Acute General Oncological Wound Healing

Surgery Clerkship Oral Exam Study Guide
Acute
Wound Healing
Cholecystitis
Nutrition
Appendicitis
Diverticulitis
General
Peripheral Vascular Disease
Inguinal Hernia
Upper GI Bleed
Refulx Esophagitis
Trauma/Shock
Amanda Mure, Mark Tuttle (2010)
Oncological
Breast Cancer
Thyroid
Colon Cancer
Lung Cancer
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
Steps of wound healing:
1. Substrate/Inflammatory/Lag/Exudate phase - 0 to 7 days in primary intention, indefinitely for secondary/tertiary until
epithelialization occurs
a. Hemostasis: Activated platelets, coagulation factors --> hemostatic plug. - 1 to 2 hours
i. Impaired in chronic liver disease and uremia
b. Inflammation: PDGF, TGF-B and fibronectin are chemoattractive. - 0 to 2 days
i. PMNs, macrophages, complement C5A, kallikrein
1. PMNs are the most prominent cell type during this period
2. Macrophages are the most important cell type, they release metalloproteinases for remodeling/
debridement of necrotic tissue as well as growth factors
ii. Impaired by steroids, immunosuppressants, congenital or acquired immunodeficiency
iii. 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.
c. 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 - 4 days to 3 weeks
a. Epithelialization must occur as the first step for the rest of the phase to continue.
b. Net production of collagen during this phase
i. Alpha helix, every 3rd AA is glycine, has unique AAS OH-proline, OH-lysine
c. Primary cell type: fibroblast
d. 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
a. Cross linking of collagen
b. “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
● 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
CHOLECYSTITIS
Obstruction, NOT infection of cystic duct: acute inflammation
10% of population have gallstones. May not be symptomatic.
10% of people with cholecystitis are acalculus: ICU patients with MOF, burns, sepsis, TPN...due to bile stasis....same workup)
Risk factors: Female, fat, fertile, forty, flatulent
Cholelithiasis
Signs &
symptoms
Diagnosis
● Biliary colic:
colicky RUQ pain, radiates
to shoulder (Boas sign),
worse w/fatty foods
● Physical exam often
unremarkable
1. Ultrasound
(95% sensitive)
Acute cholecystitis
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Cholelithiasis, but worse
Nausea/vomiting
Constant pain, not colicky
Mild fever (101F)
Mild leukocytosis (12000)
Hypoactive bowel sounds
LFTs normal except alk phos
Muscle guarding
Murphy’s sign pathognomonic
Acute ascending cholangitis
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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
1. Ultrasound (Pericholecystic
fluid, thickened gallbladder)
2. HIDA scan (4 hours)
3. CT if suspect complication
(abscess, perforation,
pancreatitis)
1. Ultrasound
Treatment 1. Elective laparoscopic
cholecystectomy
1.
2.
3.
4.
NPO, IVF
IV antibiotics
IV analgesia
Cholecystectomy in 24-48 hours
1. IV antibiotics
2. Decompress biliary tree (percutan.)
3. ERCP after acute phase: treats
underlying cause - obstruction
Complica.
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Gangrenous cholecystitis
Perforation (very bad)
Emphysematous cholecystitis
Gallstone ileus
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33% cholecystitis in 2 years
Sepsis
Hepatic abscess (very bad)
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
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
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/infarction
● 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
● Colorectal cancer
● Acute cholecystitis
● Mesenteric ischemia
● Pyelonephritis/Nephrolithiasis
● Colitis
● Diverticulitis
● Pyelonephritis/Nephrolithiasis
● Ovarian torsion, cyst
● Ovarian torsion, cyst
● Ruptured ectopic pregnancy, PID
● Ruptured ectopic pregnancy, PID
● Intussusception
● Colon Cancer
● Meckel’s diverticulum
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: ustable patients when surgery can help
APPENDICITIS
Pathophysiology:
● Hyperplasia of lymphoid tissue (60%), fecalith (35%), foreign body, parasite, carcinoid tumor (rare)
○ 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
● Peak incidence: teens to mid-20s
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:
● Acute appendicitis is a clinical diagnosis. Lab/film findings are supportive.
● Leukocytosis (mild), CT scan (sensitive 98-100%), ultrasound (90%)
Treatment:
● Appendectomy (laparoscopic) 20% false positive. Risk is ok in pregnancy (10-15% increased risk of premature labor)
● Right hemi-colectomy if cecum is involved (!), or if carcinoid tumor is discovered (>2cm or involving cecum)
Complications:
● PERFORATION (20% of all cases): Greatest risks with delay in tx and extremes in age. Atypical presentation = little pain,
present late). 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
GU DDX: 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.
● Microperforation of the diverticulum secondary to the increased pressure or obstruction by inspissated feces. Feces
extravasate onto the serosal surface but infection is usually well contained in an immune competent patient.
Symptoms: LLQ pain (subacute onset), alteration in bowel habits (constipation OR diarrhea)
● Lower GI bleeding rare (common in diverticulosis, not -itis)
Signs:
● Palpable mass (sometimes)
● Fever...sometimes peritoneal signs, leukocytosis
● If constantly having waxing and waning symptoms--will have distension, high-pitched bowel noises, severe constipation or
obstipation.
Diagnosis:
● CT with oral and IV contrast.
● Barium enema and colonoscopy are CONTRAINDICATED due to perforation risk.
Treatment: Directed at specific complication.
● Acute: medical treatment 85% of the time.
○ Admit, IVF, IV non-opioid analgesics, NPO, IV antibiotics (aminoglycoside, coverage for B. fragilis) x 5-7 days.
● Indications for surgery: Perforation, obstruction, intractability, bleeding, fistula, or recurrence
● All patients with diverticulitis must undergo a full colonoscopy 4-6 weeks after the attack to r/o malignancy
Procedure: sigmoid colectomy, temporary colostomy:
● No attempt at primary reanastamosis because of high rate of infection and bowel leak.
● Second operation for colostomy take down and anastamosis to rectal stump.
Complications:
● Perforation, abscess, fistula, obstruction
Fistula formation: colovaginal, colovesicular (pneumaturia, recurrent UTI), colocutaneous
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.
INGUINAL HERNIA
Pathophysiology:
● Most common in males and females = indirect inguinal hernia
● Occur in areas where striated muscle does not protect
● 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 IH: enters canal via weak posterior wall, does not pass thru internal ring
● Lies posterior to spermatic cord, occurs almost exclusively in males, older, smokers
● Never enters the scrotum, can damage the ilioinguinal nerve
● Protrude medial to the inferior epigastric vessels, not assoc. with processus vaginalis.
● Herniate thru Hesselbach’s Triangle:
● Inferior border: Inguinal ligament
● Medial border: Rectus abdominus
● Lateral border: Inferior epigastric vessels (lateral umbilical fold)
Indirect IH: most common in males AND females, enters thru the internal inguinal ring, travels to external ring. If
complete, can enter scrotum while exiting external ring. (congenital? Think patent process vaginalis)
● More common on right side in first decade of life (right testis descends later)
● 1/3 = bilateral
Treatment:
● Surgery = treatment of choice
● 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.
● Non-surgical: (moribund patients) “hernia truss” to keep hernia reduced, limited in use
DDX:
Abdominal wall mass, Desmoids (locally aggressive fibrous proliferation), Neoplasm, adenopathy, rectus sheath hematoma,
hydrocele (differentiate by shining a light, hernias not translucent)
UPPER GI BLEEDING
Pathophysiology:
● PUD-Duodenal ulcer (25%), gastric ulcer (20%), gastritis (25%)
● Upper GI Bleed = above ligament of Treitz; reflux esophagitis, esophageal varices (10%), gastric varices/erosions,
duodenitis, Mallory-Weiss tear, hemobilia, Dieulafoy’s vascular malformation--submucosal dilated arterial lesions that
cause massive GI bleed
● NSAIDS/Aspirin or anticoagulants
● Rare: Aortoenteric fistula following aortic graft surgery
● Neoplasm: bleeding is not rapid, usually not emergent.
● Increased morbidity with age >65, severity of initial illness, extensive comorbidities, onset or recurrence while hospitalized
for another issue, need for emergency surgery (see below), significant transfusion requirements, cause of bleed (e.g.
esophageal varices has 30% mortality rate), endoscopic stigmata of recent hemorrhage.
Symptoms/Signs:
● Hematemesis
● “Coffee ground emesis” suggests Upper GI bleed, and lower rate of bleeding
● Melena suggests upper GI bleed (DDx: bismuth, iron, spinach, charcoal, licorice)
● Hematochezia could be a very brisk upper GI bleed (blood not digested)
● Signs of volume depletion, anemia (fatigue, pallor, exertional dyspnea)
● Hypotension/tachy/etc.
Diagnosis:
● Upper GI endoscopy is initial test with hematemesis (diagnostic and therapeutic)
● NG tube (gastric lavage to see if there’s new blood/old blood--false negative possible)
● Exclude rectal source if necessary: Stool guaiac for occult blood (rectal exam!), Colonoscopy
● CBC (H/H, MCV low), PT/PTT/INR, LFTs, Renal Function
● Bun/Cr ratio elevated with upper GI bleed (if no concurrent renal issues)
● Bleeding scan (uses 99mTc to detect bleed, not good at finding location of bleed, just that there is one). Arteriography can
pinpoint source of bleeding
● Exploratory laparotomy = last resort!
Treatment:
● 80% stop bleeding spontaneously (e.g. Mallory-Weiss), only need supportive therapy.
● Resuscitation (IV fluids, transfusion)
● Endoscopy with coagulation of bleeder
● Surgery.....
Indications for surgery:
1. Hemodynamically unstable patient who does not respond to IV fluid, 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)
Ongoing transfusion requirement (5 units in the first 4-6 hours)
REFLUX ESOPHAGITIS
Pathophysiology:
● Loss of normal GE barriers... LES, secondary to low or reduced LES tone with reflux of gastric contents into esophagus.
● Causes: structurally defective sphincter, hiatal hernia, transient loss of GE barrier secondary to gastric abnormalities such
as distension with air, food. Delayed gastric emptying, increased intrabdominal pressure.
● 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:
● Diagnostic tests are not necessary for typical, uncomplicated, initial cases of GERD
● R/o cardiac and pulmonary disease (H&P, ECG, cardiac enzymes)
Endoscopy with biopsy = test of choice...but.....
● 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:
● Important in order to prevent progression to Barrett’s, cancer, pulmonary problems
● Initially: medication that decreases gastric acid production, lifestyle modification
Phase 1: Elevate head of bed, antacids. Education to avoid EtOH, coffee, chocolate, peppermint--aggravate Sx, nicotine-decreases LES tone, eat small frequent meals, don’t sleep for 3-4 hours after eating
Phase 2: Add H2 blocker
Phase 3: Switch to PPI
Phase 4: meds to promote gastric emptying (metoclopromide)
Medical therapy trial 6-12 weeks before further diagnostics
Phase 5: combination therapy (phase 2+4, phase 3+4, or increase 2, 3, dose)
Phase 6: Surgery (Fundoplication)......with goal to restore function.....
Indications for surgery: Failure of medical therapy (Nissen) OR dysplasia of esophageal mucosa (resection)
● Preoperative studies: Manometry, endoscopy, barium swallow
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
1) PRIMARY SURVEY: ABCDEF
Airway (and c-spine)
● Assess airway patency, use jaw thrust to initially open airway (protects c-spine) clear foreign bodies, insert oral or nasal
airway (temporarily, these are not definitive airways), intubate--or cricothyroidotomy when unable to intubate (extensive
facial/laryngeal trauma)
● Intubate if:
○ Inadequate respiratory effort
○ GCS < 8
○ Hoarseness, stridor, retractions
○ Inability to protect the airway
○ Severely compromised respiratory mechanics
● Assume C-spine injury until proven otherwise
● Sucking out secretions/blood/vomitus with Yankauer tip hooked to wall suction
Breathing
● Inspect, auscultate, and palpate chest
● Is trachea midline? Neck veins distended?
● First ask, is air moving in and out of the mouth... then ask, is it moving in and out of both lungs equally?
● Ensure adequate ventilation and immediate identify and treat:
○ Tension pneumothorax (chest tube, don’t wait for x-ray)
○ Flail chest and pulmonary contusion
○ Massive hemothorax
○ Open pneumothorax (dressing that is closed on 3 sides)
Circulation/Control of hemorrhage
● Place two large bore (16g or bigger) IVs
● Assess circulation (capillary refill, pulse, skin color)
● Apply direct pressure to life-threatening hemorrhage
Disability (neurologic)
● Rapid neuro exam--pupillary size/reactivity
● Establish LOC using Glascow Coma Scale (eye response, verbal
response, motor response....min 3 max 15)
○ Or, AVPU (alert? responsive to verbal? responsive to pain? Unresponsive?)
● GCS of less than or equal to 8...severe!
Exposure/Environment
● Undress patient (e.g. cut through their $200 Lucky jeans)
Foley Never without doing a rectal exam: displaced prostate (“riding high”) may be indicative of urethral transection
2) RESUSCITATION
● Performed simultaneously with the primary survey (translation: nursing staff)
● 100% oxygen administered
● IV fluids started (LR preferred)
● Warmers/Blankets to prevent hypothermia
● 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
● Portable x-ray (chest, pelvis, lateral c-spine)
3) SECONDARY SURVEY
● Detailed head-to-toe assessment
● Reassesment of the primary survey
● AMPLE Hx (Allergies, Meds, PMH/Prego?, Last meal, Events of injury)
● From Gen. Essen. of Surg: “Tubes or fingers are placed in every orifice.” (p.141)
4) DEFINITIVE CARE
● Injuries prioritized based on MOI, physiological status, comorbidities. Blood products given, surgery performed.
Diagnostic peritoneal lavage or FAST (Focused Abdominal Sonogram for Trauma) but this seems to be done in real life during
primary survey--circulation step.
SHOCK n’ Awe: inadequate organ perfusion
Hemorrhagic Shock: Hypovolemia due to bleeding. Treatment aimed at stopping bleeding and restoring intravascular volume--NOT
restoring blood pressure. Therefore, it is not appropriate to use vasoconstrictors to reach this goal.
● Use the 2 large bore needles you put in during the primary survey to deliver LR solution.
○ Why large bores? 1. Can infuse faster, and 2. blood products can hemolyze through smaller diameter catheters.
● Initially, run two 1 liter LRs wide open on the probable hemorrhagic shock patient. See their response--did their vitals
improve and urine output increase? Still hemodynamically unstable? (this means no improvement in blood pressure)
○ No response: run another bolus of 1-2L. If after second bolus of fluid there is no response in vitals or urine output,
consider type-specific or O-neg blood transfusion along with more LR.
● Adjuncts to fluid resuscitation (not really used anymore in hospital but are in the field)...PASG/MAST pants, inflate below
the abdomen (look like fighter pilot g-suits) and increase SVR and L ventricle afterload, therefore increasing BP. These are
good for pelvic fractures because they stabilize pelvis and help with hypotension, but still are controversial.
Cardiogenic shock: myocardial dysfunction due to cardiac tamponade, contusion, air embolus, MI (rare)
● Cardiac tamponade
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))
TX: Pericardiocentesis
● 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.
BURNS
● 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
ONCOLOGY: General rule: any lymph node >1cm, 4+ week, w/out infection should be biopsied.
BREAST CANCER
Workup by presentation:
● Palpable mass
○ Fine needle aspiration (for cytology)
○ If <30 years old: Ultrasound. Mammogram would be useless due to dense breast tissue
○ if >30 years old: Mammogram
○ Biopsy (stereotactic, needle guided)
Infiltrating ductal carcinoma
● Lumpectomy, nodes + radiation
● Simple mastectomy (no rad)
DCIS: lumpectomy + radiation. No nodes
● Bloody discharge
○ Mammogram
○ Galactograph, resection of papilloma
● 18 year old rubbery, movable mass: Fibroadenoma
● 35 year old, 10 year cyclic tenderness: Fibrocystic change
○ Aspirate cyst
○ Bloody fluid? send 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
● For ALL: thorough H/P, including:
○ Age, family history (first degree relatives), previous breast cancers (path results?), Hx of benign breast disease,
presence of palpable masses, history of estrogen replacement therapy, age of menarche, nulliparity.
○ Orange peel, spontaneous nipple discharge (especially bloody)
Diagnostic Studies:
● Mammography (2 views each boob)--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/malignancy: spiculated lesion 5-10% false neg. rate, so if you feel something, and have
suspicion/symptoms--> continue workup regardless of radiography
● Ultrasound: next step after mammography for a suspicious lesion (good first tool for pregnant boobs with palpable
masses). Most useful in young women (<35) with dense breast tissue....Can distinguish between a mass and a cyst, and
can be used for U/S guided biopsy. Like mammography, doesn’t replace clinical suspicion.
● Biopsy: Good choice if patient >30yo and mass is solid (do an FNA or core biopsy) but it does not tell you staging.
● FNA: 20% false negative rate, so you will probably have to go in and excisional biopsy whatever the hell it is anyway. So
really consider if this is a good option. It also 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 Dx. Can be diagnostic AND therapeutic. Costs more money, more risks b/c this is an
open surgical procedure under general anesthesia.
● Needle localization breast biopsy: good for lesions you can’t feel but see on the mammogram
Is an invasive surgical procedure under general anesthesia.
THYROID
H/P: “24 yo woman with asymptomatic 3cm neck mass she noticed 1 week ago. She is otherwise well.”
● History of childhood radiation, family history of MEN syndromes, is there a nodule or multinodule?, pain? pressure?
hoarseness or voice changes (think local invasiveness), thyroid toxicity signs? history of goiter?
● Women, aged 25-65.
Types
● Papillary - spreads via lymphatics
● Follicular (more aggressive than papillary) - spreads hematogenously
● Medullary - usually assoc. with MEN
● Anaplastic - worst prognosis
Diagnosis
● Order TSH/T3/Free T4
● Request FNA of mass.
● Ultrasound that neck.
● Family Hx of Men-2A? Order urine catecholamines (pheochromocytoma)
Treatment: Select appropriate operation--total T-ectomy? radiation? chemo?
● Smaller lesions (<1cm) can be treated with lobectomy instead of total.
Complications of thyroidectomy
● Low calcium due to inadvertent parathyroidectomy with the thyroidectomy: perioral tingling, parasthesia, MS change
● Horseness due to injury to the recurrent laryngeal nerve
GI 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
● Melena: 1) upper GI endoscopy 2) colonoscopy
● 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%), 80% stop spontaneously, ask about NSAID use, anticoagulant use
○ Reflux, varices, Mallory-Weiss, hemobilia, aortoenteric fistula (Hx of AAA repair)
● Lower GI bleed
○ 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
Treatment: IV antibiotics, NPO. Recurrent episode: resection
Complications: Bowel obstruction, abscess, fistula
○ Angiodysplasia (40%) - most common in > 60 years old
○ Colorectal cancer
○ 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)
○ 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
Treatment
● Upper: EGD with sclerotherapy, gastrografin swallow study if you suspect perforation
● Lower: r/o hemorrhoids.
○ Slow bleed (<0.5ml/hr): radionucleotide scan.
Fast bleed (2+ ml/hr): emergent angiogram.
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
● Bowel resection
○ Stage I + II (T4N0M0): radiation and chemo play NO role. Stage III + IV: Chemo is indicate
○ Baseline CEA (to help detect recurrences)
● Chest X-ray (to look for metastasis)
● Liver function tests (to look for metastasis)
Prognosis
● Stage I: 90% 5 year survival. Stage IV: <5% 5 year survival
T1: limited to mucosa/submucosa, T2: invades into, not beyond muscularis, T3: full thickness
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.
● Below the lip: Squamous cell (metastasizes, but still pretty good prognosis). Get 1cm margins.
Presentation: ABCDs
● Asymmetry
● Border
● Color (black color & multiple colors are worse)
● Diameter (greater than 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
● 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)
Staging
● Clark Level: I: epidermis, II: into papillary dermis, III: through papillary dermis, IV: into reticular dermis, V: SQ fat
● Breslow Thickness: <0.76mm 90% cure rate, >4mm 80% risk of mets/recurrence in 5 years
Treatment
● Excision. Get wide margin if > 1mm thick, go down to muscle fascia.
● Get CXR, AXR looking for mets
● Sentinel node biopsy if >1.0 mm
Adjuvant therapy: IFN-a2b
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 1-2
POD 3-5
POD 4-6
POD 5-7
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