Acute General Oncological Wound Healing

Document technical information

Format pdf
Size 2.6 MB
First found Jun 9, 2017

Document content analysis

Language
English
Type
not defined
Concepts
no text concepts found

Persons

Organizations

Places

Transcript

Surgery Clerkship Oral Exam Study Guide
Acute
Wound Healing
Biliary System/Cholecystitis
Nutrition
Acute Abdomen/Appendicitis
Diverticulitis
General
Peripheral Vascular Disease
Abdominal Wall Hernias
Gastrointestinal Bleeding
Reflux Esophagitis
Trauma/Shock/Burns
Mark Tuttle, Amanda Mure (2010)
Oncological
Breast
Thyroid
Colorectal
Lung
Melanoma
ACUTE
WOUND HEALING
General Considerations: Wounds- injury (trauma) or intentional (surgery)
● Always consider Tetanus vaccination status
○ Give tetanus toxoid always unless already given 3 doses in lifetime or at least one given in the last 5 years
○ Give tetanus immune globulin only if in a tetanus-prone wound and < 3 doses given in lifetime (or unknown)
● Only important way to decrease bacterial count in a wound is debridement, in addition to dressing changes q4hr.
● Apply no tension on skin (causes necrosis)
● Close along Langer’s lines if possible
● Absorbable suture (gut, vicryl, PDS) is more inflammatory than non-absorbable (silk, ethibond, prolene, nylon, steel)
● Tensile strength: very little until 3 weeks, level off at around 7 weeks. At 4 weeks is 85% of its maximum strength.
Steps of wound healing:
1. Substrate/Inflammatory/Lag/Exudate phase - 0 to 7 days in primary intention, indefinitely for secondary/tertiary until
epithelialization occurs
• Hemostasis: Activated platelets, coagulation factors --> hemostatic plug. - 1 to 2 hours
o Impaired in chronic liver disease and uremia
• Inflammation: PDGF, TGF-B and fibronectin are chemoattractive. - 0 to 2 days
o PMNs, macrophages, complement C5A, kallikrein
PMNs are the most prominent cell type during this period
Macrophages are the most important cell type, they release metalloproteinases for
remodeling/debridement of necrotic tissue as well as growth factors
o Impaired by steroids, immunosuppressants, congenital or acquired immunodeficiency
o MOST IMPORTANT stage to prevent wound infection: macrophages can handle small #’s of bacteria. If there
are large #s, or neutropenia, clinical wound infection occurs.
o Systemic Abx don’t work during this phase b/c they don’t penetrate granuation tissue. Use topical Abx.
2. Proliferative phase: Epithelialization, collagen synthesis, angiogenesis (VEGF-mediated) - 4 days to 3 weeks
• Epithelialization must occur as the first step for the rest of the phase to continue.
• Net production of collagen during this phase
o Alpha helix, every 3rd AA is glycine, has unique AAS OH-proline, OH-lysine
• Primary cell type: fibroblast
• Impaired by Vitamin C def, iron def, or Dz of collagen synthesis (osteogenesis imperfecta, Ehlers-Danlos, etc)
3. Maturation: Remodeling, contraction - 3 weeks to 1 year
• Cross linking of collagen
• “flattening” of the scar, takes 9 months in an adult
• No net production of collagen during this period
Factors affecting wound healing
● Aging
● Nutritional status
○ Need anabolic positive protein balance for optimal healing
○ Vitamin A deficiency: delayed wound healing, epithelial keratinization, anemia
○ Vitamin C deficiency: delayed wound healing, wound dehiscence. Is a cofactor in matrix metalloproteinases which
cleave collagen fibrils, helping it mature to full tensile strength.
○ Vitamin K deficiency: essential for carboxylation of glutamate, synthesis of X, IX, VII, II coagulation factors
● Chronic disease: ex. Diabetes
● Oxygen delivery: Peripheral vascular disease, smoking (↓ oxygen carrying capacity)
● Chronic edema: CHF
● Medications: ex. steroids
Wound Closure
● Primary Intention: edges of wound are approximated by either sutures, skin grafts, etc
○ Immediate coverage with epithelial elements. Epithelialization occurs in 12-24 hours
○ Use absorbable suture for deep closure and nonabsorbable for skin closure (less irritating)
○ Contraindicated with contaminated wound (human bite, farm injury), severe crush injury
● Secondary Intention: spontaneous wound closure. Granulation at base first, margins contract, epithelialization last
○ Contracts at 1mm/day
For wounds to large to close.
● Tertiary intention: Granulation occurs, then wound edges approximated a few days later.
○ Should only be performed in wounds with bacterial counts of less than 10^5, therefore NON-infected wounds.
Wound contamination status
Type
Characteristics
Chance of infection
Clean
<12 hours old, minimal bacteria. No GI, GU, respiratory tract.
1-4%
Clean-Contaminated
Penetration into GI, GU, respiratory, but prepped
5-15%
Contaminated
Gross contamination, > 105 organizz. Fresh traumatic wound.
16-25%
Infected
Prior infection in region of wound. Ex. perforated viscus.
50%
Types of wounds: Avulsion, Crush: need debridement
Abrasion: suture
Puncture: no closure necessary
Chronic Wounds
Types
● Diabetic foot ulcer
○ Foot architecture changes due to loss of intrinsic muscles of the foot (Charcot foot)
○ Loss of sensation and protective reflexes
● Pressure ulcer
● Arterial insufficiency ulcer
● Venous stasis
○ Usually in anteromedial leg NOT foot
○ Tx: compression stockings
● Open wounds (stalled inflammatory phase)
Wound Care
● Debridement: surgical, hydrotherapy (to separate eschar), enzymatic (Elase, Travase, Biozyme-C)
● Negative pressure devices
● Recombinant growth factors: still in clinical trials
● Hyperbaric oxygen: controversial in care of chronic wounds
● Topical agents: Hydrogen peroxide (not bactericidal, but cleanses w/bubbling), Neosporin, sulfdiazene, nitrofurazon
● Dressings
○ Conventional gauze: helps in gentle debridement. Other dressings better once granulation bed present
○ Semipermeable: minimize moisture loss
○ Impermeable hydrocolloids: Anaerobic, may improve reepithelialization rate
BILIARY SYSTEM WORKUP (CHOLECYSTITIS - Obstruction, NOT infection of cystic duct: acute inflammation)
10% of population have gallstones. May be asymptomatic. Risk factors: Female, fat, fertile, forty, flatulent.
10% of people with cholecystitis are acalculus: ICU patients, due to bile stasis) Tx: Perc. decompression and interval chole.
Indications for cholecystectomy: Symptomatic, calcified gallbladder, stones > 3cm (with or withour symptoms)
Cholelithiasis
Sx
● Biliary colic:
colicky RUQ pain, radiates to
shoulder (Boas sign),
worse w/fatty foods
● Physical exam often
unremarkable
● Mild leukocytosis (12-15k)
● Mild jaundice (2-3mg/dl)
○ In 20%. From inflammatory
cholestasis, not obstruction
Acute cholecystitis
●
●
●
●
●
●
●
Cholelithiasis, but worse
Nausea/vomiting
Constant pain, not colicky
Mild fever (101 F)
Mild leukocytosis (12,000)
Hypoactive bowel sounds
LFTs usually normal
○ except alk phos
● Muscle guarding
● Murphy’s sign pathognomonic
Acute ascending cholangitis
●
●
●
●
●
Cholecystitis, but worse
High fever (104 F), chills
Severe leukocytosis (22,000)
LFTs abnormal: ↑ bili, ↑ alk phos
Charcot’s triad: RUQ pain, fever,
jaundice (seen in 50-70%)
● Reynold’s pentad: + sepsis & MS Δ
● 60% due to choledocholithiasis
Dx
1. Ultrasound
(95% sensitive)
1. Ultrasound (Pericholecystic fluid, 1. Ultrasound
thickened gallbladder)
2. HIDA scan (4 hours)
3. CT if suspect complication
(abscess, perforation,
pancreatitis)
Tx
●
1. NPO, IVF, (NGT if N/V)
2. IV antibiotics (2nd gen ceph)
3. IV analgesia (Meperidine, not
morphine- contracts sphnicter of Oddi)
4. Cholecystectomy in 48-72 hours
1. IV antibiotics
2. Decompress biliary tree (percutan.)
3. ERCP after acute phase: treats
underlying cause - obstruction
4. Cholcystectomy
●
●
●
●
●
●
●
●
Cx.
Elective laparoscopic
cholecystectomy
No antibiotics necessary postop.
Preop: 1st gen cephalosporin
33% cholecystitis in 2 years
Hepatic a ligation: ischemia,stricture
Gangrenous cholecystitis
Perforation (very bad)
Emphysematous cholecystitis
Gallstone ileus
Sepsis
Hepatic abscess (very bad)
Other differentials
● RUQ pain and jaundice, but afebrile: Suspect Choledocolithiasis
○ Diagnosis: Some combination of: ERCP, cholangiogram (mandatory if pancreatitis), lap. chole
○ Treatment
Stones < 3mm: observe
Biliary stricture (if previous cholecystectomy): Choledochojujunostomy
● Ultrasound: gallbladder distention with internal echoes + gallstones: Empyema of the gallbladder
○ Treatment: IV antibiotics, percutaneous cholecystostomy, cholecystectomy
● Ultrasound: No gallbladder stones, but dilated ducts with air: Suppurative cholangitis
○ Treatment: IV antibiotics, ERCP for decompression
● Other therapeutic Measures:
Deoxycholic acids-help dissolve some bile salts
Lithotripsy
Antibiotics if gangrenous-use 3rd gen cephalosporins
Pain control: meperidine (morphine contracts sphincter of Oddi)
NUTRITION
Digestion:
Fat: 100g/day
Protein: 100g/day
Carbohydrates: 400g/day
Reserves:
160,000 calories stored in liver as glycogen, elsewhere as muscle, fat.
Nitrogen balance: (g) = (Protein intake (g)/6.25) - (Urine Nitrogen +4)
Caloric requirement: (Basal energy expenditure [BEE]):
Males = 25 kcal/kg/day
Females = 22 kcal/kg/day
Protein requirement: 24 hr urine nitrogen is the most accurate reflection of individual protein requirements
● .8-1.0 g/kg. More in burns, less in refeeding after starvation and hepatic failure
● Nondepleted: 1g/kg/day, calories 120% of BEE
● Depleted: 2-2.5g/kg/day, calories 150-200% of BEE
Need 1 mEq K+/kg/day, 1.5 mEq Cl-/kg/day, 2 mEq Na+/kg/day
Starvation
● 0-48 hours: Protein and fat are the only major sources of calories. Nitrogen loss: 15g/day
○ Primary sources: skeletal muscle to feed the brain, RBCs, and WBCs
○ Hepatic glycogen depleted in 36 hours. Lactate/pyruvate exchanged through Cori Cycle from glycolysis.
○ “Protein sparing effect” - Give surgical patient carbs, spares AAs released from muscle (insulin-mediated)
● 48+ hours: nitrogen loss decreases to 4g/day
○ Occurs due to switch of brain from glucose to ketoacids (produced from fat)
Switch mediated by insulin and alanine
Nutritional assessment
● Preoperative
○ Anthropometry (triceps skin fold thickness, arm circumference)
○ Lab tests: Albumin less than 3.2. Prealbumin (thyroid binding globulin) is more sensitive b/c lower half life.
○ Anergy to skin antigens
○ Patient unable to eat for 10 days or more
○ Severe trauma, burn patient
○ Major GI surgery
● Postoperative: studies are inconclusive whether this helps or not!
Indications for nutritional support
● Enteral nutrition: Used when gut is working, but oral may be difficult.... AMS, ventilator, upper GI disorder
○ Not sufficient in increased metabolic states (anorexia, sepsis, trauma, burns)
○ Decreased risk of infection compared to TPN
○ Glutamine (enterocytes), Arginine, Leucine, Isoleucine, Valine (colonocytes) important
○ Contraindicated when patient cannot protect airway
● Total Parenteral Nutrition (TPN)
○ Indications
When patients can’t tolerate adequate GI intake within 5-7 days
Newborns with catastrophic GI abnormalities or FTT
Short bowel syndrome and/or vascular compromise of bowel
GI obstruction, ileus
Acute renal failure since catabolism would overload kidneys
○ Complications
Infection
Hyperosmolar, nonketotic hyperglycemia.
● Treatment: replace volume and electrolytes, add insulin drip
Hepatic steatosis
CO2 retention aggravating respiratory insufficiency
○ Contraindications: Cardiovascular instability, Less than 8 cm of normal bowel
Signs of nutritional deficiency
● Fatty acids: Dry, scaly dermatitis
● Trace metals: Eczematoid rash in intertriginous areas, changes in taste, microcytic anemia, glucose intolerance
● Vitamin A: hair loss, night blindness
● Vitamin C: cheilosis
● Vitamin K: Ecchymosis and bleeding
● Vitamin B1 (thiamin): Ataxia, parasthesia, muscle weakness, beriberi
ACUTE ABDOMEN
Right Upper Quadrant
Epigastrium (u/s, empiric PPI... EGD)
Left Upper Quadrant
● Biliary colic/Acute cholecystitis
● GERD
● Acute pancreatitis
● Peptic ulcer disease (PUD)
● Pancreatitis (acute/chronic)
● Perforated viscus
● Gastritis
● Peptic ulcer disease (PUD)
● Myocardial infarction
● Cholangitis
● Angina, myocardial infarction
● Splenic rupture (Kehr’s sign)
● Hepatitis
● Gastroenteritis
● GERD
● Penumonia
● Perforated viscus
● Gastritis
● Pleurisy
● Esophagitis/gastritis
● Peptic ulcer disease (PUD)
Right Lower Quadrant
● Abdominal aortic aneurysm (AAA)
Left Lower Quadrant
● Acute appendicitis
● Early acute appendicitis
● Diverticulitis
● Inflammatory bowel disease
● Acute bowel obstruction
● Sigmoid volvulus
● Meckel’s diverticulum
Indications for urgent operation:
● Colorectal cancer
● Involuntary guarding, rigidity
● Acute cholecystitis
● Mesenteric ischemia
● Increasing severity/distention
● Pyelonephritis/Nephrolithiasis
● Colitis
● High fever, hypotension
● Diverticulitis
● Pyelonephritis/Nephrolithiasis
● Equivocal findings w/sepsis, bleeding ● Ovarian torsion, cyst
● Ovarian torsion, cyst
Radiology: pneumoperituneum, distension, ● Ruptured ectopic pregnancy, PID
● Ruptured ectopic pregnancy, PID
● Intussusception
space-occupying lesion, mesenteric occlus.
DPL: blood, bile, pus, enteric contents
● Colon Cancer
Workup: CBC, electrolytes, LFTs, amylase & lipase, UA, urine microscopic exam, urine culture
● All female patients need a pelvic exam and a pregnancy test
● CXR and AXR to look for free air - highly suggestive of a perforated viscus. Most common cause: PUD
● Abdominal CT scan and/or RUQ ultrasound
Expectant management: NPO, NG tube if N/V, IVF, foley. Exploratory laparotomy: unstable patients when surgery can help
APPENDICITIS
Pathophysiology:
● Hyperplasia of lymphoid tissue (60%), fecalith (35%), foreign body, parasite, carcinoid tumor (rare - 5%)
○ Obstruction leads to bacterial overgrowth, inflammation, distention can compromise blood supply (appendicular
artery is a branch of the ileocolic artery which is a branch of the SMA) .
● Complications: necrosis, infarct, perforation, abscess, peritonitis
Symptoms: Abdominal pain, mid-epigastrium, moves to umbilicus, then to RLQ, anorexia is always present. Nausea, vomiting
Signs:
● Tenderness in RLQ (most intense at McBurney’s point), rebound tenderness, guarding, diminished bowel sounds, low
grade fever (if high, think perforation)
● Rovsing’s sign (push on LLQ, referred pain to RLQ), Psoas sign, Obturator sign ,if palpate a mass on rectal, think
appendiceal abscess. Preggo women may have RUQ pain due to the location of the appendix in the gravid uterus.
● Atypical appendicitis: N/V without peritoneal signs, may mimic obstruction
Diagnosis: Peak incidence: teens to mid-20s, and elderly
● Acute appendicitis is a clinical diagnosis. Leukocytosis (mild), CT scan (sensitive 98-100%), ultrasound (90%)
● Rectal exam (retrocecal appendix), Pelvic exam (r/o gynecological cause)
Treatment:
● Appendectomy (laparoscopic) 20% false positive. Risk is ok in pregnancy (10-15% increased risk of premature labor)
● With cecum involvement: Right hemi-colectomy
● Carcinoid tumor of the appendix
○ <2cm and not involving cecum: appendectomy alone sufficient (probably +baseline 5-HIAA, octeotride scan)
○ >2cm or involving cecum: Right hemi-colectomy, baseline 5-HIAA, octeotride scan for mets.
Complications:
● PERFORATION (20% of all cases): High fever, tachycardia, marked leukocytosis, peritoneal signs, toxic appearance.
Differential diagnosis (if negative on laparoscopic appendectomy, search for other cause of symptoms):
● Gastroenteritis, Mesenteric adenitis (Yersinia enterolytica), Meckel’s, Intussusception, typhoid fever, primary peritonitis,
terminal enteritis, diverticulitis, carcinoid tumor (baseline 5-HIAA, CT, octeotride scan)
● Gynecological: Ectopic pregnancy, PID, Ovarian torsion/tumor/cyst, UTI/pyelo, ureteral stone
DIVERTICULITIS - “LLQ appendicitis”, 95% of time: sigmoid colon
Pathophysiology:
● Limited infection of one or more diverticula, including extension into adjacent tissue.
● Fecalith obstriction --> microperforation.
Symptoms: LLQ pain (subacute onset), alteration in bowel habits (constipation OR diarrhea)
○ Lower GI bleeding rare (common in diverticulosis, not -itis)
○ Fever, LLQ pain, leukocytosis (“LLQ appendicitis”)
Diagnosis/Workup
● AXR, CT with oral and IV contrast.
● Barium enema and colonoscopy are CONTRAINDICATED during acute phase (2-3 weeks) due to perforation risk, unless
signs of obstructive or fistula symptoms.
Treatment: Directed at specific complication.
● Acute: medical treatment 85% of the time.
○ Admit, IVF, IV non-opioid analgesics, NPO, IV abx(aminoglycoside, coverage for B. fragilis) x 5-7 days.
● Surgery: Resection
Indications for surgery: Perforation, obstruction, intractability (recurrence), bleeding, fistula
● All patients with diverticulitis must undergo a full colonoscopy 4-6 weeks after the attack to r/o malignancy
● Procedure: sigmoid colectomy, temporary colostomy
Complications
● Fistula: skin, vagina, bladder (most common complication - 4%. Pneumaturia, recurrent UTI)
● Perforation, abscess, fistula, obstruction
DIVERTICOLOSIS
● 70% of elderly patients may have asymptomatic diverticulosis. Increases from 50s-80s.
● 80% an asymptomatic finding on barium enema.
● 95% occur in sigmoid colon. Usually occurs where branches of marginal artery penetrate the wall of the colon.
● Etiology: higher than normal intraluminal pressures as would occur with low fiber diet.
● Symptoms: 40% of lower GI bleeds. Most common cause of lower GI bleeds in < 60 years old.
○ 25% of bleeds are massive (requires 4+ units of blood in 24 hours to maintain hemodynamics)
○ Usually asymptomatic. Recurrent abdominal pain in LLQ, change in bowel habbits. Bleeding.
○ Fever and leukocytosis MUST be absent.
● Treatment: Diet of increased fiber, psyllium.
GENERAL:
PERIPHERAL VASCULAR DISEASE
Pathophysiology:
● Patients usually have underlying CAD (with CHF, Hx of MI, etc) or other chronic problems (IDDM, lung disease, smoking,
hyperlipidemia, HTN, homocystinemia)
● Change in arterial pressure is usually small until stenosis >50% (Poiseuielle’s law)
● Most common cause of death is IC patients is cerebral or cardiac events
Types
○ Femeropopliteal: Below inguinal ligament: --> Hunter’s (adductor) canal
■
Most common site overall. Typically occurs at the adductor hiatus
○ Tibial occlusive disease: distal to popliteal artery trifercation
■
Most common in: diabetes, ESRD, advanced age
○ Aortoiliac: Leriche Syndrome: Impotence, no femoral pulse, claudication, buttock muscle wasting
■
Generally a progressive disease that will fail medical management. PTA works best here.
○ Superficial Femoral: Calf claudication
Symptoms
● Intermittent claudication: cramping leg pain with exercise that is reproducible, improved by rest (vs. neurogenic)
● Rest pain: distal metatarsals, prominent at night, awakens from sleep
Signs
● Diminished/absent pulses, muscular atrophy, decreased hair growth, thick toenails, ↓ skin temp
● Ischemic ulceration (usually on toes): local necrosis, tissue infarct/gangrene (advanced)
● Buerger’s sign: rubor when dependent, pale when elevated (advanced disease)
Diagnosis
● Doppler: Triphasic waveform (healthy). Systole, backflow as elastic arteries recoil, forward in diastole
● Ankle to brachial (ABI) index: normal 1.0, claudication <0.7, rest pain <0.4
● Pulse volume recording (assess segmental limb perfusion)
● Arteriography (contrast, X-ray): gold standard. Not performed to diagnose, but instead as preoperative study.
Treatment
● Medical management
○ Stop smoking - 50% improve!!! Graduated exercise program, foot care, atherosclerotic risk factor reduction, avoid
extremes of temperature (esp. Toledo)
○ Medicine: aspirin, Pentoxifylline (aka Trental, lowers blood viscosity)
● Surgery: bypass graft (aortobifemoral, axillofemoral). Angioplasty
Surgery indications: Failed medical Tx, pain interferes with lifestyle/occupation, impending/actual tissue loss, rest pain.
Prognosis: 70% remain stable or improve, 20% progress and require revascularization, 10% require amputation
• The more distal and more severe the disease, the more likely the graft is to fail.
ABDOMINAL WALL HERNIAS
Pathophysiology:
● Occur in areas where striated muscle does not protect
● The smaller it is, more likely to strangulate
● Inguinal canal boundaries:
○ Anterior: External oblique aponeurosis
○ Posterior: Transverse abdominal muscle aponeurosis and transversalis fascia
Symptoms:
● Pain (increases with hard work/straining/worse at end of day, relieved at night/lying down), non-specific discomfort
● Dull, dragging pain referred to testes. “Bulge in groin”
● Asymptomatic
Signs: Bulge palpated or visible upon standing and coughing.
Diagnosis: Clinical diagnosis. Radiology only used in special circumstances (obesity, clinical exam not reliable)
Types
• Direct inguinal: enters canal via weak posterior wall, does not pass thru internal ring
o Lies posterior to spermatic cord, occurs almost exclusively in males, older, smokers
o Never enters the scrotum, can damage the ilioinguinal nerve
o Protrude medial to the inferior epigastric vessels, not assoc. with processus vaginalis.
o Herniate thru Hesselbach’s Triangle:
Inferior border: Inguinal ligament
Medial border: Rectus abdominus
Lateral border: Inferior epigastric vessels (lateral umbilical fold)
• Indirect Inguinal: Need patent process vaginalis (congenital lesion) AND stress (20% of cadavers have some patency)
o Most common in both sexes
o Communicating hydrocele is same process but no bowel yet
o Noncommunicating: diagnosed by unchanged location by position or pressure
o New onset without identifiable stress should prompt workup: COPD, micturation straining, defacation straining
o More common on right side in first decade of life (right testis descends later)
o Children often bilateral
• Femoral: Very susceptible to incarceration b/c of inguinal ligament, lacunar ligament, Cooper’s (superior pubic lig)
Treatment: All hernias need surgical repair. (Even though evidence says only 0.1% strangulate.)
• Attempt to manually reduce when patient is in Trendelenburg: 60-70% successful
• Surgical: tension-free repair of defect using fascia, aponeurosis, or mesh
• Herniotomy (young, healthy, muscles): sac is freed, ligated, reduced
• Herniorrhaphy and plasty: herniotomy with repair of posterior wall and inguinal ring.
• Mesh: 50-75% decrease in rate of recurrence
• Non-surgical: (moribund patients) “hernia truss” to keep hernia reduced, limited in use
• Children: high ligation only is required
Differential diagnosis:
• Abdominal wall mass
• Desmoids (locally aggressive fibrous proliferation)
• Neoplasm, adenopathy
• Rectus sheath hematoma
• Hydrocele (transilluminate, hernias are not translucent but hydroceles are)
Other Hernias:
• Umbilical Hernia: Children: ignore, adult <1.5cm: suture, adult >1.5cm: mesh
• Incisional (Ventral) Hernia: Risk factors: deep wound infection (most common), obesity, steroid use
• Spegelian (through semilunar line @ junction of semicircular line of Douglas),
• Richter (wall only, no bowel obstruction sx)
• Lumbar: Grynfelt (superior lumbar), Petit (inferior lumbar)
• Hernia sac includes viscera: Littre (includes Meckel’s diverticulum in hernia), Armand (includes appendix)
• Obturator, Hesselback (like femoral but lateral to femoral vessels), epigastric, diasasis recti
GASTROINTESTINAL BLEEDING: 75% are upper GI.
Divider of upper/lower is Ligament of Treitz
Presentation
● Hematemesis: upper GI endoscopy
● Hematochezia: 1) r/o hemorrhoids, 2) colonoscopy, 3) upper GI endoscopy
● Melena: 1) upper GI endoscopy 2) colonoscopy (DDx: bismuth, iron, spinach, charcoal, licorice)
● Fecal occult blood test (FOBT): colonscopy
Determination of source: NG tube placement with lavage
● Bile + blood indicates upper GI source
● Bile, no blood indicates NOT upper GI source
● Clear fluid, w/no bile is equivocal
Etiologies
Upper GI bleed (75% of GI bleeds are upper)
● PUD (70%)- duodenal (25%), ulcer (20%), gastritis (25%). 80% stop spontaneously, ask about NSAID & anticoagulant use
● Reflux, varices, Mallory-Weiss, hemobilia, aortoenteric fistula (Hx of AAA repair)
● Dieulafoy’s vascular malformation: submucosal dilated arterial lesions
● Neoplasm: bleeding is not rapid, usually not emergent.
Lower GI bleed (25%)
● Diverticulosis (40%) - most common in < 60 years old
○ Asymptomatic or vague LLQ pain (20%)
○ Diagnosis: barium enema
○ Treatment: High fiber diet, psyllium
○ Complications: Painless bleed, diverticulitis
● Diverticulitis (rarely presents as bleed)
○ Fever, LLQ pain, leukocytosis (“LLQ appendicitis”)
○ Diagnosis: CT scan of abdomen and pelvis. NOT enema or colonoscopy during acute phase. Perform in 4-6 weeks.
○ Treatment: IV antibiotics, NPO. Recurrent episode: resection
○ Complications: Bowel obstruction, abscess, fistula
● Angiodysplasia (40%) - most common in > 60 years old
● Colorectal cancer – usually left sided cancers have gross blood, right sided have occult blood
● Polyp
○ Premalignant: FAP, villous adenoma, adenomatous polyp
○ Benign: Juvenile, Peutz-Jeghers, inflammatory, hyperplastic
● Acute mesenteric ischemia
○ Symptoms: acute, severe onset of pain that is disproportionate to benign physical findings
○ Diagnosis: mesenteric angiography, AXR, Barium enema showing “thumb print” sign
○ Treatment: IVF, papaverine injection into SMA (if arterial), heparin (if venous thrombosis, hx of DVT)
● Chronic mesenteric ischemia
○ Symptoms: postprandial pain (because of increased splanchnic demand for blood)
○ Diagnosis: angiography
○ Treatment: surgical revascularization
Rectal bleed
● Internal hemorrhoids: bleed, don’t hurt. Treatment: rubber band ligation
● External hemorrhoids: hurt, don’t bleed Treatment: surgery
Management: Resuscitation (IV fluids, transfusion)
● CBC, PT/PTT/INR, LFTs, Bun/Cr ratio (elevated with upper GI bleed if no concurrent renal issues)
● Upper: EGD with sclerotherapy, gastrografin swallow study if you suspect perforation
○ 80% stop bleeding spontaneously (e.g. Mallory-Weiss), only need supportive therapy.
● Lower: r/o hemorrhoids.
○ Slow bleed (<0.5ml/hr): radionucleotide (99mTc ) scan.
○ Fast bleed (2+ ml/hr): emergent angiogram.
Indications for surgery:
1. Hemodynamically unstable (no response to IVF), transfusion, endoscopic intervention, or correction of coagulopathies
2. Severe initial bleed or recurrence of bleed with endoscopic treatment
3. Continued bleeding for more than 24 hours
4. Visible vessel at base of ulcer (30-50% rebleed)
5. Ongoing transfusion requirement (4-6+ units of blood required, unstable, blood type indeterminate/Jehovah’s witness)
REFLUX ESOPHAGITIS
Pathophysiology:
● Causes:
○ Incompetent LES: Structurally defective sphincter (ex. hiatal hernia)
Type I: sliding
Type II: paraesophageal. Tx: surgery, risk of strangulation - acidosis, hypotension, gastric volvulus
Type III: Mixed
Type IV: Other visceral besides stomach herniate
○ Insufficient clearance of acid
○ Increased intragastric pressure: distension with air, food, delayed gastric emptying, ↑ abd. pressure (COPD)
● Prolonged exposure of esophagus to low pH from gastric contents (acid, pepsin, and duodenal contents such as biliary and
pancreatic secretions) leads to irritation of the esophageal mucosa (and respiratory epithelium).
● Prevalence increase with age.
Signs/Symptoms:
● Retrosternal pain after eating (heartburn)
● Exacerbated by lying down, may mimic cardiac chest pain, regurgitation
● Waterbrash (reflex salivary hypersecretion), cough, early satiety
● Atypical: N/V, post-prandial fullness, choking, chronic cough, wheezing, hoarseness
● Laryngitis (if severe), aspiration pneumonitis/recurrent pneumonia, idiopathic pulmonary fibrosis, asthma.
● If GERD is associated with dysphagia, think peptic stricture/mobility disorder/cancer
● Long term: dental erosion, gingivitis
Diagnosis:
● Rule out cardiac and pulmonary disease (H&P, ECG, cardiac enzymes)
● Diagnostic tests are not necessary for typical, uncomplicated, initial cases of GERD due to empiric treatment.
● Endoscopy with biopsy
● 24 hour ambulatory pH monitoring of the esophagus = gold standard (useful for determining severity)
● Barium swallow study to look for anatomical cause (achalasia, hernia, stricture) or complications from GERD
● Esophageal manometry = to determine competence of LES, only if mobility disorder suspected
Treatment: Goal: prevent progression to Barrett’s, cancer, pulmonary problems (recurrent aspiration)
1. Lifestyle modification, medication to reduce acid:
• Elevate head of bed, eat small frequent meals, don’t sleep for 3-4 hours after eating
• Antacids
• Education to avoid EtOH, coffee, chocolate, peppermint (aggravate), nicotine (decreases LES tone),
2. Add H2 blocker
3. Switch to PPI
4. Metoclopromide: to promote gastric emptying
Medical therapy trial 6-12 weeks before further diagnostics. 85% resolve.
5. Combination therapy (phase 2+4, phase 3+4, or increase 2, 3, dose)
6. Surgery
Indications for surgery: Failure of medical therapy (Nissen) OR dysplasia of esophageal mucosa (resection)
● Preoperative studies: EGD, Manometry, endoscopy, barium swallow
○ Manometry to demonstrate normal peristalsis for postop feeding and abnormal LES tone.
If normal LES tone, do 24 hour pH monitoring to be sure gastric reflux is present
Complications/Considerations:
● Patients who initially present with symptomatic GERD for 5+ years should have endoscopy with biopsy first. If patient has
documented Barrett’s metaplasia without dysplastic changes, surveillance endoscopy every 3 years.
● If patient suffers from recurrent aspiration pneumonia with reflux esophagitis, bronchoscopy with aspirate cytology (which
will show lipid-laden macrophages) is indicated.
TRAUMA & SHOCK
Four phases: Primary survey, resuscitation, secondary survey, definitive care
Background: Deaths are trimodal: Immediate (major vessels, brain), Early (head), Late (sepsis, MODS)
1) PRIMARY SURVEY: ABCDEF
Airway (and c-spine)
● Assess airway patency, jaw thrust to initially open airway (protects c-spine) clear foreign bodies, insert temp airway
● Intubate if: Use orotracheal (unconscious), nasotracheal (conscious, no basilar skull f.), cricothyroidotomy (facial/neck)
○ Airway compromise: supraglottic (stridor, snoring, gurgling), laryngeal (dysphonia, hoarseness), hematoma
○ Inadequate respiratory effort (Apnea, agitation = hypoxia, obtundation =hypercarbia)
○ Inability to protect the airway (GCS < 8, aspiration risk)
○ Severely compromised respiratory mechanics (Retractions, sucking chest wound)
● Assume C-spine injury if:
Perform: In-line immobilization of C-spine: Cervical collar AND backboard.
○ Head injury
Clear C-Spine by: Palpating neck, assessing neuro, No EtOH, CT
○ Altered level of consciousness
○ Multisystem blunt trauma
Breathing
● Inspect, auscultate, and palpate chest (Is trachea midline? Neck veins distended? Ventilating both lungs?)
● Ensure adequate ventilation and immediate identify and treat: pneumothorax, flail chest, etc.
Circulation/Control of hemorrhage
● Control obvious hemorrhage. Use direct pressure, no tourniquet. Don’t use vasoconstrictors.
● Assess tissue perfusion: pulse (rhythm, rate, quality), skin color, level of consciousness.
● Place two large bore (16g or bigger) IVs. Resuscitation step starts here simultaneously.
Disability (neurologic)
● Glascow Coma Scale or AVPU (alert, responsive to verbal, responsive to pain, unresponsive)
○ EYE opening: Spontaneous (4), verbal (3), painful (2), None (1)
○ VERBAL:
Orient x3 (5), disoriented (4), inappropriate (3), incomprehensible (2), None (1), intubated (T)
○ MOTOR:
Verbal (6), localize pain (5), withdraw pain (4), flexor (decort) (3), extensor (decereb) (2), none
○ Prognosis, prediction of mortality. 3-4: 97%, 5-6: 65%, 7-8: 28%
Exposure/Environment: Undress patient, give warm blankets to prevent hypothermia
Foley R/o uretheral injury with rectal exam. Do suprapubic catheter if uretheral injery.
2) RESUSCITATION Performed simultaneously with the primary survey (translation: nursing staff)
> 1500ml = transfusion
● IV fluids (LR). Need 3:1 ratio of blood loss. Percutaneous (I-III): Arm, saphenous. Central (IV): femoral, subclavian, IJ
○ Class I:
15% (750ml)
HR < 100
Urine 30ml/hr+
Crystalloid only
○ Class II:
15-30% (750-1500ml) HR 100+
Urine 20-30 ml/hr
Crystalloid only
○ Class III:
30-40% (1500-2000ml) HR 120+
Urine 5-15 ml/hr
Crystalloid AND blood
○ Clas IV
40%+ (2000ml+)
HR 140+
Urine negligible Crystalloid AND blood
● Gastric intubation (use OGT if think that the cribriform plate is fractured, don’t want to suck out brains with a NGT)
● Vitals, pulse-ox, ECG monitored during this phase
3) SECONDARY SURVEY
● Detailed head-to-toe assessment
● AMPLE History (Allergies, Meds, PMH/Pregnant, Last meal, Events of injury)
● ECG, pulse oximetry, baseline labs, NG or OG if basilar skull f. (prevents gastric dilation - vasovagal hypotension)
● Portable x-ray (AP chest, AP pelvis, lateral c-spine)
● FAST, diagnostic peritoneal lavage (DLP)(may miss retroperitoneal hemorrhage), any other radiography
4) DEFINITIVE CARE
● Thoracic trauma
○ Tension pneumothorax: needle in 2nd intercostal space, chest tube in 5th intercostal space
○ Open pneumothorax: cover with vaseline gauze. Tape on 3 sides.
○ Massive hemothorax (1500ml): insert chest tube with cell saver
○ Flail chest: respiratory problems due to lung contusion (V/Q mismatch), splinting. Intubate/spinal epidural, PEEP
○ Cardiac tamponade: pericardiocentesis, exploratory thoracotomy to find bleeding source (can be myocardium)
○ Blunt cardiac injury: ECG monitoring with antiarrhythmics and inotropic support ready
○ Aortic rupture: often @ L subclavian artery. PA CXR (wide mediastinum), helical CT, angiogram, TEE. Open repair.
○ Traumatic diaphragmatic rupture: 90% is left (liver on right). Bowel sounds in chest, NGT.
○ Tracheal laceration: crepitus, hemoptysis, pneumomediastinum. Need intubation or operative repair.
○ Esophageal: Severe epigastric, L chest pain, hematemesis, effusion, creptius. Operative repair. Risk of sepsis.
○ Nonlethal injuries: Simple pneumothorax (observe, chest t), simple hemothorax (<1500), rib fracture (pain control)
●
●
●
●
●
●
Abdominal trauma: anything below the nipple in males or scapula.
○ Diagnosis
FAST: RUQ (Morison’s pouch), LUQ (Splenorenal recess), pelvis, pericardium --> expl. laparotomy
DPL: 10ml gross blood, 100k RBCs, 500wbcs, bacteria, bile, amylase > serum. (98% sensitive) --> ex. lap.
Deteriorating vitals, falling hematocrit, worsening abdomen --> exploratory laparotomy.
Abdominal CT: use in hemodynamically stable patients
○ Treatment
Zone 1 (central retroperitoneum): Explore because likely to be aorta or pancreas.
Zone 2 (lateral retroperitoneam): Observe if stable, even if kidney is injured.
Zone 3 (pelvis): Externally stabilize. Arteriography if this fails to stop bleeding. Exploration difficult.
Splenic rupture: low-grade (expectant), moderate (contrast, embolization), instability (ex. lap)
Liver laceration: all but liver avulsion managed expectantly unless unstable (Pringle: port triad clamp)
Hollow viscus injury: Abdominal CT with free air --> repair or resection
Pancreatic: resection with temporary duodenal diverticulum
Gunshot: Exploratory laparotomy regardless of hemodynamic status.
Stab wound: Hemodynamically unstable --> ex. lap. If no fascial penetration --> treat as skin laceration!
Head trauma: most common cause of trauma death. 60% of MVA deaths.
○ SCALP (Skin, subCut fat, Aponeurosis, Loose areolar connective tissue, Periostium)
○ CBF = CPP/CVR. CPP=MAP-ICP. Normal ICP<10. ICP > 20 requires treatment. Brain death when CPP < 50 mmHg
Cushing reflex: Brain tries to protect CPP by increasing BP. Triad: Hypertension, bradycardia, resp. dep.
CVR inversely related to PCO2. Linear in 20-80mmHg.
Goal: keep ICP <20mm Hg and CPP 60-70 mmHg
○ Diagnosis
Periorbital bruise(raccoon eyes), perimastoid (Battle’s sign), hemotympanum, CSF (ring sign on paper)
CT without contrast and cervical radiographs
ICP monitoring: ventricular (“gold standard”), subarachnoid bolt, fiberoptic,
○ Types of injuries
Concussion: brief loss of neurologic funciton (59% of head injuries)
Diffuse axonal injury: Gray-white junction. 90% coma, CT scan shows no lesion. Nonsurgical mgt.
Contusion: coup-contrecoup. Focal deficits, confusion. (15% of head injuries)
Epidural: Loss of consciousness, lucid interval, depressed consciousness/contralateral paresis. Surgery.
Subdural: Clinically evident when serious underlying brain injury has occurred. (30% of head injury)
Subarachnoid: Headache, stiff neck. Not surgical because no mass lesion.
Intracerebral: Severe. Associated with diffuse axonal injury, gunshot wounds.
○ Nonsurgical treatment
Pressors, head elevation
Hyperventilation to PCO2 of 26 to 30 mmHg (only if signs of impending brain herniation)
Osmotic diuresis (Mannitol): 0.25 – 1g / kg with a goal of 300 - 310 mOsm
Hypertonic saline
Sedation: reduces metabolic demand ICP down (Barbiturates)
Neck injury: Any injury penetrating the platysma carries risk of underyling severe injury
○ Indications for surgery: vascular, airway, esophagus injury, penetrating injury in zone II
○ Zone I (below cricoid cartilage): high mortality because occult. Angiogram, especially if in subclavian area.
○ Zone II (cricoid to angle of mandible): usually obvious hematoma, easy surgery. Exploratory surgery.
○ Zone III (above mandible): hard to do surgery on. Angiogram
Spinal shock: flaccidity and areflexia instead of expected hyperreflexia. Give steroids within 8 hours.
Trauma in pregnant women
○ Resuscitation is most important variable. Once shock develops, fetus survival is only 20%.
○ Place in left decubitus to increase venous return.
○ Greatest risk of radiation-induced anomalies is during the first 16 weeks of gestation. <10 rad okay. CXR ok.
Compartment syndrome Treatment: fasciotomy. Assess renal function since myoglobinuria (alkalinize, give fluids)
○ Decreased sensation: pain first (unmyelinated C-fibers), touch, proprioception.
○ Pain on passive movement. Decreased pulse is unreliable because it is a late finding.
○ Compartmental pressure > 35-40 mmHg confirm diagnosis
SHOCK: Inadequate end-organ perfusion
Hemorrhagic Shock: Hypovolemia due to bleeding. Stop bleeding, restore volume. DO NOT use pressors.
● Large bore needles to infuse LR, blood: Infuse faster, small would hemolyze blood products
1. Infuse 2 L of Lactated Ringer and check for response in vitals.
2. No response: Bolus 1-2 L again.
3. No response: Infuse blood and/or more crystalloid.
● Field adjuncts: PASG/MAST pants, inflate below the abdomen and increase SVR and L ventricle afterload, increasing BP.
Cardiogenic shock: myocardial dysfunction due to cardiac tamponade, contusion, air embolus, MI (rare)
● Cardiac tamponade
Treatment: Pericardiocentesis
Beck’s triad: JVD, hypotension, muffled/distant heart sounds
Pulsus paradoxus (decrease of BP >10 with inspiration)
Kussmaul’s sign (an increase in CVP with inspiration, usually as jugular venous distention (JVD))
● Tension pneumothorax: produces shock by impeding venous return.
Neurogenic shock: injury to descending sympathetic pathway (caused by high thoracic and cervical spine injuries)
● UNIQUE: hypotension without tachycardia (no sympath. response)
● Unlike hemorrhagic shock, can use vasoconstrictors to achieve hemodynamic stability.
Septic shock: not really assoc. with trauma; resembles hypovolemic or normovolemic shock.
Hypoadrenal shock: adrenal hemorrhage (due to external steroids suddenly withdrawn), circulatory collapse can be triggered by
stress of injury. Not really responsive to therapies. Treatment is high dose steroids.
Systemic Inflammatory Response Syndrome
Indications for Swan-Ganz (CVP, pulmonary artery - PCWP)
SIRS
2+ of the following:
● Diagnosis of shock states, pulmonary edema
○ temp >38 or <36
● Assessing hemodynamic response to resuscitation
○ HR >90bpm
Example: post-operative normal vitals but oliguria
○ RR >20 or PCO2 <32 or mechanical
● PEEP can cause decrease in CO, oliguria
ventilation
● CVP high: cardiogenic shock
○ WBCs >12,000 or <4,000 or >10% bands
● CVP low & PCWP high (>20 mmHg): pulmonary edema
Normal values
Sepsis
SIRS + identifiable source of infection
*measured by Swan-Ganz
CVP/Right atrium: 0-6*
Right ventricle: 20-30/0-6
Severe sepsis Sepsis + organ dysfunction
Pulmonary artery: 20-30/6-12 PCWP/Left atrium: 6-12*
Septic shock
Sepsis + CV collapse requiring vasopressors
Left ventricle: 100-140/5-14
Arteries: 100-140/60-80
Burns
●
●
●
●
●
●
Criteria for referral to burn center:
○ Full thickness >5% BSA or partial thickness >20% BSA
○ Age <5 or >50. Face, hands feet, genetalia, perineum
○ Inhalational injury, Circumferential, Chemical or electrical
Epidermal burn (1st degree)
○ Red from capillary dilation. Blanches with pressure. No blister. Limited physiologic effects
○ Treatment: PO H2O, analgesia
Partial-thickness burn (2nd degree)
○ Into dermis. Superficial: eschar, deep: leathery coagulation necrosis (white)
○ Treatment: Conservative for 10-14 days to see if skin regenerates
Full-thickness burn (3rd degree)
○ Painless. Skin proteins contract when burned, creating tourniquet-like contraction
○ Treatment: require skin grafting
Fluid Replacement (Parkland Formula): 4 x %TBSA x kg of Lactated Ringer’s.
○ Give 1/2 the requirement over 8 hours, 1/2 the requirement over following 16 hours. Maintenance: D5W
○ Colloid (if the patient fails to respond to crystalloid after 24 h): 0.5ml plasma x %BSA over 8 hours
Topical antibiotics. Don’t use systemic because they don’t penetrate eschar and select for resistant bacteria.
○ Silver nitrate:
Broad spectrum. Painless - limited eschar penetration.
○ Mafenide acetate: Broad spectrum except yeast. Painful - good eschar penetration. Acidosis, hypersensitivity
○ Silver sulfadiazine: Gram + and yeast only. Painless - limited eschar penetration. Neutropenia/thrombocyto.
ONCOLOGY: General rule: any lymph node >1cm, 4+ week, w/out infection should be biopsied.
BREAST CANCER
Workup by presentation:
Palpable mass
● <30 years old: ultrasound – cystic or solid.
○ Mammogram useless due to dense breast tissue
● >30 years old: mammogram
○ Characterizes lesion as cystic or solid
○ Examines for synchronous lesion in contralateral
● Biopsy if solid (stereotactic, needle guided)
○ Infiltrating ductal carcinoma: see staging table
○ DCIS
Multicenteric: simple mastectomy
Solitary: Lumpectomy + nodes
○ LCIS: mammogram every 6 months
Bloody discharge
● Mammogram, galactograph, resection of papilloma
18 year old rubbery, movable mass
• Fibroadenoma (98%). Observe for a few menstrual cycles
35 year old, 10 year cyclic tenderness: Fibrocystic change
● Aspirate cyst, send bloody fluid for cytology
● Biopsy if cyst does not reduce or if it recurs
Cracks, abscess, fluctuant, red hot mass, fever, leukocytosis
● ONLY “allowed” in lactating women, otherwise do full workup for possible inflammatory cancer
Risk factors
● Age, family history (first degree relatives), previous breast cancers, benign breast disease, palpable masses, estrogen
replacement therapy, age of menarche, age of menopause, nulliparity.
Diagnostic Studies:
● Mammography (2 views each breast): used for screening and diagnostics. Purpose is to detect non-palpable cancer.
○ Most common finding: microcalcifications and round/smooth dominant masses (cystic lesion or fibroadenoma)
○ Suspicious finding: spiculated lesion.
○ 5-10% false negative rate so if suspicious, continue workup regardless of radiography
● Ultrasound: Most useful in young women (<35) with dense breast tissue. Can distinguish between a mass and a cyst
○ Can be used for guided biopsy. Like mammography, doesn’t replace clinical suspicion.
● FNA: 20% false negative rate. Best for cysts. It only tells you cytologic diagnosis, not histologic.
● Core needle biopsy (CNB): risk of hematoma, pneumothorax, and also has a 20% false negative rate
● Excisional biopsy: definitive histologic diagnosis. Can be diagnostic AND therapeutic. (surgery under anesthesia)
● Needle localization breast biopsy: good for non-palpable lesions detected on mammogram(surgery under anesthesia)
Screening
● Self exam: monthly, 5 days post period
● Physician breast exam: 20-30 (q 2-3 years), 40+ (annual)
● Mammogram: 35-45(baseline), 40-50(q 1-2 years), 50+ ( annual)
Stage T
N
M
Treatment
5-year
Post-op treatment
I
< 2 cm
0
0
93%
• Annual CXR, LFTs
• Lumpectomy with radiation
• Mammogram
IIA
< 2 cm
Mobile
0
72%
• Lumpectomy with radiation
every 6 weeks
2-5 cm
0
0
or,
• Tamoxifen if ER+
IIB
2-5 cm
Mobile
0
• Modified radical mastectomy
• Patients with CT
5+ cm
0
0
disease can’t have
IIIA
5+
Mobile
0
41%
• Neoadjuvant (consult oncologist)
radiation
Any
Fixed
0
• Modified radical mastectomy
Other
prognostic fx.
IIIB
Skin changes: Peu d’orange
• DNA ploidy
(lymphatics), retraction (Cooper’s)
• S-phase fraction
IV
Any
Any
Distant
18%
• Palliative radiation and
• Her-2-Neu status
chemotherapy
• ER/PR status
• Surgery maybe for debulking
THYROID “24 year old woman with asymptomatic 3cm neck ‘bump’ she noticed 1 week ago. She is otherwise well.”
Risk Factors
● Radiation, family history of MEN, solitary nodule (vs. multinodular), hoarseness or voice changes
● Cyst which is large (>4cm) or recurs - 15% risk of malignancy.
● Women, aged 25-65.
Diagnosis
● Fine needle aspiration (FNA) for cytology
○ Radiolabeled iodine uptake scan if equivocal
● Family history of Men-2A: serum calcium (PTH hyperplasia), calcitonin (medullary), epinephrine metabolites (pheo.)
● TSH, ultrasound: Not necessary for solitary nodule, but may be useful if multinodular, or hyper/hypothyroid symptoms
Cytology results:
● Papillary: Psammoma bodies - spreads via lymphatics
● Follicular (more aggressive than papillary): spreads hematogenously
● Medullary: 20% associated with MEN. Diagnosis: Amyloid deposits on FNA, serum calcitonin levels
● Anaplastic: worst prognosis
● Lymphocytic infiltrate: lymphoma or chronic thyroiditis. Differentiate with flow cytometry.
● Adenoma: Hurtle cells on FNA
Treatment:
● Papillary: Smaller lesions (<1cm) and no history of radiation: lobectomy. 100% 10-year survival in low-risk.
● Follicular: microinvasive and smaller than 4cm: lobectomy
● Other papillary, follicular, medullary, anaplastic (if resectable): Total thyroidectomy
● Anaplastic (unresectable): chemotherapy and radiation
● Lymphoma: radiation
● Adenoma: Hurtle cells are somewhat equivocal, so lobectomy is still necessary.
● Grave’s disease: subtotal thyroidectomy
Postoperative
Thyroid suppression with thyroid hormone
Possibly I131 ablation in Papillary and Follicular, NOT Medullary since it is of parafollicular C-cell origin.
Complications of thyroidectomy
● Parathyroid resection: Low calcium, high phosphate manifested as perioral tingling, parasthesia, MS change
● Recurrent laryngeal nerve damage (0.5-5% risk): Hoarseness. If bilateral, may require tracheostomy.
COLORECTAL CANCER
●
●
●
●
●
●
Screening:
○ Fecal occult blood testing annually after 50 years of age. 20% positive predictive value
○ Sigmoidoscopy at 50 and at 5 year intervals OR colonoscopy at 50 and at 10 year intervals
Presentation:
○ Most common cause of bowel obstruction in an individual without prior abdominal surgeries (generally right sided
cancers have worse prognosis due to late presentation (later obstruction vs. left-sided tumors))
○ Heme-positive stool (generally right-sided cancers)
○ Unexplained anemia in a male OR FEMALE over 40-50
○ History of inflammatory bowel disease (especially UC)
○ Family history of colon cancer, FAP, HNPCC, Peutz-Jeghers
Diagnosis: Colonoscopy & biopsy
○ 50% of colon cancer occurs in the rectum, 20% sigmoid, 15% ascending
Treatment
○ Hemicolectomy + node dissection (50% involvement)
■Stage I + II (any T, no nodes, no mets): Resection only
■Stage III + IV (nodes or mets): Neoadjuvant and postoperative
○ Baseline CEA (to help detect recurrences)
○ Chest X-ray (to look for metastasis)
○ Liver function tests to look for metastasis - liver is the most common site - 20% at diagnosis. 0% 5-year surv.
Prognosis: most important variable is lymph node involvement
○ 20% recur. 90% of recurrences in 3 years.
Stage 5-year survival
○ T1 (A): limited to mucosa/submucosa
I
90%
○ T2 (B1): invades into, not beyond muscularis
I
75%
○ T3 (B2): full thickness
II
65%
○ T4: invades other organs
II
○ Positive nodes (C)
III
50%
○ Distant mets (D)
IV
5%
Postoperative: Colonoscopy or barium enema every 6 months. Bimonthly CEA level (70% predictive). PET, CXR, LFTs.
○ Recurrence: Liver metastasis
■Resectable: 33% 5-year surival. Get 1 cm margin.
■Unresectable: alcohol, cryotherapy, RF ablation, chemoembolization
○ Anastomotic leak: persistent ileus, mechanical obstruction from adhesions, Richter’s hernia
■CT, small bowel series, Gastrografin enema
RECTAL SQUAMOUS CANCER
Diagnosis: transrectal ultrasound (wall invasion), CT (invasion of surrounding structures - prostate, bladder, ureter)
Staging: same as with adenocarcinoma
Treatment: <5cm from anal verge: can spread via inguinal lympatics, margins include sphincter mechanism
Small tumor: small resection, larger tumor: NIGRO neoadjuvant therapy
LUNG CANCER
Presentation:
● Smoker (85%) with a NEW “coin” lesion discovered on chest x ray or a rapidly enlarging one (a few months)
○ If enlarges “too fast” (e.g. a few hours), likely is an infectious process (ex. abscess)
● Pleural effusion without CHF
● Hemoptysis
Diagnosis
1. Sputum cytology
2. CT (Chest AND abdomen for mets)
3. Biopsy (percutaneous if lesion is peripheral, broncoscopy-guided if lesion is central)
Staging:
● Stage I: limited to lung (70% cure rate)
● Stage II: hilar nodes only. Mediastinal would make it IIIB (40-50% 5 year survival)
● Stage III: beyond lung
● Stage IV: distant mets
Treatment
● Non-small cell lung carcinoma:
Resection, radiation, no chemo:
14% 5 year survival
○ Preop assessment: FEV1 (800ml minimal to survive), V/Q scan to see how valuable that lung is
● Small cell lung carcinoma:
Non operable. Chemo, radiation if localized:
2 years max to live
MELANOMA
General Principles
● Above the lip: Basal cell (doesn’t metastasize, responds well to local excision). Do Moh’s excision, chemo, radiation.
● Below the lip: Squamous cell (metastasizes, but still pretty good prognosis). Get 1 cm margins.
○ Excise palpable lymph nodes only. Chemo, radiation.
Presentation: ABCDs: Asymmetry, Border, Color (black color & multiple colors are worse), Diameter (> 0.6cm is suspicious)
Risk factors
● Fair skin, sun exposure, family history, genodermatoses (Xeroderma pigmentosum), advanced age, increased number of
moles (50% of melanomas arise from existing moles), dysplastic nevi, giant congenital nevi
Types: All have the same prognosis when controlled for thickness
● Superficial spreading (75%)
● Nodular: worst prognosis, grows vertically early
● Lentigo maligna: best prognosis, typically on head & neck from a Hutchinson’s freckle (slow growing)
● Acral lentiginous (common in African Americans). Often on sole of foot. Subungual (under nail): amputate.
Stage
0
I
IB
II A
II B
III
IV
●
●
●
Clark level
I: epidermis
II: papillary dermis
III: breadth of papillary dermis
IV: into reticular dermis
V: subcutaneous fat
Breslow thickness TNM
T0N0M0
≤ 0.75 mm
T1N0M0
0.75-1.5 mm
T2N0M0
1.51-4 mm
T3N0M0
≥ 4 mm
T4N0M0
TanyN1M0
TanyNanyM1
Treatment
5-year survival
0.5-1 cm margin = cure >95%
Resect 1 cm margin
89%
75%
Resect 2 cm margin
58%
Resect 2-3 cm margin 25%
Interferon IFN-a2b
Ulceration: Bumps stage up one level. 1/3 reduction in survival regardless of thickness.
Sentinel node biopsy if palpable nodes. Dissect remainder of nodes if sentinel node is positive.
Get CXR, AXR looking for mets. CBC, LFTs.
PREOPERATIVE ASSESSMENT and POSTOPERATIVE FEVER
Prognostic Factors
Cardiac
● CHF -> JVD
● MI within 7 months
● Arrhythmia
● Age > 70
● Emergent
Pulmonary
● FEV1
Postoperative fever
● Wind (Atelectasis)
● Water (UTI)
● Walking (DVT)
● Wound
● Wonder where (Abscess)
● Wonder drug
Hepatic
● Bilirubin
● Albumin
● PT
● Encephalopathy
Nutritional
● Recent weight loss
● Albumin <3
● Skin anergy
POD 1
POD 3
POD 5
POD 7
POD 10-15
POD 7+
SOURCES:
● Essentials of General Surgery, 4th edition, 2006, Peter E. Lawrence, Lippincott Williams & Wilkins
● NMS Surgery Casebook, 2003, Bruce E. Jarrell, Lippincott Williams & Wilkins
● Step up to Internal Medicine, 2nd Edition, 2008, Steven S. Agabegi, Lippincott Williams & Wilkins
● First Aid for the Wards, 3rd Edition, 2006, Tao Le, McGraw-Hill
● Surgical Recall, 5th edition, 2009, Lorne H. Blackbourne, Lippincot Williams & Wilkins

Similar documents

×

Report this document