Mind Mapping - (From Wikipedia and www.mindmapping.com) A diagram used to visually outline information.

. Often created around a single word or text, placed in the center, to which associated ideas, words and concepts are added. Major categories radiate from a central node, and lesser categories are sub-branches of larger branches. Categories can represent words, ideas, tasks, or other items related to a central key word or idea. A natural organizational structure that radiates from the center and use lines, symbols, words, color and images according to simple, brain-friendly concepts. A Mind Map converts a long list of monotonous information into a colorful, memorable and highly organized diagram that works in line with your brain's natural way of doing things. Can be drawn by hand, either as "rough notes" during a lecture or meeting, or as higher quality pictures with software programs when more time is available. The term "mind map" was rst popularized by British popular psychology author and television personality Tony Buzan when BBC TV ran a series hosted by Buzan called Use Your Head. Buzan suggests the following guidelines for creating mind maps: Start in the center with an image of the topic, using at least 3 colors. Use images, symbols, codes, and dimensions throughout your mind map. Select key words and print using upper or lower case letters. Each word/image is best alone and sitting on its own line. The lines should be connected, starting from the central image. The central lines are thicker, organic and thinner as they radiate out from the centre. Make the lines the same length as the word/image they support. Use multiple colors throughout the mind map, for visual stimulation and also to encode or group. Develop your own personal style of mind mapping. Use emphasis and show associations in your mind map. Keep the mind map clear by using radial hierarchy, numerical order or outlines to embrace your branches. Concept maps - Mind maps differ from concept maps in that mind maps focus on only one word or idea, whereas concept maps connect multiple words or ideas. Also, concept maps typically have text labels on their connecting lines/arms. Mind maps are based on radial hierarchies and tree structures denoting relationships with a central governing concept, whereas concept maps are based on connections between concepts in more diverse patterns. However, either can be part of a larger personal knowledge base system.

General Comments on Life Threatening Abdominal Emergencies

Although not specically stated each time below, all of these require pain and emesis control as well as uid resuscitation Disposition is ICU or OR

Acute Mesenteric Ischemia

Pathophysiology lack of oxygenation of small or large intestine due to an interruption of vascular ow 3 categories Arterial occlusion: embolus to SMA (50%) and SMA thrombosis (25%) Venous occlusion: 5-15% Non-occlusive mesenteric ischemia (NOMI) (20%) usually systemically/critically ill, hypoperfusion states strangulated bowel 4 contributing factors to extent of disease hypoxic injury reperfusion injury toxic luminal factors presence of bateria Clinical Presentation Risk factors elderly post-op or ICU patients, especially if they are on vasopressors (norepinephrine) cocaine use hypercoagulable Character of the abdominal pain Abrupt onset (usually - may develop over minutes to weeks) Severe, disproportionate to physical exam localized or diffuse colicky or constant Associated symptoms fever, nausea, vomiting, anorexia, diarrhea, GI bleeding (15%) Physical exam may be normal if present in shock --> most likely will be fatal febrile, tachycardic usually have an abnormal exam, but may not be as severe as the disease process Diagnosis Labs hemoglobin - usually high due to hemoconcentration may see a very high leukocytosis modest amylase elevation lactate is elevated, but only if infarction is already present (need to suspect before this happens!) metabolic acidosis CTA = bowel wall thickness with pneumotosis, streaky mesentery and thrombosis Treatment key is rapid diagnosis and stat surgical consult for OR***

 **Discuss with patient their preference. Given the usual age group, comorbidities, and high mortality, some may opt for DNR resuscitate with IVF and blood Complications Mortality > 50% and up to 80% with a delay in diagnosis Multi-Organ Dysfunction Syndrome (MODS) Ruptured AAA Pathophysiology >50% increase in the aortic diameter or and infrarenal aortic diameter >= 3 cm < 4cm is low risk for rupture 4-5cm has a 5 year rupture risk of 3-12% >5 cm has a 5 year rupture risk of 25-40% occurs in 2% of elderly, and this number is increasing gradual increase in size occurs, followed by rupture, exsanguination and death Clinical Presentation Risk Factors smoking (strongest risk factor) atherosclerosis genetic older age male > female Start out asymptomatic at 4-5cm, 50 % are palpable at 5-6cm 76% are palpable usually an incidental nding on CT May become symptomatic if rapidly progresses in size Variable location of pain (abdomen, back, ank) may radiate to the groin/testis pain is usually not affected by movement approximately 10% have severe marked pain and TTP prior to rupture Associated symptoms syncope hematuria hydronephrosis or leg swelling - due to compression new or worsening HTN Once ruptured Classic picture is back pain, hypotension, pulsatile mass (although see all 3 together only 1/2 of the presentations) Diagnosis US - can detect presence of AAA but not rupture CT - more accurate in size and any leakage, but cannot undergo if unstable Aortography - done only for surgical planning Treatment Asymptomatic 4-5 cm = usually watch > 5 cm = usually elective repair if decent surgical candidate Ruptured Stat vascular surgery consult

straight to OR (**see below) T&C blood products resuscitation - consider permissive hypotension as long as perfusing ok **Discuss with patient their preference. Given the usual age group, comorbidities, and high mortality, some may opt for DNR Complications GI bleeding due to arotoenteric stula - usually occurs in presence of a previous repair Aortic occlusion (Leriche syndrome) Mortality untreated, symptomatic patients usually dead in 1 year (34% @ 1 mo, 74% @ 6 mo) operative mortality 2-7% rupture mortality 90% high litigation rate if missed Ascending Cholangitis Pathophysiology bacterial infection of biliary system usually associated with CBD stones and obstruction Clinical Presentation think of it in your septic patient without a source typical clinical pictures below are only seen 50% of the time Risk Factors diabetes elderly debilitated recent biliary instrumentation Charcot Triad RUQ pain (intermittent) & tenderness jaundice (though usually mild) Fever Reynolds Pentad Charcots Triad mental status changes shock Diagnosis Labs leukocytosis with left shift hyperbilirubinemia increased alk phos US stones in CBD (sensitvity 25-68% CBD dilitation (5%) Treatment antibiotics sepsis resuscitation surgical consult for urgent biliary decompression / endoscopic sphincterotomy Complications Mortality 40 % perforation, emphysema or empyema = emergent surgery

Necrotizing Acute Pancreatitis Pathophysiology autodigestion by inappropriate intrapancreatic activation of proteolytic enzymes (primarily trypsin) and release of other substances (such as lipase) resulting in coagulation necrosis and vascular injury, thereby causing hemorrhage, edema and pain Necrotizing acute pancreatitis is a systemic disease intravascular volume loss due to massive edema and exudation of uid into the peritoneal cavity, to systemic effects of released vasoactive substance or pancreatic hemorrhage - can lead to frank hypovolemic shock cardiac dysfunction, renal failure, CNS dysfunction, DIC, pleural effusion, ARDS Pancreatitis in general: Most acute cases are caused by alcohol and cholelithiasis (80-90%) Most chronic cases are triggered by excessive alcohol consumption (75%) and the rest are idiopathic, congenital, neoplasia, trauma, or metabolic disease (CF, hyperlipidemia, hyperparathyroidism) Clinical Presentation Risk Factors alcohol use cholelithiasis Abdominal pain usually severe and constant, exacerbated by recumbency and better sitting up/exing may be diffuse but more likely localized to epigastrium or LUQ may radiate to the back (retroperitoneal irritation) epigastric tenderness, guarding and peritoneal irritation on exam Associated sx N/V fever, tachycardia, diaphoresis Cullens sign (periumbilical ecchymosis) and Grey Turner sign (ank ecchymosis) are uncommon signs of retroperitoneal hemorrhage Diagnosis remember that many disease may occurs simultaneously with pancreatitis diagnosis is based upon clinical picture (H&P) and supported by labs; there is no direct measurement Labs Amylase - somewhat sensitive but not specic, rapidly clearly by kidneys (within 72h) Lipase - 99% specic (especially is 3 x normal) Imaging US - identify biliary disease and possibly pancreatic edema and uid collections CT with IV contrast - can evaluate presence and degree of necrosis/hemorrhage and associated abnormalities (pleural effusion, ascites) Ranson Criteria for predicting severity - On Admission Age >55 WBC > 16,000 Glucose > 200 LDH > 350 AST > 250 APACHE II score > 8 is high mortality Treatment

usually supportive therapy to rest the pancreas aggressive uid resuscitation correct electrolyte abnormalities (hypokalemia, hypocalcemia, hypomagnesemia) some studies advocate for antibiotics in cases of necrotizing pancreatitis to decrease incidence of sepsis and mortality Complications Mortality 5% Local Necrosis pancreatic uid collections (pseudocyst or abscess) necrotizing obstruction or stulization of colon GI bleed (ulceration, varices, rupture of pseudoaneurysm) right-sided hydronephrosis) splenic rupture/hematoma Systemic shock coagulopathy respiratory failure acute renal failure hyperglycemia hypocalcemia subcutaneous nodules retinopathy psychosis Intestinal Obstruction Pathophysiology 4% of ED presenting complaints of nontraumatic abdominal pain lasting < 7 days accounts for 20% of surgical admissions 20% involve the colon Most small bowel obstructions (SBOs) are due to adhesions (50%) In adults, other causes are inammatory bowel disease (Crohns), hernias, neoplasm In peds, intussusception, hernia, congenital The obstruction prevents ow of uid and bowel contents, so it accumulates proximally. This results in increased pressure and thus hypersecretion and a decrease in absorption. Because of the hypersecreations and poor absorption, volume loss can be up to 9 L in 24h Clinical Presentation Risk Factors >50 history of abdominal surgery or colorectal cancer Abdomen intermittent and colicky cramps Q3-10 min crescendo - descrescendo high pitched and increased bowel sounds distension and diffuse tenderness; may not notice rebound due to high levels of distension Associated symptoms vomiting (usually occurs AFTER the onset of pain) obstipation/constipation (diarrhea may occur initially or with partial obstruction)

 orthostatic hypotension if severe volume depletion Diagnosis ensure a complete PE for hernias Labs: may see a metabolic acidosis and electrolyte abnormalities if vomiting Abdominal xrays limited role; will be completely normal in 5% may see air uid levels (string of beads) and dilated loops CT allows assessment of transition point and degree of obstruction Treatment IVF resuscitation antibiotics if fever or suspected infarction correct electrolyte abnormalities NGT?? - maybe if persistently vomiting Surgical consult Complications mortality 5% (down from 60% in 1900) strangulation leading to infarction & sepsis hemorrhagic necrosis gangrene leakage of abdominal contents peritonitis & sepsis Ruptured Ectopic Pathophysiology one of the leading causes of maternal M&M frequency increased > 5-fold since 1970 (infertility treatments) results from implantation of a fertilized ovum at a site other than the endometrium most frequent site is lateral two-thirds of fallopian tube (80%) medial one-third of fallopian tube (12%) interstitial or cornual implantation (3%) extratubal (5%) = ovary, abdominal cavity or cervix interstitial and extratubal highest mortality due to hemorrhagic tendencies heterotopic = implantation both in endometrium and ectopic (infertility treatments) Clinical Presentation Risk Factors (42% have no known risk factors) abnormalities of fallopian tube (PID, prior tubal ligation, previous ectopic) advanced maternal age IUD Lower abdominal pain, vaginal bleeding & positive pregnancy test pain is most common symptom - but quality, character and location are variable abnormal bleeding occurs is 55-85% abdominal pain without bleeding occurs in 1/3 of patients tenderness on pelvic exam is common VS will likely be normal until signicant blood loss has occurred, then will see signs of hemorrhagic shock (may see paradoxic bradycardia) Diagnosis urine HCG screens for pregnancy, US locates it and serum HCG helps to date (roughly) the pregnancy and guide US ndings HCG, UA, CBC & type and screen (unless shocky then want cross)

 normal intrauterine pregnancy - bHCG increases >66% in 4 hours; if this isnt occurring they need further evaluation of abnormal pregnancy US gestational sac in normal IUP visible on transabdominal at bHCG 6000-6500 (5-6 weeks gestation) and transvaginal once bHCG is over 1000-1500 may see signs of ectopic if bHCG levels are below this cutoff. most helpful if it can EXCLUDE the diagnosis by revealing a normal IUP (unless concerned for heterotopic) Treatment based upon three categories of hemodynamic stability hypovolemic shock treated for shock and go to OR acute abdomen but stable anticipate shock BEDSIDE US stat gyn consult complaints suggesting ectopic but low risk for immediate deterioration serial HCGs in 48hrs usually most helpful here, especially if patient falls into the window of positive pregnancy test but nondiagnostic US (4-5 weeks gestation) you may consider medical management for stable unruptured ectopic in consultation with GYN Complications associated with intraabdominal hemorrhage with shock, which may be refractory hemorrhagic shock (cause of death in 85% of fatalities) other high cause of mortality is mis-diagnosis infertility