Esophageal Anatomy and Dysphagia PDF
Document Details
Uploaded by ConvincingEarth
Tags
Summary
This document provides an overview of esophageal anatomy and different types of dysphagia, including definitions and distinguishing features. It also includes information on various diagnostic and treatment procedures for these conditions.
Full Transcript
ESOPHAGEAL Anatomy: sophagus → muscular tube that connects pharynx to stomach E UES → keeps food from entering trachea LES → prevents gastric content reflux into esophagus 4 Layers:...
ESOPHAGEAL Anatomy: sophagus → muscular tube that connects pharynx to stomach E UES → keeps food from entering trachea LES → prevents gastric content reflux into esophagus 4 Layers: Adventitia Muscular ○ Outer longitudinal ○ Inner circular Submucosa Mucosa Lining → stratified squamous epithelium Squamo-columnar junction (z line)→ junction wheresquamous lining of the esophagus meets the columnar lining of the gastric mucosa Terms: 1. ysphagia→ subjective sensation of difficulty/abnormalityof swallowing D 2. Odynophagia→ pain w swallowing 3. Esophagitis→ esophagus inflam/irritation 4. Globus sensation→ non-painful sensation of a lump,tightness, FB, or retained food bolus in the pharyngeal or cervical area (functional w/o structural abnormality) Procedures Upper Endoscopy thin scope with alight + cameraat its tip A (EGD) Used to look inside UPPER DIGESTIVE TRACT Barium Esophagram Noninvasive imaging test that uses barium contrast Xrays to take images of the UPPER GI TRACT (Barium Swallow) Esophageal A thin flexible tube containingpressure sensorsispassed through the nose, down the esophagus and into the stomach anometry M 1. Evaluates motility/muscle contractions 2. Helps determinepressureof esophagus Dysphagia Definition larm sx that warrants prompt eval to define the exact cause + initiate appropriate tx, d/t structural or motility abnormality in the A passage of solids or liquids from oral cavity to stomach Inability toinitiatea swallow orsensationof hindrance NOTdue to normal aging process Acute/non acute Functional dysphagia →ROME IV CRITERIA → ALL CRITERIAMUST BE FULFILLED FOR 3 MO + SX ONSET MIN 6 MO + FREQUENCY 1/WK) 1. Sense of solid +/- liquid food lodging, sticking, or passing through the esophagus 2. No evidence that anesophageal mucosal/structuralabnormality, GERD, or eosinophilic esophagitisisthe cause 3. Absence of major esophageal motor disorder(achalasia,esophagogastric junction outflow obstruction, distal esophageal spasm, hypercontractile esophagus, absent peristalsis) istinguishing from D Oropharyngeal locations 1. Difficultyinitiatinga swallow 2. Point toCERVICALregion 3. Accompanied byregurgitation, aspiration, + sensationof residual food 4. Drooling, coughing, choking, dysphonia Esophageal 1. Difficulty swallowing several secondsAFTER initiatinga swallow 2. Sensation that foods are beingobstructedwhen theypass from UE to stomach 3. Pt points toSUPRASTERNAL NOTCHor area behind thesternum 1 4. Arises within thebody of the esophagus, lower sphincter,or cardia ifferentiating D Solids only + PROGRESSIVE sx Dysphagia 1. G radually progressive → esophageal stricture (acid reflux, radiation, tx, eosinophilic esophagitis) 2. Rapidly progressive→ cancer, may have additional sx(chest pain, odynophagia, anemia, anorexia, wgt loss) Solids only + INTERMITTENT sx 1. Maybe eosinophilic esophagitis, esophageal ring/web, vascular anomaly Solids +/- liquids 1. Maybe esophageal motility disorder, distal esophageal spasm, hypercontractile esophagus, functional disorder Dysphagia + odynophagia 1. C OMMON IN BOTHINFECTIOUS + MEDICATION-INDUCED ESOPHAGITIS 2. Less commonly present in reflux esophagitis and Crohn’s Disease Esophagitis Definition Esophagus inflam/irritation. Diff types. Causes 1. CC = GERD M 2. Infectious (hallmark sign → odynophagia) 3. Medication/pill induced 4. Eosinophilic/ allergic 5. Corrosive/caustic Diagnostics Upper endoscopy, Biopsy,Barium esophagram Treatments Cause dependent Infectious Esophagitis Definition Infection in esophagus that occurs mainly in those with immunocompromised states(HIV, post-transplant,malignancy, chemo) Etiology 1. C = CANDIDA ALBICANS M 2. CMV 3. HSV 4. Other →EBV, histoplasmosis, cryptococcosis, mycobacteriumTB/avium Clinical Presentation ODYNOPHAGIA,dysphagia, retrosternal chest pain iagnostics D Candida albicans →linear yellow-white CMV →LARGEshallow ulcers or HSV →DISCRETEshallowulcers (Upper endoscopy)+ plaques erosions Treatment Tx: Acyclovir (1st line), or Foscarnet Tx: Fluconazole Tx:Ganciclovir (1st line), or Valganciclovir, Foscarnet Eosinophilic Esophagitis Definition llergic, inflammatory, eosinophilic infiltration of the esophageal epithelium A “Chronic immune/antigen-mediated, esophageal disease characterizedclinicallyby sx related to esophagealdysfunction + histologicallyby eosinophil-predominant inflammation” 2 Epidemiology Kids + adults, MALE, increasing incidence Etiology Associated withatopic disease(asthma, eczema, etc),and other allergies (celiac) Clinical Presentation C = DYSPHAGIA TO SOLID FOODS M Chest pain, heartburn, food impaction Reflux or feeding difficulties in children +/- odynophagia (longstanding) Diagnostics ndoscopy →normal orMULTIPLE CORRUGATED RINGS, WHITEEXUDATES E Bx →presence of abundance of eosinophils Management emove foods that incite allergic response, acid suppression withPPIs,INHALED topical corticosteroids(fluticasone, R budesonide) allergy testing New →Dupilumab Medication/Pill-Induced Esophagitis Definition Esophagitis due to prolonged pill contact with the esophagus Etiology 1. BX(MC tetracyclines,PCNs, macrolides) A 2. NSAIDS 3. Bisphosphonates 4. BB, CCBs, potassium chloride, iron pills, vitamin C Clinical Presentation dynophagia, dysphagia, retrosternal pain,heartburn O Dx ENDOSCOPY →discrete, well defined ulcers of varyingdepths,KISSING ULCERS.Bx may be done Management /C offending agent(most cases will resolve) D Acid suppression withPPIs Precautions to decrease risk → 1. Upright+remainfor 10 mins, 30 if strong associationif pill eso 2. 4 oz of water,8 if pill eso Corrosive/Caustic Esophagitis Definition I ngestion of acids or corrosive substances Can be accidental (children) or intentional (suicide intention), prognosis depends onsubstance potency+ exposure duration Pathophysiology 1. A LKALINE→LIQUEFACTIONnecrosis (dead mucosa→ liquid),disintegrates mucosa early →ALLOWSdeep penetration a. PERFORATION 2. ACID→COAGnecrosis → esophageal injury reduced +perf less common d/t coagulum formed on mucosal surface limitsdeep penetration a. AIRWAY INJURIES Etiology Alkaline→MC ESOPHAGUS(pH > 12) Drain cleaning products, ammonia containing, oven-cleaning products, hair relaxers, bleachers, cement, etc Acids → MC STOMACH(pH < 2) Toilet bowl-cleaning products, automotive battery liquid, rust-removal products, metal cleaning products, etc Clinical Presentation arieson how much ingested and what was ingested V MC → odynophagia, dysphagia,hematemesis, dyspnea Caustic injury to the oropharynx → 1. Causes oropharyngeal pain + inability to clear pharyngeal secretions → persistent drooling 2. Maybe retrosternal/epigastric pain 3. Hoarseness, stridor, dyspnea from caustic burns of the epiglottis/larynx 3 Diagnostics PIto determine agent H Check airway, Oropharynx may reveal edema, erosions, deep necrosis with gray pseudomembrane, rebound tenderness CTof abdomen + chest→ eval for extensive injury Early upper endoscopy→ determine risk of strictureformation (done in patients who do not require surgery+ stable) Management dmit patient→ supportive care, pain control, IV fluids,resp support, +/- ABX (perforations) A NOinduction of vomiting (can lead to additional esophagealinjury due to repeat contact with esophagus) Emergent surgeryif perf Complications sophageal perforation, esophageal stricture, fistula, pyloric stenosis E Esophageal cancer → ~30% pts develop w hx caustic injuries Screening →every 2-3 years starting 10-20 yearsaftercaustic ingestion Low threshold for upper endoscopy in pts with dysphagia + hx of caustic ingestion Esophageal Stricture Definition bnormal tightening or narrowing of the esophagus A Gradually progressivedysphagia tosolids Etiology C = GERD (70-80% of cases have long standing GERD),esophagitis, dysfunctional LES, motility disorder, hiatal hernia, M iatrogenic Diagnostics arium Esophagram (INITIAL TEST) B Upper endoscopy(DX + TX) → determines underlyingcause, exclude malignancy, perform endoscopic dilation if needed Treatments Endoscopic dilation Boerhaave Syndrome Definition ffort rupture of the esophagus E Spontaneous perf of the esophagus d/t sudden increase in intraesophageal pressure + neg intrathoracic pressure(S EVERE STRAINING OR VOMITING) MC = Left posterolateral wall of lower esophagus Spontaneous rupture may occur in patients with normal esophagus (some may have underlying esophagus disease) 40% mortality rate Clinical Presentation 1. etrosternal chest pain worse with deep breathing + swallowing,vomiting,hematemesis R 2. Crepituson chest exam(rice crispy sound) 3. Hamman’s sign →mediastinal “crackling”accompanyingevery heart beat, present in LLD Diagnostics Contrast Esophagram→ DX TEST OF CHOICE 1. Leakage 2. GASTROGRAFINSWALLOW PREFERRED(water soluble, bariumis caustic if leaks through) Chest CT → if esophagram unable to locate/dx, pt unstable, free air, eval for drainage CXR → not sensitive for esophageal perforation, nonspecific findings Management mall + stable →NPO, IV fluids + PPI, broad-spectrumABX S Large/severe →surgical OBSTRUCTIVEDISORDERS OF THE ESOPHAGUS OBSTRUCTIVE →Esophageal Web Definition ONcircumferential thin membrane in MID-UPPER esophagus,can becongenital or acquired(associated withZenker's N diverticulum) Clinical Presentation Dysphagia to solids, many are asx Diagnostics Barium esophagram= TEST OF CHOICE 4 Treatments I f severe → Endoscopic dilation PPI tx after dilation may decrease risk of recurrence OBSTRUCTIVE →Esophageal Ring (Schatzki Ring) Definition ircumferential diaphragm of tissue that protrudes into esophageal lumen C MC LOWER ESOPHAGUS (squamocolumnar junction) Risk factors iatal herniapresent in most PTS H May havereflux or eosinophilic esophagitis Clinical Presentation any are asx M Can haveepisodicdysphagia (esp solids), food bolusmay get stuck in lower esophagus →STEAKHOUSE SYNDROME Diagnostics arium esophagram→ more sensitive, circumferentialridge a few cm above the hiatus of the diaphragm B Upper endoscopy often performed to bx for EE Treatments ilation if sx D Antireflux surgery may be done if reflux present OBSTRUCTIVE →Esophageal Neoplasms Definition Major types → 1. MC US → ADENOCARCINOMA 2. MC worldwide → SCC Clinical Presentation ALLMARK → PROGRESSIVE DYSPHAGIA,odynophagia H WEIGHT LOSS, anorexia, chest pain, cough, reflux,hoarseness Diagnostics Upper endoscopy with bx(dx test of choice) Treatments Esophageal resection may be combined with chemotx, radiation, palliative stenting to improve dysphagia (advanced cases) MOTILITY DISORDERS OF THE ESOPHAGUS MOTILITY →Diffuse Esophageal Spasm Definition sophageal motility disorder characterized by severe non-peristaltic esophageal contractions (uncoordinated contractions) E Impaired inhibitory innervation → premature + rapidly propagated contractions Can be severe or debilitating Pain similar to angina but NOT exertional(r/o MI) Clinical Presentation TABBING chest pain, worse w hot or cold liquids or food S Dysphagia to both solids + liquids(simultaneously) Sensation of object stuck in the throat Diagnostics sophagram→ severe non-peristaltic contractions →CORKSCREWesophagus E Manometry →DEFINITIVE,increases simultaneous orpremature contractionsin distal esophagus with preservationof some peristaltic activity Manometry, esophagram, + endoscopy often combined to rule out malignancy Management ntispasmodics or antihypertensives(first line) →Dicyclomine, CCBs (Dilt) , nitrates. Alt → TCAs A Botox, pneumatic dilation (second line) Surgery (Peroral Endoscopic Myotomy) → reserved for pts refractory to medical tx MOTILITY →Hypercontractile (Jackhammer) Esophagus Definition Esophageal motility disorder characterized byincreasedpressure during peristalsis 5 AkaNutcracker esophagus Clinical Presentation hest pain similar to diffuse esophageal spasm C Dysphagia to both solids + liquids Diagnostics anometry (DEFINITIVE) → increased pressure during peristalsis(jackhammer appearance) M Upper endoscopy + Esophagram usually NORMAL Management ower esophageal pressure, reduced esophageal contractility L Dicyclomine, CCBs, nitrates, botulinum toxin injection,TCAs MOTILITY →Achalasia Definition Loss of peristalsis + LES relaxation failure (degenerationofAuerbach’splexus→ ↑ LES pressure) Epidemiology MC < 50 Clinical Presentation ysphagia tobothsolids + liquids at the same time,regurgitationof undigested food D Chest pain, cough May developmalnutrition, wgt loss, dehydration(foodnot reaching stomach) Diagnostics arium esophagram→BIRD’S BEAK APPEARANCE OF LES(LES narrowing), proximal esophageal dilation, loss of B distal peristalsis Manometry→MOST ACCURATE TEST→increased LES pressure+ lack of peristalsis Upper endoscopy → usually done in achalasia prior to initiating tx to r/o esophageal cancer Management ecrease LES pressure → Botulinum toxin injection (requires tx in 6-12 mo), nitrates D Pneumatic dilation of LES Surgery (definitive) → Esophageal Myomectomy/Heller myotomy (incising in muscle of LES) Complications Esophageal cancer MOTILITY →Neurogenic Dysphagia Definition aulty transmission of nerve impulses to the pharyngeal muscles F Condition produced by weakness + incoordination of pharynx muscles that propel food into the esophagus Etiology Generally caused by associatedneuromuscular disease(MG, ALS, MS, stroke) Clinical Presentation ysphagia toboth solids + liquids D WINDPIPE ASPIRATION + NOSE REGURG MOTILITY →Zenker Diverticulum Definition Pharyngoesophageal pouch (false diverticulum) d/t weakness at junction ofKillian's triangle Outpouchingat junction MC MALES > 60 Clinical Presentation ysphagia D Regurgitation of undigested food, cough, feeling of lump in neck, choking sensation Halitosis(d/t food retention in pouch) Diagnostics Barium esophagramwith video fluoroscopy(INITIALTEST OF CHOICE) Collection of dyebehindthe esophagus at the pharyngealjunction Upper Endoscopy → usually performed for surgical evaluation 6 Management bservation if small (< 1 cm) + asx O Sx or > 1cm → surgery (diverticulectomy, cricopharyngeal myotomy) MOTILITY →Scleroderma Esophagus Definition Scleroderma → group of rare ds that causes hardening + tightening of the skin Clinical Presentation CREST SYNDROME→multisystem CT disorder - Calcinosis - Raynaud’s - Esophageal dysmotility - Sclerodactyly - Telangiectasias Causes decreased esophageal sphincter tone + peristalsis Dysphagia toboth solids + liquids Treatments Aimed at improving sx, dysphagia, underlying complication STRUCUTURALDISORDERS OF THE ESOPHAGUS STRUCTURAL →Mallory-Weiss Tear Definition ear that occurs in the esophageal mucosa at thejunctionof the esophagus + stomach T 8-15% of upper GI bleeds May be associated with hiatal hernias Pathogenesis nclear → mucosal lacerations develop secondary to a sudden ↑ in intra-abdominal pressure(FORCEFULRETCHING OR U VOMITING AFTER ETOH BINGE) Clinical Presentation pper GI bleeding preceded by retching or vomiting U Hematemesis(vomit blood), melena (black tar stool),hematochezia (blood in stool), syncope, abd pain, back pain Diagnostics Upper endoscopy(when stable)TEST OF CHOICE →SUPERFICIALLONGITUDINAL MUCOSAL EROSIONS Labs → CBC, CMP, add others depending on presentation Management ssess HD stability A Not actively bleeding →supportive care mainstay →PPIsfor acid suppression + promote healing Many cases stop bleeding w/o intervention Actively bleeding →endoscopic tx 1. Thermal coag, hemoclips, endoscopic + ligation (+/- epi) 2. Choice depends on specialist preference + underlying factors 3. IV PPIs Antiemetics reserved for persistent N/V STRUCTURAL →Esophageal Varices Definition Dilated gastroesophageal submucosal veins as a complication ofportal vein HTN Etiology MC = CIRRHOSIS 1. 90% of pts with cirrhosis develop esophageal varices 2. 30% bleed (mortality=30-50%) 3. 70% rebleed within 1st year of initial bleed (1/3 are fatal) Clinical Presentation pper GI bleed →hematemesis,melena, hematochezia U Severe → s/s of hypovolemia 7 Diagnostics Upper endoscopy (test of choice) → dx + tx - Any newly dx cirrhotic should have EGD for screening of varices Management Acute variceal bleed → 1. Stabilize patient → 2 large bore IVs, IV fluids a. If low hematocrit → may need packed RBC b. If coagulopathy (increased PT/INR) → may need FFP 2. Endoscopic variceal ligation (INITIAL TX OF CHOICE) 3. Pharmacologic vasoconstrictors →Octreotide(firstline medical management) alone or with endoscopic tx 4. Balloon tamponade →rapid bleeds or stabilize bleedingnot controlled by endoscopic/pharmacologic intervention 5. Surgical decompression →TIPS transjugular intrahepaticportosystemic shunt= done ifbleeding despite endoscopic or pharmacologic intervention + some advanced cases ABX prophylaxis → fluoro or ceftriaxone Prevention of rebleed→non-selective BB (Nadolol,Propranolol) LIVER Anatomy: argest gland in the body and largest single organ (after the skin) L Accounts for 2.5% of adult body weight Located in RUQ of abdomen, protected by rib cage and diaphragm → moves with diaphragm movement Dual blood supply enters through porta hepatis ○ Hepatic vein= 75-80% of blood to liver - Portal blood had 40% more O2 than blood from systemic circulation→sustains parenchym ○ Hepatic artery= from celiac trunk of abdominal aorta - Brings 20-25% blood and first goes to nonparenchymal structures (bile ducts) Lobes: 2 anatomic and 2 accessory ○ Midline plane defined by attachment of falciform ligament ○ Left sagittal fissure separates right from left ○ 8 functional segments based on vascular supply and bile duct distribution Liver = master multitasker Digestive: bile production and processes nutrients Hematologic: removing senescent RBCs and synthesisof plasma proteins, clotting factors, albumin Vascular: storage of blood Immunologic:produces immune factors, removes bacteria,and produces lymph Metabolic Functions:removes waste, stores glycogen,minerals, vitamins, blood sugar homeostasis, excretes bilirubin Definitions Steatosis: fatty infiltration of the liver Steatohepatitis: inflammation associated with fatty infiltration Cirrhosis: chronic degenerative disease, cells are damaged and replaced by scar tissue→ decreased function (life threatening) Liver Function Tests (LFTs) Types ost of the tests reflecting health of liver are not a direct measurement of function M ↑ enzymes reflect damage to liver or biliary obstruction 1. Biochemical markers of liver injury a. ALT Alanine aminotransferase b. AST Aspartate aminotransferase c. Alkaline phosphatase d. Bilirubin 2. Markers of hepatocellular function a. Albumin (↑↑can indicate impaired hepatic syntheticfunction) b. Bilirubin c. Prothrombin time (↑↑can indicate impaired hepaticsynthetic function) Patterns 1. Hepatocellular a. ALT,AST> Alk phos b. ↑ Bilirubin 2. Cholestatic a. Alk phos > AST,ALT 8 b. ↑ Bilirubin 3. Isolated hyperbilirubinemia a. ↑ Bilirubin b. Normal AST, ALT, alk phos 4. AST:ALT >2:1 a. Alcohol associated disease (especially with ↑ GGT) b. NASH c. Hep C d. Cirrhosis Liver Enzymes ALT and AST lanine aminotransferase and Aspartate aminotransferase A Normal levels 80g/day ○ Females: >30-40g/day Pattern of drinking, females>males, genetics (FH of alcoholism, genetic abnormalities), diet tiology/ E 1st Stage Pathophysiology Fat accumulation is response to toxic stimuli→ steatosis Reversible with cessation 2nd Stage Continued exposure→ diffuse fat accumulation in liver→ liver injury→ scar tissue Range of symptoms Reversible 3rd Stage Necrosis and scarring due to hepatocellular injury Not reversible Clinical Presentation atty liver usually asymptomatic F Cirrhosis can have jaundice, weakness, edema, distention, bleeding PE can be normal Other s/s: Hepatomegaly Stigmata of chronic liver disease ○ Spider angioma ○ Palmar erythema ○ Gynecomastia Hepatic decompensation (ascites, peripheral edema, encephalopathy) Often coexisting dysfunction in other organs-- cardiomyopathy, neuropathy, pancreatic dysfunction, skeletal muscle wasting PE in alcohol abuse: abdominal wall colateral, ascites,cutaneous telangiectasia, digital clubbing, disheveled appearance, gynecomastia, jaundice, malnutrition, palmar erythema, peripheral neuropathy, splenomegaly, testicular atrophy Diagnostics arly disease= moderate ↑ in AST/ALT, GGT E Advanced disease: severe ↑↑ in AST/ALT, GGT Also: hyperbilirubinemia, ↑ alk phos, ↓albumin, coagulopathy, macrocytosis, ↓folate Ultrasound: fatty infiltration and liver size Biopsy to confirm Treatments bstinence from alcohol (can treat AUD with medication) A Nutritional support and counseling Advanced disease: Methylprednisolone x 1 month followed by taper ○ Reduce short term mortality in patients with alcoholic hepatitis ○ Can also use Pentoxifylline (when steroids CI) Surgery (liver transplant) ○ Must be abstinent for at least 6 months Prognosis Depends on severity of disease Short term: mortality rate ~34% without steroids Long term: 5 year mortality rate of patients who recover ~85% Most important prognostic factor is continued excessive ETOH use Hepatic Fibrosis 10 Definition appens before cirrhosis, due to chronic liver injury,Can resolve H Hepatic lobules collapse→ fibrous septa form→hepatocytes regenerate with nodule formation Extracellular matrix components accumulate in liver Good to measure to guide treatment, estimate time to cirrhosis, screening for portal HTN taging and S 0= no fibrosis and F4= cirrhosis (fibrosis>2 is significant) F Diagnosis Liver biopsy is gold standard Serology: more elevated with high inflammatory activity Indirect: reflects changes in function but not metabolism of extracellular matrix Direct: markers associated with matrix deposition Imaging: Elastography (estimates stiffness by applyingmechanical waves and measures speed through tissue) Transient Elastography: shear waves created by vibration source are measures with US Magnetic Resonance Elastography Cirrhosis tiology/ E auses in US: Hep C, Alcoholic Liver disease, Non-alcoholic liver disease C Epidemiology 9th leading cause of death in the US` Clinical Presentation irectly correlate to severity of disease D Anorexia, weight loss, weakness, fatigue, anovulation, hypogonadism Decompensated: jaundice, pruritus, signs of bleeding, abdominal distention from ascites, confusion/hepatic encephalopathy ↓BP: ↓MAP→ hepatorenal syndrome Skin: 1. Jaundice (from ↑ serum bili) a. bili>2-3 mg/dL b. Urine can be dark 2. Spider angiomata (telangiectasias), on trunk, upper arms, face, a. Possibly from alterations in sex hormone metabolism b. Not specific for cirrhosis Head and neck 1. Parotid gland enlargement (alcohol use) 2. Fetor hepaticus- sweet, pungent breath→ suggests portal systemic shunting Chest Gynecomastia: benign proliferation of glandular tissue of male breast (↑ hormone production) Abdominal 1. Ascites: accumulation of fluid in peritoneal cavity 2. Hepatomegaly: absence of this does not exclude 3. Splenomegaly: caused by congestion of red pulp resultingfrom portal HTN 4. Caput medusa: blood from portal venous system getsshunted due to portal HTN 5. Cruveilhier-Baumgarten murmur: venous hum that canbe auscultated in pts with portal HTN, over epigastrum, ↑with valsalva GU:testicular atrophy in men Extremities 1. Palmar erythema: from altered sex hormones, not specific,frequently on thenar and hypothenar eminences 2. Nail changes:due to hypoalbuminemia a. Muehrcke nails: paired horizontal white bands separated by normal color b. Terry nails: proximal ⅔ of nail white and distal is red 3. Clubbing 4. Dupuytren’s Contracture:thickening and shorteningof palmar fascia→ flexion deformities of fingers Neurologic Asterixis: bilateral asynchronous flapping motions of dorsiflexed hands Lab findings ALT/AST, ↑alk phos, ↑GGT, ↑Bilirubin, ↑PT ↑ ↓albumin Hyponatremia Thrombocytopenia (most common) Treatments Slow or reverse progression- treat underlying causes when possible 11 reventing additional insults- vaccinate Hep A, Hep B, avoid hepatotoxins P Adjust or avoid medications Complications uscle cramps: quinine, BCAAs, zinc repletion M Umbilical hernia: try to reduce, if ruptured: surgery, manage ascites Hyponatremia: withdraw beta blockers, alpha blockers, diuretics, others, correct, for hypotension: Midodrine Thrombocytopenia: treatment for low plt only if active bleeding or if procedure planned with risk of bleeding anagement/ M revent, identify, treat complications P Prognosis Determine appropriateness and timing for transplant Prognostic models helpful for decision making tools when it comes to guiding care (APACHE III, Child-Pugh, MELD) MELD Score ses serum bili, serum creatinine, and INR U Predicts 3 month survival In cirrhosis→ HIGHER Meld= higher dysfunction and mortality risk Used to prioritize liver transplants MELD 3.0→ includes additional variable and slightly better than MELD-na hild-Pugh C ssess risk of non-chunt operations in pts w/ cirrhosis A Classification Correlates w/ survival (1 yr) in pts not having surgery (Class A calcium composition C Causes:Four F’s: Fat, Fertile, Female, Forties 1. Genetic→ metabolism disorders 2. Obesity/DM→ hypercholesterolemia 3. Crohn's Ds→ decreased bile salt reabsorption 4. Hypertriglyceridemia→ decreased GB motility 5. Fasting→ precipitation of bile salts 6. Pregnancy/HRT→ increased estrogen Protective: 1. Low carb, low fat, high fiber diet 2. Caffeine 3. ASA 4. Mg+ Clinical Presentation 75% asx 1. iliary Colic→ episodic pain attributed to gallstonesw/out evidence of GB wall inflam B 2. RUQ pain but may be epigastric + radiate to R shoulder 3. N/V 4. Episodes in relation to fatty meal(stims GB contraction) DDx 1. astric (ulcer, gastroparesis) G 2. Pulmonary (PNA, PE) 3. MI/angina, renal (stone, pyelonephritis) 4. Pancreatitis 5. Acute hepatitis 6. Referred from gyn etiology Diagnostics 1. UQ U/S will confirm Dx 95% of the time R 2. Shadow 3. CBC + CMP w/ LFTs 4. Amylase/lipase → indicative of pancreatic involvement 5. UA or cardiac enzymes r/o other etiologies 6. Ab XRay can show up to 15% of stones but best to r/o other etiology Treatments Asx does not requireemergenttreatment 1. OTC analgesics prn + diet mods 2. For biliary colic pain mgmt → a. Keterolac (Toradol) 30 mg IM or 15 mg IV(don’t worrymuch about this) b. Narcotic analgesics may also be necessary(MSO4, dilaudid,Fentyl) c. Glycopyrrolate (Robinul)- anticholinergic, reducesspasm. Dry mouth 36 3. Ursodeoxycholic Acid- oral bile salt to dissolve cholesterol stones a. Reserved for non-surgical option, max 2 yrs /U → F 1. Elective surgery Complications otential to develop cholecystitis, cholangitis +/- pancreatitis P GB cancer is rare but highly associated w/ gallstones Cholecystitis Definition Acute or chronic inflammation of the GB Etiology allstone impacted incysticduct- 90% G Acalculous- 10%, recent major surgery/illness, hxof vasculitis, AIDs pt w/ CMV, cryptosporidiosis, or microsporidiosis Clinical Presentation 1. UQ+/- epigastric pain after fatty foods R 2. N/V 3. +/- Fever 4. Murphy’s sign→ inhibition of inspiration during palpationof RUQ, pt will lose their breath Diagnostics 1. BC → WBC usually elevated C 2. AST/Alk Phos usually elevated 3. Amylase/lipase → indicative of pancreatic involvement 4. U/S → stones, GB wall thickening, pericholecystic fluid, + murphy 5. HIDA (hepatic iminodiacetic acid) scan→ nuclear test,best for cystic duct obstruction 6. CT scan → 2nd line to ultrasound or HIDA, r/o other pathology Treatments 1. nalgesics/antiemetics A 2. IV ABX → cephalosporin or fluoro + metro 3. Surgical resection (cholecystectomy) urgently or stent placement Complications 1. bscess or gangrene A 2. Choledocholithiasis/cholangitis 3. Perforation 4. Fistula to bowel 5. Pancreatitis 6. CA 7. Repeated attacks may lead to cholecystitis a permanent inflammatory star despite resolution of the blockage, leading to aporcelain gallbladder (calcified, nonfunctional)or CA mphysematous E Cholecystitis associated w/ gas forming bacteria(Clostridia,E. coli, Klebsiella) Cholecysitis - IV Amp/sulb (Unasyn) or Pip/tazo (Zoysn) + Metronidazole (Flagyl) - RequiresEMERGENTresection Cholangitis Definition ommon bile duct infection secondary to choledocholithiasis C Primary sclerosing cholangitis→ no stone secondaryto inflammatory bowel ds Etiology Choledocholithiasis can be primary or secondary Clinical Presentation C harcot Triad →jaundice,feverw/ rigors, RUQ pain Reynolds pentad→Charcot’s triad + altered mentalStatus + hypotension - Suggestssepticcholangitis dx Diagnostics 1. ignificant AST elevations S 2. WBC, bili, alk phos, & amylase 3. U/S →CBD > 6mm is high likelihood of obstruction 37 4. RCPEndoscopic retrograde cholangiopancreatography-dx + tx E 5. MRCP → dx,not to tx Treatments 1. BX → Metronidazole (flagyl) + pip/tazo (Zoysn) or Cipro A 2. ERCP → sphincterotomy + stone retrieval 3. Subsequent cholestectomy if cholelithasis present Complications Sepsis, stricture, pancreatitis, hemorrhage Acute Pancreatitis Definition Inflammation of the pancreas Etiology C = STONES M ETOH Hypercalcemia, hyperlipidemia Abd trauma, peritoneal dialysis, ERCP, CA Meds, vasculitis, mumps, CMV Smoking, obesity + celiac ds have some association Clinical Presentation 1. onstant dull or “boring” epigastric pains, can radiate to mid-back or shoulders C 2. May follow fatty mealor heavy ETOH use 3. Increasedw/ laying supine 4. N/V, Anxiety PE → 1. oderate epigastric tenderness to palpation M 2. Distention 3. Diminished bowel sounds 4. Guardian 5. Fever 6. Jaundice 7. Tachycardiapossible DDx Gastritis, PUD, perf, cholecystitis, MI, AAA/TAA, mesenteric ischemia, splenic infarct/rupture/splenomegaly Diagnostics 1. BC & CMP C 2. Lipase→ 3x UNL, more sensitive than amylase (but both markedly elevated) 3. EKG→ r/o cardiac 4. Ab Xray→ helpful to r/o//in ddx, some may suggestacute process (calcifications correlate w/ chronic) a. Sentinel loop (LUQ air-filled small bowel) b. Colon cutoff sign (gas-filled transverse colon) 5. Ultrasound/CT/MRI (more sensitive the U/S)→iffebrileor hx/PE/ labs not dx 6. Ranson Criteriato assess severity: (know generalidea) Treatments 1. owel Rest until resolution of sx B 2. Parental (TPN) vs enteral via nasojejunal tube 3. IV fluids, analgesics + antiemetics 4. ABX only for secondary infection 5. ERCP for sphincterotomy, stent or stone retrieval as indicated 6. Chronic ETOH avoidance 38 Complications 1. Necrotizing pancreatitis→tissue destruction and hemorrhage a. Turner’s sign→hematoma appearance noted in flanks b. Cullen’s sign→periumbilical discoloration c. Panniculitis→ red tender nodules on extremities 2. Hypovolemic/shock 3. Ileus 4. Chronic pancreatitis → pseudocyst→ abscess Chronic Pancreatitis Definition rogressive damage to pancreatic tissues secondary to repetitive inflammation resulting in fibrosis, calcification, pancreatic ductal P inflammation and/or pancreatic stone formation and eventual functional impairment Etiology hronic ETOH C Smoking Hyperparathyroidism, obstructive process (stricture, stone, CA), autoimmune Clinical Presentation Recurrent epigastric pains, anorexia/wgt loss, N/V,constipation, flatulence, steatorrhea Diagnostics 1. mylase/lipase may notbe elevated A 2. Secretin stimulation test →secrettin given IV + duodenalcontents aspirated via NG tube a. Pancreatic secretiondiminishedin chronic pancreatitis 3. Fecal Elastase test →measures pancreatic enzyme elastasein stool 4. Ab Xray/U/S/CT → may showcalcificationsin body 5. ERCP/MRCP/Endoscopic U/S → dilated ducts, intraductal stones, strictures, pseudocysts/abscess Treatments 1. TOH, low-fat diet E 2. Pain mgt → non-opioids preferred but chronic pain plan may be necessary 3. Pancreatic enzyme supplement(Viokace, Creon, Pancreaze) 4. ERCP → duct decompression, opening of strictures, pseudocyst drainage Complications evelopment of DB- 80% within 25 yrs D Narcotic addiction Pseudocyst/abscess formation Pancreatic CA Pancreatic Pseudocyst Definition terile, localized fluid collection in or on pancreas surrounded by fibrous or granulation tissue S Usually connected to the pancreatic duct system + usually containing amylase or lipase Etiology Pancreatitis, trauma, ETOH use, biliary tract ds, stones Clinical Presentation Can be asx 1. Epigastric pain 2. N/V, anorexia 3. Palpation of mass 4. Sepsis/fever 5. Pleural effusion 6. Peritonitis Diagnostics /S, CT, MRI U ERCP w/ fluid analysis Treatments upportive care if asx S Drainagefor following → 1. Persistent sx 2. Infection 39 3. H emorrhage 4. Gastric/duodenal/biliary obstruction, ascites, pleural effusion, or compression of major vessels ancreatoduodenectomy P I ndicated for malignancy contained (NO METASTASIS) within the HEAD OR NECK of pancreas (Whipple Procedure) Procedure: 1. Head of pancreas, duodenum, gallbladder,distalportionof common bile duct +occasionallypart of the stomach removed → remaining portion ofpancreas, bile duct+ intestineare reconnected 2. Complications → leakage at anastomosis, wgt loss, DB CONSTIPATION GD → esophagus → stomach → duodenum E Lower endoscopy → flexible sigmoidoscopy, colonoscopy → lower - Flexible → rectum → sigmoid - Colonoscopy → rectum → colon Transit Time Factors Hypermotility → SPEEDS UP Hypomotility → SLOWS DOWN 1. edications M 7. edications M 2. Bacterial overgrowth in colon + sm bowel producing gas 8. Bacterial overgrowth in colon + sm bowel producing gas a. HYDROGEN SULFIDE producing microbes a. METHANE producing microbes 3. Parasitic infections 9. Parkinson’s ds 4. Supplements → increase amt of water in colon 10. UC/Crohns 5. Stress- fight or flight 1 1. Delayed gastric emptying 6. UC/Crohns Bristol Stool Chart Constipation Definition < 3 BM/wk, straining, hard stools → constipation Etiology Primary Colorectal Dysfunction → 1. Slow transit→prolonged delay in stool transit throughoutthe colon d/t smooth muscle or neuronal innervation dysfunction or dyssynergic defecation 2. Dyssynergic defecation→ difficulty w/bowel movementor inability to expel stool from anorectum, prolonged colonic transit time 3. IBS-C→ab pain w/ altered bowel habits, may have slowtransit, dyssynergia, and visceral hypersensitivity 4. Chronic Idiopathic(functional)→infrequent, persistentlydifficult passage of stools or incomplete defecation not meeting IBS criteria Secondary causes ROME IV Criteria Presence of the following min 3 mo (w/ onset min 6 mo prior to dx) for Functional 1. Must include 2 or more of the following → Constipation a. Straining b. Lumpy or hard stools (bristol 1 or 2) c. Sensation of incomplete evacuation 40 d. Sensation of anorectal obstruction e. Manual maneuvers to facilitate more than 25% of defecations 2. Loose stools are rarely present w/out use of laxatives 3. Insufficient criteria for IBS Risk Factors I ncreasing age, FEMALE, Physical Inactivity, Low education/income,Consumption of fewer calories & meals,Concurrent med use, Depression, Comorbid illness, Nursing home residence,Concurrent med use, Depression, Comorbidillness, Nursing home residence Clinical Presentation LARM SX →MORE EXTENSIVE EVAL →GI A nsatisfactory defecation U REFERRAL Infrequent stools 1. >45 Difficult w/ passage 2. Hematochezia/ (+) fecal occult test Older adults may be associated w/ fecal impaction 3. Obstructive sx Abd distention/bloating 4. Acute onset 5. Severe persistent refractory to tx 6. Wgt loss >10 lbs 7. Change in stool caliber 8. Fam Hx colon cancer or IBD PE →Comprehensive + rectal exam - Palpating for hard stool, assess for masses, anal fissures, hemorrhoids, sphincter tone, prostatic hypertrophy in males/ posterior vaginal masses in females Diagnostics abs → CMP, CBC, TSH, other labs to r/o suspicion L Ab Xray → stool retention/megacolon Endoscopy (flexible sigmoid, colonoscopy) → identify lesions that narrow or occlude the bowel, bx + polypectomy if needed, colonoscopy for alarm sx + colon cancer screening + >45 Colonic Transit studies (Sitz marker study) → radiopaquemarker or wireless motility capsule Motility studies→ anorectal manometry, colonic manometry, balloon expulsion Treatments onstipation lasting >2 wks despite tx should undergo further eval C Lifestyle and dietary modification (initially) → 20-25g fiber, exercise, fluids BulkLaxatives → increases frequency + softens stoolconsistency w/ min SE - Psyllium husk, methylcellulose, calcium polycarbophil, wheat dextrin - Metamucil, citrucel, FiberCon, Benefiber OsmoticLaxatives trial→ if bulk fail - PEG Low dose polyethylene glycol, lactulose, Sorbitol Stimulantlaxatives→ effective but caution chronic Stool softeners, suppositories + enemas (limited efficacy) Biofeedback tx (dyssynergic) Fecal Impaction Definition Prolonged retention + buildup of feces in the rectum, large mass of hardened stool accumulated in colon/rectum RF CNS ds, limited mobility, low fiber, chronic narcotics, long laxative hx, polypharmacy Clinical Presentation onstipation C Ab pain/discomfort Sensation of rectal fullness or discomfort Passive fecal incontinence/overflow diarrhea→ liquid stool leaks around impaction Urinary frequency/overflow incontinence/ urethral obstruction Rare → N/V, ab distention Diagnostics RE→ reveals copious amounts of stool D Ab Xrays → if DRE nondx Treatments Manual disimpaction to remove part of fecal mass → warm water enema + mineral oil 41 - PEG admin after partial emptying outine bowel regimen (reduce recurrence) R Identify and remove cause Small Bowel Obstruction Definition artial or complete blockage of SI P MC DEVELOPED COUNTRIES = INTRA-AB ADHESIONS(SCARTISSUE→ SURGERIES. PELVIC + AB SURGERY HX) - Hernias, Crohn’s ds, malignancies, volvulus - Neoplasm risk hx, abpevlic irradiation, FB hx Etiology 1. P rocesses that are extrinsic to SI WALL→ adhesions,hernia, volvulus 2. Diseasesintrinsic to SI WALL→ tumor, stricture,intramural hematoma 3. Processes that block an otherwise normal bowel lumen→ intussusception, gallstones, FB Clinical Presentation Sx → 1. oliky (crampy) pain C 2. Ab distention 3. N/V 4. Obstipation (LATE) 5. Decreased PO intake PE → 1. IGH PITCHED “TINKLING” BS ASSOCIATED W/ PAIN H 2. Ab distention 3. TTP/rebound 4. Hypoactive BS 5. DEHYDRATION/SYSTEMIC SIGNS a. HYPOTENSION, TACHYCARDIA, DRY MUCOUS MEMBRANES, REDUCED UO, AMS (SEVERE), +/- FEVER Diagnostics Labs → 1. CBC w/ diff→ leukocytosis + anemia 2. CMP→ electrolytes, kidney fxn 3. LFTs, Lipase, Amylase→ liver, gallbladder, pancreas fxn 4. FOBT fecal occult blood test 5. ABG→ metabolic alkalosis/acidosis 6. Blood cultures→ bacteremia Ab xray → PREFERRED INITIAL STUDY TO CONFIRM - DILATED BOWEL LOOPS + AIR FLUID LEVELS “STEP LADDER APPEARANCE” (UPRIGHT) - CT ab/pelvis → characterize severity/ etiology - Transition zone→ contrast dilated loops of bowelto no contrast area US/MRI→ pts who cant tolerate CT DDx N/V, adynamic/paralytic ileus, intestinal pseudo-obstruction, large bowel obstruction Treatments Goal → relieve discomfort, restore fluid, acid base balance + electrolytes 1. Immediate surgery→bowel compromise (surgically correctablecause of SBO) 2. 60-85% of adhesions will resolve w/out surgery, difficult to predict which ones will 3. Admit, surgery consult 42 4. N PO, fluid resuscitation, electrolyte repletion, NG tube/GI decompression 5. ABX → bowel compromise, periop prophylaxis, infectious 6. Gastrografin→ reserved for adhesive SBO w/o bowel obstruction (CONTRAINDICATEDin bowel compromise+ pregnant) Surgically correctable causes of SBO → 1. Closed loop obstruction, volvulus, intussusception, incarcerated hernia, gallstone ileus, FB ingestion, small bowel tumor Complications Bowel ischemia can significantly increase mortality Paralytic (Adynamic) Ileus Definition I nterruption of the normal passage of bowel contents d/treducedperistalsisin the absence of a mechanicalobstruction MC = POSTOPERATIVE ILEUS Etiology ostoperative → inflam response to manipulation + trauma but no obstruction on imaging P Medications (opioids, anticholinergics) Hypokalemia Medical conditions(DM, stroke, spinal cord injury) Clinical Presentation ypoactive/absent BS H NOOOOOO peritoneal signs Ab distention, bloating, gassiness Diffuse, persistent ab pain N/V Delayed passage of or inability to pass flatus Inability to tolerate PO Diagnostics ame labs as SBO S Ab Xray → dilated loops of bowel w/ NO transition zone CT ab → good for distinguishing ileus fromcompleteSBO (less for partial) Treatments orrect reversible causes C Supportive care is mainstay→ NPO, pain control, fluid resuscitation, electrolyte repletion, NGT for decompression, TPN, serial ab exams Toxic Megacolon Definition Total or segmental nonobstructivecolonic dilation > 6cmthat occurs in the context ofsystemic toxicity Etiology omplications of IBD→MC = UC C Infectious→C. Diff Ischemic colitis Volvulus Diverticulitis Radiation Obstructive colorectal cancer Clinical Presentation PI →Profound bloody diarrhea, abdominal pain anddistention, tenesmus,N/V H PE → Lower abdominaltenderness+distention, AMS,FEVER, tachycardia, hypotension, dehydration, +/- signs of 43 peritonitis Diagnostics abs →CBC w/ diff, CMP,lactic acid, ESR + CRP, Lipase,TSH, stool culture L Ab Xray →evidence of colon > 6 cm T ab/pelvis C CONTRAINDICATED→ bowel prep, barium enema, completecolonoscopy (can cause perforation) Dx Criteria→ 1. Radiographic evidencePLUS 2. 3 or more of the following→ a. FEVER > 38 C/100.4 F b. Pulse >120 c. Neutrophilic leukocytosis > 10,500/micoL d. Anemia 3. PLUSat least one→ a. Hypotension, dehydration, electrolyte abnormalities, AMS Treatments upportive care mainstay→ admit, bowel rest, NG tube,ABXceftriaxone + metro,fluid/electrolyte repletion,serial labs S Tx underlying cause Surgery → colonic perf, necrosis, full thickness ischemia, intra abdominal HTN or abd compartment syndrome, clinical signs of peritonitis or worsening abd exam despite medical tx Ogilvie Syndrome Definition cutecolonic pseudo-obstructionis a disorder characterizedbyacute dilation of the colon in the absenceofan anatomic A lesion that obstructs the flow of intestinal contents Usually involvescecum + right colon MEN > 60 Hospitalized/institutionalized pts Clinical Presentation C AB DISTENTION M N/V Ab pain, constipation, paradoxical diarrhea (overflow) PE → ab distention, tympanic to percussion, high-pitched BS FEVER, MARKED AB TENDERNESS, PRESENCE OF ABDOMINAL SIGNS→ suggestive of colonic ischemia or perf or their impending development Diagnostics abs → CBC, CMP, LFTs, Serum Lactate, TSH, stool cultures L Ab X rays Ab CT→ PREFERRED→ proximal colonic dilation may extendto rectu Treatments oal → decompress colon in order to min risk of colonic perf + ischemia G Pts w/out ischemia/perforation/peritonitis (< 12cm)→ supportive, NPO, NGT, IV fluid/electrolyte repletion,tx underlying ds, serial exams xrays and labs 12-24 hrs Pts at risk for perforation (12cm)/severe ab pain/failed tx→Neostigmine - Colonic decompression → failed tx, neostigmine CI/failure 44 - Serial exams xrays and labs 12-24 hrs Pts w ischemia/perf/peritonitis/failure tx→ surgicaldecompression → cecostomy or colectomy 45
