Gastrointestinal Emergencies

TopicsAcute appendicitisAcute pancreatitisDiverticulitisInstestinal obstructionUpper/lower GI bleeding/hemorrhoidsGastroenteritisCholelithiasis/cholecystitis/cholangitisHepatitis (alcoholic and viral)Booerhaves syndrome

ABDOMINAL PAINAcute abdominal pain accounts for 5% of all ED visits.Three categoriesIntra-abdominal3GsGI.GU.GYN.Vascular emergencies.Extra-abdominalCardiopulmonaryAbdominal wall.Toxic-metabolicNeurogenicUndifferentiated

Common Causes of Abdominal Pain in the ED for All Age Groups

Cause Percentage Abdominal pain of unknown cause41.3Gastroenteritis6.9Pelvic inflammatory disease6.7Urinary tract infection5.2Ureteral stone4.3Appendicitis4.3Acute cholecystitis2.5Intestinal obstruction2.5Constipation2.3Duodenal ulcer2.0Other causes22.0

From Brewer RJ et al: Am J Surg 131:219, 1976.

Causes of Abdominal Pain in Patients Over 70 Years of Age

Cause Percentage Acute cholecystitis26.0 Malignant disease13.2 Bowel obstruction10.7 Nonspecific abdominal pain 9.6 Gastroduodenal ulcer 8.4 Acute diverticular Dz 7.0 Incarcerated hernia4.8 Acute pancreatitis4.1 Acute appendicitis3.5 Other causes12.7

ACUTE ABDOMINALPAIN

ACUTE ABDOMINAL PAINThree categories: VisceralOften poorly localized. Steady ache or dull.Vague discomfort or gaseous.Colicky or crampy.Can be excruciating.ParietalSharper and more localized. Tenderness and guarding.Rigidity and rebound.Referred

ABDOMINAL PAIN

Visceral pain Often the earliest symptom .Caused by inflammation, distention, or ischemia of nerve fibers innervating the walls or capsules of hollow or solid organs.Parietal or Somatic painIrritation of fibers that innervate the parietal peritoneum.Often initiated by chemical or bacterial inflammation.Referred PainAny pain felt in a cutaneous site distant from a diseased organ.

Pareital peritoneumLines internal surface of the walls of the abdomen and pelvic cavity

ABDOMINAL PAIN

Epigastric painForgut organsStomachDuodenumBiliary tractPeriumbilical painMidgutMost of small intestines AppendixCecumSuprapubic or hypogastric painHindgut organsMost of colon including sigmoid.Intra-peritoneal portions of GU system.Kidney, Ureters and Bladder.Pelvic organs.

hypogastrichypochondriaciliaclumbar

History.Onset and Duration of Pain.Location, radiation and migration of Pain.Quality and Severity of Pain.Aggravating and relieving factors.Associated Symptoms. Past and Current Medical History.____________________________(very important)Social History.Physical Exam.General Appearance and Vital Signs. Inspection, Auscultation, and Percussion.Palpation and Localization of Tenderness.Rectal and Pelvic Examination. Extra-abdominal Examination.

Lab & imagingWhite Blood Cell Count.Urinalysis.Electrolytes.Renal function test.Tests for Pregnancy.Amylase and Lipase.LFTs.Plain abdominal films.Abdominal ultrasound.Abdominal CT scan.

Appendicitis

cecumappendix

Acute Appendicitis Incidence

Approximate yearly incidence of 1 per 1,000 populationAffects all agesHighest incidence in second and third decades of life.Slight male predominance. Approximately 200,000 appendectomies annually in the US.Most common surgical condition in children.the most common surgical problem requiring emergency intervention during pregnancy.Less than 1% mortality rate.Mortality is higher with children

Acute AppendicitisClinical presentation (Classic)Abdominal pain Initially periumbilical RLQSevere diffuse abdominal pain

Acute AppendicitisClinical presentation (atypical)Abdominal painRetrocecal appendixBack, flank, testicular pain Pelvic appendixSuprapubic pain Long appendixThe inflamed tip may cause pain in RUQ or LLQ

Acute AppendicitisClinical presentation

Anorexia Fever (low grade)Vomiting Diarrhea (33%) Constipation (933%)

Acute AppendicitisClinical exam

Abdominal exam RLQ tenderness.McBurney's point Guarding ReboundBowel sounds Rectal exam

Acute AppendicitisClinical exam

(Special tests)Abdominal exam Psoas signObturator signRovsing's sign

Acute AppendicitisDDxAdultsundiagnosable abdominal pain, diverticulitis, urinary tract infection, ileitis, cholelithiasis, pancreatitis, bowel obstruction, and gastroenteritis.Womenabdominal pain of unknown cause, PID, ovarian cysts, endometriosis, and ectopic pregnancy.Children, abdominal pain of unknown cause, mesenteric adenitis, ileocolitis, Meckels diverticulum, testicular torsion, urinary tract infection, Henoch-Schnlein purpura, pancreatitis, and gastroenteritis.Elderly.gallstones, diverticulitis, and intraabdominal tumors.

Acute AppendicitisLab & imagingCBC.Electrolytes.Renal function test.Urinalysis. Urine pregnancy test (if woman of childbearing age). Abdominal series.RLQ ultrasound.CT scan of abdomen and pelvis.

Appendicolith

Acute AppendicitisManagement

Nothing by mouth (NPO)Saline lock (IV hydration if dehydrated) Surgical consultation Antibiotic e.g., cefotetan or cefoxitinFlagyl (or clindamycin) with ampicillin and gentamicin.

Acute AppendicitisManagement

High clinical probabilitySurgical consultationAntibiotic (e.g., cefotetan or cefoxitin)AppendectomyModerate clinical probabilitySurgical consultation UltrasoundIf positive, appendectomyIf negative, observation and serial examinations.Low clinical probabilityUltrasound if symptoms persist at time of follow-up Surgical consultation Follow-up in 12 to 24 hours for repeat examination, earlier if increased symptoms.

Standard of care for acute appendicitisAppendectomyRemember This

Acute Pancreatitis

Acute pancreatitisIn the U.S. Cholelithiasis or alcohol abuse accounts for 90% of all cases of acute pancreatitis

PathophysiologyThe central cause is believed to be the intracellular activation of digestive enzymes and autodigestion of the pancreasPancreatic digestion from activated proteolytic enzymes leads to edema, interstitial hemorrhage, vascular damage, coagulation, and cellular enzymes.

PathophysiologyIt can also cause a generalized systemic inflammatory response that may lead to shock, ARDS, and multisystem organ failure.

Clinical featuresBoring epigastric pain that radiates to the back.TachycardiaNausea and vomitingAbdominal distensionCullens signGrey Turners signBlood loss, refractory hypotension, and respiratory failure may accompany more severe forms.

Diagnosis and differentialDiagnosis is made by a suggestive history and physical exam, associated with elevated pancreatic enzymes.Amylase greater than 3x the upper limit of normal has a specificity of 75% and a sensitivity of 80-90%Lipase is more specific than amylase and is the preferred test. At a cutoff of 2x the upper limit of normal, lipase is 90% sensitive and specific.

Diagnosis and differentialLeukocytosis may be present, and an elevated alkaline phosphatase suggests biliary disease.Hypotension, tachycardia >130bpm, Po2

Diagnosis and differentialUltrasound is helpful in the identification of gallstones or dilatation of the biliary tree.CT is the study of choice for visualizing the pancreas, confirmation of inflammation, and the identification of phlegmons, abscesses, or pseudocyts. It cannot be used to rule out Acute Pancreatitis.

Diagnosis and differentialEndoscopic retrograde cholangiopancreatography (ECRP) can be useful the the etilology remains unclear after initial evaluationDDX: LLL pneumonia, rupture of a pseudocyst, gallbladder disease, peritonitis, PUD, SBO, renal colic, dissecting aortic aneurysm, DKA, and gastroenteritis.

TreatmentPancreatic rest (NPO)Fluid resuscitation with normal salinePain control; parenteral analgesia prn IV narcotics e.g. MorphinePrevention of vomiting; antiemetics e.g. Promethazine IVPressors such as dopamine are indicated for persistent hypotension despite fluid resuscitation

TreatmentO2 to maintain a pulse ox of

TreatmentPatients with significant systemic complications, shock or extensive pancreatic necrosis will need to be place in an ICU setting.

Diverticulitis

DiverticulitisIs caused by bacterial proliferation within an existing colonic diverticulum, leading to microperforation and inflammation or pericolonic tissue.

DiverticulitisClinical diverticulitis occurs in 10-25% of patients with diverticulosis.One-third of the population will have acquired the disease by age 50, and two-thirds by age 85.Only 2-4% of patients with diverticulitis are under age 40 and tend to have a more virulent form of the disease, with frequent complications requiring earlier surgical intervention.

PathophysiologyMost commonly, clinical diverticulitis results form high colonic pressures, resulting in erosion and microperforation of the diverticular wall, leading to inflammation of pericolonic tissue.

Clinical featuresThe most common symptom is LLQ pain.Other symptoms include tenesmus, diarrhea or increasing constipation.The involved diverticulum may irritate the urinary tract and cause frequency, dysuria or pyuria.If a fistula develps between the colon and bladder patient may present with recurrent UTIs or pneumaturia

Clinical featuresParalytic ileus w/abd distension.Nausea and vomitingSmall bowel obstruction and perforation can also occur.RLQ painLow-grade fever but the temperature may be higher in patients with generalized peritonitis and in those with and abscess.

Clinical featuresAbdominal exam reveals localized tenderness oftern w/voluntary guarding and rebound tenderness.A fullness or mass may be appreciated over the affected area of colon.Occult blood may be present in the stool.

Diagnosis and differentialDDX: appendicitis, PUD, PID, endometriosis, ischemic colitis, aortic aneurysm, renal calculus, IBS, lactate intolerance, colon carcinoma, intestinal lymphoma, Kaposi's sarcoma, sarcoidosis, collagen vascular disease, irradiation colitis or proctosigmoiditis, fecal impaction, foreign body granuloma, and any bacterial, parasitic, or viral infectious cause.

Diagnosis and differentialRoutine screening blood tests, UA, and an abdominal radiographic series.Leukocytosis is present in only 36% of patients with diverticulitis.CT scan of the abdomen is the diagnostic procedure of choice.

TreatmentIf patient has systemic signs and symptoms of infection, has failed outpatient management, or demonstrates signs of peritonitis, hospitalization and surgical consultation is necessary.Inpatient treatment consists of IV antibx, usually an aminoglycoside e.g. Gentamicin or tobramycin and either flagyl or clindamycin for aerobic and anerobic coverage.

TreatmentTicarcillin-clavulanic acid or imipenem have been used as alternative agents.Bowel rest, NPO, IV fluids are administered.Nasogastric suction may be indicated in patients with bowel obstruction or adynamic illeus.

TreatmentOutpatient management is acceptable for patients with localized pain without signs and symptoms of local peritonitis or systemic infection.Treatments consists of bowel rest, broad-spectrum or antibx therapy.Ampicillin, bactrim, ciprofloxacin, or keflex. One of these meds is taken in combination with an agent with anaerobic coverage e.g. Flagyl, clindamycin

TreatmentPatients should limit activity and maintain a liquid diet for 48 hours.If symptoms, improve low-residue diet then begun.Patients should seek medical care if they develop increasing abdominal pain, fever, or are unable to tolerate oral intake.

HemorrhoidsAre associated with constipation and straining at stool, pregnancy, obesity, chronic liver disease, portal hypertension, and rarely tumors of the rectum and sigmoid colon.

PathophysiologyInternal hemorrhoidal veins are located above the dentate line and drain into the portal venous system.External hemorrhoidal veins are located below the dentate line and drain through the pudendal and iliac venous system.

Clinical featuresInternal hemorrhoids are only visible through and anoscope and cause painless bright-red rectal bleeding with defecation.External hemorrhoids may be visualized on external exam and commonly cause pain and discomfort, most severe at the time of defecation.

Clinical featuresThrombosis of external hemorrhoids is the usual cause of pain.Prolapse may occur with larger hemorrhoids, spontaneously reducing or requiring periodic manual reduction.Prolapse may cause mucous discharge and pruritus ani.Common complications are strangulation, thrombosis, and severe bleeding.

Diagnosis and differentialClinical signs cannot differential colonic lesions from hemorrhoidsDDX of rectal pain: malignancy, abscess, cryptitis, anal fissure, trauma, foreign bodies, rectal prolapse, and venereal proctitis.

TreatmentFor most patients treatment is nonsurgical and includes: hot sitz baths and good hygiene. Bulk laxatives( Metamucil, stool softeners)Topical analgesics or steroids may provide temporary relief.Thrombosed external hemorrhoids require excision of clot for relief. Initial conservative treatment may be tried for less severe cases.

TreatmentSurgical referral and intervention is indicated for continued bleeding, intractable pain, incarceration, or strangulation.

Intestinal obstructionSmall bowel obstruction(SBO) is more common the large bowel obstruction (LBO)Intestinal obstruction is due to mechanical or function obstruction, with ileus being more common.Adhesions following surgery are the most common cause of SBOLBO is most commonly due to neoplasm.

Intestinal obstructionFecal impaction is common is elderly and debilitated patients.

PathophysiologyBlockage prevents passage of luminal contents and result in dilatation due to accumulation of gastric, biliary, and pancreatic secretions.With distention, intraluminal pressure rises, decreasing bowel wall blood flow. When pressure exceeds capillary pressure, absorption ceases and leakage of fluids (third-spacing) may occur.

PathophysiologyMicrovascular changes may allow entry of gut flora into the circulation, resulting in bacteremia and sepsis. Necrosis and bowel perforation may follow.With obstruction, oral fluid intake stops and vomiting occurs. This fluid loss, coupled with the third space losses, leads to hypovolemia and shock.Closed loop obstruction has a more rapid progression.

Clinical featuresClassic history includes vomiting, abd distention, and pain, with a past history of abdominal surgery or hernia.Abdominal pain is crampy and intermittent.SBO primarily periumbilical painLBO hypogastric painPain with ileus may be constant.

Clinical featuresEmesis is often bilious early and may be feculent with late SBO or with LBO.Early symptoms may include high-pitched bowel sounds, and this may decrease with time.Physical exam may be show surgical scars, hernias, or intraabdominal mass.Peritoneal signs suggest perforation.

Clinical featuresTachycardia, hypotensionRectal exam may reveal impaction,occult blood, or carcinoma.Women may have palpable gynecologic neoplasms on pelvic exam.Passage of stool does not rule out obstruction.

Diagnosis and differentialDDX: pseudo-obstruction(Ogilvies syndrome), intestinal motility due to TCAs or anticholinergic agents.Radiographs help localize SBO vs. LBO.Laboratory tests include: CBC, BUN, serum electrolytes, serum amalyse and UA. LFTs as well as cross-match and coagulation studies may also be needed.

Diagnosis and differentialSigmoidoscopy or barium enema may be useful in localizing the site of LBO.CT of the abdomen.

TreatmentWith mechanical bowel obstruction, prompt surgical consultation is required!Nasogastric tube is used to decompress the bowel.Fluid resuscitation using crystalloid.Monitor vital signs and urine output.

TreatmentAppropriate antibiotic therapy e.g. Piperacillin-tazobactam, or ampicillin-sulbactam should be started if perforation is suspected or surgery is anticipated.For adynamic ileus, conservative tx including: nasogastric decompression, fluid replacemdtn, and observation

Gastrointestinal bleedingAcute upper GI bleeding in 60% of cases is caused by PUD, followed by erosive gastritis and esophagitis, esophageal and gastric varices, and mallory-weiss syndrome.The most common cause of apparent lower GI bleeding is upper GI bleeding.Hemorrhoids are the most common cause of acutual lower GI bleeding.

GI bleedingBoth upper and lower GI bleeding are more common in males and the elderly.

PathophysiologyUpper GI bleeding is defined as that originating proximal to the ligament of treitz.Irritative factors such as ETOH, salicylates, and NSAIDs are predisposing factors for PUD, gastritis, and esophagitis.

Clinical featuresHematemesis, hematochezia, or melena.Hematemesis or coffee-ground emesis suggests a source proximal to the right colon.Hematochezia indicates a more distal colorectal lesion.

Clinical featuresWeight loss and changes in bowel habits are classic symptoms of malignancy.Vomiting and retching followed by hematemesis is suggestive of mallory-weiss tear.History of aortoenteric graft should suggest the possibility of an aortoenteric fistula.

Clinical featuresHx of ETOH or medication use may suggest PUD, gastritis, or esophageal varices.Hypotension, tachycardia, angina, syncope, weakness, and confusion.Hypotension and tachycardia suggests severe bleeding.Cool clammy skin is an obvious sign of shock.

Clinical featuresSpider angiomata, palmar erythema, jaundice, and gynecomation suggest underlying liver disease.Ingestion of iron or bismuth can simulate melena, and certain foods such as beets can simulate hematochezia; however, stool guiac testing will be negative.

DDXUpper GI bleed include: PUD, esophageal and gastric varices, esophagitis, erosive gastritis, mallory-weiss syndrome, arteriovenous malformations, Lower GI bleed include: diverticular dz, colonic angiodysplasia, crohns dz, ulcerative colitis, colorectal cancer, internal hemorrhoids, anal fissure, colonic polyps, upper GI bleeding, endometriosis.

DiagnosisThe dx may be obvious with the finding of hematemesis, hematochezia or melena.Nasogastric tube placement and aspiration.Rectal exam is mandatory!Exam of ENT to exclude swallowed blood as source.

DiagnosisType and cross-match of bloodCBC, BUNM, creatinine, electrolytes, glucose, coagulation studies LFTs.Upper GI endoscopy, H. pylori studies, barium radiography, endoscopic U/S, CT angiograpy.Colonoscopy, anoscopy, stool studies, CRP, ESR, meseteric angiography, radionuclide imaging.

TreatmentEmergency stabilization of the airway, breathing, and circulation is foremost.O2, large-bore IVs, and monitors should be applied.Replace volume loss with crystalloids.Blood products replacement depends on clinical factors.Nasogastric tube placement.

TreatmentEarly therapeutic endoscopy should be considered the treatment of choice for significant upper GI bleeding.Band ligation or injection sclerotherapy of esophageal varices.Endoscopic hemostasis for nonvariceal etiologies of upper GI bleeds.

TreatmentSomatostatin and octreotide for reducing bleeding form both varices and PUD.Other tx considerations include prevpac, helipac for tx of H. pylori.Balloon tamponade for variceal hemorrhage.In patients who do not respond to medical therapy, and endoscopic hemostasis fails, emergency surgical intervention is indicated.

TreatmentPts with GI hemorrhage will require hospital admission, and early referral to an endoscopist is advisable.

Esophageal PerforationBoerhaaves syndrome

Boerhaaves syndromeIs a spontaneous esophageal rupture, is rare but serious condition, with a mortality rate ranging from 25%-89%.Increased incidence in men as compared with women, with a ratio approximately 2:1.It is more common in the middle-aged; 80% of patients are middle-aged men.

PathophysiologyThis syndrome is characterized by a complete transmural rupture of the esophagus resulting from barogenic trauma (ie, forceful vomiting). A sudden rise in intraluminal pressure caused by uncoordinated vomiting with pyloric closure and diaphragmatic contraction against a cricopharyngeal muscle is theorized to be the underlying cause.

PathophysiologyPerforation usually occurs at the weakest point of the esophagus; therefore, the most common site of rupture is the left posterolateral wall of the third of the esophagus.This is seen in 90% of patients.

Clinical presentationIncludes a history of nausea and vomiting, followed by severe unrelenting, and diffuse, in the chest, neck, and epigastric area.Pain can radx to the back & shoulders, or back pain may be the predominant symptom.Swallowing often exacerbates pain.

Clinical featuresHematemesis is typically not a complaint with esophageal rupture, and this can help to differentiate it from a Mallory-Weiss tear.SOB can be a common complaint, resulting from pleuritic chest pain or pleural effusion. The Mackler triad is a term that defines the classical presentation of vomiting, lower chest pain, and subcutaneous emphysema.This sign is mostly noted in those patients that present later in the disease course.

Physical examPhysical exam varies with the severity of the rupture and the elapsed time between the rupture and presentation.Abdominal rigidity with hypotension and fever often occur early.Tachycardia and tachypnea are common.Nonspecific findings diaphoresis, fever, and hypotension, especially as the condition evolves.

Physical examThe Hamman crunch, a crackling sound heard on auscultation of the chest, demonstrates pneumomediastimum and can be present in 20% of patients. It is caused by air in the mediastinum being moved by the beating heart.More advanced stages of rupture typically present as sepsis with progression toward multi-organ failure.

DDXMI, pulmonary embolus, peptic ulcer disease (PUD), aortic castastrophe, or acute abdomen, acute coronary syndrome, mallory-weiss tear, pericarditis, acute pancreatitis, and spontaneous pneumothorax.

DiagnosisCXR, and contrast esophagography with contrast most often make the DX.Endoscopy, CT of the chest, and thoracentesis can be useful adjuncts.

TreatmentIn the ED, resuscitation of shock and broad-spectrum parenteral antibiotics should be given to cover both aerobic and anaerobic organisms.Keep the patient NPO.Examples include piperacillin-tazobactam, cefotaxime or ceftriaxone plus clindamycin or metronidazole.Emergent surgical consultationAdmission to the hospital.

Esophageal bleedingMallory-Weiss tear

PathophysiologyArterial bleeding from longitudinal mucosal lacerations of the distal esophagus/proximal stomach that usually follows forceful vomiting.Account for 5-15% of upper GI hemorrhages.

Clinical features

Acute onset of upper GI bleeding is the usual presentation, although some patients can present with melena or hematochezia.The spectrum of severity of bleeding is broad.Less than half of patients with Mallory-weiss tears will report a history of vomiting prior to hematemesis.

DiagnosisIs made by hx and the presence of acute upper GI bleeding.Gastric aspiration may aid in the dxEndoscopy may be both diagnostic and therapeutic.

TreatmentThe vast majority of mallory-weiss tears stop bleeding spontaneously, thus requiring only supportive care.

vomiting & diarrheaViral gastroenteritis, caused by norwalk viruses, astroviruses, rotaviruses, and enteric adenoviruses are the most common form of food-borne disease.Food-borne viruses are usually transmitted person-to-person by the fecal-oral route.

Vomiting & diarrheaThe most common causes of bacterial food-borne illnesses in the U.S. are campylobacter, salmonella, shigella, and E.coli.

Clinical featuresVomiting with blood can represent gastritis, PUD, or carcinoma.Aggressive non-bloody vomiting followed by hematemesis is more consistent with a mallory-weiss tear.Bilious vomitus can rule out gastric outlet obstruction.Associated with fever may be caused by and infectious or inflammatory cause.

Clinical featuresAssociated with chest pain may suggest MI or pneumonia.Associated with back pain may be seen with aortic aneurysm or dissection, pancreatitis, pyelonephritis, or renal colic.Associated with headache suggests increased intracranial pressure, such as subarachnoid hemorrhage or head injury.

Clinical featuresIn a pregnant patient is consistent with hyperemesis gravidarum in the 1st trimester; in the 3rd trimester it could represent pre-eclampsia.Associated medical conditions are also useful in discerning the cause.Diabetes mellitus( DKA)Peripheral vascular disease (mesenteric ischemia)Previous abdominal surgery(intestinal obstruction.)

Clinical featuresMedication use (eg. Lithium or digoxin) suggests toxicity.Physical exam includes careful assessment of the GI,GU, and pelvic systems.Dermal exam (eg, hyperpigmentation w/ addisons disease).Pulmonary examination (eg, signs of consolidation, suggesting pneumonia.

Clinical featuresBy definition, diarrhea represents a daily stool out put of >200 g, but generally refers to any increase in frequency or liquidity.Acute diarrhea of

Clinical featuresAssociated with fever, pain presence of blood, or type of food ingested may suggest infectious diarrhea or diverticulitis.Associated with neuroglogic symptoms such as seizure with shigellosis or theophylline toxicity.Paresthesias with ciguatoxin.Detail about the host can also better define the diagnosis.

Clinical featuresDietary practicesCertain medications, particularly antibx, colchicine, lithium, and laxatives.Travel historySocial history

Physical examinationThe physical examination should initially focus on assessment of hydration status.Abdominal examination.Rectal examination.

DDXGASTROENTERITIS mnemonicGastrointestinal disease Appendicitis or aortaSpecific disease (eg, glaucoma)Trauma medications (Rx)OB/GYN disordersEndocrine disordersNeurologic diseaseToxicology

DDXEnvironmental disordersRenal diseaseInfectionTumorsIschemiaSupratentorial

DiagnosisIn a presumed food-borne illness, determining the exact time of exposure may suggest a particular causative agent.Refer to table 48-1 p. 171.All women of childbearing age warrant a pregnancy test.LFTs, UA, lipase or amylase.

DiagnosisElectrolytes, renal function tests. EKG, CXRAbdominal seriesStool cx, stool O & PLevels for theophylline, lithium, or heavy metals.

TreatmentReplacement of fluids can be IV with normal saline solution in seriously ill patients.Oral rehydration in mildly dehydrated patients.Nutritional supplementation should be started as soon as nausea and vomiting subside.BRAT diet (bananas, rice, apples, toast)

TreatmentAntibiotics for adult patients with severe or prolonged diarrhea, or patients that have traveled from tropical or third world countries Ciprofloxacin 500mg PO bid x3days is recommended.Flagyl 250-750mg PO tid x5-14days is indicated for C. dificile, Giardia, or Entamoeba infection.

TreatmentAntidiarrheal agents, especially in combination with antibx have been shown to shorten the course of diarrhea such as Loperamide. Diphenoxylate and atropine for more severe diarrhea.Antiemetic agents are useful in actively vomiting pts w/dehydration such as promethazine, prochlorperazine, or metoclopramide.For severe or refractory cases, ondansetron may be uses.

TreatmentAdmission is dependent on toxic appearance and response to therapy, as well as concomitant and preexistent medical conditions.

CHOLELITHIASISCholecystitisCholangitis

CholelithiasisThe presence of stones in the gallbladder.Gallstones cause four major biliary tract emergencies biliary colic(symptomatic cholelithiasis), cholecystitis, gallstone pancreatitis, and ascending cholangitis.

CholelithiasisRisk factors associated with formation and complication include increased age, female sex and parity, pregnancy, obesity, marked weight loss or prolonged fasting, familial tendency, oral contraceptives, clofibrate, ceftriaxone, asian descent, chronic liver dz and hemolytic disorders (sickle cell disease)

PathophysiologySymptomatic cholelithiasis or biliary colic occurs when a gallstone is forced from the gallbladder into the cystic or common bild duct, producing obstruction,

CholecystitisIs an acute gallbladder inflammation caused by cystic duct obstruction.

Clinical featuresPatients typically complain of nausea and abdominal pain that lasts more than 3-6 hours, which is unremitting and associated with fever.Abdominal pain is severe and steady.Physical exam may reveal RUQ tenderness or a palpable mass.

Clinical featuresA positive murphys sign( increased pain or inspiratory arrest during deep subcostal palpation of the RUQ with inspiration)Persistent pain, fever, or chills and more severe localized or generalized tenderness may indicate complicated disesase (eg. Abscess formation or gallbladder perforation)

DiagnosisUltrasound is the definitive initial test and preferred diagnostic technique; HIDA scanning and MRI may be helpful in cases where dx is unclear.CBC, C-reactive protein, LFTs, RUQ U/S scan, bhcg

Treatment Administer isotonic crystalloid IV fluids to correct volume deficits and electrolyte abnormalities.In some cases (eg, septic shock) pressor support may be required.Antiemetics or antispasmodics should be given for vomiting.

TreatmentMeperidine has traditionally been the preferred drug for analgesia.Antibiotics should be given.Immediate surgical consultation and hospital admission.

CholangitisAscending cholangitis is a life-threatning illness, usually resulting from obstruction of the common bile duct and reflux of bacteria into lymphatics and hepatic veins.The most common etiology is cholelithiasis leading choledocholithiasis and biliary obstruction.

CholangitisIs a surgical emergency!

Clinical featuresMost patients have fever, jaundice and RUQ pain (Charcot triad).Other symptoms may also be present, acholic stools, pruritus,hypotension, mental status changes.

DiagnosisCBC, BUN, creatinine, ABG analysis, LFTs, electrolytes, blood cx, coagulation panelRight upper sonography is the diagnostic procedure of choice and shows dilated, obstructed intrahepatic billiary ducts.

TreatmentTreat shock with infusion of IV crystalloid solution. Nasogastric tube if patient is vomitingInsert foley catheter to monitor urine output.Administer antimicrobialsClassical treatment has included an aminoglycoside, a penicillin and flagyl

Viral hepatitisHepatitis A is one of the most frequently reported diseases in the U.S. Transmission primarily occurs via fecal-oral route.After ingestion and absorption, the virus replicates in the liver and is excreted in bile, reaching extremely high concentrations in the stool.

Hepatitis ATransmission usually precedes symptoms by 2 weeks when stool concentrations are highest. Patients are considered noninfectious 1 week after onset of jaundice.Symptomatic patients may present with abrupt-onset fever, abdominal pain, malaise and jaundice.

Hepatitis ACommon exam findings are hepatomegaly and clinical jaundice with marked elevation of serum transaminases. Serum IgM anti-hepatitis A virus antibodies is the test of choice for diagnosis.No specific therapy is available and treatment is supportive. Personal hygiene is the key to prevention.

Hepatitis APassive immunization with intramuscularly administered polyclonal immune globulin give within 2 weeks of exposure is at least 80% effective in preventing Hepatitis A.

Hepatitis BMost people are asymptomatic, although some will present with complications such as cirrhosis, hepatocellular carcinoma or liver failure.People from endemic areas (Asia, Africa, eastern Europe) or injection drug users and those with high-risk sexual behaviors are at an increased risk.

Hepatitis BSerologic markers are essential in making the diagnosis and evaluating disease activity, including differentiating between acute and chronic infection, and chronic asymptomatic carriers.Therapy for acute inection is almost always supportive care alone.Therapy for chronic infection includes nucleoside analogs and interferon-alfa.

Hepatitis CMost common route of transmission is through illicit injection drug use.Following acute exposure, about 55-85% of patients develop chronic hepatitis C.Most infections are asymptomaticTreatment usually includes interferon and ribavirin, with goal of eradicating viremia.

Hepatitis CLong-term complications include cirrhosis or hepatocellular carcinoma.

ED care and disposition for viral hepatitisMost patients can be successfully managed as outpatients with emphasis on rest, adequate, oral intake, strict personal hygiene, and avoidance of hepatotoxins(ETOH and drugs)Close follow-up arrangements should be made.

ED care and dispositionPatients with following should be admitted:Encephalopathy, PT prolonged by more than a few secondsIntractable vomitingHypoglycemiaBilirubin>20mg/dlAge >45 years old

ED care and dispositionImmunosuppressionSuspected toxin-induced hepatitisVolume depletion and electrolyte imbalances should be corrected w/ IV crystalloid.Hypoglycemia should be treated with dextrose and careful monitoring.

ED care and dispositionFulminant hepatic failure should warrant admission to the ICU with aggressive support of circulation and respiration, monitoring and treatment of increased intracranial pressure if present.Correction of hypoglycemia and coagulopathy, administration of oral lactulose or neomycin, and protein-restricted diet.

ED care and disposition Consultation with a hepatologist and liver transplant services are indicated.

PERFORATED VISCUS

Greater omentumintestinesappendix

Cystitic ductcbd

TopicsCholelithiasis/Cholecystitis/Cholangitis.Acute Pancreatitis.Hepatitis (alcoholic and viral).Acute Appendicitis. Diverticulitis.Intestinal obstruction. Upper and lower GI bleeding/hemorroids. Gastroenteritis.Boerhaaves syndrome.Mallory-Weiss Syndrome.

Cholelithiasis

Kehrs signIrritation of the diaphragm perceived as pain in the side of the neck and proximal shoulder area. iliopsoas sign obturator sign Murphys sign Rovsings sign,pain is caused in the RLQ while palpating the opposite side of the abdomen, is another indicator of appendicitis.

*Acute abd pain is pain of