SURGERY - EOR Study Guide PDF

Summary

This study guide details various surgical procedures, including those related to the gastrointestinal tract, such as appendicitis, cholecystitis, and bariatric surgery. It covers definitions, diagnostic procedures, therapeutics, and preventative measures, providing a comprehensive overview of these medical conditions.

Full Transcript

SURGERY GASTROINTESTINAL/NUTRITIONAL Abdominal pain Renal o CC: colicky right sided flank pain, nausea, vomiting, hematuria, CVA tenderness o Workup: UA, BUN/Cr, CT abdomen, renal US, KUB, blood cultures...

SURGERY GASTROINTESTINAL/NUTRITIONAL Abdominal pain Renal o CC: colicky right sided flank pain, nausea, vomiting, hematuria, CVA tenderness o Workup: UA, BUN/Cr, CT abdomen, renal US, KUB, blood cultures o Ddx: nephrolithiasis, renal cell carcinoma, pyelonephritis, GI etiology, glomerulonephritis, splenic rupture Pancreas: o CC: dull epigastric pain that radiates to the back o Workup: CT abdomen, CBC, electrolytes, amylase, lipase, AST, ALT, bilirubin, alkphos, U/S abdomen o Ddx: pancreatitis, pancreatic cancer, peptic ulcer disease, cholecystitis/choledocholithiasis Gallbladder: o CC: RUQ pain o Workup: RUQUS, CBC, CMP, HIDA scan, MRCP/ERCP, amylase, lipase, alk phos, bili o Ddx: cholecystitis, choledocholithiasis, hepatitis, ascending cholangitis, fitz-hugh-curtis syndrome, acute subhepatic appendicitis Liver: o CC: RUQ pan, fever, anorexia, nausea, vomiting, dark urine, clay stool o Workup: CBC, amylase, lipase, liver enzymes, viral hepatitis serologies, UA, U/S abdomen, ERCP, MRCP o Ddx: acute hepatitis, acute cholecystitis, ascending cholangitis, choledocholithiasis, pancreatitis, primary sclerosing cholangitis, primary biliary cirrhosis, glomerulonephritis Spleen: o CC: severe LUQ pain that radiates to left scapula w hx of infectious mono o Workup: CBC, CXR, CT/US of abdomen o Ddx: splenic rupture, splenic infarct, kidney stone, rib fracture, pneumonia, perforated peptic ulcer Stomach: o CC: burning epigastric pain after meals o Workup: rectal exam (occult blood in stool), amylase, lipase, lactate, AST, ALT, bili, alk phos, upper endoscopy (H.pylori biopsies), upper GI series o Ddx: peptic ulcer disease, perforated peptic ulcer disease, gastritis, GERD, cholecystitis, mesenteric ischemia, chronic pancreatitis Intestines: o CC: crampy abdominal pain, vomiting, abdominal distention, inability to pass flatus o Workup: rectal exam, CBC, electrolytes, CT abdomen/pelvis, colonoscopy o DDx: intestinal obstruction, small bowel / colon cancer, volvulus, gastroenteritis, food poisoning, ileus, hernia, mesenteric ischemia/infarction, diverticulitis, o w/ alternating disrrhea/. Constipation: diverticulitis, Crohn’s disease, ulcerative colitis, abscess, IBS, celiac disease, GI parasitic infection (amebiasis, giardiasis) Pelvis: o CC: RLQ pain, nausea, vomiting, dysuria, hematuria o Workup: pelvic exam, urine hCG, doppler U/S, rectal exam, UA, CBC, CT abdomen, laparoscopy, chlaymdia and gonorrhea testing o Ddx: ovarian torsion, appendicitis, ectopic pregnancy, ruptured ovarian cyst, pelvic inflammatory disease, bowel infarction / perforation, endometriosis, vaginitis, cystitis, pyelonephritis Cholecystitis Definition: gall bladder (cystic duct) obstruction by stone à inflammation / infection o 50-80% = E.coli History and Physical Exam: o Biliary colic: episodic RUQ / epigastric pain beginning abruptly, continuous in duration, resolves slowly lasting 30m-hours assoc with nausea precipitated by fatty foods or large meals o Low grade fever, nausea/vomiting, palpable GB, murphy’s sign; boas sign (referred pain to subscapular area due to phrenic never irritation) o Hypoactive bowel sounds are an indicator that a perforation has occurred. Other symptoms include high fever, systemic signs of toxicity (tachycardia and increased respiratory rate), and increased abdominal pain with rebound tenderness. Diagnostics: o US = initial test of choice: thickened GB 130bp à grave prognosis o Hemorrhagic pancreatitis: may cause bleeding into flanks (Grey turner) or umbilical (Cullen sign) o Chronic = fat malabsorption / steatorrhea o Triad of calcifications, steatorrhea, diabetes mellitus o Left sided exudative pleural effusion Diagnostics: o Elevated amylase – may be transient / return to normal after 48-72 hrs o Lipase = more sensitive but only with elevations 3x or greater – increases 7-14 days o Abdominal CT = diagnostic test of choice o AXR: sentinel loop = localized ileus – dilated small bowel in LUQ – colon cutoff sign o WBC count elevated; liver enzymes may increase – mild hyperbilirubinemia / bilirubinuria, hyperglycemia, hypocalcemia o Chronic: calcification on US / gallstones; amylase and lipase usually not elevated Therapeutics: o Stop oral intake; fluid resuscitation – 90% recover with supportive measures only o Pain management (analgesics and Demerol) consider abx but not used prophylactically – when necessary, broad spectrum imipenem (necrotizing pancreatitis) o ERCP if biliary sepsis suspected; only effective in obstructive jaundice o Monitor for complications o Chronic: oral pancreatic enzyme replacement; low fat diet; surgical removal of damaged part for pain control / pain control; STOP DRINKING o Indications for surgery: severe pain that limits functioning; intractable pain despite non-narcotic analgesics + absence of alcohol intake Health Maintenance: o STOP DRINKING Acute vs chronic: Acute pancreatitis: isolated episode of abdominal pain accompanied by elevations in blood enzyme levels. o inflammation of the pancreas. >80% of the cases of acute pancreatitis are related to biliary stones or alcohol use. Acute pancreatitis may lead to chronic pancreatitis. Chronic pancreatitis is a painful disease of the pancreas in which inflammation has resolved, but with resultant damage to the gland characterized by fibrosis, calcification and ductal inflammation. It is possible for patients with chronic pancreatitis to have episodes of acute pancreatitis. Anal Fissure Definition: o Painful, linear lesions in the distal anal canal most commonly found on posterior midline o May involve full thickness of mucosa if untreated History and Physical Exam: o Severe tearing pain on defecation, often accompanied by hematochezia o bright red blood often noted on stool or toilet paper o skin tags seen in chronic o MC = posterior midline Diagnostics: o severe painful BM causing pt to refrain from having BM à constipation, bright red blood per rectum, rectal pain Therapeutics: o >80% resolve spontaneously o 1st line: analgesics, sitz bath, bulking agents and increased fluids to avoid straining o 2nd line: topical nitroglycerin.4% ointment or topical styptic, such as silver nitrate 1% or 2% may help with healing; gentian violet solution 1% may help with healing; nifedipine ointment, botox Health Maintenance: o High fiber diet Anorectal Abscess / Fistula Definition: Often results from bacterial infection of anal ducts / glands. MC staph aureus, e.coli MC posterior midline History and physical: throbbing rectal pain worse with sitting, coughing, defecation Treatment of perirectal abscess: incision and drainage – no antibiotics Appendicitis Definition: o obstruction of the appendix à inflammation / infection o MC due to fecalith, or inflammation, malignancy, foreign body (collagen vascular dz, IBD) o MC surgical emergency History and Physical Exam: o Initial sx = anorexia, periumbilical / epigastric pain à constant and worsened RLQ pain (McBurney’s point), nausea, vomiting (vomiting usually occurs after pain) and rebound tenderness o Diarrhea may occur but not common o Low-grade fever is common; high grade fever = unlikely o Retrocecal appendicitis = pain on rectal exam o 20% = perforation / peritonitis (high grade fever, generalized abdominal pain, increased leukocytosis) o MC 10y-30y o Physical: rebound tenderness, rigidity, guarding o Rovsing sign: RLQ pain with LLQ palpation o Obturator: RLQ pain with internal and external hip rotation with bent knee o Psoas sign: RLQ pain with right hip flexion / tension (raise leg vs resistance) o McBurney’s point tenderness: the point 1/3 the distance from ASIS and navel Diagnostics: o Abdominal US is preferred initial imagining o CT is more sensitive and confirms diagnosis (will also help locate abnormally placed appendix) o Leukocytosis (10,000-20,000) – higher levels suggest perforation and peritonitis o Some microscopic hematuria and pyuria Therapeutics: o Appendectomy o Reason to suspect abscess or perforation, broad spectrum abx administered before and after surgery o A single dose of cefotetan 2 g intravenously (2nd gen cephalosporin) is recommended for preoperative administration for prophylaxis against infection. This is given to prevent intra-abdominal and wound infections. The targeted florae represent those that are found within the colon. In acute appendicitis without perforation, only a single dose within 60 minutes of the initial incision is indicated. Antibiotics are not indicated postoperatively in these uncomplicated cases of appendicitis. In patients with a penicillin or cephalosporin allergy, the recommended antibiotic regimen is clindamycin and one of the following: ciprofloxacin, levofloxacin, gentamicin, or aztreonam. Bariatric Surgery Definition/diagnostics: only proven method to maintain weight loss and reduce obesity-related morbidities and mortalities; usually last resort due to risks guidelines: BMI >40 (100lb over ideal body weight); BMI >35 with medical problem sequelae of obesity; failed other non- surgical programs; must be psychologically stable and able to follow post-op instructions; obesity NOT EXPLAINED by medical organic cause (ie endocrine) Therapeutics: in US most common are RNYGB, AGB, VSG, BPD/DS Restrictive procedures: less weight loss, not as much morbidity o Adjustable gastric banding (AGB): SMALLEST AMOUNT WEIGHT LOSS § Indications: BMI >30-35 with comorbid conditions; ideal for volume eater; trains you to eat / chew slower § Proximal gastric pouch created using inflatable band and access port placed § 35-45% excess body weight lost in first few years § Fewer complications but need for more follow up for band adjustment § Complications: regurgitation, prolapse, must be seen annually for upper GI band checking; less risk but less weight loss o Vertical banded gastroplasty (VBG) o Sleeve gastrectomy (SG): 85% stomach removed and stomach takes shape of sleeve; weight loss less than RNYGB but higher than AGB – MEDIUM AMOUNT WEIGHT LOSS § Reduces stomach to 35 § Complications: lack of hunger, 70% weight loss at 2y Malabsorptive: more weight loss than restrictive but issues with malnutrition / nutrient absorption o Biliopancreatic diversion (BPD + Biliopancreatic diversion with/without duodenal switch (BPD/DS) § Not popular bc of malnutrition issues associated; about 70-90% weight loss Combo of restrictive / malabsorptive – MOST WEIGHT LOSS o Roux-en-Y Gastric Bypass (RNYGB): MC used bariatric surgery for tx of severe obesity in US – proximal gastric pouch created by transecting stomach; 75-85% excess body weight lost in first two years; less severe nutrition problems § Bypass of most of stomach, entire duodenum, and part of small intestine § Pouch is restrictive, causing fullness; roux limb limits absorption § Indications: BMI>35 § Complications: dumping syndrome, lifelong micronutrient supplementation (B1, B12, folate, vitamin C) and vitamins A,D,E,K and minerals Complications: Early: anastomotic leak, DVT, PE, bleeding, infection, splenic injury Late: malnutrition / nutritional problems, marginal ulcer and anastomotic strictures, internal hernia, cholelithiasis, band slippage, band erosion, esophageal dilatation, dumping syndrome (usually occurs when pt attempts to eat large amount of simple sugars – they move from stomach to bowel too quickly à fullness, cramping/pain, n/v/d, seating, flushing, rapid heartbeat) Bowel Obstruction Definition: o Most small bowel are caused by adhesions or hernias; other causes: neoplasm, inflammatory bowel disease, volvulus o Post-surgical adhesions MC (60%); hernias, crohn’s disease, malignancy (although malignancy is MC cause of large bowel obstruction is may cause SBO) o Lg. bowel obstruction more likely caused by neoplasm; others causes are strictures, hernias, volvulus, intussusception, fecal impaction o Complete strangulation of bowel: infarction, necrosis, peritonitis, death History and Physical Exam: o SBO: abdominal pain, distention, vomiting of partially digested food, obstipation (severe constipation) o Crampy, abdominal pain, vomiting, usually follows the pain, diarrhea (early finding); mild pain à severe o High pitched tinkles on auscultations and visible peristalsis à hypoactive bowel sounds in late obstruction o Bowel sounds = high pitched and in rushes; later on = absent o LBO = distention and pain, afebrile and tachycardic; shock may ensue Diagnostics: o Dehydration and electrolyte imbalance o Upright radiographs à air fluid levels and multiple dilated loops of bowel o XR: air fluid levels in step ladder patterns; dilated bowel loops o If radiography inconclusive, abdominal CT with contrast should be obtained Therapeutics: o 1. NPO, nasogastric suctioning, IV fluids, monitoring o 2. Partial obstruction in hemodynamically stable pt may be managed with IV hydration and nasogastric decompression o 3. Urgent surgical consultation is necessary when mechanical obstruction is suspected, especially of the large bowel (esp. if strangulated) o Pain management necessary for pt. with bowel obstruction Metabolic alkalosis would be the most likely acid-base disturbance to develop postoperatively in SBO. Volume contraction combined with gastric fluid loss is the most common cause. During this type of surgery, aggressive third-spacing of fluid into the peritoneal cavity, as well as the intestinal lumen, is the cause of volume contraction. Postoperatively, nasogastric decompression of the stomach causes acid loss. As the stomach works to replenish hydrochloric acid, bicarbonate (HCO3-) is released into the serum. The patient also loses potassium from the gastric fluid during nasogastric suctioning. The combination of the volume contraction and the postoperative measures causes a hypochloremic, hypokalemic metabolic alkalosis. Compared to a complete bowel obstruction requiring intestinal decompression and electrolyte regulation, most early postoperative bowel obstructions are partial and resolve spontaneously. Patients who experience ileus, return to normal bowel function, and then present with obstructive symptoms are more likely to have a true postoperative bowel obstruction Volvulus Twisting of any part of the bowl in itself; MC = sigmoid, cecum s/sx: abdominal pain, distention, n/v, fever, tachycardia management: o 1. Endoscopic decompression o 2. Surgical correction Primary Sclerosing Cholangitis Autoimmune, progressive cholestasis with diffuse fibrosis of intrahepatic and extra hepatic ducts – RARE MC associated with inflammatory bowel disease – 90% have ulcerative colitis +/- Crohn’s MC men 20-40yo Clinical manifestations progressive jaundice, pruritus, RUQ pain, hepatomegaly, splenomegaly Diagnosis: increased ALP (3-5x normal), increased GGT (cholestasis), increased ALT, AST, increased Bili, increased IgM; +P- ANCA o ERCP = GOLD STANDARD (increased risk developing cholangiocarcinoma) Management: liver transplant; meds (steroids, immune meds) = no significant benefit Ascending Cholangitis: Definition: biliary tract infection secondary to obstruction by gallstone o Dx: ERCP o Charcot’s triad: fever/chills, RUQ pain, jaundice, increased liver enzymes o Reynold’s pentad: shock + AMS o Tx: abx (PCN + aminoglycoside), decompression of biliary tree via ERCP stone extraction Cholelithiasis Definition: gallstones in the gall bladder (NO INFLAMMATION) o 90% cholesterol History and Physical Exam: o Risk factors = 5Fs: fat, fair, female, forty, fertile: OCP’s (increased estrogen), Native Americans, bile stasis, chronic hemolysis, cirrhosis, infection, rapid weight loss, IBD, TPN, fibrates, increased triglycerides o MC asymptomatic (may be incidental finding) Diagnostics: o Ultrasound = test of choice o Biliary colic: episodic RUQ / epigastric pain beginning abruptly, continuous in duration, resolves slowly lasting 30m-hours associated with nausea precipitated by fatty foods or large meals Therapeutics: o If asymptomatic may observe or use oral bile dissolution treatment o Cholecystectomy in symptomatic pt (usually laparoscopic) Complications: o Choledocholithiasis: gallstones in biliary tree à +/- biliary colic or jaundice o Dx = MRCP o Tx = stone extraction via ERCP Diarrhea Definition: increased frequently or volume of stool 3+ liquid or semisolid stools daily for at least 2-3 consecutive days o Causes: infectious, toxic, dietary, other GI dz o Food borne / waterborne: norovirus, rotavirus, staph aureus, clostridium perfringens, vibrio (cholera), E. coli, giardia lamlia, cryptosporidium, cyclospora, salmonella, E. coli, shigella, campylobacter History and Physical: o Include all current meds and illnesses among others who have shared meals with the patient + travel history!! o Secretory (large volumes without inflammation) indicates infection, pancreatic insufficiency, ingestion of preformed bacterial toxins, laxative use o Inflammatory (bloody diarrhea with fever, dysentery) indicates invasive organisms or IBD o Abx associated is almost always caused by c. diff colitis which in the most severe cases causes the classic psuedomembranous colitis Diagnostics: o WBC in stool = inflammatory process o Cultures for bacterial agents, microscopy for parasites, toxin identification (if enterotoxic E. coli or C. diff I suspected) can identify infectious agents in stool Therapeutics: o IV fluid repletion = mainstay of gastroenteritis management; PO preferred o Diet: bland low residue (BRAT / crackers, boiled vegetables, soup) o Anti-motility agents: in pt. 50yo with new onset constipation should be evaluated for colon cancer History and Physical: +/- tender, hard abdomen Diagnostics: +/- KUB, hypercalcemia Therapeutics: o Increase in insoluble fiber (up to 10-20g/day) and fluid intake (up to 1.5 to 2L/day) and increased exercise Health Maintenance: o Lasting longer than 2 weeks or with constipation refractory to modifications in diet, exercise, and fluid intake should undergo further investigation to detect the underlying cause o If treatable underlying cause is found, constipation will resolve with treatment of the disease process Diverticular Disease Diverticula: small mucosal herniations protruding through intestinal and smooth muscle layer along natural openings of the vasa recta of the colon; sigmoid colon MC area due to highest intraluminal pressure; onset usually >40y Diverticulosis: uninflamed diverticula (assoc w low fiber diet***, constipation and obesity); usually asymptomatic but MC causes of acute lower GI bleeding o MC area = sigmoid Diverticulitis: inflamed diverticula secondary to obstruction/infection (fecaliths) à distention s/s: fever, LLQ pain, nausea, vomiting, diarrhea, constipation, flatulence, bloating dx: CT = test of choice; increased WBCs, +guaiac management: o diverticulitis: clear liquid diet, broad spectrum abx (cipro / Bactrim) + metronidazole o diverticulosis: high fiber diet, fiber supplements; bleeding stops in 90% (+/- vasopressin if not) Esophageal Neoplasms Squamous cell: 90-95% worldwide assoc w tobacco and alcohol use, decreased fruits/vegetable intake, achalasia, hot beverage ingestion, exposure of esophagus to noxious stimuli in men, nitrates o Decreased incidence with NSAIDs and coffee consumption o MC in upper 1/3 esophagus; peaks 50-70yo; increased incidence African Americans Adenocarcinoma – 50-80% in the US; presents in younger patients and usually presents early o Usually a complication of GERD / Barret’s esophagus, obesity o Lower 1/3 esophagus o Most serious complication of barrett’s is esophageal adenocarcinoma clinical manifestations: solid food dysphagia (fluids / soft foods usually tolerated initially); odynophagia o weight loss, chest pain, anorexia, cough, hoarseness, reflux, hematemesis, +/-Virchow’s node o hypercalcemia in patients w squamous cell (due to ectopic PTH related protein tumor secretion) diagnosis: upper endoscopy with biopsy = test of choice management: esophageal resection, XRT, chemotherapy **commonly spreads to mediastinum; endoscopy screening n pts w Barrett’s every 3-5 years o Barrett’s = transition of squamous to columnar epithelium Esophageal Strictures Esophageal web: thin membranes in mid-upper esophagus, may be congenital o Plummer-vinson syndrome: dysphagia + esophageal webs + iron deficiency anemia; atrophic glossitis, angular cheilitis, koilonychias, splenomegaly Schatzki ring: mucosa lower esophageal constrictions at squamocolumnar junction; MC assoc with hiatal hernia s/s: dysphagia (esp to solids) dx: barium esophagram (swallow): dx test of choice for esophageal webs management: endoscopic dilation of the area Gastric Carcinoma adenocarcinoma = MC worldwide 99%; MC males >40 and usually present in late disease r/f: H.PYLORI = MOST IMPORTANT R/F – salted, cured, smoked, pickled foods containing nitrites; pernicious anemia, chronic atrophic gastritis, achlorydria, smoking, ETOH, blood type A s/s: indigestion, weight loss, early satiety, abdominal pain / fulness, nausea, post-prandial vomiting, dysphagia, melena, hematemesis; iron deficiency anemia o signs of metastasis: virchow’s node, sister mary joseph’s node, ovarian METS, palpable nodule on rectal exam (blumer’s shelf); left axillary lymph node involvement (irish sign) dx: upper endoscopy with biopsy; linitis plastica – diffuse thickening of stomach wall d/t cancer infiltration (worst type) tx: gastrectomy, XRT, chemo; poor prognosis Disease encasement of the hepatic artery is considered an indicator of unresectability of gastric cancer. Gastric cancer is typically surgically resected along with regional lymph nodes with complete disease eradication representing the best chance for positive outcomes. During gastric and lymph node resection, complete abdominal exploration should occur. Indicators of unresectability include vascular involvement of the aorta, hepatic artery, or proximal splenic artery. Distant metastases are also an indicator of unresectability, although locoregional metastases are not always unresectable. Lymph nodes that are located in the aorto-caval region, in the porta hepatis, or behind the pancreas are also considered unresectable. GERD Definition: o transient relaxation of LES à gastric acid reflux à esophageal mucosal injury History / Physical Exam: o typical symptoms: heartburn (pyrosis) hallmark often retrosternal and post prandial (MC 30-60min post eating, increased in supine position and often relieved with antacids); regurge (water brash or sour taste in mouth), dysphagia, cough at night (acid aspiration into the lung causes lung irritation o halitosis, cough, hiccupping, sore throat, laryngitis, atypical chest pain o atypical symptoms: hoarseness, aspiration pneumonia, “asthma” (bronchospasm from lung contact with acid), noncardiac chest pain, weight loss o ALARM SYMPTOMS: dysphagia, odynophagia, weight loss, bleeding Complications: o esophagitis, esophagus stricture, barrett’s esophagus, esophageal adenocarcinoma o barrett’s: esophageal squamous epithelium replaced by precancerous metaplastic columnar cells from the cardia of the stomach Diagnostics: o clinical diagnosis based on history especially if present with classic, simple symptoms o endoscopy: often 1st used: useful to evaluate persistent symptoms, GERD with culture, malignancy, new sx >50y etc o use with: pt older than 45 with new onset sx, long standing or frequently recurring symptoms, failure to respond to therapy or symptoms indicating more severe conditions like anemia, dysphagia, or recurrent vomiting o make sure to eval / rule out MI o esophageal manometry: decreased LES pressure – often done if normal upper endoscopy o 24h ambulatory pH monitoring: gold standard (not usually done) Therapeutics: 1. As needed pharm therapy: antacids and OTC H2 receptor blockers: if alarm of atypical sx upper endoscopy is next appropriate step 2. Initiation of scheduled pharmacologic therapy: PPIs are drug of choice in severe disease 3. H2 blocker at bedtime and PPI in the daytime may be helpful in pt with significant nighttime symptoms 4. Avoid: beta agonist, alpha adrenergic antagonist, nitrates, calcium channel blockers, anticholinergics, theophylline, morphine, meperidine, diazepam, barbiturate agents (decrease LES pressure) 5. Nissen fundoplication if refractory Health Maintenance: 6. Lifestyle modifications: elevate head of bed by six inches, avoid recumbency for 3 hours after eating, eating small meals, avoid fatty/spicy, citrus, chocolate, caffeinated products, peppermint; decrease fat and alcohol intake, weight loss, smoking cessation 7. Predisposing factors: obesity, pregnancy, diabetes, hiatal hernia, connective tissue disorders Scientific Concepts: o multifactorial: increased gastric acid, incompetent lower esophageal sphincter (LES), esophageal motility disorders and delayed gastric emptying +/- hiatal hernia o reflux esophagitis is result of recurrent reflux of gastric contents into distal esophagus bc of mechanical or functional abnormality o present in ~10% of the population o infants: 50% o protective factors: gravity, lower esophageal sphincter tone, esophageal motility, salivary flow, gastric emptying, tissue resistance o can à barrett’s which can predispose to malignancy Hematemesis / GI bleed Diagnostics: usually pt with upper GI bleeding s/sx: vomiting blood, coffee ground emesis, melena (black/tarry stools), orthostatic dizziness, confusion, angina, severe palpitations Eval: HEMODYNAMIC STABILITY Causes: peptic ulcer, esophageal ulcer, Mallory-weiss tear, variceal hemorrhage/portal hypertensive gastropathy, malignancy Physical exam: look for signs of hypovolemia o Mild/moderate (15%): orthostatic hypotension o severe (>40%): supine hypotension Labs: CBC, chemistries, liver tests, coags, ?cardiac enzymes/ECGs for those at risk for MI Treatment: o NGT lavage: if unclear pt has ongoing bleeding o IV access: 2 large bore (18 gauge) IVs, FLUIDS!! o Transfusion: § RBC: if unstable, high-risk and hgb W, risk increases with age; greater incidence in smokers, **cigarette smoking and alcohol abuse MC ductal adenocarcinoma located at pancreatic head presentation: painless jaundice = pathognomonic, weightloss/epigastric abd pain, clay-colored stools, jaundice + palpable non- tender gallbladder (Courvoisier’s sign), virchow’s node = lymph in left supraclavicular fossa diagnosis: abdominal CT scan (75% shows tumor at the head of the pancreas) – ERCP, pancreatic biopsy, abdominal MRI, elevated serum bilirubin, abnormal LFTs CA 19-9 present in about 80% of patients with pancreatic cancer Treatment: only about 20% can be removed by pancreaticduodenectomy (whipple); when can’t be removed with surgery à combination of radiation therapy and chemotherapy Pancreatic Pseudocyst Definition: cystic collection of tissue, fluid, and necrotic debris surrounding the pancreas Causes: acute/chronic pancreatitis, trauma to chest (steering wheel trauma), classically occur 2-3 weeks after acute pancreatitis Sx: abdominal pain Physical exam: abdominal mass Diagnosis: CT = test of choice Tx: if pseudocyst persists for 4-6 weeks or continues to enlarge à percutaneous drainage, surgical decompression (pancreaticogastrostomy), cyst fluid drained Complications: can become infected and lead to peritonitis Peptic Ulcer Disease Definition: secondary to imbalance of 1. Decreased mucosal protective factors 2. Increased damaging factors (acid); gastric ulcers more common in elderly History and Physical: o Etiology: h. pylori, NSAIDs, Zollinger Ellison syndrome (suspect GI malignancy in nonhealing GU-ZES and gastric cancer) o Asymptomatic, dyspepsia, worse at night o Ulcer-like or acid dyspepsia: relief with food, antacids, anti-secretory agents; worse before meals or 2-5h after meals; nocturnal symptoms o Food provoked: pain 1-2 hours p meals and weight loss o GI bleed: PUD = MC cause of upper GI bleed Diagnostics: o Endoscopy = gold standard / most accurate diagnostic test o Bx to r/o malignancy – alarm sx: >50yo, dyspepsia, history of UG, anorexia, wt loss, anemia, dysphagia o Upper GI series: all GU seen on UGI serious should be followed with endoscopy to r/o malignancy o H. pylori testing: o Endoscopy with biopsy = gold standard + rapid urease test o Urea breath test to confirm eradication after therapy o H. pylori stool antigen = >90% specific – confirm eradication after therapy o Serologic antibodies: confirm infection not eradication o Complications: bleeding (melena, hematemesis, dizziness), perforation (sudden onset severe, diffuse abdominal pain, rigid abdomen, rebound tenderness), penetration (pain radiating to back), obstruction (vomiting) Therapeutics: o H.pylori: clarithromycin + amoxicillin + PPI (CAP) o H. pylori negative: PPI, H2RA, misoprostol, antacids, bismuth compounds, sucralfate o PPI: drug of choice / most effective drug to treat PUD – 30m before meals; s/e = B12 deficiency o H2 blocker: cimetidine = lots of drug interactions + anti-androgen effects o Misoprostol: good for preventing NSAID related ulcers but not for healing already existing ulcers; CI in premonopausal women bc abortifactent o Antacid: milk of magnesia à diarrhea; amphogel à constipation; Maalox, Mylanta o Bismuth compounds: antibacterial and cytoprotective; s/e = darkening tongue / stool, constipation o Sucralfate: forms viscous adhesive ulcer coating; promotes healing / protects mucosa; may reduce bioavailability of H2RA, PPI o Parietal cell vagotomy if refractory o Weight loss is experienced by up to 30% of patients post-surgically. Patients may limit food intake due to early satiety. Distention or discomfort may occur shortly after even a moderate-sized meal as the residual gastric pouch is smaller. Patients should be counseled to eat smaller and more frequent meals. Additionally, weight loss can be a result of other postsurgical complications such as maldigestion or dumping syndrome. Pilonidal Cysts Chronic pilonidal disease, for which the definitive treatment requires surgical excision of all sinus tracts. Pilonidal disease occurs when the skin and subcutaneous tissue at or near the upper region of the natal cleft of the buttocks becomes infected, often in the setting of ongoing inflammation and damage of local hair follicles. This problem is most common in young adults and often occurs in patients with sedentary occupations, obesity, or a positive family history. Patient presentations can range from asymptomatic to chronic pain and drainage. Acute abscess formation can also occur. Pilonidal disease is a clinical diagnosis that does not require any imaging or laboratory procedures. Incision and drainage is necessary in the setting of an acute pilonidal abscess, but is not the definitive step in management due to high recurrence rates after incision and drainage treatment alone. Pyloric Stenosis Presentation: infants feed well for first 2-3 weeks then present with nonbilious vomiting after most or every feeding Pediatric pt 6cm o at least 3 of the following: fever >101.5F, HR >120, neutrophilic leukocytosis >10.5 x 10^9, anemia treatment: decompression of colon is required – in some cases, colostomy or even complete colonic resection may be required PREOPERATIVE/POSTOPERATIVE CARE Acid Base Disorders Baseline values: easy way to remember – 24/7 40/40 24 (HCO3 à base) 7.4 pH 40 (CO2 à acid) 1. LOOK AT PH (7.35-7.45 = normal) a. 7.45 = alkalosis 2. LOOK AT PCO2 à normal, low, or high (35-45 = normal) a. Increased CO2, decreased pH = respiratory acidosis i. pH low, high PCO2, normal bicarb ii. lungs fail to excrete CO2: slow breathing, pulmonary disease, neuromuscular disease, drug-induced hypoventilation (opiates, barbiturates) iii. can result in hyperkalemia - potassium exchange for hydrogen ions in intracellular space causing increase in potassium b. Decreased CO2, increased pH = respiratory alkalosis i. pH high, low PCO2, normal bicarb ii. excessive elimination of CO2 à hyperventilation, pulmonary embolism, fever, hyperthyroid, anxiety, salicylate intoxication, septicemia iii. can result in hypokalemia / hypokalcemia à paresthesias, carpopedal spasm, tetany c. No change in CO2 in relation to pH à look at HCO3 3. LOOK AT HCO3 à normal, low, high (20-26 = normal) a. Decreased HCO3, decreased pH = metabolic acidosis i. Low pH, normal PCO2, low bicarb ii. CALCULATE ANION GAP 1. Na – (Cl + HCO3) = 10-16 2. Increased anion gap (>16) à MUDPILES a. Methanol, uremia, diabetic ketoacidosis, paraldehyde, infection, lactic acidosis, ethylene glycol, salicylates 3. Low anion gap (2 o Other r/f: age, smoking, abnormal cardiac stress test, long-term beta-blocker therapy, COPD Hx of MI = 5-10% increased risk of post-op MI o Pre-op EKG on pt >40, avoid surgery with current unstable angina, control stage 2 HTN prior to surgery, take antihypertensive meds day of surgery, provide prophylactic abx therapy with rheumatic heart disease; send to cardio for clearance Noninvasive stress test before noncardiac operations for pt with: active cardiac conditions, pt who need vascular operations Coronary revascularization before noncardiac operations with: left main coronary artery stenosis, stable angina with 2 vessel coronary disease, stable angina with two vessel disease, significant LAD coronary artery stenosis with EF 30 = compartment syndrome § Tx: fasciotomy = only treatment Deep Venous Thrombosis Definition: caused by clot formation in veins r/f: virchow’s triad – stasis (post-surgical, immobility, venous insufficiency), hypercoagulability (factor V leiden, cancer, OCP + smoking, pregnancy), trauma (surgery, cellulitis presentation: edema of one extremity, positive Homan’s sign (extend leg and push foot towards the head à elicits pain) dx: vneous duplex ultrasound = 1st line o d-dimer: r/o DVT in low risk pt o venography = gold standard tx: IV heparin then bridge to warfarin o recurrent DVT = lifetime anticoagulation Electrolyte Disorders Definition: serum sodium of < 135 mmol/L Peripheral and presacral edema, pulmonary edema, JVD, hypertension, decreased hematocrit, decreased serum protein, decreased BUN/CR Presentation: Muscle cramps and seizures § Hypervolemic hyponatremia – CHF, nephrotic syndrome, renal failure, cirrhosis § Euvolemic hyponatremia – SIADH (steroids, hypothyroid) § Hypovolemic hyponatremia – sodium loss (renal, non-renal) Treatment: § Asymptomatic à free water restriction § moderate hyponatremia à IV normal saline, loop diuretics may be added § severe hyponatremia à hypertonic (3%) saline Hyponatremia Serum Na should be corrected slowly—by ≤ 10 mEq/L over 24 h to avoid osmotic demyelination syndrome Definition: serum sodium of > 145 mmol/L Etiology: Diarrhea, burns, diuretics, hyperglycemia, diabetes insipidus, a deficit of thirst Poor skin turgor, dry mucous membranes, flat neck veins, hypotension, increased BUN/CR ratio > 20:1 § Decrease circulating volume = decrease of flow to kidneys means more bound urea in the blood which means ↑ BUN Treatment: intravenous (IV) 5% dextrose in water (D5W). Rapid overcorrection causes cerebral edema and pontine herniation.* Diabetes insipidus - Low urine sodium (but high serum sodium) and polyuria usually indicate diabetes insipidus § Neurogenic (central) is caused by deficient secretion of vasopressin (ADH - anti-piss-hormone) from the posterior pituitary § Nephrogenic DI is caused by kidneys that are unresponsive to normal vasopressin levels - usually inherited X-linked or from lithium or renal disease Hypernatremia § Urine osmolality of less than 250 despite hypernatremia, indicated Diabetes Insipidus Hyperkalemia Definition: serum potassium of > 5-5.5 mEq/L Presentation: Peaked T waves prolonged QRS, muscle fatigue Treatment: Insulin, sodium bicarbonate and glucose (drive potassium back into cell), calcium gluconate (antagonize effect of potassium on heart), kayexalate Give calcium gluconate with EKG changes Definition: serum potassium of < 3.5 mEq/L Presentation: Muscle cramps, constipation, flattened/inverted T waves, U waves Treatment § Potassium repletion remember to NOT use dextrose-containing fluids as this will stimulate insulin release and shift potassium within the cell which worsens the hypokalemia Hypokalemia § Replace magnesium in magnesium deficiency Definition: § serum total calcium < 8.4 mg/dL § ionized fraction of calcium < 4.4 mg/dL Presentation: QT prolongation, Trousseau’s sign, Chvostek’s sign § Labs: ↓ Ca+ ↓ PTH ↑ phosphate § EKG = Prolonged QT Treatment: IV calcium gluconate or calcium chloride Hypocalcemia Definition: § serum total calcium > 10.5 mg/dL § ionized fraction of calcium > 5.6 mg/dL Presentation: “Stones, bones, abdominal groans, psychiatric moans”, EKG: shortened QT interval. § Blood: ↑ PTH, ↑ Calcium, ↓ phosphorus § Associated with malignancy and hyperparathyroidism Hypercalcemia Treatment: IV normal saline and furosemide Definition: serum magnesium < 1.8 mg/dL Presentation: Muscle weakness, hyperreflexia, prolonged QT, PR and wide QRS, ventricular tachycardia, torsades de pointes Hypomagnesemia Treatment: IV magnesium sulfate (acute) or oral magnesium oxide (chronic) Definition: serum magnesium > 2.6 mg/dL Presentation: Muscle weakness, prolonged QT, PR and wide QRS Hypermagnesemia Treatment: IV isotonic saline, loop diuretics can be considered Definition: serum phosphate > 4.5 mg/dL Etiology: Chronic kidney disease Presentation: typically asymptomatic Hyperphosphatemia Treatment: calcium carbonate, restrict potassium Definition: serum phosphate < 2.5 mg/dL Presentation: weakness, muscle and bone pain, osteomalacia, rickets Hypophosphatemia Treatment: IV phosphate replacement Hematologic Disease DVT diagnosed in 20% general surgery pt and 30% colorectal pt without prophylaxis TX: o Compression devices o Subcutaneous heparin and LMWH are equivalent in reducing both DVT and PE § LMWH has simpler dosing and decreased risk heparin-induced-thrombocytopenia BUT more expensive and ? dose-related increased risk of bleeding § Fondaparinux is new Xa inhibitor with efficacy for prophylaxis § No enough evidence to say one is better than the other o Very low risk: early ambulation o Low risk: mechanical prophylaxis with intermittent compression devices o Moderate: LMWH or low-dose unfractionated heparing or IPC o High risk: IPC + LMWH or low-dose heparin o Extended course (4 weeks) or LMWH may be indicated for pt undergoing abdominal resection / pelvic malignancy Risks with treatment: wound hematomas (MC risk), mucosal bleeding, reoperation Fluid / Volume Disorders ~1% pt have reduced kidney function post-op o Reduce risk by pushing fluids, avoiding NSAIDs, exposure to IV contrast minimized/avoided o Blood transfusions may be necessary before surgery, esp with active hemorrhage / anemia CALCULATING FLUIDS: daily sensible / insensible loss in adult = 1500-2500mL depending on age, gender, weight o Pt weight (kg) x 30 = fluid over 24 hours o Increase for fever, hyperventilation o Measure intake and output / weight pt daily o General rule: 2000-2500mL of 5% dextrose in normal saline or LR solution daily o Re-evaluate IV fluid orders q24 hours Don’t have to measure electrolytes postop, unless extra fluid loss, sepsis, preexisting electrolyte abnormalities, renal insufficiency o Don’t add potassium during first 24 hours because K is already increased during surgery (from stress) with increased aldosterone activity o Otherwise, 20 mEq potassium added to each liter if pt has good urine output o Replace post-op ionized serum calcium in pt with thyroidectomy or parathyroidectomy Indications for catheter placement: long procedure, urologic / low pelvic surgery, need to monitor fluid balance Metabolic Disease Pt should be assessed at admission for hx of diabetes (with blood glucose testing) Blood glucose may be elevated preoperatively in DM pt esp with physical trauma + emotional stress o Perioperative hyperglycemia treated with IV short-acting insulin or SQ sliding scale insulin Elevated postop blood glucose in diabetic pt à increased chance postop infection and longer hospital stays and higher risk heart disease o Risk surgical site infection increases with degree of hyperglycemia, levels >140 = predictor of site infection IV insulin = best for perioperative glucose control bc of rapid onset, short half-life, immediate availability Post-op glycemia control o Normal: 90-100mg/dL – control with IV insulin o Moderate control: 120-200mg Post-op monitering for : hyperglycemia, hypoglycemia, infection, poor healing, wound issues, CVD (double risk for men, quadruple for women) Pulmonary Disease MC perioperative complications = pulmonary r/f: operative site and presence of pre-existent lung disease OPTIMALLY STOP SMOKING AT LEAST 8 WEEKS BEFORE SCHEDULED SURGERY COPD: o Treat aggressively to get to best possible baseline o Minimum of one week of therapy: smoking cessation, administration of antibiotics for purulent sputum, bronchodilators if indicated Asthma: poorly controlled = increased risk for postop complications; well-controlled = confers little additional risk o Poorly controlled: step-up in asthma therapy (course of steroids if FEV1 or PEFR are below predicted value) o Elective surgery à free of wheezing with PEFR > 80% of predicted / personal best prior to surgery o For those who need endotracheal intubation à administer inhaled rapid-acting beta agonist 2-4 puffs / neb treatment 30 min prior to intubation o 1-2 days systemic steroids sometimes advised to prevent acute bronchoconstriction at time of intubation Pulmonary fibrosis / restrictive lung disease: treat infection, remove sputum, stop smoking Acute lower respiratory tract infection (tracheitis, bronchitis, pneumonia): CONTRAINDICATIONS TO ELECTIVE SURGERY o Emergency surgery: humidification of inhaled gas, remove lung secretions, bronchodilators, antibiotics Diagnosis: done by PFTs before hospital admission o Do with exceptional dyspnea, exercise tolerance, cough, production of sputum, hx of smoking, previous pulm complications, asthma, age, body weight o Mild pulmonary compromise for non-abdominal / thoracic surgery don’t need PFTs o Test via simple spirometry with forced expiratory outflow o If airflow reduced à measure response to bronchodilators / get an ABG § Increased risk if FEV1 45 Treatment: o Preop: cigarette cessation, optimize underlying condition, patient education § Antibiotics for lower respiratory tract infections (purulent sputum / change in sputum character) o Intraop: increased risk for surgeries >3-4 hours; upper abdominal / open AAA repair, open thoracotomy, head/neck surgeries = GREATEST risk for postop complications § Lung protective ventilation for those undergoing abdominal surgery à low tidal ventilation of PEEP at 6-8cm water to reduce adverse pulmonary events o Postop: lung expansion, incentive spirometry, CPAP for some patients, early mobilization Substance Use Disorder Key features: substance taken in large amounts over longer periods than intended, unsuccessful efforts to cut down, lot of time spent obtaining substance / recovering from effects, craving, recurrent despite hazards, tolerance / withdrawal Alcohol / drug dependence = 5-10% of population; males >females (15% of pt seen in primary care have at-risk pattern of drug/alcohol abuse) Surgical issues: venous access, arterial injury, DVT, abscess formation, tissue compression, crush injury, ischemia (compartment syndrome), poor wound healing, altered consciousness, difficulty with pain management) Patients with known opioid use disorder on methadone should be advised to continue the use of methadone, including on the day of surgery to avoid precipitating withdrawal. For this reason, it is advised to continue chronic narcotics on the day of surgery. Dx: screen for alcohol / drug use in ALL patients à quantity, frequency o >2 drinks per day in men and >1 drink per day in women or anyone >65yrs o CAGE questions: need to cut down; annoyed by people criticizing behaviors, guilt about use, eye opener right in the morning o Blood alcohol content ( 2 drinks = 0.08%) o Tox screen o MCV, GGT, AST/ALT can be useful to diagnose / monitor Treatment: hx of drug abuse = contraindication to surgery o Avoid surgery if pt is acutely intoxicated if possible o Pharmacological agents: Naltrexone (antagonist), acamprosate, disulfram (causes nausea, headache, flushing, respiratory distress when combined with alcohol), topiramate, methadone (opioid agonist), buprenorphine (partial agonist), naltrexone § Opioids work on mu receptor o Combine pharmacotherapy with counseling o Treatment of comorbid psychiatric disorders improves outcome Anesthesia: o Opioid use: predicting analgesic needs = difficult o Sympathomimetic drug use (cocaine, amphetamine) à greater pressor response to stimuli like oro-tracheal intubation and surgical incision à may need more anesthetic o Volatile solvents: can mimic alcohol intoxication – chronic use à cardiomyopathy and dysrhythmia § Sensitivity to sympathomimetic agents and myocardial depression with volatile anesthetic agents o Patient controlled anesthesia (PCA pumps) usually involve morphine – risky for opioid-abusing patients / those in recovery to relapse § Avoid IV bolus of opioids Tobacco Use / Dependence Epidemiology: 1 in 5 smokes cigarettes in US, ~30% those undergoing general surgery smoke Smoking within 1 year of surgery: increased postop complications, increased hospital cost, higher resource use, decreased wound healing ability Optimally stop smoking at least 8 weeks before surgery o HIGHEST rate of pulm complications for those who had stopped smoking 1-8 weeks pre-op o Recent smoking cessation may pose greater risk pulm complication bc of increased cough / sputum production o Short-term cessation à reduction in vasoconstriction / irregularly heart activity; decreased risk of blood clot, better wound healing, improved PFTs Perioperative nicotine replacement = controversial à nicotine gum / lozenge helpful even on morning of surgery for a preop fast from cigarettes Use of NRT in hospitals not necessary to treat withdrawal symptoms but may be good setting to initiate treatment To help quit: bupropion 1-2 weeks before quit date Post-operative fever 5 W’s: wind, water, wound, walking, wonder drugs/whopper. o Wind (atelectasis): first 24-48 hours § Bronchial breathing / ipsilateral tracheal deviation could occur § Tx: prevent with smoking cessation at least 2 weeks before surgery, incentive spirometry, mycolytic, expectorant, inhaled beta-agonists o Water (UTI): 48-72 hours à MOST COMMON § Usually from catheter / GU instrumentation § MC nosocomial infections in the hospital § Tx: antibiotic therapy based on urine culture / sensitivity; remove infected indwelling catheter o Wound (infection): >72 hours § Staph = MC organism implicated o Walking (thrombophlebitis): >72 hours § Superficial and deep can occur à venography = most accurate for diagnosis in lower leg § Dx: ultrasound = initial diagnostic tool § Anticoagulant using heparing/ LMWH o Wonder drugs: 1 week § Anesthetic, sulfa drugs o Whopper (abscesses): 1+ week § Can cause ileus / anastomotic leak § Tx: percutaneous drainage / surgical debridement with abx Diagnosis: physical exam, CXR, UA, blood cultures, CBC, abdominal CT, cultures (sputum, wound, abscess) Wounds / infections Usually appears 5-10 weeks after surgery s/sx: fever (first sign), pain at incision site, erythema, drainage, induration, warm skin common bacteria: staph aureus (20%), e. coli (10%), enterococcus (10%), clostridium – bronze-brown weeping, tender wound dx: CBC (leukocytosis / leukopenia), blood cultures, imagine studies (CT to locate abscess) tx: remove skin sutures/stpales, rule out fascial dehiscence, pack wound open, send wound culture, administer abx o delayed course: usually wounds that open due to infection are left to heal by secondary intention At risk for infection risks: diabetes ASA score: CARDIOVASCULAR Aortic Aneurysm / Dissection AAA trifecta = back pain, pulsatile mass, hypotension (usually male >60yo); sometimes syncope; males = 8x more likely o Involves all 3 layers – intima, media, adventitia o Screening: ultrasound, if male >65 and ever a smoker o Diagnosis: ultrasound = initial imaging; CT for further eval; angiography = gold standard § >3cm if considered aneurysmal § Monitor annually if >3-4.4cm; monitor q6mo if >4.5-5.0cm and refer to vascular surgery; monitor q3mo if 5- 5.4cm; >5.5cm or >0.5cm expansion in 6 months = immediate surgical repair even if asymptomatic o Treat: § Surgical repair if >5.5cm or expands >0.6cm per year § Treat with beta blocker Dissection = severe, tearing (ripping, knife-like) chest pain radiating to the back between scapula; pulse variation between right and left arm o Just 2 layers – intima, media o Ascending aorta = surgical emergency; descending = medical therapy (beta blocker) o Dx: CXR shows widened mediastinum; MRI angiography is gold standard for evaluation o Tx: lower blood pressure § Type A (proximal aortic dissection): surgical management § Type B (distal aortic dissection): medical management initially, surgery only if needed Arterial Embolism / Thrombosis Caused by arterial occlusion: 6p’s: pain, paralysis, pallor, paresthesia, poiklothermia, pulselessness Risk factors: afib, mitral stenosis o MC site of arterial occlusion by embolus = common femoral artery o MC cause embolus from the heart = afib o Sources of embolism: heart (85%), aneurysms, atheromatous plaque Lower extremity > upper extremity Dx: angiography = gold standard; ECG, echocardiogram to look for clot, MI, valve vegetation Tx: anticoagulated with IV heparin (bolus followed by constant infusion) o surgical embolectomy via cutdown/fogarty balloon (bypass if embolectomy failed) § Fogarty balloon catheter – catheter with balloon tip that can be inflated with saline; used for embolectomy o Immediate preop management: anticoagulated with IV heparin; A-gram § Look for these postoperative after reperfusion of limb: compartment syndrome, hyperkalemia, renal failure from myoglobinuria, MI Arterial / Venous Ulcer Disease Venous ulcer: chronic defects of the skin that last longer than 4 weeks à usually on lower leg just above ankle o Physical exam: irregularly shaped wound with well-defined borders, painless, brown-stained skin, dry, itchy, reddened o r/f: obesity, age, family hx chronic venous insufficiency, hx of DVT o dx: hx and clinical signs and symptoms § measurement of ankle-brachial index (ABI): ABI 1 mm § Coronary angiography provides a definitive diagnosis If severely symptomatic despite medical therapy and being considered for PCI Patients with troublesome symptoms difficult to diagnose Angina symptoms in a patient who has survived a cardiac death event and patients with ischemia on noninvasive testings Treatment: Nitroglycerin sublingual → IV NTG Beta-blockers Severe: angioplasty and bypass Prognosis: § Depends on LVEF: < 50% (increased mortality) § Vessel(s) Involved: left main (poor, 2/3 of the heart) Unstable angina Chest pain or discomfort, heaviness, pressure, squeezing, tightness that is increased with exertion or emotion § Previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest Chronic angina—increasing in frequency, duration, or intensity of pain New-onset angina—severe and worsening Angina at rest § O2 demand unchanged, supply decreased, secondary to low resting coronary flow Workup: § EKG: ST-segment or T-wave abnormalities § Cardiac enzymes: normal troponin, CK-MB Treatment: § Admit to the unit with continuous cardiac monitoring, establish IV access, O2 § Pain control with NTG and morphine § ASA and/or clopidogrel - (Plavix reduces the incidence of MI in patients with unstable angina compared with ASA alone 9-12 months of therapy) § LMWH continued for at least 2 days § β-Blockers § LMWH § Replace electrolytes § If the patient responds to medical therapy → stress test to determine if catheterization/revascularization necessary § Revascularization if symptoms persist despite medical therapy § Reduce risk factors: stop smoking, weight loss, treat DM/HTN § ACE inhibitors and statins - start patients with unstable angina or NSTEMI with high LDL on HMG-CoA reductase inhibitor (statin) Prinzmetal variant angina Coronary artery vasospasms causing transient ST-segment elevations, not associated with clot § Smooth muscle constriction (spasm) of the coronary artery without obstruction → leads to MI, ventricular arrhythmias, sudden death § Known triggers: hyperventilation, cocaine or tobacco use, provocative agents (acetylcholine, ergonovine, histamine, serotonin) § Nitric oxide deficiency → increased activity of potent vasoconstrictors and stimulators of smooth muscle proliferation 50-y- old, females Nonexertional chest pain similar to unstable angina § Preservation of exercise capacity § Look for a history of smoking (#1 risk factor) or cocaine abuse § Pain is cyclical (mostly occur in morning hours, no correlation to cardiac workload) Diagnostics: § EKG may show inverted U waves, ST-segment or T-wave abnormalities § Cardiac enzymes: normal troponin, CK-MB § Check Mg level, CBC, CMP, lipid panel Treatment: § Stress testing with myocardial perfusion imaging or coronary angiography § Pharmacotherapy SL, topical, or IV nitrates (initial) § Antiplatelet, thrombolytics, statins, BB § Once diagnosis made—CCB and long-acting nitrates used for long-term prophylaxis (amlodipine) Claudication Reduced arterial blood supply can’t meet metabolic demand of muscles utilized during walking Reduction in blood flow to leg muscles (mostly lower extremity but sometimes upper extremity), MC by atherosclerotic plaque; NOT due to blood clot / embolization, chronic limb ischemia Usually lower extremities r/f: smoking, diabetes, hypertension, hypercholesterolemia, advanced age, male gender, obesity, sedentary lifetstyle, family history vascular dz, heart attack, stroke s/sx: pain in leg with walking, relieved within few minutes of rest, reproducible at the same walking distance each time; calf muscle atrophy, hair appendages die, dry scaly skin, prolonged cap refill dx: ABI 6mm, non-healing ulcer in sun-exposed area (face, trunk, lower legs) Risk factor: fair-skinned individuals with hx of sun exposure Dx: shave/punch biopsy Tx: depends on type, size, location o Most treated surgically à photodynamic therapy, tissue scraping, electrosurgery, mohs, wide local incision Burns Rule of 9’s: head, each arm, chest, abdomen, each anterior leg, each posterior leg, upper back, lower back all = 9% o genitals =1% o palm = 1% (palmar method) degree involvement: o 1st degree (sunburn): skin blanches with pressure, skin may be tender o 2nd degree (partial): skin red and blistered, skin is very tender o 3rd degree (full thickness): burned skin is tough / leathery; NON-TENDER o 4th degree: into bone and muscle Minor burns: 10% full thickness burn à burns involve face, hands, perineum, feet, cross major joints / circumferential Tx: monitor ABCs (airway, breathing, circulation, disability, environment/exposure), fluid replacement, topical antibiotic o Cleanse with mild soap / water, don’t apply ice directly o Irrigate chemical burns with running water for 20 minutes o Topical antibiotic cream applied to superficial burns o Fingers / toes should be wrapped individually o Escharotomy indicated for eschar restricting airway, ventilation, causingishcemia o DO NOT ASPIRATE BULLAE but leave in place until rupture on own then debride Children with >10% total body surface area and adults >15% burns need formal fluid resuscitation o 4mL x % body surface burned x weight in kg à– ½ in 1st 8 hours and other ½ in remaining 16 Urine output should be 0.5mL per kg weight per hour Cellulitis definition: acute bacterial skin/skin structure infection of dermis and subcutaneous tissue caused by S. aureus, group A strep, or children with H.flu/strep pneumo s/sx: pain, erythema, warmth, swelling; flat margins, not well demarcated o systemic: fevers, chills, LAD, lymphangitis, myalgias, hemorrhage, necrosis tx: antibiotics asap + culture (then follow up in 48 hours) o oral for mild: cephalexin or dicloxacillin o suspected MRSA: start empiric and culture § clindamycin, Bactrim, doxycycline, IV vanco/Linezolid o cat bite – augmentin or doxy if PCN allergy o puncture wound (cover for pseudomonas): ciprofloxacin o modify with known pathogens, underlying conditions/diseases, animal bite exposure Discharge breast/nipple discharge o mastitis/breast abscess: nipple discharge, redness, warmth o breast CA: nipple discharge, breast discomfort, breast mass o gynecomastia: nipple discharge, breast enlargement, overweight o inflammatory breast cancer: nipple discharge, breast enlargement, redness o hypogonadism: nipple discharge, sexual dysfunctional, reduced sex drive GU: o Vaginal infection: yeast, BV, trichomoniasis, HPV, herpes o Cervix: cervicitis o Foreign body: tampon o STI: chlamydia / gonorrhea o Vaginal medicines / douching o Menopause: discharge, absence of menstruation, anxiety Other skin conditions: abscess = red, painful, +/- discharge Postoperative Drug Eruptions Drug-induced exanthems: MC cutaneous reactions to drugs, responsible for ~90% of all drug rashes (abx, sulfonamides) Ddx: SJS, early TEN, erythema multiforme, viral exanthems, drug rash Dx: skin biopsy: shows necrotic epithelium; often obvious on physical exam Tx: stop all offending medications!!! o Early admission to burn unit, manage fluid/electorlytes/nutrition, airway stability, eye care o Ophthalmology/dermatology consult o IVIG o Steroids used to be treatment of choice but now ? increased risk sepsis Melanoma Definition: tumor from malignant transmoration of melanocytic cells à mostly skin but can’t be on any tissue (ocular, GI, GU, lymph, leptominentes) MC sites: back for men, calves for women Likes to metastasize and spread to any sit on body – MC tumor responsible for metastasis to the heart r/f à HARMM: hx prior melanoma, age >50yo, absence of regular dermatologist, mole changes, male gender Dx: BIOPSY! à excisional is preferred - with doubt biopsy full depth of dermis and extend slightly beyond edges of lesion o Microstaging is important part of staging / clinical management o Physical exam: ABCDE (asymmetry, border irregularity, color varied, diameter increasing or >6mm, elevation raised – doesn’t have to meet all criteria to be suspicious Prognosis most strongly associated with depth of the lesion Tx: excision and wide margins (stage I-III), but for stage IV systemic tx with chemotherapy Prevention: avoid sunburns, use sunscreen, avoid tanning beds Pressure Ulcers Soft tissue injury from pressure between external surface + bony prominence Pt usually >65yo with hip fracture / ICU care; sacrum and hip = MC sites r/f: age >65, impaired circulation, immobilization, undernutrition, incontinence Dx: observation o Stage 1: erythema of localized area, non-blanching over bony surface (stays red) o Stage 2: partial loss dermal layer; pink ulceration o Stage 3: full dermal loss often showing subcutaneous tissue / fat o Stage 4: full thickness ulceration exposing bone, tendon, muscle à osteomyelitis may be present Tx: manage based on stage of ulcer o Stage 1: aggressive preventive measure, thin film dressings for protection o Stage 2: occlusive dressing to maintain healing, hydrocolloids, transparent films o Stage 3/4: debridement of necrotic tissue; exudative ulcers benefit from absorptive dressings; dry ulcers need occlusive dressing to maintain moisture o Debridement: incisional with scalpel when extensive and dry; mechanical with wet-dry dressings § Surgical closure may be necessary; vacuum-assisted closure; negative pressure; remove necrotic debris; negative pressure wound therapy shows efficacy Prevention: reposition q2hrs Rash Difficult to diagnose, esp if generalized Ddx: o Abx side effects – fever, skin rashes, AMS o zinc deficiency – perioral pustular rash o paget disease: pruritus, well-demarcated, erythematous, eczematous rash o herpes zoster: classic vesicular lesions; dermatomal distribution o herpes simples: clear vesicles on erythematous base, crusting o systemic rheumatoid disease (still’s): multiple (>5) joint involvement, fever, LAD, hepatosplenomegaly, rash, subcutaneous nodules, pericarditis o fat emboli from long bone fracture: respiratory insufficiency, coagulopathy, encephalopathy, upper body petechial rash tx: observe / treat empirically, diagnostic testing, refer to dermatology for workup Redness / Erythema Causes: infection, massage, electrical treatment, acne medication, allergies, exercise, solar radiation (sunburn), photosensitization, cutaneous radiation syndrome, mercury toxicity, blister agents, niacin administration, waxing/tweezing, radiotherapy treatment Ddx: clcer, eczema, stasis / contact dermatitis, drug allergy, cellulitis / MRSA, chemical burns, angioedema / urticaria, venous insufficiency, herpes zoster, scarlet fever, tinea infections, psoriasis, acne, polycythemia vera, paronychia, osteomyelitis, abscess, autonomic hyperreflexia, lymphadenitis, carbuncle, furuncle, neutropenia Osteomyelitis Infection of bone à spreads via spinal arteries Bones of vertebral spine = MC affected May originate in urinary tract and IV drug use can carry it to the spine frequently caused by pseudomonas (puncture wound to foot) – treat with ciprofloxacin caused by breakdown of coagulation factors à decreased fibrinogen / platelet count, prolonged PT and PTT, and presence of firing split products à bleeding/oozing from multiple sites DIC caused by breakdown of coagulation factors à decreased fibrinogen / platelet count, prolonged PT and PTT, and presence of firing split products à bleeding/oozing from multiple sites dx: thrombocytopenia, high PTT, high PT, high d-dimer, decreased plasma fibrinogen tx: correct underlying cause o replace platelets, coagulation factors, fibrinogen to control severe bleeding o heparin in pt with slowly evolving DIC who at risk for DVT Squamous cell carcinoma malignant epithelial tumor arising from epidermal keratinocytes à enlarging hyperkeratotic macule, scaly or crusted lumps usually from pre-existing actinic keratosis; much faster growing than BCC s/sx: erythematous, indurated, scaly/ulcerated papules on sun exposed skin (face, lips, ears,h ands, forearms, lower legsi – often tender/painful – size varies exam: basal cell = telangiectasia with central ulceration and rolled border vs scaly papules of SCC dx: biopsy tx: surgical excision +/- mohs, radiotherapy, cryotherapy, electrodessication and curettage good prognosis with immediate treatment Urticaria pruritus and urticaria frequently occur during paranesthesia period causes: anesthetic agent, widespread use of potent opioids, latex, abx, LMWH, cold compresses, underlying systemic disease dx: clinical tx: identify and stop offending agent – treat/monitor anaphylaxis urgently; antihistamines / steroids may be needed NEUROLOGY Change in Speech aphasia: inability to comprehend / form language due to damage of specific brain regions o usually caused by postop CVA (trouble speaking / numbness and face drooping / one arm weakness) OR head trauma o other causes: MS, intracerebral hemorrhage, migraine headache, carotid disease, recurrent laryngeal nerve injury (thyroidectomy), apraxia of speech dysarthria: motor speech disorder resulting from neurological injury of motor component or moto-speech system o causes: § toxic/metabolic: wilson’s, hypoxic encephalopathy (drowning), central pontin myelinolysis § degenerative: parkinsonism, ALS, MS, huntington’s, niemann-pick disease, friedreich’s ataxia § others: TBI, thrombotic/embolic stroke, brain tumor, cerebral palsy, Guillain-barre, hypothermia, lyme disease, stroke, intracranial hypertension (pseudotumor cerebri), tay-sachs disease Change in Vision perioperative o vision loss = very rare § ischemic optic neuropathy: caused by ischemia / poor circulation to short posterior ciliary blood vessels that supply the front, anterior, portion of optic nerve à painless abrupt reduction in vision and optic disc pallor / swelling o visual changes: range from transient blurring of vision to irreversible blindness § transient: usually from ocular ointments, excessive drying of cornea, corneal trauma § complete / partial: surgical trauma, embolic events, acute anemia, hypotension postop o ocular injury / vision loss § injury: MC = corneal abrasion (+/- associated with vision loss) § vision loss: MC = central retinal artery occlusion, ischemic optic neuropathy, cerebral vision loss other causes: sickle cell, syphilis, Bechet disease, local anesthetic toxicity, general anesthesia, orbital fracture, cataract, optic neuritis, polyarteritis nodosa, myocardial infarction, migraine headache, cardiac valvular disease, hypotentsion ,internal carotid disease, vasculitis, collagen vascular disease, sleep apnea, anemia, diabetes mellitus, herpes zoster infection, acute nagle closure glaucoma, retrobulbar hemoatoma, pituitary apoplexia, glycine induced vision loss r/f: long duration prone position, excessive blood loss, hypotension, anemia, hypoxia, excessive fluid replacement, use of vasoconstricting agents, elevated venous pressure, head positioning, patient-specific vascular susceptibility dx: o complete history and eye exam (pupils and opthalmoscoy, color vision and amsler grid, visual field testing) o labs: ESR (temporal arteritis), CRP, fasting blood glucose, VDLR, fluorescent treponemal antibody absorption, ANA Epidural Hematoma Transient loss of consciousness from injury, then lucid period followed by increasing drowsiness, headache, and unilateral (contralateral) weakness. Blood in the space between dura and skull Cause: traumatic intracranial hemorrhage after temporal bone skull fracture à tearing of middle meningeal artery Dx: non-con head CT à lenticular, unilateral convexity (lens-shape) usually in temporal region – usually doesn’t cross suture lines but may cross midline Tx: o surgical craniotomy o medical to decreased intracerebral pressuer: mannitol, steroids/ventricular shunt, hyperventilate Motor and Sensory Loss Spinal Cord Injuries Anterior cord syndrome: § Loss of pain and temperature below the level with preserved joint position/vibration sense Central cord syndrome: § Loss of pain and temperature sensation at the level of the lesion, where the spinothalamic fibers cross the cord, with other modalities preserved (dissociated sensory loss) Complete cord transection: § Rostral zone of spared sensory levels (reduced sensation caudally, no sensation in levels below injury); urinary retention and bladder distention Brown-Sequard syndrome (hemisection of the cord): § Loss of joint position sense and vibration sense on the same side as lesion and pain and temperature on the opposite side a few levels below the lesion § Lesion of half-ipsilateral cervical cord lesion § Contralateral sensory findings: pain and temperature loss Neuropathies Distal sensory polyneuropathy o Stocking-glove: sensory loss affecting distal lower and upper extremities Axonal: MC due to diabetes melltius, alcohol, vitamin B12 deficiency, HIV, lyme, uremia, chemotherapy, vasculities, amyloidosis Other sensory neuropathies: sjogren’s, guillain-barre, chemoterapy induced (esp platinum drugs), vitamin B6 toxicity Subarachnoid Hemorrhage Sudden, severe (often excruciating) HA à “worse headache of my life” s/sx: sudden, transient LOC (~50% of pt), blood pressure rises, fever, confusion, stupor, coma, nuchal rigidity (meningeal irritation) herald bleed (~40% of pt) à less severe but atypical headache with focal neurologic signs – usually happens 1-3 weeks before severe SAH causes: o ruptured cerebral arterial aneurysm or AVM à bleeding into CSF in subarachnoid space o ruptured saccular (berry) aneurysm = ~75% nontraumatic cases with mortality rate of 50% - during 5th/6th decade of life § r/f: smoking, HTN, hypercholesterolemia, heavy alcohol use dx: non-con head CT = initial o LP if CT is unrevealing / negative with high clinical suspicion § Elevated opening pressure, grossly blood fluid in all four tubes o Cerebral angiography to evaluate entire vasculature o EEG may show side/site of hemorrhage Tx: manage hypertension, surgery to clip/wrap aneurysm, remove/embolize AVM by intra-arterial catheter Subdural Hematoma Caused by head injury (fall, MVA, assault) à tearing of blood vessels Usually elderly pt with hx of multiple falls + neuro sx (chronic) Acute: sx within 48 hours of injury Subacute: 3-14 days Chronic: 2+ weeks (common in alcoholics / elderly) Dx: non-con head CT à crescent shaped, concave hyperdensity that can extend across suture line Tx: depends on severity o Small + mild sx: no tx other than observation; repeat imaging to monitor o Severe: surgery to reduce pressure in brain § Burr hole trephination: hole drilled in skull and blood suctioned § craniotomy: larger section of skull removed for better access to hematoma to recuce pressure § craniectomy: section of skull removed for extended period of time to allow injured brain to expand / swell without permanent damage (rarely used) Pituitary Adenoma located at sella turcia à applies pressure on optic chiasm à diminished temporal vision / bitemporal hemianopsia lactotrophy adenomas (prolacintomas) à hypersecretion of prolacting à amenorrhea, galactorrhea, headache dx: MRI, CT, eval hormone levels tx: 1st line = dopamine agonists (cabergoline / bromocriptine); estrogen for women with hypogonadism o if medical fail à consider transsphenoidal resection Vascular Disorders carotid artery narrow (stenosis) caused by atherosclerotic plaque build up à necrotic core with weak fibrous cap à disruption of cap à thrombosis / embolization r/f: male gender, family hx, hyperlipidemia, smoking, HTN, diabetes associated conditions: PAD, coronary artery disease sx: transient visual disturbance (amaurosis fugax), unilateral muscle weakness or paresthesia, dizziness, tinnitus, aphasia physical exam: carotid bruit, motor / sensory defects dx: o duplex doppler UA = best initial test to determine level of stenosis § >50% = moderate, >70% = severe o Angiography is US unavailable / unclear Screening: not recommended for asymptomatic pt à optimize therapy for underlying dz (HTN, hyperlipidemia) Tx: smoking cessation, antiplatelet therapy (aspirin / Plavix), statins for all pt o Operative: carotid artery revascularation for stenosis >70% § Carotid endarterectomy (CEA)= 1st line; carotid artery stenting if can’t tolerate CEA Transient Ischemic Attack Definition: transient episode of neurologic dysfunction without acute infarction Low flow TIA: from stenotic atherosclerotic lesion at internal carotid artery origin à usually short lived (minutes) and recurrent o Sx: hand, arm, face numbness, weakness; aphasic syndromes when dominant hemisphere effected Dx: CT indicated for all; also MRA, carotid cuplex ultrasound, transcranial doppler ultrasound Tx: resolve symptomatic carotid atherosclerotic dz o CEA (carotid endarterectomy) for symptomatic carotid stenosis 70-99% with life expectance 5 yrs § Low dose aspirin should be started prior to procedure and continued for at least three months after CEA is done o Recently symptomatic 70-99% stenosis à carotid artery stenting preferred if: carotid lesion not suitable for surgery, radiation-induced stenosis, cardiac/pulmonary/other disease at risk with anesthesia Symptomatic stenosis 3.5g/day § Heart failure: swelling of legs, abdomen, lungs à shortness of breath § Cirrhosis: obstruct blood flow through liver à ascites / peripheral edema in lower legs § MC causes: chronic venous insufficiency; complication of DVT § Sx: “heavy legs”, itching, pain, hyperpigmentation, stasis dermatitis, thick brawny skin, increased abdomen size, trouble breathing § Dx: § U/S = initial test of choice § Low suspicion – d-dimer § Color duplex ultrasound, ABI § Urine dipstick to r/o nephrotic syndrome § Tx: treat underlying cause § Leg edema à compression stockings, elevate legs above heart 30 min 3-4x/day § Sodium restriction § With chronic without volume overload avoid diuretics § May enhance sodium retention through increased secretion of renin and angiotensin à AKI / oliguria Fluid and Electrolyte Disorders § IV or orders re-evaluated every 4-6 hours on first day of surgery and q24hrs thereafter § 2000-2500 5% dextrose daily = general rule § Don’t add potassium during first 24 hours after surgery (due to increased amounts in circulation from stress and increased aldosterone activity) § Fluid loss through NG tube 20mm systolic bp, 10mm diastolic bp, or both à 2-5 minutes after change from supine to standing § Dx: measure BP and heart rate after 5 min of supine and 1 and 3 min after standing (or sitting if can’t stand) § Hypotension without compensatory increase in HR suggests autonomic impairment; marked increase to >100bpm or by >30 beats/min suggests hypovolemia § ECG, electrolytes and glucose routinely checked § Tilt table testing when autonomic dysfunction suspected § Tx: identify cause and treat accordingly à physical measure to reduce venous pooling, increased Na intake, sometimes steroid / midodrine § Causes: autonomic dysfunction, medications, postprandial (from insulin response to high carb meals / blood pooling in GI tract – worse with alcohol intake), vagal / carotid sinus hypersensitivity, hypovolemia, adrenal insufficiency § Drugs: alcohol, alpha blockers, anti-depressants, antihypertensives, antiparkinsonism, antipsychotic, beta-blocker, diuretic, muscle relaxers, narcotic analgesic, phosphodiesterase inhibitors, sedatives / hypnotic drugs, vasodilator drugs Renal Cell Carcinoma § Renal clear cell = most common type (80%); transitional cell = second most common § r/f: smoking § s/sx: hematuria = most common presenting symptom (~60%) flank pain + abdominal pain = ~30%, palpable abdominal / renal mass § dx: ultrasound or CT then biopsy = gold standard § tx: surgery with radical nephrectomy = curative Hypovolemic Shock § decrease in circulating blood volume in intravascular system à decrease CVP pressure (amount of blood in right ventricle) § less blood = decreased bp § body compensates by increased pulse rate Renal Vascular Disease § renal artery stenosis: narrowing of one or both renal arteries à most often caused by atherosclerosis / fibromuscular dysplasia § narrowing of renal artery can impeded blood flow to target kidney à renovascular hypertension § dx: § renal artery bruit on auscultation § HTN resistant to 3+ drugs § If on ACE-I and pt develops acute renal failure / sharp rise BUN:Cr, think renal artery stenosis § Ultrasound = initial imaging § Renal arteriography = gold standard § Tx: stenting of renal arteries § Percutaneous transluminal angioplasty (PTA) + stent placement with surgical bypass of stenotic segment § Extensively infarcted kidney must be removed if revascularization not expected to result in functional recovery Testicular Carcinoma § MC solid tumor in young men ages 15-40 (average 32 yo); 5 year survival = 90% § Seminoma = MC type (60%) § r/f: history of cryptochordism § s/sx: firm, painless, nontender testicular mass § dx: § tumor markersBHCG (+) and afp (+) in non seminoma germ cell tumors § scrotal ultrasound § other radiologic studies to look for mets (common to belly, brain, lung) § tx: § orchiectomy +/- chemotherapy / radiation depending on cell type § orchiectomy and radiation are the most effective combination § seminomatous tumors = radiosensitive and can be treated with radiation therapy § nonseminomatous = radioresistant § AFP can be used to identify early relapse / monitor Urinary Retention § Causes: § Obstructive: urethral stricture, bladder calculi, neoplasm, foreign body § Neurogenic: MS, Parkinson, CVA, postop retention § Post-op urinary retention (POUR) à common after spinal / epidural anesthesia à prolonged blockage of parasympathetic fibers that innervate the bladder with resultant urinary retention / need for urinary bladder catheter § Traumatic: urethral, bladder, spinal cord injury § Extra urinary: fecal impaction, AAA, rectal / retroperitoneal mass § Infectious: local abscess, cystitis, genital herpes, zoster § Acute urinary retention: can’t void despite full bladder § r/f: male gender, prostatic enlargement, epidural, spinal or prolonged anesthesia; antihistamine / narcotic use; pelvic / perineal procedures § sx: suprapubic discomfort with urgency / inability to void (8 hours after surgery / catheter removal), pain, vomiting, palpable bladder on exam, hypotension, bradycardia, cardia dysrhythmias § complication: infection, ischemia, long term bladder dysfunction § dx: bladder u/s 500mL of urine; post-void residual >500mL; urine culture; CBC if suspected infection § tx: immediate sterile catheterization for 24h then void trial; identify and treat underlying cause § chronic urinary retention: painless, develops gradually, fullness sensation, overflow incontinence, suprapubic dullness, rounded midlines mass § dx: postvoid residual bladder volume by cath or u/s; abdominal US or CT to identify masses, stones, hydronephrosis § tx: immediate sterile catheterization for 24h then void trial; identify and treat underlying cause § detrusor sphincter dyssynergia: usually from neurological pathway (SCI / MS) § urethral sphincter muscle dyssynergically contracts during voiding causing flow to be interrupted and bladder pressure to rise § s/sx: daytime and nighttime wetting, hx of UTI / bladder infections; associated constipation / encopresis § PE: palpable bladder, bladder residual volume upon placement of foley catheter § Dx: post-void residual volume >150mL § Tx: botulinum A toxin injections; surgical incision of bladder neck (can cause incontinence) Wilms Tumor § Nephroblastoma (wilms tumor); MC solid renal tumor of childhood (5% childhood cancers younger than 15) § Arise from kidney and seen in otherwise healthy children 90% from clots in deep veins of lower extremities (homan’s sign – dorsiflexion foot = calf pain) § r/f: virchow’s triad – hypercoaguable state, trauma, venostasis (surgery, cancer, oral contraceptives, pregnancy, smoking) § dx: spiral CT = initial method of identifying § ABG = respiratory alkalosis secondary to hyperventilation § EKG: S1Q3T3 (rare); non-specific ST wave changes § CXR: Westermark sign or Hampton hump (triangular or rounded pleural base infiltrate adjacent to hilum) § VQ scan: perfusion defects with normal ventilation (normal VQ rules out PE; abnormal – non-specific) § D-dimer § Pulmonary angiography = gold standard definitive § Tx: heparin = anticoagulant of choice or warfarin (INR 2-3) § Duration: minimum of warfarin 3 months with reversible risk factor § Unprovoked: warfarin recommended for at least 6 months then reevaluate § 2 episodes unprovoked, long term with warfarin Shortness of Breath § MANY CAUSES – some to do with underlying disease; others not (exercise, altitude, tight clothing, prolonged bed rest, sedentary lifestyle § Disease: asthma, COPD, pneumonia, CHF, acid reflux, pneumothorax, PE, foreign body aspiration, interstitial lung disease, obesity, pulmonary hypertension, sarcoidosis, tuberculosis, anemia, cardiomyopathy, pericarditis, epiglottitis, generalized anxiety, myasthenia gravis, fractured rib, sudden blood loss Bronchospasm § Common post-op complication § Causes: exacerbation of chronic lung condition, aspiration, histamine release from medications, trachea stimulation from secretions, suctioning, endotracheal intubation § s/sx: dyspnea, wheezing, chest tightness, tachypnea, hypercapnia § Tx: treat underlying cause à short acting beta-2 agonist (albuterol) + bronchodilator = 1st line therapy for asthmatic Weight Loss / Fatigue § MANY CAUSES – some to do with underlying disease; others not (dieting, exercise, malnutrition, lack of access to food, lack of sleep, heavy exertion, jetlag, large meal, aging) § Disease: COPD, chronic fatigue syndrome, sarcoidosis, interstitial lung disease, pulmonary hypertension, tuberculosis, HIV, sleep apnea, RA, hyperthyroidism, T1DM, T2DM, clinical depression / seasonal affective disorder, anorexia, insomnia, anemia, anxiety OBSTETRICS / GYNECOLOGY Adenopathy § Enlargement of lymph nodes due to gynecologic infections, malignancy, inflammation § Most commonly seen adenopathy in breast disease is axillary adenopathy (85%) § Other adenopathies seen: internal mammary, parasternal, supraclavicular Benign Breast Disease § Fibroadenoma = most common benign breast condition in young adolescent women (10-20%) § Young, reproductive age women, associated with cyclic history, breast pain resolves with menses § s/sx: painless, firm solitary (rubbery feeling) well-defined mobile mass; grows slowly over time and doesn’t wax/wane with menses; no axillary involvement / nipple discharge § dx: ultrasound / mammogram + fine-needle biopsy or excision biopsy § rare, but malignant neoplasms have occasionally been found in fibroadenoma § Fibrocystic breast disease = 2nd most common § Lumps develop in breasts that come and go § No increased risk breast cancer § s/sx: painful, swollen, lumpy breasts bilaterally, intermittent to constant pain; well-circumscribed rubbery lumps, round, discrete, and relatively moveable § may increase or decrease in size with menstrual hormonal changes § ovarian hormones are causative agent; usually resolves with start of menstrual cycle § dx: breast cyst aspiration + U/S and/or mammogram; straw colored fluid with no blood § tx: no definitive cure; bra with extra support for pain relief; caffeine may worsen condition; montly breast exams one week after period § NSAIDs, heat/ice, supportive bra, decrease caffeine/fat/chocolate § OCPs with low estrogenic activity and potent progestin § Most resolve spontaneously; +/- fine needle aspiration for removal of fluid Breast Carcinoma § MC cancer and 2nd MC cause of death in adult women § Rf: 70% pt diagnosed have no risk factors § First degree relative with hx breast CA, obesity, ETOC, >65yo, late >17 or early 75 yrs § Dx: § Aspirate if cystic, mammography, U/S, breast biopsy = definitive § Tx: segmental mastectomy (lumpectomy) followed by breast irradiation in all patients with adjunctive chemotherapy in women with positive nodes is appropriate therapy and just as effective as modified radical mastectomy for stage I and II and tumor

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