GI module
Jane R. Perlman Fellowship Program Nurse Practitioner and Physician Assistant Fellowship in Emergency Medicine
Jennifer S. Foster PA-C Dina Mantis PA-C
Acute Abdomen – causes
Acute appendicitis Acute mesenteric ischemia/ischemic colitis Perforated bowel, acute peptic ulcer or tumor Spectrum of cholecystitis Asymptomatic gallstones Biliary colic Acute Cholecystitis Choledocholithiasis Cholangitis Pancreatitis Hemoperitoneum – perforated AAA, trauma, surgery Abcess Bariatric surgery complications
Acute abdomen Worry about abdominal pain in elderly, children, HIV infection, immune suppressed from steroids or chemotherapy History questions to ask: MerckManuals.com Where is the pain? What is the pain like? Have you had it before? Yes – recurrent problem such as ulcers, biliary colic, diverticulitis, mittelsherz No – think perforated ulcer, ectopic pregnancy, torsion How severe is pain? Pain out of proportion – mesenteric ischemia Does pain travel to other body parts? Right scapula – gallbladder pain Left shoulder – ruptured spleen, pancreatitis Other questions re abdominal pain: What relieves the pain? Sitting up right and leaning forward, think acute pancreatitis What other sx occur with the pain? a) vomiting before pain, then diarrhea = gastroenteritis b) delayed vomiting, no bowel movements, no gas = acute intestinal obstruction, SBO c) severe vomiting, then intense epigastric left chest or shoulder pain = perforation of esophagus
Other historical questions the surgeon will want to know: Prior surgeries Surgical history, when – how recently, what, where, who did it? Also postop complications, postop course Pregnant or not Physical exam General, are they texting and talking and telling you pain is 10/10 or quiet, pale and diaphoretic? Ask patient where most tender area is, then start away from there, listen first, then percuss and palpate. Guarding or rigid? Check groin area for bulges, hernias Even if they are very tender/distended, always check for inguinal hernias Red flags Severe pain, abdominal distention Shock, tachycardic, hypotensive, diaphoretic, confusion Signs of peritonitis Tricks with this, go back and examine patient, distract them by asking a question, re-evaluate their tenderness Notice if when ask them to take deep breaths during lung exam if they do it easily and without pain or do they sit up in bed really easily and without wincing. Or are they really having pain and tenderness? Appendicitis Appendectomy most common general surgery performed in US. 7% of all surgeries annually. Most common cause of acute abdominal pain Historically: Mortality for appendicitis in 1886? 45% died!
Signs and symptoms of acute appendicitis Classic Symptoms: Epigastric/periumbilical pain Brief nausea/vomiting/anorexia Pain moves to RLQ Increased pain with cough and motion Classic Signs: RLQ tenderness Rebound tenderness at Mcburney’s point – pain worse when let go Rovsing sign – pain in RLQ when push in LLQ Psoas sign/obturator sign – tests for retrocecal appendicitis. Obturator sign not a very good diagnostic tool.
Non classic signs, symptoms Elderly patients, patients with dementia, pregnant women – pain may be less severe and local ttp less severe Hamburger sign – Ask patients with suspected appendicitis if they would like a hamburger or pizza/favorite food: if they are hungry, seriously question diagnosis This only lasts for a few hours
Diagnosis of acute appendicitis Clinical evaluation CT findings: Thickened appendix > than 6 mm Fat stranding Cecal thickening Appendicolith No contrast in appendix Arrowhead sign – contrast in cecum forms an arrowhead pointing to the occluded appendiceal orifice Acute appendicitis
Acute appendicitis Time to appendectomy and risk of perforation Study looked at time to treatment and perforation, analyzed hospital arrival time, time of diagnostic imaging, operating room start times. (Drake et al. 2014) 9048 patients Mean time from presentation to OR was 8.6 hrs 15.8% were perforated
No association between time from presentation to surgery and risk of perforation Higher risk of perforation associated with: male sex, increased age, 3 or more comorbid conditions, and lack of insurance. New hypothesis, perforation is most often a prehospital occurrence, not strictly time-dependent.
Acute mesenteric ischemia Interruption of blood flow Causes: Thrombus – blood clot that forms in a vein Embolism ie small piece of clot, fat, air, tumor, foreign body Low flow state Then inflammatory mediator release Infarction
Interesting fact: intestinal mucosa uses 20-25% of cardiac output (high metabolic rate) Acute mesenteric ischemia Ischemia – disrupts the mucosal barrier - allows bacteria, toxins, vasoactive mediators to leaks out Within 10-12 hours, Myocardial depression, systemic inflammatory response, multiorgan failure, death Acute mesenteric ischemia 3 major blood vessels involved I: Celiac trunk, supplies esophagus, stomach, prox duodenum, liver, gallbladder, pancreas, spleen
II: SMA: supplies distal duodenum, jejunum, ileum, colon to splenic flexure
III: IMA: descending colon, sigmoid colon, rectum Most common areas for ischemia ? Most common area?
How is acute mesenteric ischemia different from ischemic colitis?
Which areas least likely to be ischemic?
What test do you use to test for ischemia? Most common areas for ischemia Most common area = splenic flexure, watershed area Why? The splenic flexure is supplied by the area btwn the SMA and IMA
Acute mesenteric ischemia involves clots or emboli in the bigger gut vessels
Ischemic colitis is only small vessels – causes mainly necrosis and bleeding
The stomach, duodenum and rectum are least likely to be ischemic because many collateral vessels. Risk factors of acute mesenteric ischemia based on cause Arterial embolus (40% of cases): CAD, CHF, Afib, valvular heart disease
Arterial thrombosis: atherosclerosis
DVT: hypercoagulable states, inflammatory conditions like pancreatitis
Non-occlusive ischemia: Low flow states - shock, heart failure, cocaine, vasopressors Acute mesenteric ischemia: symptoms, signs Early – lots of pain, benign abdominal exam findings, abd soft, min ttp (Pain out of Proportion)
Later findings signs of peritonitis, markedly ttp, guarding, rigid, no bowel sounds Stool heme postive Shock Death Diagnosis, acute mesenteric ischemia
CTA (if renal function allows) might need to hydrate first Mesenteric angiogram (if renal function allows)
Serum markers: creatinine kinase, lactate New test: intestinal fatty acid binding protein
Early diagnosis important
Very high mortality if infarction occurs Summary acute mesenteric ischemia Early diagnosis important CTA or mesenteric angiogram Surgical exploration
Treatment: resuscitate – IVF, cipro/flagyl for bacterial gut translocation
embolectomy, resvascularization and resection GI tract perforation Etiology: Blunt and penetrating trauma Swallowed foreign body ex toothpick Anatomical location and causes: a) esophagus – forceful vomiting aka Boerhave syndrome, iatrogenic (EGD), ingestion corrosive material b) stomach/duodenum: PUD (peptic ulcer disease) 1/3 of patients, no prior hx of ulcer sx, 20% don’t have free air on xray!!!!
GI perforation, stomach cont b) stomach – PUD, ingestion corrosive material c) Intestine – strangulating obstruction, possibly acute, ex. Appendicitis, sbo, obstruction, meckel’s diverticulum ex. free air, rarely visible on xrays d) Symptoms of esophageal, gastric, duodenal perf ’s: sudden onset abrupt onset severe pain, peritoneal signs, may radiate to shoulder Symptoms of perforation (not in esophagus, stomach or duodenum) Usually small initially, omentum walls them off
Pain develops gradually, may be localized, tenderness is focal too. Often exam is very distended, but NO tenderness
Nausea, vomiting, anorexia common Bowel sounds quiet to absent Diagnosis of GI tract perforation Obstructive series, 50-75% show free air
Abdominal ct +/- po and iv contrast, and/or rectal contrast Case study - perforation 64 yo male Hx Etoh, diabetes Recent ORIF shoulder after fall, postop had PE/DVT discharged on lovenox, coumadin Came back to ER with abdominal pain, possible SBO on xray at NH CT extensive free air
Perforated colon Case study Perforated right colon Treatment – exploratory lap, right colectomy Postop septic, abdominal compartment syndrome, went back to OR for ex lap, washout Intubated, sedated for weeks, finally extubated, then transferred to floor approx HOD 20 Treatment GI tract perforation Immediate surgery, NGT, resuscitate, IV abx, typically broad spectrum, unasyn, zosyn
There are cases where we’ve successfully treated patients with only IV antibiotics, bowel rest,
esp. when body has walled it off. Or elderly patient, too many medical comorbidities Causes of Colon perforation Colon – causes: obstruction from colon mass, diverticulitis, IBD (Crohn’s, ulcerative colitis), toxic megacolon, constipation – stercoral ulcer.
most common area to perforate = cecum.
High risk greater than 13 cm, patients on prednisone or other immune suppressed patients.
GI tract perforation Clinical pearl: People on steroids could still have a bad problem, even though physical exam without peritoneal signs. Case study 67 yo male PMhx: htn ER complaint: abdominal pain, rectal bleeding, nausea Wbc 18.8 CT – diffuse bowel wall thickening, inflammatory changes Colon ischemia Initial treatment in ER IV antibiotics, Zosyn or cipro/flagyl NPO IVF Case study - Flexible sigmoidoscopy – significant ischemia Repeat CT - more infl changes, new ascites, entire colon involved Case study - Surgical treatment - total abdominal colectomy, end ileostomy - Ended up with renal failure, on dialysis Spectrum of Gallbladder disease
Asymptomatic gallstones – expectant management Biliary colic – 20% of patients progress to acute chole if untreated Choledocholithiasis – stone lodged in CBD, admit or close followup Acute cholecystitis – admit, iv abx, early chole (less than 24 hrs) Cholangitis – admit, IV abx, urgent ercp Gallstones Cholesterol stones – common, 80% Pigment stones – less common, 20% Risk factors – elderly, female, obesity, parity, OCP’s, family hx, rapid wt loss Acalculous chole risk factors – prolonged fasting, ICU patients, DM, HIV, vascular disease, TPN
Cholelithiasis 1% per year have complications Biliary colic – stone passes into cystic duct, 50% associated with meals, symptomatic cholelithiasis, MC manifestation of gallstones Symptoms: RUQ or epigastric pain N/V RUQ ttp Biliary colic - treatment Outpatient surgery referral Symptom prevention Analgesia Nsaids, opioids, anticholinergics, active spasmodics Acute cholecystitis Pathophysiology: Caused by cystic duct obstruction – leads to GB distention, inflammation, ischemia, infection – acute chole Signs and symptoms: Biliary colic pain that doesn’t resolve Guarding/rebound Murphy’s sign Fever/leukocytosis Acute cholecystitis Treatment: Admit Analgesia Antibiotics – Unasyn, PCN allergy cipro, flagyl or 3rd generation ceph + flagyl E Coli, Klebsiella, Enterococci, Anaerobes
Surgery – early lap chole = preferred approach
Biliary colic vs cholecystitis Classic teaching – Constant long lasting RUQ pain Fever Increased wbc count Murphy’s sign
Recommendations for treatment - wait on biliary colic New recommendations for Symptomatic cholelithiasis 1059 patients underwent lap chole for sx gallstones in Seoul Korea July 2004-December 2007 Main outcome measures – acute cholecystitis vs operative outcomes Risk factors for worse outcomes: Male sex, age > 60 yrs, diabetes, hx of CV disease, hx of CVA, ischemic stroke, cerebral hemorrhage Lap cholecystectomy in patient with Acute chole vs chronic chole group Longer mean operative times 60.5 vs 40.3 minutes (P < .001) More difficult in acute chole vs chronic Complication rate higher in acute chole group 34 acute chole group vs 26 chronic chole group (P < .001)
Recommendation: patients with symptomatic gallstones and adverse risk factors, early cholecystectomy before disease progresses to acute cholecystitis Case study – Mergener, K M.D. 47 yo healthy woman Epigastric pain x 2 hrs, increasing in severity, radiates to back, vomited x 3-4 times No meds or etoh Vitals: heart rate 115 (supine), 125 (upright) WBC 17,500/mm3 Bilirubin 3.2 mg/dL ALT – 283 IU/L AST – 182 IU/L Alkaline phosphatase 321 IU/L Serum amylase – 10,250 IU/L Serum lipase - 22,300 IU/L DIAGNOSIS? Case study cont What approach? A) Do nothing else and await surgical consultation and recs B) Patient is stable, needs pain meds, cont to observe in ER, possibly discharge to home later C) Immediate ERCP, without further workup D) Worried about patient, admit, close monitoring, aggressive fluid replacement (6-8 L/day of fluid containing appropriate electrolytes may be required) Correct answer • D) Worried about patient, admit, close monitoring, aggressive fluid replacement (6-8 L/day of fluid containing appropriate electrolytes may be required)
Acute Pancreatitis Inflammation of the pancreas caused by release of activated pancreatic enzymes MCC – biliary tract disease (gallstones and chronic heavy alcohol intake) 80% of causes Range of condition from mild – just abdominal pain and vomiting to severe – pancreatic necrosis, pancreatic pseudocysts and a systemic inflammatory process with shock and MOF Overall mortality 5-10% Pathophysiology of acute pancreatitis Obstruction of sphincter of oddi by a gallstone or sludge Prolonged alcohol intake >100g/day for >3-5 years – can cause precipitation of pancreatic enzyme proteins inside small pancreatic ductules
this ductal obstruction can cause premature activation of pancreatic enzymes
Signs and Symptoms Acute pancreatitis Steady upper abdominal pain (better with leaning forward) Nausea, vomiting Sudden onset = gallstone pancreatitis Several days of pain = alcoholic pancreatitis Signs Tachycardia – 100-140 beats/min Tachypneic Postural hypotension Mental status changes Upper abdominal distention 20% cont. Pancreatitis signs and sx Marked abdominal ttp Rigid boardlike abdomen Bowel sounds (hypoactive) Grey turner sign – ecchymoses of flanks Cullen sign – belly button ecchymosis
DDX anytime severe abdominal pain Suspect pancreatitis Perforated gastric or duodenal ulcers Ischemic SBO, strangulated Dissecting aneurysm Biliary colic Diverticulitis/appendicitis Inferior wall MI
Triage for pancreatitis Evaluate hemodynamic status Early, aggressive IVF for acute pancreatitis
Urgent ERCP – if evidence of persistent obstructing biliary obstruction
Necrotizing pancreatitis – prolonged hospitalization
Intestinal obstruction – SBO, HGSBO, PSBO Causes: #1 adhesions, #2 hernias #3tumors. Other causes: diverticulitis, foreign bodies (gallstone ileus stuck at ileocecal valve, saurkraut, rubber glove), volvulus (twisting on mesentery), intusseption (think telescoping), fecal impaction – which leads to stercoral colitis. SBO, PSBO pathophysiology A) Simple mechanical obstruction – ingested fluid, food + digestive secretions and gas in proximal segment, distal segment collapses, bowel wall becomes edematous and congested 80% of SBO’s resolve within 48 hrs without surgery Strangulating SBO, high grade SBO B) Strangulating obstruction, blood flow compromised 25% of patients with SBO Usually associated with volvulus, internal hernia, intusseption Gangrene occurs within 6 hrs Venous obstruction, arterial obstruction then rapid ischemia of bowel wall Bowel wall becomes edematous, infarcts Then gangrene, perforation commonly at site of tumor of diverticuli High grade SBO High grade SBO SBO, symptoms and signs A) Small bowel obstruction, immediate sx: Cramps, vomiting, obstipation, PSBO – might have diarrhea If pain is severe, constant – likely strangulated bowel Diffuse tenderness, hyperactive high pitched bowel sounds with rushes Shock and oliguria are serious signs of strangulation Large bowel obstruction signs, sx Milder symptoms, develops gradually Increased constipation, obstipation, abdominal distention, NO tenderness or minimal Uncommon to have vomiting, happens later Lower abd cramps, no bm’s Distended abdomen, loud borborygmi (stomach rumbling) Empty rectum Large bowel obstruction - volvulus Volvulus – abrupt onset, continous, colicky pain - Happens in sigmoid and cecum - Cecal volvulus requires immediate surgery - Sigmoid volvulus can have c’scope decompression first, usually keeps happening so will need sigmoid resection within a short time frame Large bowel obstruction diagnosis Supine, upright xrays – air fluid levels, dilated loops Leukocytosis, acidosis Infarcted bowel may produce a mass effect on xray Gas in bowel wall – pneumatosis intestinalis = gangrene Large bowel obstruction xray findings Distention of proximal colon prior to point of obstruction Cecal volvulus – large gas bubble in mid abdomen, LUQ Contrast enema will show point of obstruction with both cecal and sigmoid volvulus Contrast enema – can be therapeutic for sigmoid volvulus or c’scope decompression – bird beak deformity at site of twist Treatment of intestinal obstruction NGT, IVF, sometimes IV abx if suspect bowel ischemia, strict I/O’s Replete lytes – gut motility functions best with: K at 4.0 meq/L and Mg of 2.0 mg/DL Obstructing tumors – GI stent to bypass, or colostomy to bypass Obstruction key points MCC of obstructions are adhesions, if no history of prior surgery think hernia or tumor If pt vomiting, they will be third spacing – resuscitate Prolonged obstruction – worry re bowel ischemia, infarction, perforation Hemoperitoneum Abdominal Trauma – Blunt or penetrating Blunt – direct blow (kick), fall on bike handlebars Penetrating – GSW, knife Iatrogenic injuries, intraop Surgery, serosal tears or other injuries – Anne Lindstrom
Perforated AAA Traumatic abdominal injuries Most common blunt abdominal injury – splenic injury, splenectomy used to be commonly done Now, if stable, observe patients, serial exams, keep npo, serial cbc’s, transfuse prn, Unstable patient, laparotomy and/or angio/embolization, depending on severity of splenic injury Left shoulder pain, think splenic injury Grading system – Grade I-V, size of subcapsular hematoma, depth of capsular injury, injury of trabecular or hilar vessels, devascularization. Grades IV and V – most severe, Grade V, spleen is shattered Abdominal trauma – blunt vs penetrating (Malinowski, D., Dec 2013). Etiology Blunt abdominal trauma – direct blow, fall Penetrating – stab wounds less likely to be intraperitoneal than GSW
Signs/symptoms: abd pain and tenderness, can be mild if patient has more painful injuries (fractures) or mental status changes, shock, head injury – may not be able to communicate their pain. Inspect abdominal wall, AND look for entrance wounds on back, buttocks, perineum, lower chest
Abdominal trauma Rectal exam – gross blood think penetrating colon injury Hematuria, blood at meatus Perineal hematoma Diagnosis: Clinical evaluation – peritonitis, evisceration, unstable – xlap or diagnostic laparoscopy if GSW is etiology CT or Ultrasound CXR – look for free air under ______? Abdominal trauma Treatment: Rescusitate, surgery, monitor for complications Complications: abcess, ileus, obstruction (usually delayed and after laparotomy), hematoma rupture, bile leak or biloma (rare), abdominal compartment syndrome Abdominal aortic aneurysm (Rahimi, et al. Nov 2014) Affects 5-9% of population > 65 yrs Commonly found incidentally Think Ruptured AAA if pt’s history is: Sudden onset of severe low back pain, flank, abdominal or groin pain Syncope, even transient Hemoperitoneum Perforated AAA – surgical emergency Most fatal surgical emergency – 15,000 deaths per year, 13th leading cause of death 90% mortality rate Symptoms: pain, hypotension, pulsatile mass (found on exam > 50% of time) 5-9% of population > 65 yrs Most common patient: elderly male smoker*** Other risk factors: family history, increased height, increased weight, higher BMI, copd, CAD, htn, prior aneurysm repair (femoral or popliteal) Diagnosis of Ruptured AAA Physical exam, pulsatile mass, only 38% diagnosed this way Imaging studies: US standard imaging tool, if suspect ruptured – abdominal, pelvis CT Treatment of AAA >50% die before coming to ER, survival rate drops 1% per minute if present to ER in shock Emergent open repair if perforated, patient unstable Sometimes can be done endovascularly in these cases, going thru femoral vessels, Goretex or polyester graft If AAA found incidentally, often monitor and electively repair when Abscess Abdominal abscess (Ansari, P, 2014) Causes: Perforated viscus – appendix, intestine Trauma Iatrogenic – recent surgery serosal tears, anastomotic leak PID Inflammatory bowel disease Higher risk in trauma, perforations and weak immunity Signs, symptoms of abscess Leukocytosis Abdominal pain, tenderness Nausea, vomiting, anorexia Diarrhea
Diagnosis with CT abdomen, pelvis, esp with po and iv contrast if possible CBC, blood cultures should be done Treatment of abdominal abscess IV antibiotics, if abcess less than 4 cm in dimensions, should heal with abx alone Call IR department, percutaneous drainage Bariatric surgery patients in the ED
Dehydration/dumping syndrome:
Electrolyte/nutrient imbalance
Postop complications – early and late
Gastric balloon complications
Postop complications Roux en Y GBP Early complications: anastomotic/staple line leaks postop bleeding/infections bowel obstruction incorrect Roux limb reconstruction Late complications: anastomotic stricture marginal ulcers fistula formation weight gain nutritional defificiencies – vit B12, folate, Iron 1/3 of obese patients develop gallstones Bibliography www.merckmanuals.com/professional/gastrointestional www.medscape.com Advanced Surgical Recall by Lorne H. Blackbourne The ASCRS Manual of Colon and Rectal Surgery Editors: David E. Beck, Patricia L. Roberts, John L. Rombeau, and Michael J. Stamos www.medscape.com A Pancreatic Emergency, Mergener, Klaus M.D. November 4th, 2003 Drake et al. Time to appendectomy and risk of perforation in acute appendicitis, JAMA Surgery 2014 Aug: 149(8):837-44. www.medscape.com Abdominal Aortic Aneurysm, Rahimi et al. November 19th, 2014. Merck Manual professional version. Abdominal trauma. Darren Malinowski M.D. Dec 2013
Bibliography Intra-abdominal Abscesses. Merck Manual, Professional version. Ansari, P. June 2014.