 \212Primary hemorrhage : I.e., continuous bleeding, starting during surgery. Replace blood loss. If severe, return to the operating room for ade- quate hemostasis. Treat shock vigor ously (p. 745). \212Reactive hemorrhage : Hemostasis appears secure until BP rises and bleeding starts. Replace blood and reexplore wound. \212Secondary hemorrhage occurs 1 \200\2232 wks postop and is the result of infection. Table 13.15 Discharging patients after day-case surgery After day-case surgery, don \200\231t discharge until \200\234LEAP-FROG \200\235 establish ed: L ucid, not vomiting, and cough reflex established E asy breathing; easy urination A mb ulating P ain relief + postop drugs dispensed + given. Do they understand doses? F ollow-up arranged R hythm, pulse rate, and BP checked one last time. Is trend satisfactory? O perat ion site checked and explained to patient G ive the primary care provider a call is 3 If a patient has a stoma, this should be attended to by a stoma thera- pist by at least 4 wks after surgery because the size of the stoma often changes. 4 If patient is being treated for a cancer and requires further adjuvant ther- apy, the onc ologist appreciates a check from the surgeon prior to initiat- ing therapy. For day-case surgery, see Table 13.15. The acute abdomen An acute abdomen refers to any sudden manifestation of a nontraumatic dis order involving pain in the abdominal area for which urgent surgical exploration may be nec essary and repeated examination is essential. Begin by obtaining a careful history of the p ain Ask about the location of the pain, any spreading or shifting, duration, mode of onset, progression, character (dull, sharp, crampy), and any other associated symptoms including nausea, vomiting, diarrhea, obstipation, constipation, hematuria, etc. Types of pain Viscer al pain is mediated by the afferent C fiber and usually is felt in the midline. It is slow in onset and dull. It can be elicited by distension, inflam- mation, or ischemia. Parietal pain is mediated by both C fibers and A delta nerve fibers. Abdominal parietal pain is more focused as a result of direct irritation of the somatically innervated parietal peritoneum by pus, bile, GI secretions, etc. It is conventionally described as occurring in four abdo minal quadrants (see Figure 13.4). 466 Other relevant aspects of history include: \212 \212 \212 \212 \212 Physical exam Obse rve patient: Lying still or writhing, pallor, sweating, feverish? Inspect the abdomen for d istension, bruising; look for gray Turner \200\231s sign for hemorrhagic pancreatitis. Ausc ultate for bowel sound: Hypoactive indicates intra-abdominal infection; hyperactive sounds are noted in bowel obstruction. Palpate in a sequential pattern with the most tender area b eing touched last. Specific signs on palpation include: \212 \212 y r e g r u S Medical and surgical history Menstrual history Drug history Family history Travel history Peritoneal inflammation causing rectus muscle rigidity. Guarding: Rebound tenderness: gentle pressure; acute appendicitis. Murphy \200\231s sign: a brupt arrest of inspiration secondary to pain; acute cholecystitis. Iliopsoas sign: psoas a bscess in Crohn \200\231s disease. Obturators sign: discomfort in the groin area; incarcera ted obturator hernia. Costovertebral angle tenderness: angle; renal colic. Discomfort is felt upon releasing your hands from \212 Palpation in the right subcostal area while inspiring causes \212 Active flexion or passive extension of the hip illicit pain; \212 Internal or external rotation of the flexed thigh may cause \212 Punch tenderness of the costovertebral Tests CBC, electrolytes, amylase, LFT, \222 -HCG, urinalysis; laparoscopy may avert open s urgery. CT can be helpful provided it is readily available and causes no delay. Preop care Anesthesia compounds shock, so resuscitate properly first, unless blood is being lost faste r than it can be replaced in ruptured ectopic pregnancy or a leaking abdominal aneurysm (p. 475). Also do the following: 1 Establish good IV access (two 18-g IVs) and begin resuscita tion with 0.9% saline. 2 Insert Foley and NGT. 3 Type and cross-match. 4 ECG, AXR, CXR 5 Begin broad-spectrum anti biotics if infection is suspected. 6 Consent and manage pain. Clinical syndromes that usual ly require urgent surgical exploration \212 Spleen, aorta, ectopic pregnancy. Shock secondary Rupture of an organ: to cardiovascular co llapse (e.g., faints or orthostatic BP \206\223 by \200\234 20 mm Hg on standing) is a le ading sign. Abdominal swelling may be seen. Delayed rupture of the spleen may occur weeks a fter trauma. Perforation of peptic ulcer, diverticulum, appendix, bowel, or Peritonitis: ga ll bladder. Signs: Prostration, shock, lying still, tenderness ( rebound/ percussion pain ), board-like abdominal rigidity, guarding, and no bowel sounds. Erect CXR may show gas und er the diaphragm on the right side usually or free intraperitoneal air (see Figure 13.3). N B: Acute pancreatitis (p. 487) may cause these signs, but does not require a laparotomy, so always check serum amylase. 467 \212 Syndromes that may not require urgent exploration \212 E.g., diverticulitis, cholecystitis, salpingitis, and appendici- Local peritonitis: tis. If abscess formation is suspected (palpable mass, fever, and WBC \206\221 ), arrange a diagn ostic US or CT. Drainage can be percutaneous (US- or CT-guided) or by laparotomy. Look for a \200\234sentinel loop \200\235 on the plain AXR. \212Colic is a regularly waxing and waning pain caused by muscular spasm in a hollow viscu s; e.g., gut, ureter, uterus, or gallbladder. (In the latter, pain is often dull and consta nt.) Colic causes restlessness, unlike peritonitis. Other causes of abdominal pain that may masquerade as an acute surgical abdomen in which su rgery is not indicated Myocardial infarction Pneumonia (p. 160) Sickle-cell crisis (p. 618) Pheochromocytoma Gastroenteritis or urinary tract infection (UTI) Tabes (p. 576) (p. 315) Diabetes mellitus (p. 268) Zoster (p. 558) Pneumococcal peritonitis Tuberculosis (p. 552) T yphoid fever (p. 590) Porphyria (p. 682) Henoch \200\223Sch nlein Thyroid storm Narcotic a ddiction Malaria (p. 549) Cholera (p. 585) Yersinia enterocolitica (p. 583) Lead colic PAN (p. 417) Accuracy in diagnosing acute abdomen is 45% so always maintain a high index of suspicion. It is better to have a negative surgical exploration than to miss a surgical emergency. Wit h newer minimally invasive techniques in surgery, patients recover quickly. These diagrams go over the causes of an acute abdomen manifested as free intra-abdominal air or peritoniti s. Intestinal ischemia Acute onset of severe abdominal pain should always suggest the idea of bowel ischemia. Etiology can be classified as the following: \212 Strangulated bowel, large-vessel embolic or thrombotic event, Occlusive: ligation of the IMA during aortic surgery Vasospastic: titis, pancreatitis, acal culous cholecystitis Inflammatory: \212 Small-vessel nonocclusive intestinal ischemia, ischemic hepa- \212 Acute intestinal ischemia The most common cause is arterial embolism. Emboli originat e from the heart in >75% of cases and lodge preferentially just distal to the origin of the superior mesenteric artery (SMA) (see Figure 13.5). Low-flow states usually reflect poor c ardiac output but there may be other factors, such as DIC. Venous thrombosis is uncommon an d tends to affect smaller lengths of bowel. The incidence of acute colonic ischemia after a ortic surgery is 5 \200\2239%. Other risk factors include atrial fibrillation, recent myoca rdial infarction, valvular heart disease, recent cardiac or vascular catheterization, ather osclerotic disease, hypercoagulable state. A classical clinical triad of occlusive ischemia : Acute severe abdominal pain, no abdominal signs, and rapid hypovolemia (causing shock). P ain tends to be constant and central or in the right lower quadrant. The degree of pain is often out of proportion to the clinical signs. Nonocclusive ischemia: Ischemic colitis; usu ally presents with generalized abdominal pain, anorexia, bloody stools, and abdominal diste nsion. Tests: There may be Hb \206\221 (due to plasma loss), WBC \206\221 , modestly elev ated plasma amylase, elevated lactate, elevated creatine phosphokinase (CPK), and a persist ent metabolic acidosis. Early on, the AXR shows a gasless abdomen. Arteriography helps, but many diagnoses are made at laparo- tomy. CT/MR angiography may provide a noninvasive alter native to con- ventional arteriography. Lupus, Beh et \200\231s disease, angioedema 468 Treatment: Fluid replacement, antibiotics (broad spectrum) secondary to the risk of translo cation and, usually, heparin. If arteriography is performed, thrombolytics may be infused l ocally via the catheter. At surgery, dead bowel must be removed. What needs to be removed c an be a difficult surgical decision and often the Woods \200\231 lamp can help. Revasculari zation of potentially viable bowel should be attempted but is difficult. A second-look lapa rotomy may be required. Chronic intestinal ischemia Small bowel chronic ischemia is typical ly due to SMA disease. Less common causes of ischemia include vasculitis, trauma, radiother apy, and strangulation (e.g., hernias). Chronic ischemia presents quite a different picture from acute ischemia, with severe, colicky postprandial abdominal pain ( \200\234gut claudi cation \200\235) with weight loss (food hurts). Auscultation may reveal abdominal bruits. D iagnosis can be made by duplex US scan of the aorta or on angiography. Treatment requires r evascularization with either endovascular or open surgical techniques. Colonic ischemia usu ally follows low flow in the watershed areas between the inferior mesenteric artery and the superior mesenteric branches . Griffith \200\231s (splenic flexure) and Sudeck \200\231s ( rectosigmoid) points (see Figure 13.5). Patients present with left -sided abdominal pain an d bloody diarrhea. There may be fever, tachycardia, blood per rectum, and a leukocytosis. U sually this \200\234ischemic colitis \200\235 resolves, but it may progress to gangrenous ischemic colitis. Colonoscopy will demonstrate a spectrum of findings beginning with hypere mia and ending with frankly dead mucosa. Barium enema may show \200\234thumb-printing \200 \235 indentation of the barium due to submucosal swelling. CT will demonstrate diffuse colo nic thickening. Symptoms may be mild and result in stricture formation. Treatment may be su pportive, with fluid replacement and antibiotics, or involve surgical removal of the colon with formation of an ileostomy in severe cases. Gangrenous ischemic colitis This may follow ischemic colitis and is signaled by more severe pain, peritonitis, and hypovolemic shock. After resuscitation, necrotic bowel should be resected and a colostomy or ileostomy formed. y r e g r u S Figure 13 .3 Erect 469 Figure 13.4 The causes of parietal pain in the four quad- rants of the abdomen Gastrointestinal bleeding GI bleeding is manifested as hematemesis, melena, or hematochezia . Melena can be from a gastroduodenal source, as well as from the colon. Small bowel bleedi ng is rare (<5%). The most common causes of gastrointestinal bleeding are listed below: Upp er gastrointestinal tract: \212 \212 \212 \212 \212 \212 Small intestinal bleeding: \212 \212 \212 \212 \212 470 Peptic ulcer disease Gastritis Gastric neoplasia Mallory \200\223Weiss syndrome (see Table 13.16) Delafore lesion Varices Angiodysplasia Meckel \200\231s diverticulum Crohn \200\231s enteritis Neoplasia NSAID abus e Large intestinal bleeding: \212 \212 \212 \212 \212 \212 Initial management Directed toward resuscitation and includes the following: 1 Establish IV access with two large-bore IVs (16 g). 2 Draw blood for type and cross-match, CBC, PT, PTT, and electrolytes. 3 NGT as pirate to rule out (R/O) upper GI source, although can be y r e g r u S Diverticulosis (30 \200\22350%) Colitis \200\224inflammatory, infectious, or ischemic (20%) Angiodysplasia (10%) Arteriovenous (AV) malformations Anorectal disease Neoplasia inaccurate. 4 Foley catheterization and O administration is based on the severity of the bleed. 5 Obtain history regarding the use of warfarin, Plavix, aspirin, or NSAIDs. Diagnostic test s For bleeding <1 cc/min: esophagogastric-duodenoscopy (EGD) and colonoscopy For bleeding \211 1 cc/min: Angiography for localization and possible treat- ment, radionucleotide blee ding scan, endoscopic evaluation, surgery. Therapeutic interventions Most causes of upper g astrointestinal bleeding are managed endoscopically with either electrocautery, heater prob e, banding, or injection of epinephrine. Similarly, lower tract bleeding can also be manage d endoscopically but more frequently will require surgery. Arterial embolization or coiling is routinely performed for gastroduodenal bleeding because of the low risk of end-organ is chemia. However, only highly selective embolization can be performed for colonic bleeding s econd- ary to the risk of ischemia following embolization (20%). Surgical intervention for colonic bleeding from a source that has not been identified either colonoscopically or angi ographically is a subtotal colectomy . If the bleeding source has been identified, a coloni c segmentectomy can be performed. The decision of whether to re-anastomose the bowel is bas ed on the overall health of the patient and the amount of bleeding that has occurred. A tra nsfusion requirement of >10 units is associated with a higher anastomotic leak rate. The co llateral arterial blood supply to the intestinal tract 471 Figure 13.5 Grifiiths point Phrenic a. Celiac a. Pancreatico-duodenal a. Ao Arc of Riolan SMA IMA Marginal a. Sudeck s point IIA Superior Middle Inferior Hemorrhoidal aa. Table 13.16 Mallory \200\223Weiss syndrome A 1 \200\2234 cm submucosal tear occurring at the gastroesophageal junction usually followi ng forceful retching. The lesion is diagnosed on EGD. Brisk bleeding will require surgical repair by the creation of an open high gas- trotomy and oversewing the bleeding ends. Alter natively, with less brisk bleeding, the lesion can be controlled with endoscopic electrocau tery. 472 Trauma Trauma is the leading cause of death in the United States for individuals <45 yrs. D eath as a result of trauma can occur immediately as a result of hemorrhage, severe head inj ury, loss of airway, pneumothorax, and fatal heart injury. Other causes of death can be les s immediate and include sep- sis and multiple organ system failure. Surgical training under the auspices of Advanced Trauma Life Support (ATLS) has produced an algorithm for maximizi ng the care of the trauma patient. The basics of this algorithm are the ABCDE of primary su rvey in trauma care: A. Airway and cervical spine protection An airway can be maintained wi th a simple jaw thrust and bagging. A definitive airway can be established either by orotra cheal, nasotracheal, or surgical means and is indicated in apnea, inability to maintain air way or oxygenation by other means, and for airway protection in inhalation injuries, head injuries, etc. i. Spina l cord injuries must be assumed in all patients and therefore inline manual cervical tracti on should be used during intubation. ii. A surgical airway should be performed through the cricothyroid membrane when oral or nasotracheal intubation cannot be success- fully perform ed. y r e g r u S B. Breathing and ventilation Expose the chest to assess breathing. Keep an eye out for the following disorders that will inhibit adequate breathing: i. Tension pneumothorax: Hypotens ion with distended neck veins; treat initially with large-bore IV placed in the second inte rcostals space in the mid-clavicular line. ii. Flail chest: Multiple rib fractures often associated with pneumotho- rax and pulmonary contusion. iii. Massive hemorrhage and hemothorax: Requires thoracostomy and possibly thoracotomy if > 1,000 cc drain immediately or patient becomes hemodynamically unstable. iv. Open pneumothorax: Initial treatment is the placement of a sterile occlusive dressing t aped on three sides with a flutter valve. Definite treatment is a chest tube. C. Circulation i. Shock: Recognize and resuscitate with 0.9% NS or LR. Assume hemor- rhage and be prepared to give O-neg blood. Other causes of shock in trauma include tamponade, ten sion pneumothorax, air embolus, myo- cardial contusion, and spinal cord injury resulting in neurogenic shock. Cardiac tamponade can be diagnosed on bedside US (focused assessment wit h sonography for trauma \200\224FAST). Management usually requires peri- cardial window. ii. Interventions: 1. Apply direct pressure to external bleeding. 2. Two large-caliber IVS and possibly cordis for large-volume rapid infusion. 3. Infusion of warmed crystalloid using 3:1 rule and give type-specific or O-neg blood for class III or IV shock (see Table 13.17). 4. Send patient \200\231s blood for type and cross-match, hemoglobin, chemis- tries, \222 -HCG in female patients. Table 13.17 Classes of shock 473 Class I . Blood volume loss <15% associated with mild tachycardia Class II . Blood volume l oss 15 \200\22330%. Signs include tachycardia, tachyp- nea, \206\223 pulse pressure Class III . Blood volume loss of 30 \200\22340%. Marked tachycardia and tachyp- nea, hypotension and confusion Class IV . Blood volume loss of >40%. Severe tachycardia, hypotension, narrow pulse pressure, obtundation Table 13.18 Glasgow Coma Scale Assessment of eye opening (1 \200\2234) Assessment of verbal response (1 \200\2235) Assessm ent of motor response (1 \200\2236) If total is >8, high potential for severe CNS injury. D. Disability Refers to a brief neurologic assessment via a measurement for the level of co nsciousness, also known as the Glasgow Coma Scale (see Table 13.18). Altered mental status may be the result of hypoxia, shock, drugs, alcohol, but consider injury to the central ner vous system until proven otherwise. E. Exposure Undress the patient to evaluate every area to make sure no injury is missed. Br oken bones are commonly missed in the intoxicated trauma patient. Once this is done, the pa tient should be covered to prevent hypothermia. Following the primary survey for trauma, a secondary survey is undertaken. This begins with an AMPLE history: Allergies, Medicines, Past medical and surgical history, Last meal, Expo sures (tetanus). A complete head-to-toe examination is performed and vital signs are reasse ssed. Any further inter- ventions are arranged. F. FAST (Focused Assessment with US in Trau ma) Exam Bedside US examination of the chest and abdomen to evaluate for free fluid in the pericardium or abdomen. Indications: Thoracoabdominal trauma in an unstable patient. Evaluation: Rapid, sequential exam of the pericardial sac, right upper quad- rant (RUQ) interface between the liver and k idney, left upper quadrant (LUQ) splenorenal fossa, pelvic area around bladder. Aortic aneurysm and dissection Aortic aneurysm True aneurysms are abnormal dilatations of a rteries. They should be distinguished from \200\234false \200\235 aneurysms, which are col lections of blood around a vessel wall (e.g., following trauma). Aneurysms may be fusiform or sac-like (e.g., berry aneurysms in the Circle of Willis). Common sites: Aorta, iliac, fe moral, and popliteal arteries. Atheroma is the usual cause; also connective tissue disorder s (e.g., Marfan \200\231s, Ehlers \200\223Danlos) and infections (e.g., endocarditis or ter tiary syphilis). Complications from aneurysms: Rupture, thrombosis, embolism, pressure on o ther structures, infection. Symptomatic and ruptured abdominal aortic aneurysm (AAA) Signs and symptoms: Intermittent or continuous abdominal pain (radiates to back, lower abdomen, o r groins), collapse, an expansile abdominal mass (i.e., the mass expands and contracts: Swe llings that are pulsatile merely transmit the pulse; e.g., nodes overlying arteries), and m ottling over the lower extremities. Other associated findings in patients with AAA include hypertension 40%, peripheral aneurysms 20%. The main differential diag- noses are myocard ial infarction and pancreatitis. If in doubt, assume a rup- tured aneurysm. Management: 1 S tart two large-bore IVs. 2 Send type and cross-match for 12 units, CBC, electrolytes, ECG, and, if in doubt, cross-table lateral plain movie of the abdomen, which will demon- strate aortic calcification. 474 3 Take the patient to the operating room. Do not order other investiga- tions. You will waste precious time. 4 The patient is prepped and draped while awake and only put to sleep when the surgeon is r eady to cut. Surgery involves clamping the aorta above the leak (usually at the diaphragmat ic hiatus). Alternatively, a large-bore Foley can be placed in the proximal end of the aort a and inflated to tem- porarily tamponade the bleeding. A Dacron graft (e.g., \200\234tu be graft \200\235 or, if significant iliac aneurysm also, a \200\234trouser graft \200\235 with each \200\234leg \200\235 attached to an iliac artery)may be used to replace the ruptured aorta. Presently, the role of endolu minal placement of stent grafts for ruptured AAA is being investigated (see below). y r e g r u S Outcomes: Mortality when treated: 21 \200\22370%; untreated: 100%. Asymptomatic AAA Prevale nce: 3% of those >50 yrs. Trials suggest that aneurysms <5.5 cm across might safely be moni tored by regular examination and US/CT. Risk of rupture below this size is <1%/ yr, compare d with 25%/yr for aneurysms >6 cm across. Aneurysms larger than this, rapidly expanding (> 1 cm/ yr), or symptomatic should be considered for elective surgery. It should be noted tha t 75% of aneurysms monitored in this way will eventually need repair. Elective operative m ortality is 5%. Studies show that age >80 yrs is not a reason to decline surgery. Open ele ctive and emergent operations can be avoided by the placement of an endoluminal stent, also known as EVAR (endovascular aneurysm repair). 60% of all aneurysm repairs are done via EVA R. Indicated in patients with suitable anatomy and at high risk for conventional repair. 50 % will not have suitable anatomy. EVAR is associated with shorter hospital stays and fewer transfusions than conventional surgery. There is also a risk that the stent will leak. Type s of Endoleaks Type I II III Description Inadequate seal at proximal or distal attachment site Flow into aortic aneurysm al sac from branch vessel (lumbar) Endograft fabric tear or failure of seal between compone nt grafts IV Endograft fabric porosity Preparation for surgery is similar to the above preparation, with the addi- tion of a preop erative cardiac and pulmonary evaluation. A mechanical bowel prep is preferred. Urinalysis should be performed and antibiotics given prior to incision. Postoperative care and complic ations: Patients will usually spend time in the ICU postoperatively. Peripheral pulses are monitored. The most common complications following aortic surgery include: 1 Renal insuffic iency: Usually hypovolemic, but you must be concerned about injury from aortic cross-clamping leading to embolization. 2 Ischemic colitis: Secondary to inferior mesenteric artery (IMA) ligation. 475 Can start as early as 12 h after surgery. 3 Spinal cord ischemia: Occurs when the blood supply to the distal spinal cord is compromis ed and results in paraplegia. The injured artery is the artery of Adamkiewicz and can arise anywhere from T8 to L4. Aorta dissection Blood splits aortic media with sudden tearing chest pain ( radiation to back). As dissection unfolds, branches of the aorta occlude, leading sequen- tially to hemi plegia (carotid), unequal arm pulses and BP, paraplegia (ante- rior spinal artery), and anu ria (renal arteries). Aortic valve incompetence and myocardial ischemia may develop if diss ection moves proximally. Aortic dissection is classified according to the Stanford classifi cation (Table 13.19). Management: Type A dissections: Because of the risk of intrapericardi al rup- ture and left ventricular failure, all patients with type A dissections should be c onsidered for surgery. Cross-match 10 U blood; do ECG and CXR (expanded mediastinum is rare ). Perform CT/MRI or transesophageal echocardiography (TEE). Admit to ICU. If hypertensive: Keep systolic at Table 13.19 Stanford classification Type A. Primary intimal tear located in the ascending aorta Two-thirds of all dissections E hlers \200\223Danlos syndrome, Marfan \200\231s Type B. Dissection limited to the descendin g thoracic aorta with the intimal tear located near the subclavian artery One-third of all dissections Ruptured atherosclerotic plaque 100 \200\223110 mm Hg; labetalol (p. 135) or esmolol (p. 122; t is ultra-short) by IVI i s helpful here. Perioperative mortality: 12%. Type B dissections: May extend and cause symp toms as a result of poor flow to peripheral vessels. Symptomatic extension is treated surgi cally or by endovascular techniques with fenestration, stenting, or bypass. To prevent exte nsion, antihypertensive therapy is started. Limb ischemia Chronic ischemia is due to atherosclerosis. Its chief feature is intermittent claudication (from the Latin meaning \200\234to limp \200\235). Cramping pain is felt in the calf, thigh, or buttock after walking for a fairly fixed distance (the claudication dis tance). Ulceration, gangrene, and foot pain at rest (e.g., burning pain at night relieved b y hanging legs over side of bed) are cardinal features of critical ischemia. See Figure 13. 6. Signs: Absent pulses; cold, white leg(s); atrophic skin; punched out ulcers (often painf ul); postural color change. Tests: Exclude DM, arteritis (erythrocyte sedimentation rate/c- reactive pro- tein [ESR/CRP]). Do CBC (anemia, infection), electrolytes (renal disease), li pids (dyslipidemia), syphilis serology, ECG (cardiac ischemia). Do coagu- lation profile an d type and cross-match if planning arteriography. Ankle \200\224 brachial pressure index (D oppler): Normal = 1. Claudication = 0.9 \200\2230.6. Rest pain = 0.3 \200\2230.6. Impending gangrene 0. 3 or ankle systolic pressure <50 mm Hg. Do arteriography, digital subtractio n arteriography, or color duplex imaging to assess the extent and location of stenoses and the quality of distal ves- sels (run off). If only distal obliterative disease is seen, wit h little proximal atheroma, suspect arteritis, previous embolus, or diabetes mellitus. Mana gement: Symptoms improve with conservative treatment; i.e., quit smoking, lose weight, get more exercise \200\224ideally a supervised exercise pro- gram. Treat diabetes, hypertension (avoid \222 -blockers), and hyperlipidemia. Aspirin has a role. Vasodilators rarely help. Percutaneous transluminal angioplasty is good for short stenoses in big arter- ies (a ball oon is inflated in the narrowed segment). Stents maintain artery patency after angioplasty and are beneficial for iliac artery disease. If ather- omatous disease is extensive but dis tal run off is good (i.e., distal arteries filled by collateral vessels), the patient may b e a candidate for arterial recon- struction by a bypass graft. Vein grafts are often used b ut prosthetic grafts are an option. Aspirin helps prosthetic grafts to remain patent; warfa rin may be better after vein grafts and in high-risk patients. Sympathectomy (chemical or s urgical) may help relieve rest pain. It may not be appropriate in diabetic patients with pe ripheral neuropathy. Amputation may relieve intractable pain and death from sepsis and gang rene. The decision to amputate must be made by the patient, usually against a background of failed alternative strategies. The level of amputation must 476 be high enough to ensure healing of the stump. Rehabilitation should be started early with a view to limb fitting. Acute ischemia may be due to thrombosis in situ (in 41%), emboli ( 38%), graft/angioplasty occlusion (15%), or trauma. There is little difference in presentin g signs. Mortality: 22%. Amputation rate: 16%. y r e g r u S Figure 13.6 inguinal ligament common femoral superficial femoral profunda femoris popliteal anterior tibial posterior tibial 477 peroneal dorsalis pedis Signs and symptoms: The 5 Ps: The limb is p ulseless, p ainful, p allid, p araes- thetic, a nd p aralyzed. Onset of fixed mottling implies irreversibility. Emboli commonly arise from the heart (infarcts, atrial fibrillation [AF]) or an an- eurysm (aorta, femoral, or poplite al). The limb may be red, but only when dependent, leading to disastrous misdiagnosis of go ut or cellulitis. Management: This is an emergency and may require urgent surgery or angiop lasty. Ischemia of <12 h is associated with 93% limb salvage rate, whereas ischemic time of >12 h is associated with only a 78% limb salvage rate and a 30% mortality. If diagnosis is in doubt, do urgent arteriography. If the occlusion is embolic, the options are surgical e mbolectomy (Fogarty catheter) or local thrombolysis (e.g., t-PA [p. 622]). Anticoagulate wi th heparin before and after either procedure. Later, look for the embolic source: Echocardi ogram; US of aorta and popliteal and femoral arteries. Ischemia following trauma and acute thrombosis may require urgent reconstruction. Acute appendicitis Appendicitis is primarily a disease of adolescents and young adults and is uncommon in individuals >55 yrs. The : ratio is 1.2:1.5. Although the incidence of acute appendicitis approaches 20% in some reports, there has been a notable decline in the incidence for all age groups over the past 30 yrs. genetic, Epidemiologists have demonstra ted Pathogenesis dietary, and infectious factors are associated with development of acute a ppendicitis. Appendiceal inflammation results from luminal obstruction of the appendiceal o rifice lymphoid hyperplasia, fecalith, or filarial worms. This inflammation allows for inva sion of GI organisms through the appendix wall. There may also be impaired ability to preve nt invasion. Symptoms Often referred to as the \200\234great masquerader, \200\235 the dia gnosis of acute appendicitis is not always straightforward. A careful review of symptoms is essential. See Table 13.20. Pain is the most important symptom. In general, as inflammatio n begins, central abdominal colic occurs as a result of stimulation of the visceral pain fi bers. Once the peritoneum becomes inflamed, the pain shifts to the right lower quadrant (RL Q) and becomes more constant. On examination, RLQ point tenderness ( \206\221 pain on palp ation) or rebound tenderness ( \206\221 pain on release) may be present. Look for Rovsing \200\231s sign (pain more in the RLQ than in the left LQ (LLQ) when the LLQ is pressed). RL Q pain may also be elicited on rectal exam. In women, do a vaginal examination: Does she ha ve cervical motion tenderness or discharge? Reexamine frequently if unsure of diagnosis. that 478 Table 13.20 Other signs and symptoms of appendicitis \212 \212 \212 \212 \212 \212 \212 Tachycardia Lying still Flushing Low-grade fever Leukocytosis Anorexia Rare vomiting, diarr hea, or constipation Essential studies CBC: To evaluate for a leukocytosis Urinalysis : Evaluate for WBCs and ba cteria indicating bladder infection (can be misleading), and red blood cells (RBCs), which may suggest kidney stone. \222 -HCG: R/O pregnancy (ectopic) Additional studies Abdominal X-rays: Usually demonstrates a paucity of gas in the RLQ. May also see fecalith. Abdominal CT scan: Highly sensitive (0.94) for appendiceal inflammation (thickening of appendiceal wa ll) but cannot always separate acute and chronic inflammation. CT signs of acute appendicit is: 1. Thick wall >2 mm 2. Increased diameter (7 mm) with target sign 3. Appendicolith (see n in 25%) 4. Phlegmon, abscess, or free fluid Abdominal US: Sensitive for evaluation of ova rian cyst or abscess, hydrosalpinx. y r e g r u S Differential diagnosis Cholecystitis Diverticulitis Ectopic pregnancy Salpingitis Mesenteri c adenitis Menstrual cramps Meckel \200\231s diverticulitis Cystitis Crohn \200\231s disease Ovarian cyst or abscess Kidney stone Complications of acute appendicitis Perforation (does not appear to cause later infertility in girls), appendix mass, appendix abscess. An appendix mass may result when an inflamed a ppendix becomes covered with omentum or loops of small bowel. The mass is palpable on exam and easily seen on abdominal CT scan. Some advocate early surgery, but initial management i s usually conservative \200\224NPO and antibiotics (e.g., cefuroxime 1.5 g/8 h IV and metro nidazole 500 mg/8 h IV). Mark out the size of the mass and proceed to drainage if the mass develops into an abscess (see below). If the mass resolves, some perform an interval (i.e., delayed) ap- pendicectomy. See Table 13.21. An appendix abscess may result if an appendix mass fails to resolve. Signs of abscess formation include enlargement of the mass or the pa tient becom- ing more toxic (pain \206\221 , temperature \206\221 , pulse \206\221 , WBC \206\221 ). Treatment usu- ally involves drainage, either surgical or percutaneous (under radiological guidance). Antibiotics alone may bring about resolution (e.g., in >90% of chi ldren). 479 Table 13.21 Appendicitis in pregnancy Appendicitis occurs in 1/1,000 pregnancies. Mortality is higher, espe- cially from 20 wks of gestation. Perforation (15 \200\22320%), and \206\221 fetal mortality from 1.5% (for s imple appendicitis) to 30%. As pregnancy progresses, the appendix migrates, so pain is oft en less well localized. Prompt assessment is vital; laparotomy should be performed by an ex pe- rienced surgeon. Surgical treatment Once decision is made to operate, make patient NPO and hydrate with NS. Metronidazole 1 g/8 h + cefuroxime 1.5 g/8 h, 1 \200\2233 doses IV starting 1 h preop reduc es wound infections. Appendectomy is performed laparoscopi- cally or through a RLQ incision at McBurney \200\231s Point (one-third the distance between the anterior superior iliac cr est and the umbilicus). Some surgical hints include: \212 Laparoscopic appendectomy reduces recovery time and incidence of wound infections, but incr eases risk of intra-abdominal abscesses. If the appendix is perforated, most advocate closi ng the fascia but leaving the wound open for closure by secondary intention. If the appendi ceal stump is difficult to locate and close, and the appendix has ruptured, leave a drain b ecause patient is at risk to develop GI leak and fistula. If the appendix is associated wit h an unusual mass, always think of carci- noid or cystadenoma of the appendix. These tumors may cause luminal obstruction and lead to appendicitis. Larger tumors (>2 cm) will require formal right hemicolectomy, which should be performed at the time of surgery or once patho logy is confirmed. \212 \212 \212 Diverticular disease A diverticulum is an out-pouching of the wall of the gut. The term div erticu- losis means that diverticula are present, whereas diverticular disease implies that they are symptomatic. Diverticulitis refers to inflammation within a diverticulum. Althoug h diverticula may be congenital or acquired and can occur in any part of the gut, by far th e most important type is acquired colonic diverticula, to which this section refers. Pathog enesis Most occur in the sigmoid colon, with 95% of complications at this site, but right-s ided, as well as small bowel diverticula, do occur. Lack of dietary fiber is thought to lea d to high intraluminal pressures that force the mucosa to herniate through the muscular bow el wall near where vessels penetrate the wall. Nearly 50% of the population in the Western world >50 has diverticulosis. Symptoms 15 \200\22330% of patients with diverticulosis have symptomatic diverticular disease. The most common symptoms is LLQ pain. Pain usually occurs after eating and persists. Associated symptoms include low-grade fever, diarrhea or obstip ation, and anorexia. Rarely do patients experience nausea or vomiting. On exam, LLQ point a nd rebound tenderness may be present. Complications of diverticular disease Free perforatio n: A free communication exists between the colon and the peritoneal cavity. There is ileus, peritonitis shock. Free fluid in air is noted on imaging studies. Hemorrhage: Is usuall y sudden and painless. It is a common cause of big rectal bleeds. Bleeding usually stops wi th bed rest. Fistula: \212 480 Colovesical: Complaints of pneumaturia (air in urine stream) or fecaluria (feces in urine s tream) Colovaginal: Complaints of fecal vaginal discharge Coloenteric: Complaints of persis tent diarrhea \212 \212 Abscess: E.g., with swinging fever, leukocytosis, and localizing signs (e.g., b oggy rectal mass). Postinfective strictures may form in the sigmoid colon and present with large bowel obstruction. Studies CBC, urine analysis and culture. Uncomplicated diverticulitis: \212 \212 Complica ted diverticular disease: \212 \212 \212 \212 \212 Treatment Uncomplicated diverticula r disease: \212 y r e g r u S ABD and pelvic CT scan initially Colonoscopy or barium enema once symptoms resolve to R/O c ancer. AXR to R/O free air CT cystogram to R/O colovesical fistula Barium enema to R/O colovaginal fistula Small bowel series to R/O coloenteric fistula Colonoscopy to R/O cancer. A 7 \200\22314 d course of IV or oral antibiotics (ciprofloxacin 500 mg bid and Flagyl 25 0 \200\223500 mg PO tid) Keep NPO till pain resolves. Avoid narcotics, which may constipate . Encourage a \212 \212 \212 \212Antispasmodics such as Bentyl 10 mg PO 4 \227 a day. \212 high-fiber diet with dietary supplements (Metamucil ) Repetitive attacks requiring hospitalization of documented diverticular disease should be t reated with either laparoscopic or open surgical resec- tion of the diseased colon. Recurre nce of LLQ pain after surgery is more common in patients who have not had a complete resect ion of the distal sigmoid and in patients with irritable bowel syndrome (IBS) as well as di verticular disease. \212 Complicated diverticular disease Free perforation: Laparotomy, a Hartman \200\231s procedur e may be used (tempo- rary end colostomy + partial colectomy or \200\234perforectomy \200 \235). It is sometimes possible to do on-table colon lavage via the appendix stump, then im medi- ate anastomosis (so avoiding repeat surgery to close the colostomy). Hemorrhage: Tran sfusion may be needed. Highly selective embolization or colonic resection may be necessary after locating bleeding points by angiog- raphy or colonoscopy (cautery local epinephrin e injections may obviate the need for surgery). If bleeding site is identified and surgery is necessary, a limited resection can be performed. Otherwise, a total abdominal colec- tom y with either an ileostomy or ileorectal anastomosis is performed. Fistula: Treatment is su rgical (e.g., laparoscopic or open colonic resection, as well as removal of the fistula). S uccessful laparoscopic resection is less likely when a fistula is present. The most common site for a colovesical fistula is the dome of the bladder. The trigone may on occasion be i nvolved and, if so, consider urology consult for stents and reconstruction. Consider urolog y consult for stents and reconstruction. Abscess: Antibiotics CT- or US-guided drainage may be needed. This should be followed by definitive resection in 6 wks or sooner if no cli nical improvement (<25%). Postinfective strictures: Stent colon if necessary and prep if po ssible to per- form a primary anastomosis. 481