Pale sores inside the mouth (apthous ulcers)

Painful skin rash – dermatitis

What is Celiac Disease

Celiac disease is considered autoimmune disorder as well as a disease of mal-absorption because nutrients are not absorbed. Celiac disease is also known as celiac sprue, non-tropical sprue and gluten sensitive enteropathy. Celiac disease is genetic disease sometimes triggered for the first time after surgery, pregnancy, childbirth, viral infection or severe emotional stress.

What Are the Symptoms?

Celiac disease affects people differently. Some people develop symptoms as children, others as adults. Often diarrhea is the first to present.

The body makes antibodies to gluten. The antibodies are anti-gliandin, anti-endomysium, and anti-reticulin. Serum testing determines the diagnosis. If the tests and symptoms suggest celiac disease, the physician may remove a tiny piece of tissue from the small intestine (biopsy) to check for damage to the villi. THE GOLD STANDARD IS ENDOSCOPY WITH BIOPSY TESTING.

11/18/08

Screening for Celiac Disease

Screening for celiac disease involves testing asymptomatic people for the antibodies to gluten in serum. If the antibody tests come back +, removal of a tiny piece of small intestine tissue is the next step (biopsy). Americans are not routinely screened for celiac disease. Consider that celiac disease is hereditary.

Gluten Diets

Gluten Free Diets can be very helpful for people with Celiac Disease. Thickening agents (things that make things sticky), boxed products, wheat based products all contain gluten. Meats (not prepared meat), fruits, vegetables all appear fairly safe.

*** Articles on Celiac Disease in Test #4 Folder ***

Italians

Celiac disease is common to Italians. In Italy, all children are screened by age 6 so that even asymptomatic disease is caught early. Additionally, Italians of any age are tested for the disease as soon as they show symptoms. As a result of this vigilance, the time between symptom onset and disease diagnosis is only 2 to 3 weeks. In the US, the time between first symptoms and diagnosis averages about 10 years.

Treatment

Gluten-free diet is a lifetime requirement. Eating any gluten, no matter how small can have an affect.

How Common is the Disease

We don’t know, because we don’t test for it (the people we find, have the problem for many years)…Celiac disease is the most common genetic disease in Europe. In Italy about 1 in 250 and in Ireland about 1 in 300 people have celiac disease. It is rarely diagnosed in Africans, Chinese and Japanese people. Estimated 1 in 4,700 Americans may have, but the number may not be credible as we don’t test for it.

Points to Remember

People with celiac disease cannot tolerate gluten, a protein in wheat, rye, barley and possibly oats

Celiac disease damages the small intestine and interferes with nutrient absorption

Treatment is important because people with celiac disease could develop complicates like cancer, diabetes, etc.

TROPICAL SPRUE

Need to have been to tropical area for diagnosis to be made

DISSARCHARIDASE DEFICIENCY

The condition may be genetically linked. Northern and Western Europeans have a 10-15% incidence of dissacharidase deficiency. Mediterraneans, Asians, Blacks can show populations as high as 70-80% lactose intolerant. The message is to know your community and know who you are treating.

History, physical exam and diagnostic testing help make the diagnosis. Management includes not eating foods with disssacharidases. They can drink titrated milk (Lactaid) or eliminate milk altogether. There are supplements available that hope to use gastric emptying delay time and available enzyme to decrease symptoms

Typical presentation shows is cramping pain, flatulence and diarrhea. In adults, we particularly need to check for underlying disease.

Eliminate the twin sugar via elimination diet. Further management involves patient education. Testing is expensive. Elimination diets are cheaper and effective to help make the diagnosis and provide treatment.

WHIPPLE’S

Whipple’s is both an inflammatory bowel disease and a cause of enteropathic arthritis. This condition is in 3rd place as a cause for enteropathic arthritis (following Ulcerative Colitis and Crohn’s). Whipple’s has gender bias towards elderly, Caucasian men. Diarrhea can be severe. Whipple’s patient’s can also get lipodystrophy.

Proper management is antibiotic therapy (tetracycline). We think the condition is bacteria based, but we don’t know the specific bacteria.

APPENDICITIS

Presents just like Meckel’s Diverticulitis. The big difference between the two presentations is location. Appendicitis hangs off the cecum (R Lower) and Meckel’s Diverticulum is in the distal couple feet of the ileum (typically). Otherwise, peri-umbilical pain that localizes, diarrhea followed by constipation, fever, rebound tenderness, spikes in white cells are all indicators of the disease.

Another difference in presentation is where they point. Acute abdominal pain is appendicitis until proven otherwise in R lower quadrant. You try to identify the condition before it bursts or pressure builds so high it spits the stone. We can’t predict which patient will rupture or which patient will regurgitate back into the cecum.

Appendicitis is filled with bacteria and with pus. Explosion of content can lead to abscess formation and peritonitis. The most common serious complication is abscess formation.

Radiographic Exams

Abscess formation visible on KUB exam indicates huge accumulation of fluids and material. Ultrasound may find it in the bladder or midline structures. Gas or loops of bowel probably won’t show the condition of appendicitis because ultrasound is impacted by air. CT (Spiral CT) is a good choice. MRI is coming into play to show the appendicitis (must be 3 Tesla or higher and a fast MRI). MRI is also very expensive.

They now tag WBC with radionucleotides . We take blood, spin it down, tag it with radioactive material, injecting them back into the body. We check for a hot spot on the film. If no abscess, uniform dispersion of the material would occur. Concentrated hot spots in the appendix indicates abscess formation.

Overall, there is no 1 agreed upon way to find abscess.

GASTROENTERITIS

A key finding is fluid loss and electrolyte imbalance. Gatorade and Pedilyte can help restore electrolyte and fluid loads to the body. Other key findings are: irritable stomach, delay of emptying with proteins and fats, prolonged HCL elevation, vomiting, and diarrhea. Ask the patients to stay away from raw fruits and vegetables. Mechanical stretch from fruits and vegetables can enhance the diarrhea phase. The condition can last a couple of days.

COMBINATION OF UPPER GI PAIN WITH DIARRHEA = GASTROENTERITIS

The kidneys are more vulnerable during gastroenteritis because of lack of surface volume

Examples of More Famous Versions of Gastroenteritis

1. Cholera: Seen typically in poor areas of Asia, Middle East and Africa. We have good water sources in the US, whereas in the other parts of the world water settles and can contract bacteria. There is high morbidity and mortality, directed related to electrolyte imbalance and dehydration. Cholera has profuse and frequent vomiting and diarrhea. Cholera patients evacuate fluid loads from both ends. Management involves restoring the ratio of fluid volume and electrolyte imbalance. In the US, cholera comes in from other countries. Normally, cholera is (not much of a problem here. Morbidity and mortality can occur from cholera .

2. E. Coli: Spinach, tomatoes, lettuce, hamburgers and other foods may contain levels of E. Coli. Untreated water is often used on farms allowing bacteria to spread into the food supply.

a. Traveler’s Diarrhea: A form of E. Coli linked to travel. It usually lasts for 3 days and is not particularly hard on people. The condition is often self limiting. Nothing has to be done for the patient, as the condition passes with time. Over the counter remedies may also be tried.

b. Nursery Diarrhea: Lethal complications can occur with children. It is often a new organism to their system. Epidemic numbers occur in daycare and nursery settings. 13 is the key number for a nursery to have an epidemic level. County and state systems are alerted at 9 with 13 to classify as epidemic. The sooner we begin looking for the source, the sooner we cut it off and sooner people get better. We can get federal and state money from the epidemic classification. Increased alert, quick reporting, looking for the cause, and financial assistance comes with government help. Nursery diarrhea is spread by contact. The condition is spread due to breakdown in controls (improper glove use, infrequent changing), spread from kid to kid by attendants.

3. Staph Food Poisoning: One of the most common causes of food poisoning is staph. Custard and processed meats and fish are common sources. Labor Day is the #1 day for food poisoning, with Memorial Day #2. We think warm weather holidays are linked to staph spread. We see a spike after Thanksgiving. Custard is made by cultureable media. Leaving the meat out, or cutting on a cutting board infected with staph are other sources of infection. The most spectacular feature is the exotoxin. The toxin is a neurotoxin, stimulating the vomiting center of the brain directly. This patient tends to vomit violently even after the stomach is empty (VIOLENT RETCH). Vomiting does not grant relief. They throw up over and over. Rib damage, costochondral cartilage damage and costal muscle strain can occur form violent vomiting.

4. Botulism: Botulism has a nastry neurotoxin. Botulism causes the D’s (Diplopia, Dysphagia, Dysphonia).Trouble speaking, swallowing, double vision occur. The organism can directly attack the phrenic nerve and cause respiratory problems. Botulism is a rare cause of gastroenteritis. There are some examples in poorer areas of the United States due to canning. The worst complication is respiratory distress.

5. Salmonella: Poultry is linked to the salmonella. Salmonella is a common form of food poisoning. Patients can be tested + and deny symptoms indicating low grade exposure with asymptomatic presentation. Not everyone gets sick as a consequence of exposure. Blood testing is not useful here. Fecal analysis is the path to the proper diagnosis of salmonella. Salmonella food poisoning has been associated with septic arthritis. Immuno-compromised patients or patients with sickle cell anemia are more likely to get septic arthritis. Overall, salmonella is a self limiting condition. Gut rupture of the chicken during slaughter lets salmonella out. Chicken coups contain mass large numbers of chickens in a small area leading to spread of the bacteria. The more food that you eat with salmonella, the more bacteria goes into your system. Overall, it is unusual for food poisoning to hit within 2 hours. By 6-8 hours, there can be enough organism load to create disease levels.

6. Viral Origin (Montezuma’s Revenge): The virus is an irritant. The virus replicates and becomes sited within the stomach (showing gastric problems), small intestine (mal-absorption), large intestine (profuse diarrhea). Electrolyte and water loss tends to be the biggest problems with infants and elderly at greatest risk.

7. Miscellaneous: Mushrooms, Poisons, House Plants (a problem for kids), Animals

CONGENITAL MALROTATION OF THE COLON

In some patients, the colon may not have rotated to the correct position. For example, the cecum can end up under the liver. Mal-rotation (incomplete rotation) changes the location of presenting signs and symptoms

HIRSCHSPRUNG’S/AGANGLIONIC MEGACOLON

The condition shows a portion that cannot dilate, acting as low grade obstruction. Early on dilation forces material through the narrowing. Adding bulk to the diet makes the problem more painful (after age 1). After age 1, fecal bulk increases and they dam up. They show colicky pain with unsatisfied contraction.

Lack of development of Meissner’s and Auerbach’s is the core of the problem. Endoscopic biopsy helps answer the question. Surgical removal may be necessary to remove necrosed tissue. Watchful waiting may occur in less serious situations.

The abnormal part is the narrow part, NOT THE LARGE PART. The only fix is surgical removal with re-anastomosis, otherwise the child fails to thrive. Surgical decision is based on endoscopy with biopsy that documents quantity and quality of nervous tissue.

DIVERTICULOSIS/DIVERTICULITIS

An out pocket in the small intestine or large intestine. The sigmoid is the most common area for diverticulosis and diverticulitis. The GI system stores material in the sigmoid colon. Stool becomes more viscous and takes up the shape of the sigmoid colon. Firmer, more dry stool requires powerful contractions to move forward. The sigmoid’s contraction can be very strong to push firm, dry stool out.

Herniation of mucosal tissue through the mucosal wall can also lead to diverticulum formation. Herniations occur as a direct result of peristaltic activity. Highly processed diets lack fiber and show low pliability, high viscosity and greater pressure to evacuate fecal material from the sigmoid. Greater pressures can lead to herniation of mucosal tissue. . A fiber poor diet can force normal mucosal tissue through the muscular wall.

Diverticulosis vs. ITIS

-ITIS is inflamed diverticulum. We go from osis to itis because of obstruction. Sigmoid diverticulum is smaller than the appendix diverticulum. It is often termed “size of a tear drop.”

Contrast exam can show the diverticulum. We force contrast in checking for emptying (emptying is based on fiber). Fiber poor diets may show residual contrast for weeks. Often seeds (kiwi, raspberry seeds, popcorn kernels, strawberry seeds) and shells (peanuts, walnuts, etc.) can get stuck and be irritants.

Presentation

Living tissue taps into local blood supply and shows dilation. It is possible to have a single diverticulum get enlarged, but often several plug up at the same time with bacterial growth causing the inflammatory process. The level of pain is high (8/10) with pain lasting hours to days. The pain may be so great that the patient may need to go to the hospital.

Classically, L lower pain syndrome is present. #1 on the list of L lower pain syndrome is diverticultis. Testing is by KUB, Barium Enema, Spiral CT with vascular contrast, or ultrasound (decent option).

Treatment

Patients may go to the hospital during acute episodes. One of the bad things that can happen is dissection. Inflammation in multiple diverticulum can destabilize the layers of tissue leading to separation. The lumen collapses on itself causing loss of blood supply. Removal of some length of sigmoid colon is necessary and is a surgical emergency. Another complication is gangrenous necrosis (dead bowel).

Diverticulitis

1st step = Make sure they are safe

2nd step = IV antibiotics (if necessary)

3rd step = When they are home, educate them about the condition, prevention and diet. The condition is acquired, not congenital. Pressure works against the mucosal tissue due to peristalsis. Potent peristaltic activity occurs in the muscular sigmoid colon. We often see this in patients with fiber poor diets (eating highly refined foods). We need to change the diet (add more fiber). In the elderly, we should incrementally add fiber to the diet. You can create high grade obstruction if you don’t control the increase of fiber. Changes should occur over 2-4 weeks fiber fiber poor to fiber rich diet . Diverticulitis shows over-proliferation of bacteria (due to blocked communication). Keeping the openings open through addition of bulking agents, dilating the colon and increasing the size of the osteums allows for exchange.

Medical management

They do nothing regarding prevention. They wait for it to happen again and then want to intervene quickly. As chiropractors, we can offer preventative strategies. At 6-8 weeks, you can offer bran products for fiber instead of supplements. As they learn, replace with a greater variety of bulking agents. Use Citracil and Metamucil early on, because they help control the amount of bulk and later progress to bran products to add bulk.

Complications

Peritonitis is the most common result of rupture in the abdomen and ruptured diverticulum.

*** X-ray of Ruptured Diverticulum – TEST QUESTION ***

Below diaphragm on R, we can’t tell where liver ends and the diaphragm begins. Free air between liver and the diaphragm, think ruptured diverticulum (most likely).

POLYPOSIS SYNDROMES

5 FAMOUS VARIETIES

1. Familial Polyposis: A lethal form of the disease with very high malignant potential. They say you will get carcinoma. Carcinoma is limited to the colorectal area. High concentration of large polyps in colorectal area with family members with same condition = Familial Polyposis till proven otherwise. Removal is the best course of action. They may even wan to resect the part of the GI tract.

2.Gardner’s Syndrome: Osteomas in the frontal sinus, fibromas in the abdomen and multisystem problems are linked to Gardner’s Syndrome. The lesions are typically benign. We must consider polyps with osteoma identification. Gardner’s syndrome has highly malignant polyp presentation. The distribution is wide and can be colorectal back to the esophagus. Gardner’s syndrome is the 2nd most lethal of the multiple polyposis syndromes. Polyp + osteoma + fibroid disease is the trigger to think Gardner’s

3. Peutz Jegher’s Syndrome: Some report low to no evidence of malignant degeneration. This patient has pigmentation in the peri-oral area. They have dark “lipstick” purple pigmentation around the mouth typical of Peutz-Jeghers. The condition is benign.

4.Juvenile Polyposis: The situation is not malignant (low to no malignant potential). Younger patients are often affected. The condition occurs almost exclusively in the colorectal area. Protein loss via the feces occurs leading to protein enteropathy and weight loss.

5.Cronchite Canada Syndrome No malignant potential and no controversy. We find this stomach to colon. We can see on CT and endoscope. Skin pigmentation changes occurs all over the body. THIS IS A BENIGN CONDITION WITHOUT MALIGNANT POTENTIAL.

11/14/08

GI-COLONCANCER

The #2 leading cause of cancer death is colon cancer. Tumors are often in the distal segments of the GI tract . The most important tool to visualize colon cancer is flexible fiber optic. 50% of colon cancer are within reach of an examining finger. 75% of the cancers are within reach of the early imaging tools (recto-sigmoidoscope – a rigid tool of about 18 inches length).

Rectal bleeding is a common sign. Unexplained weight loss and anemia can also be signs. There can also be alteration in bowel habits. Cancer is often written off as hemorrhoids. Both conditions present with rectal bleeding.

Another name for colon cancer is SILENT KILLER. It has moved from 6th to 2nd on the list of cancer death. If we don’t go looking for it, the survival and prognosis is not good. We can find cancer early through proper screening. Polyps are typically 2-3 cm in diameter. Early polypoid removal has 5 year survival rates above 95%. If they have signs of local metastasis, survival rates at 5 years decrease to less than 15%. Finding the cancer early gives the best prognosis. The single biggest reason for increased survival rates amongst colon cancer patients is finding colon cancer early.

Risk Factors

Age: Increased age, increases the likelihood.

History of Inflammatory Bowel Disease: Malignant degeneration can occur.

Family History

Gynecological Cancer: Increases the risk in females for Colon Cancer.

Behavior/Diet: High fat, high meat diets can lead to GI cancer. A greater percentage of colon carcinomas occur in this. Also low fiber diets with low fruits and vegetables are linked to increased risk for GI cancer.

Low Amounts of Calcium, Selenium, and Vitamin D

Physical Inactivity: Modest, low-moderate physical activity has been shown to decrease risk. There is little downside to increasing physical activity.

Treatment and Management

Early identification is the single most important thing to do for them. We need to screen for colon cancer. You may want to start checking before age 50 in patients with known risk and family history.

Hemoccult is a simple tool that is filter paper with GUIAC resin. Prepare the patient in advance for the test. Have them slightly increase fiber and decrease NSAID use before the day of the test. You want fiber meals to increase the chance for leakage of blood through the colon and rectum. Check 3 bowel movements. The test adds peroxide and the doctor looks for color change. It only takes 7 mL per day of blood to turn the hemoccult blue.

Hemoccult and DRE

+ Hemoccult test demands more investigation. DRE is the next step in the investigation. If both hemoccult and DRE come back positive, you may need to refer them.

IN some cases, mucus can be made by adenocarcinmas. IBS is also associated with increased mucus production, but IBS does not produce blood. BLOOD + MUCUS DESERVES WORK UP.

Signs

Abdominal pain does not occur early with colon cancer. If they do have pain, the pain is colicky and leads to unsatisfied contraction. Change in bowel movements occurs sooner rather than later. The process is slowly evolving. Anemia and weight loss are good signs, but they occur in middle and late disease phases.

Diagnostic Exams

DRE is typically followed by endoscopy. Spiral CT can be used with sagittal and coronal cuts to aid in disease interpretation. Helical CT can also be used. “Virtual Colonoscopy” is a properly cleansed, fasted patient that is put in a helical CT scanned throughout the system. Virtual colonoscopy has shown good early results and is a viable option.

Lateral X-rays of the lumbar spine can include sacrum. Check the pre-sacral space. It should be less than 2 cm in non-obese and less than 3 cm in obese patients. As the cancers grow into the lumen they grow out and become round lesions.

Management Advice

Hot Spots = Educate patients in areas of the country with poor diet and heart disease (because of diet and lack of activity). We need to educate patients in these areas about lifestyle choices and management.

Increased Fruits and Vegetables

Vit A, C, E need to be increased = These are recognized to decrease tumor growth

Selenium, Vit D and Calcium = Increased levels can help prevent tumor growth

HEMORRHOIDS

Benign and serious causes of hemorrhoids exist. 2 venous systems exist in the rectal area: 1). Portal system --- NO valves…the problem can be in the liver and dilation of peri-rectal veins can occur 2). Systemic – Has Valves.

Causes

Straining at the stool

Constipation: A minority of cases show constipation as a cause. The increased in IAP leads to venous dilation. Constipation is not the main cause.

Hepatic Damage: Cirrhosis, Liver Failure, Hepatitis

Prolonged Sitting: Computer Operators and others who sit have increased chances for hemorrhoids. Cushions can help to decrease the incidence

Obesity

Pregnancy

Portal Hypertension

Lethargy/Couch Potato

Hemorrhoids are the MOST COMMON CAUSE OF RECTAL BLEEDING across AGE GROUPS. As patients age, the malignancy becomes more of a concern. In children, the bias is towards Meckel’s diverticulum.

There is a genetic bias to constipation. Blacks suffer more bouts of constipation than whites, with the caucasians suffering more hemorrhoids than blacks. High level of education patients with greater income have greater chance for hemorrhoids. Less education, less income, less chance for hemorrhoids.

Symptoms of Hemorrhoids

Pruritis = Burning or Itching Pain

Bleeding

We need to first confirm the diagnosis with DRE. Sigmoidoscope can also help make the diagnosis. Ruling out cancer in the right demographic group and risk profile group is imperative.

Cautions

Preparation H and other self-management items are not good for the patients. Over the counter hemorrhoid agents have topical anesthetics. Topical anesthetics often lead to prolonged behavior that prolongs the condition.

Hygiene

Hygiene becomes important. Take soap, washcloths and luke warm water using them to decrease the irritation following defecation. Hygiene can help decrease the pruritis (itching).

Decrease Friction

2-3” inch foam cushion or pillows can help decrease the friction that can irritate the hemorrhoid.

Sitz Bath

SITZ Bath = Lukewarm bath with osmotic agents/salts that cleanse and reduce the bulk of material. Be cautious that the water is not too hot because increased dilation occurs. Hot water can lead to more engorgement of veins that already do not drain sufficiently.

Medical Management

1. Rubber Band Ligation with Suturing = For the patient than can’t manage hemorrhoids anymore… The patient must be patient and wait till the hemorrhoid falls off after the procedure is done.

2. Ligation with Cryotherapy = Tying the hemorrhoid down, freezing it and removing the hemorrhoid with a scalpel.

3. Hemorrhoidectomy = Most aggressive choice. Removal of the tissue and dilated vein occur stitching the tissue back together or allowing the area to scar. There can be a scar in the area that may require anoplasty years later due to the scar.

CONSTIPATION PATIENT

About ¼ of the year meets the definition. Less than 3 bowel movements per week meets the definition, but context must be considered (fiber poor, stress, etc.). There is no “gold standard definition.” We also need to obtain information on comfort level at the time of bowel movement. Bowel movements may be difficult and show hard, non-malleable stool.

Primary/Idiopathic Constipation

3 categories

1. Slow Transit: Colonic Inertia due to autonomic irregularities. Sympathetics stimulated or parasympathetics lose tone. The functional affect is the same (when sympathetics are stimulated or parasympathetics lose tone).

2. Outlet Delay/Obstructive Constipation/Pelvic Floor Dys-synergy: This patient does not have coordinated effort between abdominal muscles, pelvic floor and sigmoid colon muscles.

3. Functional Constipation: Patient complains of constipation, but we don’t find a motor problem upon exam. This can be the functional/adynamic ileus patient. We should check for –itis conditions (diverticultis, peritonitis, appendicitis, etc.).

Intervention

Food diaries can help. Info on diuretics, foods, timing of meals, snacks and supplements is helpful.

Dehydration plays a role…Increase Hydration

Low fiber diets play a role…Increase fiber slowly

Increased physical activity can also help bowel health

Another management is setting aside a regular time/regular schedule. Some patients seek convenient bowel movement and want to wait till later.

Drugs: Pharmaceutical agents can lead to constipation. Note your concern to the patient and prescribing physician.

Probiotics: Can be good for bowel health.

Type 2/Secondary Constipation

Type 2 is acquired un-coordination because the system works against itself. Drugs can impact the central nervous system and autonomics.

________________________________________END OF TEST #4 MATERIAL ___________________________________

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