Chapter 1: Nausea, Vomiting, and Left Groin Mass – Hernia

Differential Diagnoses for a Groin Mass (MINT)

 M (malformation) – Hernia, Undescended testicle, Varicocele, hydrocele
o Hernias protrudes with straining and can reduce with pressure
 I (infection/inflammation) – mononucleosis, abscess, sarcoidosis, lymphogranuloma verneum
o Typically, “shotty” reactive inguinal lymph nodes with mass with be this differential
 N (neoplastic) – lymphoma, lipoma, metastatic lymphadenopathy (anal/cutaneous/genital)
o Testicular cancer will NOT produce inguinal lymphadenopathy as it often metastasizes to
retroperitoneal lymph nodes
 T (traumatic) – hematoma, femoral artery aneurysm, pseudoaneurysm
o Femoral aneurysm will have a pulse on palpation of the mass
Pathophysiology
 There are three components to a hernia – abdominal wall defect, hernia sac, and contents of the sac
 The ‘neck’ of the hernia sac is the portion that is actually protruding through the defect.
o Wide neck – more common for abdominal contents to come through, but easier to reduce
o Narrow neck – less common for protrusion, but harder to reduce/higher chance of
incarceration/strangulation of the herniated abdominal contents
 Strangulated hernia – hernia where protruding bowel contents have compromised blood supply
o More common in old folks, hernias of short duration (new defect often narrow), femoral
hernias (narrow/rigid canal), and with narrow necks
o Signs – fever, tachycardia, elevated WBCs, erythema of skin, and pain
o This is a surgical emergency and requires emergent bowel resection
Types of Hernias
 Direct Inguinal Hernia – protrusion thru Hesselbach’s triangle (inguinal ligament, inferior epigastric
artery/vein, medial border of rectus abdominus) through an abdominal wall defect medial to the
inferior epigastric artery. They pass through the wall and enter into the inguinal canal to exit via the
external (superficial) inguinal ring
o Typically, due to an acquired weakness in the transversalis fascia in the anterior abdominal wall
(straining, injury, etc.). Hesselbach’s triangle is only composed of a thin layer of transversalis
fascia, making it the prime place for defect/herniation
o Abdominal Peritoneum lines the hernia sac
o Least likely to incarcerate (flabby walls to protrude through) and more common in men
 Indirect Inguinal Hernia – protrusion thru internal (deep) inguinal ring lateral to the inferior epigastric
artery and eventually trough the external (superficial) inguinal ring
o Typically, due to congenital defect of the processus vaginalis allowing for hernia to slip into the
inguinal canal and possibly into the scrotum/labia following the path of the spermatic
cord/round ligament (respectively)
o Processus vaginalis lines the hernia sac
o Most common hernia in all people (men, women, and children!)
 Umbilical Hernia – protrusion through the umbilicus
o Typically occur in children. Associated with congenital hypothyroidism (cretinism)
o In children, often are asymptomatic and resolve spontaneously without intervention
o In adults, associated with high intra-abdomnial pressure (ascites, pregnancy, weight gain, etc.)
 Femoral Hernia – protrusion thru the femoral canal into the empty space (NAVEL) medial to the
femoral vein and below the inguinal ligament
o Typically occur in women with multiple pregnancies, as the femoral veins dilate with pregnancy
causing dilation of the entire canal
 o Abdominal Peritoneum lines the hernia sac
o Most common to become incarcerate/strangulate
due to thick fibrous lining of the canal!
 Ventral (incisional) Hernia – herniation at the side of
previous surgical incision; may appear weeks to months to
years after actual procedure that caused the defect
 Richter’s Hernia – hernia where only a portion of the
bowel wall has protruded into the hernia sac
 Spigelian Hernia – herniation through two layers of the
abdominal wall (not all of them). Is NOT palpable, thus
must be diagnosed with imaging and clinical suspicion
 Sliding Hernia – when a retroperitoneal organ herniates
with the sac, making up the posterior wall of the
herniated contents through the wall defect. Often
posterior wall of hernia feels “thickened”
Workup
 Hernias are clinically diagnosed with H&P
o A reducible abdominal mass is practically diagnostic
o A non reducible mass that bulges with straining (Valsava) is also another very clear sign
o In an infant, the diagnosis can be made by observing a bulging mass with crying or lifting the
infant’s arms to they struggle (revealing the mass)
 Imaging can be used when H&P does not yield diagnosis
o Often it’s hard to appreciate the mass in obese patients or in a Spigelian hernia
o Ultrasound + Valsalva – cheap and can often diagnose an inguinal hernia easily
o Cross-sectional CT/MRI – can be used for any hernia diagnosis.
Management
 Often operative management is sought when hernia is symptomatic or risk of damage to organs
 Direct Hernia – simple reduction of the sac with repair of the weakened wall of the inguinal canal with
tension free mesh placement or a tensioned-tissue based repair
 Indirect Hernia – operatively open up the sac, assess herniated contents (often bowel) for viability,
resect non-viable contents, reduce viable contents, and perform high ligation of inguinal canal (at
internal ring) to close the patent processus vaginalis
o If muscles in area are weak, tension free mesh may be placed for reinforcement of abd. wall
o If present in a child/adolescent, there is a 5-10% chance of bilateral indirect hernia, thus the
contralateral side should be assessed and corrected as needed
 If hernia is acutely incarcerated an attempt for non-operative reduction should be made, however if
this is not possible, prompt operative reduction with repair of hernia should be sought
 Umbilical hernias in infants often close by age 2; repair should occur if it does not resolve by age 4, a
>2cm defect is present or progressive enlargement after 1yr occurs
Complications
 Nerve Injury – transection, stretching, compression by adhesions/suture are not uncommon
o Genital Branch of genitofemoral nerve – cremaster reflex loss & anterior scrotum or labia
majora loss of sensation
o Ilioinguinal Nerve – base of penis, mons pubis, and inner thigh loss of sensation
o Iliohypogastric Nerve – suprapubic loss of sensation
o Lateral femoral cutaneous nerve (meralgia paresthetica) – lateral thigh loss of sensation
extending down to the knee (often with laproscopic repair)
  Damage to testicular artery/vas deferens – indirect hernias must be separated from these structures,
thus making them prone to damage during separation. Note that testicular artery damage will rarely
cause ischemia to the testicle due to other avenues of perfusion
 Disruption of venous drainage of testicle – often in indirect hernias with a large hernia sac, the distal
portion of the sac will be adherent to the scrotum. The dissection needed to remove it can damage the
testicular veins, leading to failure of drainage and ischemia/death (swollen painful testicle after
surgery). Often this portion is left adherent while the rest of the sac is dissected for this reason.

Chapter 2: Abdominal Pain, Nausea, and Vomiting – Small Bowel Obstruction (SBO)
Presentation
 Acute onset colicky abdominal pain, nausea, vomiting, & constipation with high-pitched bowel sounds
o If due to strangulated hernia: fever, tachycardia, leukocytosis, and localized abdominal
tenderness can all be present
 Often with dehydration (dry mucous membranes, pre-renal azotemia [high BUN:Cr])
 Recurrent emesis may result in hypochloremic-hypokalemic metabolic acidosis
 Differentiating different types of Bowel Obstruction
o Complete SBO – acute onset of symptoms
o Partial SBO – slower onset of symptoms with passage of stool/gas 6-12hr after onset
o LBO – if proximally involved, presentation may be similar; however, symptoms are typically
chronic/progressive and may involve constipation, bowel distention/suprapubic cramping, and
rarely feculent vomiting
o Post-operative Ileus – typically the small bowel (24hr), stomach (48hr), and large bowel (3-5
days) all take their own amount of time to “re-start” after surgery/anesthesia. While this may
present with similar symptoms to SBO, pain is often constant and dull with mainly hypoactive
bowel sounds from the beginning of complaint.
 If patient initially was fine post-op, then complaints occurred, SBO is considered
 CT is often used to distinguish SBO from POI in equivocal cases
Pathophysiology
 Hernia is the most common cause of SBO worldwide due to closed loop obstruction
 Prior abdominal surgery is the most common cause of SBO in industrialized countries due to adhesions
o Appendectomy is the most common surgery to cause this complication; followed by colon
resection and gynecologic procedures
 Crohn’s disease (stricture/fistulas), gallstone ileus (direct obstruction/pneumobilia), intussusception
(target sign/palpable mass), volvulus (omega sign), and neoplasms (Hx) may all cause SBO
 When the bowel is obstructed, fluid/gas accumulate causing dilation, prompting the bowel to increase
motility in an attempt to relieve the blockage
o Bowel dilation = nausea, abdominal pain with contractions (colicky), and emesis
o Initially bowel sounds increase from increased peristaltic activity (high pitched/tinkling)
o Progressive dilation causes inability to contact leading to eventual decrease/absence of sounds
 Major problem is fluid loss due to emesis and third spacing (blockage/bacterial overgrowth  dilation
 starling forces moving solute into bowel wall  movement of blood serum into bowel wall)
Work-Up
 Labs – CBC, CMP, and serum lactate to assess dehydration (hemoconcentraction, pre-renal azotemia,
hypoCl/K acidosis) and bowel ischemia severity (leukocytosis, elevated serum lactate)
 Imaging – abdominal series followed by abdominal/pelvic CT with oral & IV contrast
o What are each of these tests looking for?
 Upright chest radiograph – free air under diaphragm  bowel perforation
 Upright abdominal radiograph – air-fluid levels  obstruction
  Supine abdominal radiograph – assess level/area of distention
 CT w/contrast – assess level/area of distention
o Small bowel shows lines going the full length of the tube (plica circularis) while large bowel will
only have lines going partially through (haustra)
o Pneumatosis (CT) is presence of gas in the intestinal wall, often indicating ischemia/necrosis
o Portal venous gas (CT) is a late presentation of pneumatosis where the air passed into the
portal venous circulation because it had been there for some time
Management
 First Step – aggressive isotonic IV fluid replacement, nasogastric tube placement (suction of bowel
gas), and placement of IV catheter to monitor urine output
o Partial obstruction – conservative management for up to 2-3 weeks
o Complete obstruction – conservative management with close watch on clinical status for 24hr
 Lack of improvement or clinical deterioration should prompt surgical resolution, likely with a bowel
resection for non-viable small bowel
o Non-viable bowel appears blue/pale, has no peristalsis, & lacks mesenteric arterial pulsation
o Ultrasound doppler is useful to assess bowel blood-flow when assessing questionable bowels
o IV fluorescein dye with Wood’s Lamp can be used, as bowel that lights up is getting blood
o If you still can’t make up your mind, but the section in question is small it’s acceptable to
simple remove the small section and call it a day
o If you can’t make up your mind, but the section is large, it’s acceptable to terminate the
operation, further resuscitate the patient, and have a second look surgery.
 Should re-operation be necessary:
o 10-14 days post-op = OK
o After 10-14 days post-op = not OK due to highly vascularized adhesion formation.
 Instead initiate conservative treatment for 4-6wk to allow for less vasularization to be
present on re-opteration
 Emergent re-operation may be necessary if peritonitis ro bowel compromise are seen

Chapter 3: New Palpable Mass in Breast – Breast Cancer

A new breast mass can be MANY things and the differential can be big. Make sure to review the following on
Pages 25-26 in regards to benign and malignant differentials:
 Benign: fibrocystic change, fibroandenoma, indaductal papilloma, fat necrosis, abscess, galactocele
 Malignant: DCIS, LCIS, IDC, ILC, mucinous carcinoma, inflammatory carcinoma, phyllodes tumor
Key physical features of benign vs malignant breast nodules
 Benign: well circumscribed, rubbery, mobile mass with no gross abnormalities of the breast
 Malignant:
o Overall breast: asymmetry, overlying skin changes, nipple discharge/crusting
o Mass itself: single dominant lesion that feels hard, immobile, and has irregular borders
o Lymph nodes: painlessly enlarged, firm, immobile, and/or matted
Different Types of Nipple Discharge
 Physiologic: clear, bilateral, multiductal often from hormonal changes in the body (post-lactation,
regular cycling/puberty nipple stimulation)
 Milky: can be physiologic (post-birth) or from prolactinoma, hypothyroidism (TRH can act like PRH), or
medications (DA inhibitor anti-psychotics come to mind)
 Bloody: most commonly from intraductal papilloma, up to 15% can be from invasive breast cancer.
 Purulent: may be the result of infection!
Risk Factors for Breast Cancer largely have to do with two things:
 Estrogen exposure: menarchal age <12, menopause >55, nulliparity, obesity, hormone replacement
therapy, age of first birth >30
 DNA damage/defect: mother/sister with breast cancer, previous breast cancer, radiation exposure,
known BRCA1/BRCA2 mutation, age >70yr
Pathology/Patholophys
 While fibrocystic changes are often benign, ductal hyperplasia, sclerosing adenosis, and atypical
hyperplasia all carry a risk of cancer if seen histologically
 Peau d’Orange: red-orange discoloration of the breast skin, swelling, dimpling and nipple retraction
due to compromised lymphatic outflow due to malignant invasion. Often caused by inflammatory
carcinoma of the breast
 Nipple retraction: malignant invasion of the Cooper’s ligaments causing thickening and pulling back,
resulting in retraction of the skin of the nipple, signifying breast cancer
Workup
 Triple Test: a clinical tool for physical exam of new breast mass consisting of exam, imaging, and tissue
sampling giving 1 (benign), 2 (suspicious), or 3 (malignant) ratings to each test.
 Imaging:
o Under 30yr: young breasts are denser with fibrous tissue, making mammography less useful.
Ultrasound is first line for imaging these women, mainly to differentiate cystic vs solid masses
o Over 30yr: mammography is most useful here
 Biopsy:
o Simple cystic masses may be left or drained if symptomatic; clear fluid with the mass reducing
is a normal finding; bloody fluid or a non-reducing mass require further cytology and biopsy
o Solid or suspicious masses are assessed via core needle biopsy
 Tumor Antigen testing: testing for estrogen (Er), Progesterone (Pr), and HER-2neu receptors are done
to determine options for treatment and prognosis in a malignant breast mass. If none of these
receptors are present the tumor is deemed ‘triple-negative’ and often a poor prognosis
 Metastatic Workup: LFTs (liver), alkaline phosphatase/serum calcium (bone), CXR (lung) are used as a
basic workup in low-stage cancers without symptoms
o CT, and other symptom driven testing may be undergone based on clinical situation
o Stage 3 cancer requires an additional CT C/A/P + bone scintigraphy
 Staging: can be reviewed on page 29
Management
 Lumpectomy + SLNB + chest wall radiation – basically cutting out the cancer with clean margins,
making sure there aren’t mets, and radiation for anything residual
o Contraindications: multiple primary tumors in 2+ quadrants, diffuse malignant
microcalcifications, previous chest wall radiation, positive surgical margins with repeat
excisions, and 1st trimester of pregnancy
o Nipple/Breast Skin sparing can be part of the operation, especially in lower risk cases
 Simple mastectomy + SLNB (no radiation) – more tissue gone but a more definitive treatment
 Simple mastectomy + ALND +/- neoajuvant chemotherapy – used for stage 3 or greater tumors,
especially with larger tumors that need to be shrunk for better surgical outcomes
 Chemotherapeutic Drugs
o There can either be hormonal treatments or classic chemo drugs listed on Pages 32 and 33
o Note that before starting Trastuzumab (Herceptin) all patients should receive an
echocardiogram and MUGA scan (assess left/right ventricular function) to determine ejection
fraction as there is significant risk of cardiomyopathy
Complications
 Nerve Damage due to Lymph Node Dissection
o Long Thoracic nerve – weak upward rotation/abduction, and winged scapula
o Thoracodorsal nerve – weak extension/adduction/internal rotation of the shoulder
o Medial pectoral nerve – weak internal rotation of humerus
o Lateral pectoral nerve – weak flexion, adduction, and internal rotation of humerus
 Lymphedema (swelling, pain, compromised immune system) is the most morbid comorbidity of lymph
node dissection. Also lymphangiosarcoma risk is increased with lymphedema
Things that can get you in Trouble
 Mistaking Inflammatory Breast Carcinoma for Cellulitis – don’t do it
 Ignoring a breast mass in pregnancy
o First trimester – make the diagnosis; but you can’t treat
o Second trimester – make the diagnosis; chemo can be given
o Third trimester – make the diagnosis; wait till birth until treatment
o Note that hormonal therapy and therapeutic radiation are total contraindicated in pregnancy
 Ignoring a breast mass in an elderly male – old men can definitely get breast cancer (esp. in 60s/70s).
Sadly, it’s often diagnosed in later stages, sometimes giving a worse prognosis

Chapter 4: Abnormal Screening Mammogram – DCIS/LCIS

Recommendations for Breast Cancer Screening
 While fairly controversial, most guidelines advise:
o Regular breast awareness and/or exams starting at age 20
o Mammograms at some yearly interval starting around either age 40 or 50
 It is thought that after age 50, the radiation risk of a mammograms outweighs the risk of breast cancer
 While helpful, the use of mammograms can be dependent on the patient and the skill of the tech and
interpreter of the films, lending unwanted variability
Pathophysiology
 Several reasons for abnormal findings on mammogram are listed on page 38
 Benign calcifications on mammogram are often larger and more dense
 Malignant calcifications are more often smaller and more “hazy” as they are the result of individual cell
death & calcification from malignant overgrowth
 DCIS
o Malignant epithelial cells within the mammary ducts that have not invaded the basement
membrane of the tissue; considered a pre-malignant lesion
o Often presents as incidental micro-calcifications on mammorgram
o Comedo pattern is highly suspicious of malignancy and is the most worrisome for metastasis
o Treatment includes excision to a negative margin with SLNB in some cases as this can
technically be invasive, but only in small amounts
 LCIS
o Malignant epithelial cells within the mammary lobules, often incidentally found on biopsy
o Not considered pre-malignant, but is a major risk factor for development of breast cancer in
either breast
o Treatment is excisional biopsy to search for surrounding malignancy with tamoxifen use in
some to decrease the risk of malignancy development.
Chapter 5: Chest Pain, Diaphoresis, Nausea – Heart Attack
Risk factors – increased age, male, HTN, hypercholesterolemia, diabetes, smoking, family Hx of CAD
 A patient presenting with acute chest pain can be scary, but the lack of these risk factors may mean
you should search of other etiologies!
 Young age (men <40, women <50), female gender, no cardiac risk factors (smoking, diabetes, family Hx,
etc.), and character of chest pain (exertional, relieved with rest, signs of angina) that suggest non-
cardiac etiology put people at LOW RISK for MI
 Postmenopausal women are at increased risk for MI as estrogen helps maintain the vascular intimal
layer. The loss of this maintenance leads to stiffening of arteries, thus heighted risk!
Presentation
 Chest pain (radiation to neck/left arm), diaphoresis, anxiety, tachycardia, tachypnea, nausea/vomiting
 Heart failure may occur in large MIs (dyspnea, rales, JVD, new S3/S4, new murmur, shock)
 Women most often have atypical (‘silent’) presentations (dyspnea, epigastric pain, N/V, no chest pain!)
Pathophysiology
 Acute Coronary Syndrome – pathologic process involving narrowing/damage to the coronary arteries
resulting in varying degrees of myocardial ischemia
o Unstable Angina – non-occlusive thrombosis causing ischemia but NOT myonecrosis
o NSTEMI – occlusive thrombosis where only part of the myocardium (sub-endocardial segment)
is damaged causing myonecrosis/cardiac enzyme elevation, but not ST-segment elevation
o STEMI – occlusive thrombosis affecting the entire myocardial wall causing myonecrosis/cardiac
enzyme elevation/ST-segment elevation. This is the classic heart attack.
 There are two major mechanisms for MI
o Primary coronary event – plaque rupture with thrombosis; often needs immediate intervention
to re-establish myocardial perfusion
o Non-primary – decreased O2 supply (hypoxia, hypotension, anemia, etc.) or increased
myocardial oxygen demand (tachycardia, tachyarrythmia, sepsis, etc.); often addressing the
primary problem is needed for resolution of ischemia
 Variant (Prinzmetal) Angina
o A vasospatic angina that typically occurs in young women without cardiovascular risk factors,
onset in the middle of the night, and often exacerbated by smoking.
o May be precipitated by exercise, hyperventilation, emotion, cold exposure, cocaine abuse; but
will not be consistently exacerbated with exercise like Typical Angina
o EKG can show transient ST elevation w/ complete return to baseline after ischemic vasospasm
o May be associated with other vasospastic disorders (migraines or Raynaud’s phenomenon)
o Tx: nitrates or Ca++ channel blockers (vasodilation)
Workup
 First Steps: relevant H&P + 12-lead EKG + cardiac enzyme blood assay QH8 for 24hr + chest radiograph
(rule out non-MI causes of acute chest pain) +/- echocardiogram (if not delaying treatment!)
 Cardiac enzyme characteristics
o Troponin-I – slower rise (3hr) and peak (6hr) and gradually decreases over 1 week; highest
sensitivity/moderate specificity
o Creatinine phosphokinase Myocardial fraction (CKMB) – quickly rises (peak 12-40hr) and
quickly falls (48-72hr); low specificity/moderate sensitivity; best used to diagnose re-infarction
o Note that in renal failure, the half-life of these enzymes will be increased
 EKG
o Left-anterior descending (LAD) – most common site of thrombosis; branch of Left coronary
artery; supplies anterior L.ventricle & anterior 2/3 of septum; V2, V3, V4 changes
 o Circumflex branch – branch of left coronary artery; supplies lateral/posterior L/ventricle and
left atrium (including SA node); aVL, V5, V6 changes
o Posterior Descending Artery – branch of right coronary artery (80% of people); supplies inferior
L.ventricle and posterior 1/3 of septum; II, III, aVF changes
Management
 Initial Steps (initial stabilization for STEMI or as total management for NSTEMI):
o Aspirin (chewed) + Clopidogrel + IIb-IIIa inhibitor – inhibits platelet aggregation
o Heparin – prevents further clot formation
o B-blocker – decrease heart rate/contractility (less O2 demand); contraindicated in shock
o Nitroglycerine – vasodilatation (decrease pre-load/afterload) to decrease O2 demand
o ACE inhibitor (or ARB if not tolerated) – prevents cardiac remodeling, reduces mortality
o Supplemental O2 – increase O2 saturation (if O2 sats are low)
o Morphine – alleviate pain (give if 3 doses of nitroglycerine don’t do the trick!)
o Atorvastatin – decreased cardiac events and speeds resolution of ST-elevation
 Percutaneous Coronary Intervention (PCI) - threading a catheter into the heart and inflating a balloon
on the end to open up a stenotic artery causing MI. A stent is usually placed to keep it upon until about
3 months when it’s removed, as the artery has adapted
o Indication
 STEMI – emergent PCI, always!
 NSTEMI – not needed unless pt has recurrent angina, CHF, high-risk findings, ejection
fraction <40%, hemodynamic instability, V-tach, PCI within past 6 months, or prior CABG
o Timing
 Within 90 minutes of onset of the MI; can be done up to 6hr with decreasing benefit
 If 90 minutes has passed, patient should be considered for IV tPA thrombolysis
o If PCI is unsuccessful  emergent CABG
 Coronary Artery Bypass Graft (CABG) – taking a blood vessel from somewhere else to create a route
around the area of blockage in the coronary artery
o Indication for emergent – rare
 presentation after 12hr of symptom onset
 cardiogenic shock upon presentation
 failure of PCI to resolve ischemia
o Indication for elective – more common
 >50% stenosis of L.main coronary or >70% stenosis in any coronary artery
 stenosis of the LAD + another coronary artery or stenosis of 3 or more coronary arteries
 obstruction at a place where you cannot stent (like a bifurcation point!)
o Best conduit for CABG is the internal mammary artery (off the subclavian) which 95% of these
guys are patient >10yrs post-CABG
 Greater saphenous vein, radial artery, and gastroepiploic arteries may also be used
 >2 coronary grafts being placed has been shown to increase long-term survival versus 1
o CABG is more invasive, but has better outcomes than stenting
 Use of aspirin, B-blockers, statins, and Abx post-op have better outcomes
 You must stop clopidogrel before CABG
o Preoperative shock, emergent surgery, >65%, and low LVEF denote higher M&M post-op
 Complication of MI include:
o Immediate - Cardiogenic shock, CHF (both often from cardiac hypomobility)
o 2-3 days – pericarditis, arrhythmia (V-fib most deadly; common cause of death the hospital)
o 3-14 days – cardiac tamponade, rupture (intraventricular septum, free wall, or papillary muscle)
o Long term – ventricular aneurysm, Dressler’s syndrome
Areas to get you in trouble
 Not evaluating for aortic dissection – note that Stanford Type A (toward the heart) can compress the
coronary vasculature and cause a full blown MI. CXR as initial work-up can help find this.

Chapter 6: Chest Pain + Syncope – Aortic Stenosis/Disease

Presentation
 Typical symptoms:
o Chest pain: LV hypertrophy may result causing increased O2 demand and angina
o Exertional syncope: pt will be doing something (jogging) and will get lightheaded/pass out
without confusion afterward
o Pulsus parvus et tardus (“delayed and diminished carotid pulse”): because the aortic valve is
obstructing bloodflow the carotid pulse will be delayed after the S1 sound; the bicuspid valve
closes but the blood won’t make it out of the heart until later
o Signs of CHF: pumping against that stenotic valve can cause buildup of pressure and LV
dysfunction result in typical CHF signs
 Heart Murmur: mid-systolic crescendo-decreshendo murmur; heard best in upper right sternal border
o Single/soft S2 with an S4: the S2 is diminished as the aortic valve doesn’t “click” shut, it’s fused
together. S4 from increased pressure of contraction to maintain perfusion (LVH)
o Intensity of the murmur has NO correlation with severity of disease
o Timing of murmur can indicate severity with later being worse (takes more systolic pressure to
finally pop open the valve)
o Valsalva (decreases sound with decreased preload), Handgrip (decreases sound with increased
afterload), and Leg raise (increases sound with increased preload)
o HOCM may mimic aortic stenosis but will be affected in the opposite way with
Valsalva/handgrip/leg raise.
 Special Signs
o Pulsus alternans – alternating strong/weak peripheral pulses. Occurs with LV dysfunction
(possible with aortic stenosis); poor ejection fraction in one beat leads to overfilling and better
ejection in the next beat
o Pulsus bisferiens – “double peak” pulse during systole seen with aortic regurgitation (can be
part of aortic stenosis). The mechanism is actually not well understood.
 IV drug use may be an important history component, as it may result in infective endocarditits
(discussed below). Valvular vegetations may result in outflow obstruction – stenosis.
Etiology
 Senile calcific aortic stenosis: accumulation of calcium deposits in the aorta due to aging. Only affects
people aged >70
 Bicuspid aortic valve: an inborn abnormality of the valve results in easier calcification…occuring in
those aged <70yr (usually younger than this though!). If the patient is in their 40s…has no history or
signs of Rheumatic fever…and has aortic stenosis  consider bicuspid aortic valve!
 Rheumatic heart disease: classic infectious cause of aortic stenosis, especially in immagrants with poor
healthcare! Presents with several signs and aortic stenosis (while uncommon and severe) can occur.
Will nearly always occur alongside mitral valve damage. Rheumatic damage to the aorta is actually less
commonly than bicuspid aortic valve!
Workup
 Labs: CMP, Coagulation panel, and cardiac biomarkers (troponin, CK-MB, BNP, and D-dimer) to check
for signs of underlying disease processes and CHF
 EKG to rule out MI or search for signs of heart failure
  Imaging
o CXR: can show signs of CHF (large heart, increased lung markings, etc.) and can rule out other
causes of chest pain (aortic dissection, etc.)
o Echocardiography: thickened aortic valve leaflets and hypokinesia of the heart
Management
 Asymptomatic aortic stenosis: medical control of HTN/cardiac risk factors; echocardiography every 3-
5yr; elective replacement of valve if undergoing heart surgery for another reason
o Note that while statins may help in decreasing complication risk, they DO NOT stop calcification
of the aortic valve. This process is not dependent on atherosclerosis!
 AS + CHF (“symptomatic AS”): immediate aortic valve replacement
Things to Get You in Trouble
 Drugs to avoid: any drug that decreases BP can result in significant hypotension in aortic stenosis
(diuretics, B-blockers, vasodilators, etc); thus decreased dosing with warning about this complication is
considered safe
 Elective non-cardiac surgery: remember that anesthesia causes vasodilatation (thus hypotension), thus
those with aortic stenosis may enter into shock under GAS; it’s important to identify AS pre-operatively
to avoid such a terrible complication

Tips From UWorld

4668: Infective endocarditis can present with weird, vague symptoms that may not be entirely obvious
 Systemic emboli (cerebral, pulmonary or splenic infarcts)
 Mycotic aneurysms or infections due to septic emboli
 Janeway lesions: nontender, red, raised lesions on palms/soles from emboli in superficial emboli
 Roth’s spots: hemorrhages of the retina from emboli
 Osler nodes: painful fingertips, sometimes with nodules
 Arthritis: swollen joints, especially of the hands/feet
 Proteinuria or hematuria from kidney damage
3068/3014: Infective endocarditis is easy to spot on exams but classic bacterial associations must be
memorized.
 S.aureus: implanted devices (catheters, valves, defibrillators, etc.) and IVDU
 Viridians Group Strep: dental/respiratory procedures, esp with previously damaged valve
 Coagulase-neg staph: implanted devices (catheters, valves, defibrillators, etc.)
 Enterococci: nosocomial UTIs (classic is after UG procedures)
 Strep. Bovis (gallolyticus): colon carcinoma/IBD

Chapter 7: Chest + Back Pain – Aortic Dissection

Risk Factors: hypertension, connective tissue disease (Marfan’s, Ehlers-Danlos), old age, atherosclerosis,
pregnancy, cocaine use, aortic injury, bicuspid aortic valve, or aortic coarctation
Presentation
 Classic Symptoms: sudden painful ‘tearing’ sensation in chest, radiating toward the back; uneven
pulses either between arms (aortic arch), or arm vs leg (infra-renal abdominal aorta)
 Symptoms due to surrounding tissue compression/involvement:
o Cardiac Ischemia (coronary arteries): signs of acute MI; most often the RCA
o Cerebral ischemia (brachiocephalic or carotid arteries): signs of stroke
o Spinal Cord Ischemia (Artery of Adamkiewicz): paraplegia
o Kidney failure (renal artery): oliguria, elevated BUN, elevated Cr
o Mesenteric Ischemia (SMA): out of proportion abdominal pain/nausea/bloody diarrhea
o Limb ischemia (subclavian or iliac arteries): 5 Ps of ALI
 o Aortic regurgitation (aortic root dilatation): widened pulse pressure/”water hammer pulse”
o Pericardial Tamponade (pericardial sac): hypotension, JVD, muffled heart sounds,
hepatojugular reflex, pulsus paradoxus, & electrical alterans; narrowed stroke volume (<30)
Pathophysiology
 Intimal Layer tearing is typically in inciting event in an aortic dissection; the small tear gives access to
the medial layer, allowing for high-pressure arterial blood to rip apart the aortic medial layer
 Formation of a false lumen with an inner layer (intima + inner media) and outer layer (outer media +
adventita) propagates down the aorta, causing symptoms
 Marfan’s syndrome (fibrillin-1 malformation) is one of the most common connective tissue diseases;
the malformation of connective tissue can cause cystic medial necrosis of the CT laden media later of
the aorta (needed for stretching to accommodate high pressure flow)
Classification
 Stanford classifications are based on how we would clinically treat a dissection
o Stanford A – any ascending aorta/aortic arch involvement (may also involve descending)
o Stanford B – only descending aorta involvement
 DeBakey classifications are based on more specific anatomic involvement
o DeBakey I – involves ascending/arch/descending aorta
o DeBakey II – involves only ascending aorta/arch
o DeBakey III – involves only descending aorta
Workup
 Labs: blood type/cross, cardiac biomarkers, EKG (these are to rule out other causes)
 Imaging
o CXR (first image): widened mediastinum (15-20% will be NORMAL)
o CT chest w/contrast: can show false lumen and better characterize location of disease
o MRI: may be used, but often less widely available in emergency settings
 If hemodynamically unstable: take to OR immediately for intervention; but get a transesophageal
echocardiography (TEE) in the OR to confirm diagnosis. If (+) then immediately proceed to operate
Management
 First Step: IV B-blocker – allows for decreasing BP to decrease propagation of dissection
o Contraindicated in tamponade or severe regurgitation (may result in severe hypotension
resulting in cardiac arrest or shock!)
 Type A dissection – urgent trip to OR for median sternotomy + aorta removal & grafting/aortic valve
replacement/coronary artery re-implantation (bad prognosis)
 Type B dissection – ICU admission with close blood pressure monitoring; open thoracotomy with
endovascular repair may be done should complications arise (good prognosis)

Chapter 8: Incidentally Discovered Adrenal Mass on CT scan

History and Physical
 Adrenal “Incidentaloma” – non-functional adrenal tumors are very common (85% of all adrenal
tumors) and about 5% of CT scans (and 10% of autopsies) will incidentally show an adrenal mass.
 Cushing’s Syndrome (ACTH) – central obesity, buffalo hump, moon facies, skin atrophy with purple
striae/ eccymoses/easy bruising, proximal muscle weakness, hypertension (mineralocorticoids),
glucose intolerance (glucocorticoids), skin hyperpigmentation, women may have hirsutism/menstrual
irregularities
 Conn’s Syndrome (aldosterone) – hypertension (increased Na+), hypokalemia, high aldosterone, low
renin, adrenal changes on CT scan, and metabolic alkalosis (hypoK increases bicarb reabsorption/H+
secretion)
  Pheochromocytoma (Epi/Noreepi) – episodic hypertension, palpitations, sweating, pallor classically
with increase intraabdominal pressure (urination, palpation, positional change) or anesthesia/surgery
 Adrenocortical Carcinoma – often grow unnoticed until lethal; 60% are functional (Cushing’s syndrome
>>> virilization > feminization) but may be non-functional (abdominal mass, abdominal pain, nausea,
anorexia, early satiety); typically they’re >6cm on abdominal CT
Pathophysiology
 Functional regions of the Adrenal Cortex (GFR  Salt, Sugar, Sex)
o Glomerulosa – mineralocorticoids
o Fasiculata – glucocorticoids
o Reticularis – sex hormones
 Adrenal medulla synthesizes catecholamines (epinephrine, norepinephrine, etc.)
Imaging
 CT scan with fine cuts preferred; but MRI is an acceptable alternative
 Benign lesion: size <4cm, homogenous appearance, well-defined borders, high levels of intracellular
lipid (based on Hounsfield unit density), rapid washout of contrast, low vascularity
 Malignant Lesion: size >6cm, irregular borders, necrosis/calcification/hemorrhage in the mass, ill-
defined borders, invasion of adjacent tissue, low intracellular lipids, high vascularity
Management for a non-functional adrenal mass
 Size - <4cm (watch with interval CTs), 4-6cm (either watch or resect based on perioperative risk), >6cm
(resect as it’s more likely to be malignant)
 Follow-up imaging if not resecting  6, 12, 24 months
 Follow-up labs if not resecting  every year for 4 years
Adrenalectomy
 May be done laproscopically, but open is preferred in malignancy or in tumors >8cm
 Adrenal blood supply is from inferior phrenic artery (superiorly), aorta (medially), and the renal artery
(inferiorly)
 Venous drainage
o Left adrenal vein  left renal vein  IVC
o Right adrenal vein  IVCf.

2592/4721/4419: Cushing’s Syndrome

 Presentation: central obesity, buffalo hump, moon facies, skin atrophy with purple striae/
eccymoses/easy bruising, proximal muscle weakness, hypertension (mineralocorticoids), glucose
intolerance (glucocorticoids), skin hyperpigmentation, women may have hirsutism/menstrual
irregularities
o Labs: hyperglycemia, hypokalemia
 Etiology: exogenous corticosteroid administration (most common), ACTH-producing tumor (Pituitary
adenoma “Cushing’s disease”), ectopic ACTH-production (small-cell lung cancer), or adrenal
adenoma/hyperplasia
 Dx:
o Establish hypercortisolism with midnight salivary cortisol assay (positive is >5mcg), 24-hr free
urine cortisol (positive is >150mcg), and low-dose dexamethasone suppression test (positive is
>5mcg in morning following dexamethasone admin)  2/3 must be positive for diagnosis
o If hypercorticolism present  ACTH level measurement (positive is <5 pg/mL) to see if process
is ACTH dependent or independent
o If ACTH is elevated  high-dose dexamethasone suppression test to determine if source of
ACTH is pituitary (will be suppressed) or ectopic (won’t be suppressed, likely lung cancer)
 Imaging: CT scan with fine cuts; but MRI is an acceptable alternative
  Tx: aimed at underlying cause, but likely resection of the mass
o Note that glucocorticoid replacement perioperative/postoperatively is required due to tumor’s
suppression of normal adrenal function, possibly for months/years following surgery!

3231/2725/3230/3832/8897: Hyperaldosteronism
Primary Hyperaldosteronism (Conn’s syndrome)
 Typically, from an adrenal adenoma or bilateral adrenal hyperplasia
 Presentation: hypertension (increased Na+), hypokalemia, high aldosterone, low renin, adrenal
changes on CT scan, and metabolic alkalosis (hypoK increases bicarb reabsorption/H+ secretion)
 Dx: CT findings + aldosterone:renin ratio >20 or persistently elevated after oral saline/oral salt tablet
administration (would normally be suppressed by the Na coming in)
o Adrenal venous sampling can distinguish bilateral from unilateral dysfunction
o Best first test is the aldosterone:renin ratio
 Tx:
o Unilateral: surgical excision
o Bilateral or surgery not an option: aldosterone antagonists (K-sparing diuretics) spironolactone
or eplerenone (note that spirono has anti-androgen effects, but eplerenone will have less of
these. Spirono is still the preferred first-line treatment)
 Note that these patients may be on a non-K-sparing diuretic simply because they seem to have
hypertension. But K-wasting due to diuretic use will not approach the degree that
hyperaldosteronism will achieve. Often the two combined will cause the hypokalemia

Secondary Hyperaldosteronism
 Typically, from reno-vascular HTN, malignant HTN, renin-secreting tumor, or diuretic use (basically the
kidney’s normal response to poor perfusion)
 Presentation: hypertension (increase Na+), hypokalemia, high aldosterone, high renin

Pseudo-hyperaldosteronism
 What looks like aldo, smells like aldo, but isn’t aldo? Basically things that increase other “corticoids”
that aren’t mineralocorticoids…but can act as mineralocorticoids. CAH, deoxycortisone-secreting
tumor, Cushing’s syndrome, or exogenous mineralocorticoid use
 Presentation: hypertension (increase Na+), hypokalemia, low aldosterone, low renin

3598/2170: Androgen Producing Adrenal Tumor

 Women generate androstenedione (AS)/dehydroepiandrosterone (DHEA)/testosterone (T) in the
adrenals and the ovaries. Dehydroepiandrosteone-sulfate (DHEA-S) is only produced in the adrenals,
thus elevated DHEA-S is the most specific for an adrenal androgen producing tumor
 Presentation: signs of virilization (pubertal hair, menstrual suppression, cliteromegaly), negative
pregnancy test, and no abnormalities of the uterus/ovaries
 Dx: adrenal tumor on CT scan with presentation
 Tx: excision

Chapter 9: Fatigue, Constipation, and Depressed Mood – Hypercalcemia/Hyperparathyroidism

Differential for Hypercalcemia
 Thyrotoxicosis (most common outpatient) – hypermetabolic state causing increased bone breakdown
 Primary hyperparathyroidism – results in too much PTH secretion (familial, sporatic, or in MEN 1 or 2)
 Malignancy (most common inpatient)
o PTH-rP secretion (80%) – effectively too much PTH secretion (lung, head&neck, renal cancers)
 o Direct osteolysis (20%) – cancer spreads to the bone causing breakdown (breast, multiple
myloma, prostate cancer)
 Hypervitaminosis A – works on RAR or RXR receptors to stimulate osteoclasts/inhibit osteoblasts,
resulting in increased bone turnover (vitamin A over-supplementation or Analogue acne treatments)
 Immobilization – poorly understood, but thought to be a lack of osteoblast activation due to poor
bone stimulation without loss of osteoclast activation. (post-surgery, elderly, paralyzed for any reason)
 Paget’s Disease of Bone – excessive remodeling of bone causing large Ca2+ release into serum
 Hypervitaminosis D – increased absorption of Ca2+ (over-supplementation)
 Granulomaous Disease (Sarcoid, TB, Hodgkins disease) – epitheliod histiocytes/granulomas can
convert 25-OH VitD  1,25-OH VitD
 Milk-alkali syndrome – calcium over-supplementation (Ca-antacids or osteoporosis supplements)
 Mediations
o Thiazides (HCTZ or chlorthalidone) – decreased calcium excretion based on mechanism
o Lithium – poorly understood, but may affect both the kidney and parathyroids
 Rhabdomyolysis – massive myocyte hemolysis causing Ca2+ release into blood
 Adrenal Insufficiency – poorly understood; possibly from hemoconcentration secondary to loss of
aldosterone production and diuresis

Anatomy and Embryology of the Parathyroid Glands

 Superior Parathyroids – 4th pharyngeal pouch; 95% located adjacent to the tubercle of Zuckerkandl
posterior to the terminus of the recurrent laryngeal nerve; 5% along esophagus, prevertebral fascia,
near the super thyroid artery, or intrathyroidal
 Inferior Parathyroids – 3rd pharyngeal pouch; less consistent with location (65% on inferior thyroid
gland, 35% on thymus, thyrothymic ligament, carotid sheath, behind the esophagus or partially
intrathyroidal)
 15% of people will have more than 4 parathyroid glands!

4308/4134/4309/3102: Evaluation of Hypercalcemia

 Step 1: Confirm hypercalcemia (repeat Ca2+ level/measure serum albumin to correct for it)
 Step 2: Determine the source (measure PTH)
o High/normal PTH: PTH dependent hypercalcemia
 Primary hyperparathyroidism, familial hypocalciuric hypercalcemia, or lithium
o Low PTH: PTH independent hypercalcemia
 Malignancy (Ca >15) from bone mets or PTHrP production (suppression of PTH)
 Vit D toxicity (too much Ca++ retaining), granulomatous diseases (makes Vit. D),
thiazide toxicity (Ca+ resorbtion), milk-akali syndrome (over ingestion of Ca++),
thyrotoxicosis (increased bone resorbtion), Vit. A toxicity (direct osteoclast simulation
in high doses), prolonged immobilization (increased osteoclastic activity without
matching osteoblastic activity) – often more mild elevations

3083: DON’T FORGET!!! THIAZIDE DIURETIC HYPECALCEMIA IS MILD AND WON’T CAUSE SYMPTOMS.

2599: Treatment of Hypercalcemia

 Mild (<12), Moderate (12-14) or asymptomatic – no emergent treatment. Avoid diuretics/lithium and
give hydration to ensure hemoconcentration does not occur. Initiation of bisphosphonates helps slow
osteoclastic activity and decrease risk of pathologic. Classically due to bone lesions from metastatic
cancer.
  Severe (>14) or symptomatic (hypercalcemic crisis) – immediately give IV saline + calcitonin (dilute it
out)  after euvolemic, loop diuretics to aid in peeing out Ca2+  Long-term give bisphosphonates to
decrease the amount of Ca2+ being introduced to the body through bone resorption.

Hyperparathyroidism is a common cause, especially on tests; so let’s examine how it happens:

 1o – typically parathyroid adenoma (one dominant thyroid gland with other atrophy)
o Constitutional PTH overproduction; kidney responds to it
o Hyper-calcemia, hypo-phosphatemia, high PTH
 2 – hypocalcemia or low Vit.D; classically from end-stage renal failure; parathyroid glands are normal
o

sized
o PTH overproduction via physiologic response to low Ca2+; kidney responds poorly
o Normal/hypo-calcemia & hyper-phosphatemia, high PTH
 3 – long-standing renal failure resulting in constitutional parathyroid hyperplasia with symptoms
o

present after with renal transplant to correct the problem

o Parathyroids got so ripped during time of secondary hyperparathyroidism, they can’t stop
pumping out PTH…so the underlying cause is fixed, but parathyroids are still crushing it
o Hyper-calcemia, hypo-phosphatemia, low PTH

2176/4304: Primary Hyperparathyroidism

 Presentation: typically, asymptomatic, but may present with fatigue, constipation, abdominal pain,
renal stones, bone pain, or neuropsychiatric symptoms
o “Stones, bones, groans, psychiatric overtones”  Hypercalciuria (renal stones), bone pain
(resorption of calcium from bone), nausea/vomiting/constipation/pain (intense absorption)
and confusion/depression/psychosis/sleep disturbance/memory impairment/stupor/coma
(often represents hypercalcemic crisis!)
o Typically found in post-menopausal women
o Labs: hypercalcemia, low phosphate elevated PTH, elevated chlorine, elevated urinary calcium
excretion
 Serum Cl:Phos ratio of >33 is suggestive of hyperparathyroidism (PTH causes excretion
of bicarb and phosphate alongside resorption of chloride and calcium)
 DEXA scan may show osteopenia/osteoporosis
o MEN1a (menin mutation) or PRAD1 mutation is associated with parathyroid adenoma! Note
that MEN1a will likely cause all 4 parathyroids to be mutated and possibly abnormal
 Physiology: PTH causes excessive Vit D activation, leading to renal calcium resorption, GI absorption,
and bone breakdown
 Etiology: parathyroid adenoma (or other tumor), parathyroid hyperplasia
 Dx: diagnostic labs with clinical picture
o Sestamibi scan (99-m Technetium) – radioactive scan that can show abnormal parathyroid
activity. May also by take up by thyroid gland, obscuring parathyroid localization.
o Ultrasound may also be used to localize parathyroid adenomas
 Tx:
o Medical – bisphosphonates used to decrease response to PTH in the bones with regular
monitoring of electrolyte levels and DEXA scanning
o Surgical - parathyroidectomy if symptomatic (osteoporosis, renal manifestations), age <50,
extremely high serum (>1mg/dL) or urine (>400g) calcium, BMD with T-score of -2.5 at any site.
Or if patient cannot undergo surveillance
  May be removal of adenoma (if present) or if 4-gland hyperplasia, removal of 3.5 glands
with the last 0.5 of a gland implanted into the arm or SCM. If patient develops high PTH
again, doing surgery again is less risky in those implantation spots
 Note that even if localizing scans are negative, surgery can still be considered with high
suspicion
 Complications – hematoma, hoarseness (recurrent laryngeal), perioral numbness, or
tingling in the fingers (hypocalcemia)
 If post-op hypocalcemia: Ca2+ supplementation post-op & hospitalization to monitor

2165: Familial Hypocalciuric Hypercalcemia

 Benign, autosomal dominant mutation in the calcium-sensing receptor (CaS-R) of the parathyroid
glands. This causes increased elevation of serum Ca2+ to activate them to stop PTH secretion. This
results in increased Ca2+ resorption in the renal tubules
o Differentiated from primary hyperparathyroidism by calcium urine excretion
 Presentation: asymptomatic with normal renal function
o Labs: hypercalcemia with low urine calcium excretion (<100mg/24hr)
 Dx/Tx: lab abnormalities, no treatment needed in the absence of symptoms

4307: Hyperthyroid Bone Disease

 Excess thyroid gland activity sitmulate osteoclastic acivity, thus causing bone resorbtion. The resulting
hypercalcemia inhibits PTH production ultimately leading to hypercalciuria and net calcium wasting.
 Brittle bones, tenendcy toward bone fracture, and decreased bone density are all possible problems!
 Note that a hot nodule (functional, likely toxic goiter) is nearly NEVER NEOPLASTIC, as it’s an area of
isolated hyperacitivty/hypertrophy. A cold nodule is an area of low activity but growth, which is high
suspicious of thyroid cancer.

3083: Milk-Alkalai syndrome

 Occurs due to over-supplementation with calcium and absorbable alkalai. Essentially you take too
much result in renal vasoconstriction, decrease in GFR, Na/K/2Cl inhibition (diuresis)
 Presentation: N/V, constipation, polyuria/polydipsia, AKI, suppressed PTH in the setting of calcium
supplementation (this patient was taking supplements for osteoporosis)
o Labs: hypercalcemia, hypomagnesiemia, hypophosphatemia, metabolic alkalosis
 Dx: clinical presentation
 Tx: discontinue supplementation with IV fluids/furosemide to flush out the kidneys
Hyperthyroidism-Jaw Tumor syndrome
 Odd genetic condition that predisposes patients to parathyroid carcinoma + fibroma of the jaw
 May be predisposed to other cancers

8876: Hypocalcemia
 Presentation: fatigue and weakness; may classically occur after parathyroidectomy to treat
hypercalcemia
o Labs: low Ca2+
o Chvostek’s sign – facial twitch in response to tapping the facial nerve (early tetany sign due to
hypersensitivity of neurons)
o Trousseau’s sign – flexion of fingers/wrist in response to inflation of a blood pressure cuff
 Dx:
o Low magnesium? Drugs that cause hypoCa? Recent Blood transfusion?  correct it if yes.
 o If no, measure PTH level
 Low/normal PTH – surgical damage to parathyroids, autoimmune destruction of
parathyroids, or some infiltrative disease (Wilson’s, hemochromatosis, etc.)
 High PTH – Vit D deficiency (check 25-Vit D levels), CKD, sepsis, tumor lysis syndrome

Chapter 10: Intermittent Episodes of Sweating, Palpitations, and Hypertension

3976: Pheochromocytoma
 Neuroendocrine tumor of chromaffin cells producing catacholamines (typically Epi/Noreepi)
o Association with MEN2a/MEN2b, Neurofibromatosis type 1, and von-Hippel-Lindau
 Presentation: “pressure (episodic OR constant hypertension), palpitations, perspiration, pallor, pain
(headache)”, classically with increase intraabdominal pressure (urination, palpation, positional
change) or anesthesia/surgery (may present with intra-operative crisis!)
o Constant HTN = catecholamines are slowly/constantly released
o Episodic HTN = catecholamines are released in bursts with elevated intra-abdominal pressure
o May rarely produce dopamine which does NOT present with hypertension, but instead shows
water diarrhea as the major symptom due to gastric hyper-motility
o Labs
 Elevated hematocrit (constant a-activity or EPO production) and hyperglycemia
(constant a-activity) are common lab abnormalities
 Anatomy
o Adrenal medulla > abdomen > bladder/prostate > thorax > head/neck
o Commonly, abdominal pheo occur in the para-aortic Organ of Zuckerkandl explaining an
alternative name for the tumor of “para-gangliomas”
o These tumors theoretically can occur anywhere along the sympathetic nervous system
 Pathophysiology
o Norepinephrine/Epi will stimulate all of the following receptors
 a1 receptors – smooth muscle contractions, gluconeogenesis/glycogenolysis
 a2 receptors – smooth muscle contraction, platelet aggregation
 B1 receptors – increasing heart rate/contractility, sweat gland activation
 B2 receptors – smooth muscle relaxation
o Note that norepinephrine is produced predominantly, as N-methyltranferase (converts norepi
 epi) isn’t always very present in tissues where the pheochromocytoma pops up
o The adrenals are a common place for pheo because norepi production is dependent on
glucocorticoids…which are produced in high concentrations in the adrenals
 Imaging: CT or MRI abdomen/pelvis with contrast
o Nuclear imaging (I131-MIBG or 18F-DOPA PET/CT) can be used for better imaging & localization
of other areas of neoplastic growth
 Dx: 24hr urine metanephrines (>x2 normal limit) +/- imaging of mass
o Biopsy is NOT advised as it can set off a hypertensive episode
o Note that b-blockers, decongestants, antidepressants, and antipsychotics can all cause false
elevation of catecholamines and should be discontinued 2 weeks prior to testing
o Plasma chromogranin A may be a useful adjunctive test
o Metanephrines = metanephrine, normetanephrine, and vanillylmandelic acid
 Tx: pre-treatment of phenoxybenzamine and surgical removal
o Must give a-blockers for 10-14 days before surgical removal (phenoxybenzamine)
o Beta blockers alone will cause hypertensive crisis (Epi/noreepi activate a-receptors)
o In a patient with multiple tumors (like MEN2), the pheochromocytoma is taken care of first!
  Follow-up:
o Pts should always be referred to genetic counselling with testing after surgical resection
o Catecholamine levels should be measured 2 weeks post-surgery to measure success; then every
3 months for the first year, then every 1 year
o Complications include hypertension (residual disease), hypotension (residual a-blockade, loss of
catecholamines), hypoglycemia, and arrhythmia

3587/3520/2630/3494: Multiple Endocrine Neoplasia (MEN)

 MEN1:
o Primary Hyperparathyroidism (hypercalcemia, high urine calcium, high PTH)
o Enteropancreatic tumors (most commonly gastrinoma causing Zollinger-Ellison syndrome;
VIPoma, glucagonoma, and insulinoma all possible)
o Pituitary adenomas (most commonly prolactin secreting)
 MEN2a: RET-protooncogene mutation
o Medullary Thyroid Cancer (parafollicular C-cells, produce calcitonin)
o Pheochromocytoma (elevated plasma metanephrines, episodic hypertensive crises),
o Parathyroid Hyperplasia
 MEN2b: RET-protooncogene mutation
o Medullary Thyroid Cancer
o Pheochromocytoma
o Mucosal/cutaneous neuromas, Marfanoid habitus

Chapter 11: Neck Mass that Moves with Swallowing

Hyperthyroidism
 Signs: progressive nervousness, difficulty concentrating, palpitations, weight loss, moist skin, fine
resting tremor, dyspnea on exertion, diarrhea, and heat intolerance
 Symptoms: Rapid pulse, elevated BP (systolic > diastolic), and rarely atrial fibrillation
Hypothyroidism
 Signs: lethargy, depressed affect, sluggish mentation, forgetfulness, weight gain, dry skin, constipation,
cold intolerance; may be confused with depression (women) or dementia (elderly)
o 1o hypothyroidism will show a high TSH but low T3/T4 (poor thyroid function)
o 2o hypothyroidism will show a low TSH  TRH administration is used diagnostically
 A normally functioning pituitary will respond and TSH will rise. If it doesn’t then there’s
something wrong with the pituitary (get imaging of the pituitary)
 If the pituitary responds then there may be something wrong with the hypothalamus
(not making TRH, thus no TSH production)
 Symptoms: low blood pressure, bradycardia, non-pitting edema, hair loss, dry/cracked skin, slowly
relaxing reflexes, and rarely myoedema
 Tx: thyroid hormone replacement (typically 1.7 mcg/kg daily)
o Children (use a lot for growth) and pregnant women (increased TBG) may need increased doses
o Elderly (decreased TBG) may need decreased doses
o TSH is regular follow-up for adequate response 4 weeks after any changes in dose

4324/4588: Evaluation of Hyperthyroidism

 Any suspicion of thyroid problems should begin with TSH/T4 lab values
o TSH low/T4 normal with signs of hyperthyroid  measure T3
 Normal T3  subclinical hypothyroid, early pregnancy, non-thyroid problem
  High T3  If signs of Grave’s disease, it’s Grave’s disease. If no signs, do a Radioactive
Iodine Uptake (RAIU) scan
o TSH low/T4 high with signs of hyperthyroid  consider primary hyperthyroidism
 If signs of Grave’s Disease, then you’re good; if not then RAIU scan
o TSH normal - high/T4 high with signs of hyperthyroid  consider secondary hyperthyroidism
 MRI of pituitary for TSH secreting tumor
 Radioactive Iodine Uptake (RAIU) scan performed when hyperthyroid is considered, but Grave’s
disease is not likely due to symptoms
o Low uptake  measure thyroglobulin (Tg) levels
 Low Tg  likely exogenous use of thyroid hormone
 High Tg  thyroiditis, extra-glandular production, or iodide exposure
o High uptake diffuse  Grave’s disease
o High uptake nodular  Toxic adenoma, or multinodular goiter

4324: Central Hyperthyroidism (TSH secreting adenoma)

 Presentation: signs of hyperthyroidism (weight loss, tachycardia, palpitations, etc) with tumor mass
effect signs (headache, visual symptoms, impaired secretion of other pituitary hormones)
 Dx: TSH high with high T4 & MRI showing mass location
 Tx: surgical excision or ablation

4415/3488/4726/4132/2179: Grave’s Disease

 Presentation: hyperthyroidism, exophthalmos, diffusely enlarged thyroid gland
o Low TSH with high T3 or T4
 Dx: clinical picture with confirmed TSH receptor-antibodies
 Tx: three major options
o Radioiodine ablation – basically goes in and destroys the thyroid gland cells. Apparently the
point of this treatment is to become euthyroid and complete destruction is NOT intended.
However, pts very often have the side-effect of hypothyroidism.
 Initial worsening of symptoms/exophthalmos (10%) in first week or so due to release
of stored thyroid hormone from cell destruction. Often OK in young, healthy pts.
 Pre-treatment with glucocorticoids often minimizes treatment symptoms
 Hypothyroidism (80%) may develop, and is most likely in Grave’s Disease as the entire
thyroid gland is dysfunctional, instead of just part.
o Surgery – removal of the thyroid is always on the table
 Risk of damage to recurrent laryngeal nerve or hypoparathyroidism due to damage or
unintentional removal of parathyroids
o Propylthiouracil (PTU) or methimazole (MMA) – thioamides that block production of T3/T4
 MMA a teratogen in the 1st trimester, may cause cholestasis
 PTU can cause hepatic failure, ANCA-associated vasculitis, and agranulocytosis
 Does not permanently cure disease. Typically used in pts that cannot tolerate other
treatments (old people that cannot handle worsening symptoms or surgery)

2178/3487: The life-threatening side-effect of Propylthiouracil/Methimazole is agranulocytosis (0.3%). This

classically presents with fever and sore throat within 90 days of treatment initiation. Should this occur:
1. Stop PTU/MMA immediately and check WBC levels.
a. WBC >1,500 – PTU isn’t causing the problem
b. WBC <1000 – PTU should be discontinued for life
 2. Get throat culture, give oral penicillin/acetaminophen, administer broad spectrum antibiotics before
even knowing the result as lack of immune response could be fatal. Pseudomonas is especially
worrysome in these patients

3952: Thyrotoxicosis can largely affect the heart causing changes in rhythm (atrial fibrillation, PACs/PVCs, and
sinus tachy), hemodynamics (increased CO  systolic HTN and increased myocardial O2 demand), heart
failure, and angina.

4307: Hyperthyroid Bone Disease

 Excess thyroid gland activity stimulate osteoclast activity, thus causing bone resorption. The resulting
hypercalcemia inhibits PTH production ultimately leading to hypercalciuria and net calcium wasting.
 Brittle bones, tendency toward bone fracture, and decreased bone density are all possible problems!
 Note that a hot nodule (functional, likely toxic goiter) is nearly NEVER NEOPLASTIC, as it’s an area of
isolated hyperacitivty/hypertrophy. A cold nodule is an area of low activity but growth, which is high
suspicious of thyroid cancer.

4286/10958/11277: Thyroid Storm

 Presentation: high fever, cardio (tachycardia, HTN, CHF, atrial fibrillation), CNS (agitation, delirium,
coma), hyperthyroid (goiter, lid lag, tremor), GI (nausea, vomiting, diarrhea, jaundice)
o Typically caused by: thyroid/non-thyroid surgery, acute illness, childbirth, or acute iodine load
(such as in IV contrast!)
o Most common cause of death is high output cardiac failure (often post-op patients with
undiagnosed Graves’ disease)
 Dx: clinical presentation with precipitating factor
 Tx: propranolol (decrease adrenergic effects), propylthiouracil (decrease thyroid hormone
production), glucocorticoids (suppress TRH/T3T4 conversion), and ID trigger to treat/remove

3483: Metabolic changes in hypothyroidism include hyperlipidemia (decrease in LDL receptors),

hyponatremia, and asymptomatic elevations of CK (>10x normal).
 Note that hyperlipidemia may persist for months despite adequate replacement therapy
 Statins will increase the chance of hypothyroid myopathy, thus are used with caution

3878/4382: Hypothyroid Myopathy

 Presentation: normal hypothyroidism signs with elevated CK (mild) to rhabdomyolysis/polymyositis
o CK elevation can be present years before clinical signs of hypothyroidism
o Typically, normal reflexes
 Dx: any pt with unexplained elevated CK/myositis should have TSH/T4 checked as this may be the
manifestations of hypothyroidism early on.
o If normal, then muscle biopsy should be considered
 Tx: treat underlying cause

4154: Oddly enough, oral estrogen replacement therapy will increase Thyroid Binding Globulin (TBG) levels
due to decreased breakdown of TBG in the liver.
 Pts with a normal thyroid function will make more and compensate without trouble.
 Pts on levothyroxine for hypothyroidism will have to increase the dose (as the TBG increase will mean
less free T4 present). The increased dose will saturate the increased TBG, and restore euthyroidism.
 *transdermal estrogen does not have this effect as it bypasses the liver
3495: Euthyroid Sick Syndrome (“Low T3 syndrome”)
 Presentation: acute, severe illness accompanied by abnormal thyroid function tests
o Labs: low T3 with normal T4 and TSH
o Result of of decreased deiodination of T4 from caloric deprivation, glucocorticoids, and acute
phase reactants
 Dx: typically thought to be hypothyroidism, but often thyroid levels are unreliable in acute illness
 Tx: treatment of underlying disease should resolve the abnormal tests

3496: Thyroiditis
Hashimoto’s Thyroiditis
 Presentation: predominantly hypothyroid symptoms with non-tender diffuse goiter
 Dx: Anti-thyroid peroxidase (TPO) or anti-thyroglobulin antibodies in high-titer
o Note that nearly 10% of the normal population is (+) for anti-TPO antibodies
o The most common cause of hypothyroidism is the USA
Silent (painless) Thyroiditis
 Presentation: variant of Hashimoto’s with a mild, brief hyperthyroid phase (destruction and release of
T3/T4), with a small, non-tender goiter and slowly going back to euthyroid
 Dx: Anti-TPO antibodies and low radio-iodine uptake
Subacute (DeQuervain’s) thyroiditis
 Presentation: post-viral inflammatory disease causing prominent fever / hyperthyroidism with
painful/tender goiter
 Dx: presentation with elevated ESR/CRP and low radioiodine uptake

2191: Struma Ovarii

 Rare thyroid hormone producing ovarian teratoma. Classically in women over age 40 with pelvic mass,
ascites, and abdominal pain

4318: Toxic Adenoma

 Presentation: thyrotoxicosis with single hot thyroid nodule on exam
 Dx: demonstration of single, hot nodule on radioactive iodine scan
o Note that toxic multinodular goiter would have a patchy distribution on RAIU scan
 Tx: ablation or removal

Evaluation of a Thyroid Mass

 Always start with careful H&P and TSH/T4 levels to get your baseline for thyroid function
 Imaging: bedside ultrasound (characterize mass, lymph nodes, and guide FNA)
o If signs of malignancy  consider cross-sectional CT or MRI
o Nuclear imaging (I123 RAIU scan) may be useful to differentiate a “hot” from “cold” nodule, but
apparently aren’t as widely used today; most useful when FNA is non-diagnostic
 Fine needle aspiration (FNA)
o Yes: Nodules >1cm, malignant ultrasound features (microcalcification, hypoechoic, irregular
margins), or with recent history of growth
o Yes: suspicious cervical lymph nodes
o No: <1cm, purely cystic, benign sonographic features
 Interpreting FNA results & Management
o Malignant  total thyroidectomy with possible neck dissection
o Suspicious for malignancy  totally thyroidectomy OR diagnostic thyroid lobectomy
o Suspicious for follicular neoplasm  diagnostic thyroid lobectomy
  Simple biopsy is NOT recommended as you’ll likely not be able to control bleeding, you’ll
likely seed the tumor cells, and lobectomy doesn’t affect thyroid function
o Undetermined significance (AUS/FLUS)  Repeat FNA (often benign); if still undetermined,
proceed to diagnostic thyroid lobectomy
o Benign  annual follow-up + ultrasonography
o Inadequate  Repeat FNA (often benign); if still undetermined, proceed to diagnostic thyroid
lobectomy

3498/3499/3497: Thyroid Malignancy

 Papillary – arises follicular cells (epithelial), unencapsulated, most common, best prognosis
o Typically metastasizes to the lymph nodes, but prognosis is based on local invasion presence
o Increased risk from family history and childhood radiation of head/neck
o FNA often reveals large cells with pale, grooved nuclei; Often has Psamomma bodies
o Management  lobectomy if small (<1cm); total thyroidecetomy if large, multiple nodules,
high malignancy, family history, or history of ionizing radiation
 Concentrates iodine (thus this may be used therapeutically)
 Follicular - arises follicular cells (epithelial), encapsulated, decent prognosis
o Early hematogenous spread (lung/brain/bone) and invasion of thyroid capsule
o FNA often shows normal looking follicular cells. Invasion through capsule/hemotgenous
spread is necessary for diagnosis of carcinoma (vs adenoma), thus surgical diagnosis must be
made to see if invasion outside the capsule occurs (FNA/frozen sections are non-diagnostic)
o May demonstrate Hurthle Cells (large eosinophilic epithelial cells; worse prognosis!)
o Management  total thyroidectomy
 Concentrates iodine (thus this may be used therapeutically) unless it’s a Hurthel cell
subtype (these rarely concentrate iodine)
 Medullary – parafollicular c-cell origin, good prognosis, produces calcitonin, 80% are sporadic
o Associated with MEN2a/MEN2b; screening for these diseases is recommended
o Typically contains amyloid & commonly spreads to regional lymph nodes
o Symptoms often include diarrhea and flushing due to high calcitonin levels!
o Management  total thyroidectomy
 Does NOT concentrate iodine (it’s make of C-cells!!)
 Anaplastic – epithelial origin, rare, classically in old people
o Poor prognosis, death within 6 months typically
o May involve other adjacent structures (trachea/esophagus/etc.) due to rapidly enlarging
thyroid mass
o Management  often palliative but can include tumor shrinking therapies for symptom
management. Often early tracheostomy is done as tumor invades airway!
 Primary Thyroid lymphoma – rare, typically in the setting of Hashimoto’s thyroiditis
o Has rapidly enlarging thyroid gland but good prognosis
o Typically occurs as B-cell non-Hodgkin lymphoma
 Metastases to the thyroid – primary often the kidney, breast, lung, or skin (melanoma)
 Fast facts
o Note that because thyroid cancers are often indolent, it can be prudent to wait till after
pregnancy to evaluate and treat the problem in a pregnant woman
o The greatest risk factor for thyroid cancer is exposure to ionizing radiation before age 15. The
developing thyroid gland is very sensitive to mutagenesis. Most common sources are childhood
radiation exposure, lymphoma treatment, and nuclear fallout
o Typically, patient with thyroid carcinoma are euthyroid!
 o Worrisome sign is that the thyroid mass does not move on swallowing. This can indicate that
the mass has invaded local tissue and is not moving alongside the thyroidcartilage/lig. of Berry
o Frozen sections are typically NOT useful in evaluating thyroid cancer! Most cancers can be
diagnosed via FNA, and with follicular (FNA won’t work), the frozen section will only show a few
slices…making evaluation of the capsule impossible.
o If lymph nodes are palpable, they should be dissected out with either lateral or central neck
dissection. Frozen section IS helpful when used on suspicious lymph nodes
 Post-surgical management
o Radioactive iodine ablation  useful only in tumors that concentrate iodine, but can reduce
recurrence
o Suppressive thyroxine therapy  suppresses TSH, thus suppressing thyroid tissue growth
 Follow-up
o Thyroglobulin and anti-TG antibody tests every 6 months
o If medullary carcinoma  serum calcitonin every 6 months
o Neck ultrasound every year
 If recurrence  labs + ultrasound eval + RAIU scan

Complications of Thyroid Surgery

 Recurrent laryngeal nerve damage – branch of CNX; innervates most larynx muscles below vocal
cords, thus damage results in vocal cord paralysis. Unilateral damage = hoarseness & aspiration risk;
bilateral damage = airway compromise needing tracheostomy
 External branch of superior laryngeal nerve damage – allows speaking/singing in high pitch; often
damage isn’t a big deal unless patient is a singer/voice professional
 Parathyroid glands damage – hypoparathyroidism needing calcium/calcitrol supplementation
 Post-op ‘tense’ looking wound – likely from hematoma and may cause airway compromise. Needs
emergent bedside decompression with return to OR for evacuation/irrigation/hemostasis

Chapter 12: Progressively Hoarse Voice – Laryngeal Cancer

Differential for Hoarseness
 Viral laryngitis – acute fever, hoarseness, sore throat, cough or other URI symptoms (most common)
 Vocal Cord Paralysis – hoarseness with breathy voice & no other obvious signs; typically idiopathic or
iatrogenic (recurrent laryngeal nerve damage)
 Vocal cord nodules/polyps/cysts – often due to damage to vocal cords (singing/screaming/intubation)
 HPV of the vocal cords – unfortunate but totally possible (typically HPV 6 or 11)
 Spasmodic dysphonia or Parkinson’s Disease – often more ‘vocal tremor’ but may sound hoarse
 Laryngeal Cancer – often hoarseness in older person, Hx of smoking, +/- lymphadenopathy
Presentation
 Hoarseness, Hx of tobacco/alcohol use, hemoptysis, possibly cancer ‘B signs’ (weight loss, etc.)
 Characterizing “hoarseness”
o Breathy – incomplete closure of vocal cords causing excess air to escape when phonating.
Often the result of one vocal cord being dysfunctional
o Aphonia – inability to phonate due to lack of airflow, can be from locked-in abduction, swelling
(causes stiffening so they can’t move), or irregularities of the vocal cords stopping vibration
o Strained – narrowed vocal cords like forced adduction or mass causing narrowing
o Tremulous – neurologic disorder causing abnormal vibration (Parkinsons, spasmotic dysphonia)
 Note the most common type of laryngeal cancer is squamous cell carcinoma (remember how it’s
mucosal tissue encountering a noxious stimulus, causing metaplasia  neoplasia? The mucosal cells
want to become squamous cells as squames are more durable against damage)
  The most common site of malignant laryngeal lesions is the glottis
Pathophysiology
 Superior laryngeal nerve – branch of CNX with sensory (supraglottis) and motor (inferior constrictors,
cricothyroid muscles) functions
 Recurrent laryngeal nerve – branch of CNX with sensory (glottis and subglottis) and motor (all intrinsic
laryngeal muscles save cricothyroid) functions
Work-up
 You should consult an ENT when hoarseness lasts >3-4wk (viral laryngitis rarely lasts >2wk)
 Typically, if hoarseness in not self-limited, then Flexible laryngoscopy is undergone
o Here, the vocal cords and other structure can be visualized in a minimally invasive way
 If Laryngeal cancer is suspected on flexible larngyscopy  intraoperative direct layngoscopy and
biopsy is needed to histologically characterize the lesion
o If cancer, TNM staging is done and therapy is based on early or late staging
o CXR is routinely done to search for lung mets
o CT neck is often done for late-stage cancers to search for metastatic lymph nodes
Management
 Early stage (TNM I or II) – surgical resection of tumor OR radiation of tumor; both with good outcomes
 Late Stage (TNM III or IV) – any two or all three of surgery/radiation/chemotherapy are used
 Note that the goal of treatment is preservation of the larynx
 Note that the larynx is the narrowest part of the human airway. A mass may very easily compromise
the airway and emergent airway management with tracheostomy may be necessary at any time!

Chapter 13: Lump on Neck Increasing in Size – Head and Neck Cancer
Differential for ‘Lump on Neck’ – “KITTENS”
 K – Congenital – thyroglossal duct cyst, branchial cleft cyst, dermoid cyst, laryngocele, thymic cyst
 I – Infection/Inflammation – abscess, lymphadenitits, TB, toxo, cat scratch disease, antinomycosis
 T – toxin – metals/drugs (esp. cigarette smoking)
 T – trauma – hematoma, foreign body, aneurysm
 E – endocrine – thyroid hyperplasia/tumor, ectopic thyroid gland
 N – neoplastic – (any kind)
 S – systemic – AIDS (lymphadenopathy) or Kawasaki disease
Salivary Gland Tumors
 Most frequent site is parotid glands, but may occur in any salivary gland
 Subtypes
o Pleomorphic adenoma (mixed tumor) – most common benign tumor
o Papillary cystadenoma (Warthin’s tumor) – 2nd most common benign tumor
o Mucoepidermoid carcinoma – most common malignant tumor
o Adenoid cystic carcinoma – 2nd most common malignant tumor
Head and Neck Abscesses
 Peritonsilar – typically occurs in older children (fever, odynophagia, trismus); should be aspirated
through the tonsillar bed for drainage
 Retropharyngeal – typically occurs in younger children (fever, odynophagia, drooling, airway
obstruction); should be treated with intubation and drainage for posterior-pharyngeal wall
 Parapharyngeal – all age groups, esp with dental infections/tonsillitis; should be drained through the
lateral neck
Risk Factors (head & neck cancer)
 Male, Age >40, poor dental hygiene, radiation exposure, African American race
 Leukoplakia and Erythroplakia are pre-malignant lesions
Quick Facts
 Note that Virchow’s Node (left supraclavicular node) may appear in metastatic head & neck cancer; it
always appears on the left side due to the cisterna chyli (dilated lymph sac) being at the base of the
thoracic duct
 The oral cavity is the most common site of head & neck cancer followed by larynx, & pharynx
 Note that a new neck mass represents metastatic spread until proven otherwise (85% of tumors)
 Most common type of head and neck cancer is squamous cell carcinoma (90%)
Pathology
 Typically the upper aerodigestive tract (pulmonary + mouth/oropharynx/etc.) is constantly exposed to
carcinogens (food, smoke, etc.); this constant regular exposure can produce a grossly normal appearing
organ with a field of interspersed cancerous cells that have acquired mutations (field cancerization)
Symptoms
 Otalgia (ear pain) – due to nerve compression of CN IX (Jacobson’s branch), CN X (Arnold’s branch), or
CN V3 (supplies external auditory ear canal)
 Dysphagia (difficult swallowing) – physical compression of esophagus or interference with swallow
mechanism due to nerve compression
 Odynophagia (painful swallowing) – tumor-related inflammation can cause irritation
 Dysphonia (difficulty speaking) – lesion on vocal cords or nerve paralysis
 Trismus (difficulty opening mouth) – pterygoid muscle invasion
 Stridor (high pitched breath sounds) – airway compression/invasion narrowing the airway
 Hemoptysis (bloody sputum) – tumor ulceration in upper airway or lower airway tissue destruction

Workup
 An enlarged cervical lymph node can be observed: if 1the patient has red flag symptoms (listed above)
and 2has had the enlarged node of less than 3 weeks. When encountering these patients, schedule
follow-up in 3 weeks; if persistent, then further investigation is needed.
 If node is suspected to be due to metastatic head/neck cancer
o Imaging (CT of head/neck with contrast + CXR) are used to look for primary tumor and any
further signs of metastases; can also allow for staging
 If initial imaging does not show primary tumor in the head and neck  CT chest (it may
be lung cancer)
 Whole body PET may be useful for finding mets, but is controversial
o Labs (CBC, Coags, LFTs, CMP with renal function, TSH) are to gain baseline info
o FNA is done as soon as possible to gain histologic diagnosis.
 If initial FNA, FNA with ultrasound should be performed
o In addition to the physical exam, flexible nasopharngoscopy is used when a suspected
metastatic lymph node is detected to help find the primary tumor site
 If the above fail to show primary tumor site panendoscopy (triple endoscopy) is done
o Laryngoscopy, esophagoscopy, and bronchoscopy under general anesthesia to find primary
o Allows for visualization of primary and biopsy of primary tumor
 If the above fail an open neck biopsy should be performed and the frozen section is examined
o It’s hard to control bleeding in the head/neck and open biopsy risks the chance of tumor
seeding. It’s advised to use these as a final diagnostic technique
o Note is squamous cell carcinoma is found, an immediate open neck dissection for removal of
malignant tissue to minimize seeing of tumor cells from biopsy site
Management
 Tailored to specific cancer type; you’d hand the reigns over to oncology here.
Chapter 14: Aural Fullness, Hearing Loss, and Tinnitus
Differential for Childhood Hearing Loss
 Acute otitis Media (AOM) – discussed below
 Otitis Media with Effusion – discussed below
 Chronic Otitis Media – often recurrent bouts of AOM result in TM damage/perforation/otorrhea
 Cholesteatoma – formation of yellow-ish mass of keratinized, desqamated epithelium in middle ear.
Often the result of Eustachian tube dysfunction or COM
 Labyrinthitis – often viral with vertigo, gait instability, N/V, hearing loss, and nystagmus
 Otitis externa – discussed below
 Congenital hearing loss (hereditary, acquired like TORCH infections)
 Cerumen impaction/foreign body, or trauma causing damage to ear – most typically presenting with
unilateral fullness/ear pain/hearing loss
Additional Differential in Adult with Hearing Loss
 Exposure to loud noises over the years
 Drugs – aminoglycosides, aspirin, loop diuretics, or cisplatin are all known to cause hearing loss
 Tumors – vestibular schwannoma (CNVIII involvement)
 Meniere’s disease – hearing loss, vertigo, “fullness” of the ear, tinnitus
Note that sudden deafness is associated with viral infections (often herpes viruses); mainstay of Tx is steroids
and antivirals

Testing for Hearing Loss

 Conductive - sound waves of 512Hz fork cannot vibrate the basilar membrane of the cochlea properly
o Rinne: abnormal (bone > air)
o Weber: localizes to the affected ear
o Causes:
 Ear wax/foreign object - soundwaves can’t get to the eardrum; removal fixes problem
 Tympanic membrane perforation - can’t vibrate! May be fixed surgically
 Otitis media w/ effusion - fluid in middle ear dampens vibrations
 Otosclerosis - overgrowth of staples bone, causing stiffening/sound transmission failure
 Cholesteatoma - overgrowth of keratin debris within the middle ear space; may erode
ossicles/mastoid air cells
 Sensorineural - neural transmission interrupted either from failure of 2o sound waves or nerves
o Rinne: normal (air > bone)
o Weber: localizes to the unaffected ear
o Causes:
 Cochlear/CNVIII disorders or damage
 Prebyacusis - general. Progressive loss of high frequency hearing with aging
 Viral infection - Measels, Mumps, Rubella, CMV, HIV
 Ototoxic drugs
 Meniere’s disease or vestibular schwannomas (discussed below)
 Noise-Induced - damage to the hair cells w/stereocilia in the organ of Corti
o Isolated high frequency hearing (around 4000Hz) lost first; may progress if damage continues
o Eardrum perforation may occur with sudden, extremely loud noises

Acute Otitis Media (AOM)

 Presentation: ear pain, fever, and sometimes URI symptoms with duration <3wk
o Tympanic membrane: immobile without air-fluid levels, opaque, bulging/”full”, redness
 Dx: clinical presentation
  Tx: similar to OME

2839: Otitis Media with Effusion (OME or Serous Otitis Media)

 Epidemiology
o Most commonly occurs between ages 2-6yr & is pretty rare in adults
o Risk factors: male, African American, cigarette exposure, low birth weight, low SES, lack of
breastfeeding during infancy, supine feeding position
o The most common middle ear pathology in HIV/AIDS due to lymphadenopathy obstructing the
Eustachian tube; also common caused by cancer obstruction of Eustachian tube in adults
 Pathophysiology
o AOM and Eustachian Tube Dysfunction are the two major causes of OME as fluid persists within
the ear canal leading to bacterial growth and chronic inflammation
o Normal function of the Eustachian tube is to allow for pressure equalization & drainage in the
middle ear to the throat.
 Children <6yr have shorter/flimsier tubes, thus the chance for dysfunction and failure of
the tube causing OME is more common
o Micro: typically, viral (URI pathogens) but may become bacterial (superimposed)
 Presentation: Middle ear effusion resulting in conductive hearing loss without infectious symptoms.
o Tympanic membrane: immobile with air-fluid levels, opaque, but no bulging/redness
o Language regression or language developmental delay are also common presentations. Classic
is an infant who stops babbling or a child with poor speech skills and trouble in school
o Otorrhea is suggestive of TM perforation and should be evaluated seriously!
o Tympanosclerosis can result in permanent conductive hearing loss due to inflammation
o Complications (rare) – mastoiditis, meningitis, brain abscess, subdural empyema
 Dx: clinical presentation, ear swab/culture, pneumatic otoscopy
 Tx: often resolves spontaneously within 3 months
o Autoinflation – pinching the nose and gentle blowing out to raise pressure and drain the
middle ear. Can be used to speed spontaneous resolution
o Antibiotics – only 33% of these are bacterial; thus it’s not routinely recommended
 While steroids/antibiotics give short-term benefits, antihistamines and decongestants
are not useful
o Tympanostomy Tubes – little tubes to allow the Eustachian tube to remain patient. Typically
reserved for pts with 1hearing impairment, 2significant symptom impact on quality of life,
3recurrent disease, or 4children at risk (Down’s syndrome, etc.)

Otitis Externa (Swimmer’s Ear)

 Presentation: ear pain/itching worse with manipulation, sometimes with inflamed/swollen external
ear canal with drainage and discharge. Tympanic membrane typically appears normal.
o Classically occurs after warm water exposure or instrumentation in the ear canal
o Micro: Staph, Strep, and rarely Pseudomonas (swimmer’s ear; most common in diabetics)
 Dx: clinical presentation
 Tx: irrigation, debridement, and antibiotics (IV for 4-6wk if bones involved)

2828: Malignant (necrotizing) Otitis Externa

 Presentation: intense, unrelenting ear pain that’s worse at night. Purulent drainage/feeling of fullness
that does not respond to topical medication. Ear canal shows granulation tissue/edema. May
progress to osteomyelitis of the skull base with cranial nerve involvement (facial droop) or TMJ
involvement (pain worsened by chewing)
 o Associated with poorly controlled diabetes/immunosuppression in elderly patients
o Typically caused by Pseudomonas Aeruginosa (classic in diabetics)
 Dx: clinical presentation with swab/culture and CT/MRI evidence of infection
 Tx: IV ciprofloxacin (first line)
o Fluoroquinolone resistant: other IV anti-pseudomonals (Pip-tazo/cefepime/ceftazidime)
o Failure to respond to Abx: surgical debridement/biopsy to exclude cancer

Chapter 15: Post-Prandial RUQ Pain – Biliary Colic and Gallstone Disease
Risk Factors for Developing Gallstones (Classic the the 4Fs – Fat, Female, 40, fertile)
 Obesity – decreases bile salts (unknown mech) leading to formation of cholesterol supersaturation
 Crohn’s Disease/Terminal ileum resection – bile salt loss in the inflamed/resected bowels leads to
cholesterol supersaturation
 Female Gender/Pregnancy/OCPs – estrogen increases cholesterol secretion into the biliary system
and progesterone slows gallbladder emptying. Thus, these two together can cause cholesterol super-
saturation and stasis, resulting in cholesterol stones!
 Total Parenteral Nutrition – without protein/nutrients entering the duodenum, secretin (which could
cause gallbladder contraction) is not released and gallbladder stasis can result in it’s contents to
coalesce into stones!
 Partial/Full Bowel resection – results in a decreased ability to absorb/recycle bile acids. This can occur
to a point where the cholesterol:bile acid ratio increases to the point of cholesterol super-saturation!
 Hemolytic anemia – the huge amount of heme released from massive RBC destruction results in huge
amount of bilirubin to be conjugated in the liver and sent into the bile (heme  bilirubin). Thus
bilirubin can become super saturated causing pigmented gallstones.
Physiology
 Remember that fatty foods trigger release of Cholecystokinin (CCK) trigger gallbladder contraction.
When this contraction occurs, gallstones are pushed into the biliary duct, causing gallbladder
obstruction/distention/compression of capillaries/ischemia/inflammation
 The three main components in bile are bile salts, cholesterol, and lecithin; water, electrolytes,
proteins, pigment, and bacteria are all present as well
 Types of Gallstones
o Cholesterol: most common in USA & form when cholesterol cannot be properly dissolved by
bile salts/lecithin (too much cholesterol or not enough bile salts/lecithin)
o Black stones: pigmented stones associated with hemolytic disease (high amounts of
unconjugated bilirubin isn’t dissolved well). Found within the gallbladder.
o Brown stones: larger/softer/found in ducts; bacteria/parasites cause these; common in Asia
Micro: E.coli, Bacteroides fragilis, Klebsiella, Enterobacter, Enterococcus, and Pseudomonas spp

Note that asymptomatic gallstones should not be treated

4433: Biliary colic (Symptomatic Cholelithiasis)

 Presentation: post-prandial RUQ pain with tenderness to palpation, shoulder/subscapular pain
(referred pain), nausea/vomiting with resolution within 4-6hr after onset
o Occurs due to gallbladder contraction in response to fat in meal. Classically a gallstone gets
stuck in the cystic duct, causing the pain. Resolution is with gallbladder relaxation.
o NO fever, leukocytosis, changes to vitals, and Murphey’s sign (-)
o Classic question of “what’s a better term” due to the fact that colicky pain waxes and wanes
during it’s course, when this pain is constant but resolves.
 Dx: RUQ ultrasound showing gallstones without other signs
  Tx: symptomatic treatment or cholecystectomy

2904: Acute Cholecystitis

 Presentation: RUQ pain after a fatty meal, referred pain to the shoulder, Murphey’s sign (halt on
inspiration with palpation of gallbladder), fever, nausea/vomiting, leukocytosis
o 90% are caused by gallstone impaction in the cystic duct  uncomplicated, causes mild
elevations of LFTs/bilirubin
o If gallstone goes into the common bile duct  complicated, icterus & very high Alk.phos
o Gangrene, perforation, abscess, or peritonitis may be complications
 Dx: RUQ ultrasound showing stones, fluid surrounding the gallbladder, gallbladder wall thickening (>4
mm), and possible dilation of the common bile duct (CBD)
o Normal CBD – 4-5mm which increases 1mm every decade after 40yr
o CBD of >6mm nearly always abnormally dilated
o Emphysematous Cholecystitis – air in gallbladder wall due to necrosis from Clostridia spp.
 Tx: hospital admission  NPO/IV fluids/IV Abx (gram -)  laparoscopic cholecystectomy within 48hr

2978: Acute Cholangitis

 Biliary stasis due to any number of reasons (commonly gallstone obstruction, malignancy, bile duct
stenosis) but all of them cause backup. The fear is that disruption of the blood-bile barrier could allow
for dissemination of bacteria/toxins
 Presentation: [fever, jaundice, RUQ pain], [confusion, hypotension] (Charcot triad, Reynold’s pentad)
o Labs: neutrophilia, elevated alk.phos/GGT/AST/ALT/direct bilirubin
 Dx: presentation/labs with biliary dilatation (ultrasound FIRST, then CT if not diagnostic)
 Tx: [ERCP with sphincterotomy or percutaneous transhepatic cholangiography] + broad spectrum
antibiotics

3732: Porcelain Gallbladder

 Characteristic pathologic deposition of Calcium salts intra-luminally in the gallbladder; often occurs due
to chronic irritation/inflammation from gallstones
o Appears with a “bluish” color and “brittle” consistency on gross specimen
o Increased risk of gallbladder adenocarcinoma
 Presentation: RUQ pain with firm, non-tender RUQ mass
o CXR/CT: hyper-dense rim-like calcification on the gallbladder
 Dx: imaging studies with characteristic findings
 Tx: cholecystectomy (esp. if symptomatic)

2946: Acalculous Cholecystitis

 Acute inflammation of the gallbladder WITHOUT gallstones typically in critically ill, hospitalized pts
resulting in cholestasis or ischemia  distention, necrosis, 2o infection of gallbladder
 Predisposing factors: recent surgery, severe trauma, extensive burns, sepsis/shock, prolonged
fasting/TPN, mechanical intubation
o Thought to be due to biliary stasis (NPO status) and ischemia (hypovolemia/shock)
 Presentation: unexplained fever, leukocytosis, RUQ abdominal pain/mass, jaundice, abnormal LFTs
o Gallbladder inflammation may cause gangrene, perforation, or emphysematous cholecystitis
(infection with gas-producing bacteria causing gas in the gallbladder)
 Dx: Abdominal ultrasound is preferred (thickening and pericholecystic fluid); CT abdomen or
cholescintigraphy (HIDA scan) are more sensitive/specific and can be used in unclear ultrasound (lack
of gallbladder visualization is positive
  Tx: medical management (abx/anti-inflammatory)  urgent cholecystectomy (percutaneous,
laproscopic, or open depending on how sick the patient is)

2930: Gallstone Management

 Gallstones without symptoms  no treatment necessary, simply monitor
 Gallstones with biliary colic  elective laparoscopic cholecystectomy or ursodeoxycholic acid
 Complicated gallstones (acute cholecystitis, choledocolithiasis, or gallstone pancreatits) 
cholecystectomy within 48hr

Post-Op for Lap. Chole.

 Common Bile Duct injury – feared complication of surgery.
o Recognition during surgery  If <50% of duct is damaged, stenting is acceptable. If >50%
damage then a Roux-en-Y hepaticojejunostomy must be done to place the intestines above the
area of damage.
o Recognition later  abdominal pain, anorexia, bloating, elevated LFTs often occur.
 Abdominal ultrasound or CT to search for fluid collection
 If yes or LFT elevation  are they septic?
 If yes then drain fluid then do a HIDA scan
 If no then do a HIDA scan
 If bile leak or no bile flow to duodenum  ERCP to find major problem for fixing

2943: Post-cholecystectomy syndrome

 Presentation: persistent pain/dyspepsia/nausea/vomiting/pruritis following cholecystectomy
o Can occur immediately months, or even years post-operatively
o The pain “never went away”, “is new after surgery”, or “has come back!”
o Caused by biliary (retained stone/sludge/etc, inflammation, dyskinesia) or extra-biliary (PUD,
pancreatitis, coronary artery disease, etc.)
 Dx: imaging (endoscopic ultrasound, endoscopic retrograde cholangiopancreaticography [ERCP], or
MRI cholangiopancreatography) to elucidate the underlying cause
 Tx: directed at underlying cause

Chapter 16: Right Upper Quadrant Pain, Fever, Nausea, and Vomiting – Impacted Gallstone
Presentation
 Charcot’s Triad (50%) – fever, RUQ pain, jaundice
o Pain often acute onset; jaundice most prominent in eyes/palms/soles/tongue base
o Jaundice clinically visible when >2.5
 Reynold’s Pentad (5%) – fever, RUQ pain, jaundice, hypotension, and altered mental status
o Essentially the triad + SIRS
 SIRS criteria
o Temp <96.8 or >100.4
o HR >90bpm
o RR >20 or PaCO2 <32mmHg or pt mechanically ventilated
o WBC >12 or <4 or >10% bands
o Remember that sepsis is SIRS criteria with suspected infection
Pathophysiology
 Gallstones can easily harbor bacteria and clog the biliary tree, thus they’re the most common cause
 If stone persists, abscess formation, severe sepsis, and death may all occur
Work-Up
 Labs: CBC, CMP, LFTs (AST, ALT, GGT), alk. phos
 Imaging: RUQ ultrasound  gallstone visualization or ductal dilation of >4mm
o 4mm rule occurs till age 40yr; then add 1mm for every decade past 40
o Good rule in but not good rule out test
Management (if presenting with Triad + SIRS) – all steps should be done in this order
 Aggressive IV fluid resuscitation
 Broad spectrum abx within the first hour of arrival
 Two sets of blood cultures (ideally before abx)
 ICU admission
 Drain infected bile
o Preferred: ERCP with spincterotomy and stenting
o Alternatives: percutaneous transhepatic drainage or operative placement of T-tube in common
bile duct
 Laproscopic cholecystectomy (prevent future attacks)  used to be the initial step of treatment, but
higher mortality rates were seen when putting septic patients under general anesthesia. Better to
control the sepsis, then go under the knife.

Chapter 17: Severe Epigastric Pain with Nausea/Vomiting

2982/4434/2965/2929: Acute Pancreatitis
 Pathophysiology: intra-pancreatic activation of pancreatic enzymes causes autolysis of pancreatic
tissue, and eventually peripancreatic tissue. This results in massive inflammation and damage.
o Premature Trypsin Activation  damage to pancreas  damage to rest of body
o Gallstones causing pancreatitis are often small and don’t get stuck in the Ampulla of Vater.
They are there transiently, causing enough backup to damage the pancreas, but almost always
pop out to be digested. ERCP is NOT useful in evaluation because of this.
o Ethanol’s mechanism isn’t fully understood, BUT it’s proposed that EtOH metabolites cause
damage to the pancreas, eventually resulting in enzyme activation after years of damage
o Hypocalcemia – due to fat necrosis sequestration of calcium (saponification)
 Presentation: severe acute abdominal pain, fever, nausea/vomiting, abdominal guarding, hypoactive
bowel sounds, sometimes xanthomas
o Causes (“GET SMASHED”) Gallstones (40%), Ethanol (40%), Tumors (obstruction of pancreatic
head), Scorpion stings (lol), Mycoplasma/Mumps, Autoimmune (SLE or polyarteritis nodosa),
Surgery/Trauma, Hypertriglyceridemia (classically >1000), Embolism (ischemia), Drugs/toxins
o Imaging: sentinel loop (dilated loops of bowel near the pancreas) or colon cutoff (bowel
distention until sudden collapse in upper left splenic flexure) on plain films
o Labs: elevated WBCs, elevated amylase/lipase, elevated LFTs
 Dx: two of the following
o Acute epigastric abdominal pain radiating to the back
o Increased amylase or lipase (more spec) x3 the normal limit  typically the first step in workup
o Diffuse pancreatic enlargement with contrast enhancement (CT) or hyperechoicity (ultrasound)
and sometimes with fat-stranding; Ultrasound is preferred in patients suspected with
gallstones as underlying cause (fat/40/fertile/female = gallstone)
 Prognosis (Ranson Criteria)
o At Admission: Glucose (>200), Age (>55), LDH (>350), AST (>250), WBCs (>16,000)
o At 48hr: Ca (<8.0), Hct drop (>10%), PaO2 (<60), BUN rise (>5), Base deficit (>4), Fluid
sequestration (>6L)
o Each individual value is worth 1 point  0-2 (2% mortality), 3-4 (15%), 5-6 (40%), 7-8 (100%)
 o Most common cause of mortality in 1st week  multiorgan failure resulting from SIRS/sepsis
o Most common cause of mortality after 1st week  pancreatic necrosis/abscess  often a
patient develops fever/leukocytosis 3wk into course  stat CT to assess
 Tx: supportive care (pain control/fluids) as most cases are self-limited (4-7 days)
o If caused by something that can be treated (gallstone, EtOH, drug, infection, etc) then treat that
once initial episode begins to resolve
o Meperidine (over morphine) may be preferred for pain control as it doesn’t cause contraction
of the Sphincter of Oddi; however, it lowers seizure threshold

4603: Severe Acute Pancreatitis

 Pancreatitis + evidence of organ failure due to release of pancreatic enzymes into the vasculature.
This causes increased vascular permeability in/around the pancreas, causing shock & organ failure
o Shock – systolic blood pressure <90mmHg
o Organ failure – PaO2 <60mmHg; Creatinine >2.0 after rehydration; GI bleed >500cc/24hr
 Presentation: pancreatitis symptoms with additional ones
o Organ dysfunction due to fluid overload (dyspnea, tachypnea, abdominal distention, etc.)
o Cullen sign: periumbilical blue-ish coloration indicating retroperitoneal hemorrhage
o Grey-Turner sign: red-brown coloration around the flanks indicating retroperitoneal bleed
o Remember! The Pancreas is retroperitoneal…thus bleeding goes into this area!
 Risk factors: >75yrs, obesity, alcoholism, pulmonary infiltration on X-ray
o Labs at 48 hrs  CRP >150mg/dL, Rising BUN and Creatinine
 Tx: aggressive IV fluid resuscitation to replace lost volume

3833: Drug induced Acute Pancreatitis

 Anti-seizure (valproate), Diuretics (furosemide, HCTZ), Drugs for IBD (sulfasalazine, 5-ASA),
Immunosuppression agents (azathioprine), HIV-medications (didanosine, pentamidine), Antibiotics
(metronidazole, tetracyclines), and possibly many others!

4362/4919: Chronic Pancreatitis

 Etiology: alcoholism (most common adults), cystic fibrosis (most common kids), duct obstruction
(malignancy or stones), autoimmune
 Presentation: chronic epigastric pain radiating to the back, improved with leaning forward/sitting up
(intermittent remission/relapses), malabsorption (steatorrhea, AEDK deficiency, weight loss), diabetes
o Amylase/lipase may be normal or decreased (“burnt out pancreas”)
o CT/MRCP showing pancreatic calcifications, dilate ducts, enlarged pancreas
o May result in fat-soluble vitamin (AEDK) deficiencies
o Steatorrhea occurs with 90% loss of pancreatic function
 Dx: clinical presentation with radiographic evidence (calcifications are the best thing to see)
o Fecal fat assays (Sudan Stain) may sometimes be used
 Tx: pain management, alcohol/smoking cessation, frequent small meals, pancreatic enzyme
supplementation during meals

2897: Pancreatic Pseudocyst

 Presentation: palpable mass in epigastrum following acute pancreatitis or in chronic pancreatitis, often
with pain radiating to the back
o “Cyst” actually lacks a proper epithelium and is covered by a thick, fibrous capsule
o Filled with fluid/tissue/debris that contains high levels of pancreatic amylase/lipase, thus it can
leak into the circulation causing elevation of pancreatic enzymes
 o If cyst erodes into a blood vessel, hemorrhage into pseudocyst may occur as an acute
complication, requiring immediate surgical attention
 Dx: presentation with ultrasound visualization
 Tx: often symptomatic as cyst will resolve itself
o Drainage indicated if: persistence for >6wk, size >5cm, or secondary infection

Chapter 18: New Onset of Painless Jaundice

There’s a long differential for jaundice but it can be conveniently divided into three types (page 192):
 Prehepatic – hemolytic anemia, Gilbert’s syndrome
 Hepatic – ischemic/viral/toxic liver injury, primary biliary cirrhosis, Wilson’s disease
 Posthepatic – choledocholithiasis, chronic pancreatitis, mirizzi syndrome, pancreatic/ampullary
carcinoma, cholangiocarcinoma
Presentation
 Fatigue, mild vague abdominal pain or no pain, low appetite, weight loss, jaundice, itching
o Jaundice is often noticeable at bilirubin >2.5 mg/dL, most prominent on palms, soles, under
tongue, and sclera of the eyes (less photodegeneration)
o Courvoisier’s sign – palpable non-tender RUQ mass due to enlarged gallbladder. Enlargement
due to distal biliary tree obstruction
o “Sandy” stools – poor bilirubin entry into gut  less stercobilin to color the stool
o “Tea colored” urine – back-up of direct (conjugated) bilirubin which gets filtered out by kidneys
o Sister Mary Joseph Nodule – periumbilical mass, sometimes seen w/ metastatic GI malignancy
o Blumer’s Shelf – ‘step off’ felt in rectal exam due to metastatic disease in Pouch of Douglas
 Labs: elevated total bilirubin/direct bilirubin/LFTs/alk.phos
 Risk factors: chronic pancreatitis > smoking > high-fat diet > male gender > family history
Pathophysiology
 Bilirubin is a heme breakdown product and its metabolism drives much of the symptoms here
o Heme  unconjugated bilirubin (albumin bound) that goes to the liver
o Un-bili  conjugated bilirubin in the liver, then stored in the gallbladder
o Con-bili  excreted into the small intestine and converted into urobilinogen
 Urobili  absorbed and converted into urobilin (makes pee yellow)
 Urobili  metabolized by bacteria in large intestine to stercobilin (makes poop brown)
Workup
 Labs: CBC, LFTs (AST, ALT, GGT), Alk. Phos, bilirubin levels
 Imaging:
o Painful jaundice = RUQ ultrasound (most likely gallstone)
o Painless jaundice = Triple Phase CT +/- endoscopic ultrasound
o ERCP is not routinely needed for diagnosis, but can be helpful in unequivocal cases and if stent
placement/biopsy are needed for delination
 Tumor markers CA 19-9 and Carcinoembryonic Antigen (CEA) may be used to monitor treatment
response but are not useful in diagnosis/prognosis
Management
 Pancreaticoduodenectomy (Whipple Procedure) – removal of the pancreatic head, duodenum,
proximal jejunum, distal stomach, and gallbladder
o Complications: Gastroparesis (most common, treat with metoclopramide), pancreatic leak
(milky grey-white fluid drainage with “sheen”; test for pancreatic amylase), biliary leak (green
leakage), hemorrhage (sanguinous leakage), malabsorbtion, weight loss & weight loss are all
possible complications of surgery
o Yellow-red drainage is normal post-surgically
  Typically, resectability is determined by review of triple-phase CT +/- endoscopic ultrasound
 Things that make pancreatic cancer unresectable (not a surgical candidate)
o Superior mesenteric, celiac, or hepatic artery invasion
o Any sign of metastatic disease
 If patient is unresectable, palliative procedures may be done to relieve symptoms/suffering
o Chronic abdominal pain – celiac nerve block, external beam radiation
o Gastric outlet obstruction – gastrojejunostomy, gastric tube or PEG tube placement
o Symptomatic biliary obstruction – ERCP + biliary stent is preferred
 Patients who are borderline resectable may receive neoadjuvant chemotherapy to shrink to tumor to
an appropriate size before surgical intervention (33% of patients will become resectable; this does NOT
increase survival)

2977: When assessing jaundice, positive urine bilirubin means conjugated (direct) bilirubinemia
 This makes sense, as only conjugated bilirubin is made to be water soluble, unconjugated (indirect)
bilirubin is inherently not water soluble, thus it cannot be filtered by the kidney into the urine.
 However, a positive urine urobilinogen indicates unconjugated (indirect) bilirubinemia, as the huge
amount of unconjugated bilirubin goes through it’s normal metabolism in the large intestine, a large
amount of urobilinogen (a normal by-product) will be made. This is NOT the case in a direct bilirubin, as
a direct bilirubinemia is caused by some obstructive process, and it would never make it to the large
intestine to become urobilinogen!

Chapter 19: Bright Blood per Rectum (may want to just read again; doesn’t translate well into notes)
Differential Dx  diverticulosis, neoplasia, iatrogenic, colitis (infectious, ischemic, inflammatory, or radiation),
angiodysplasia, anorectal bleeding (hemorrhoids, anal fissure, rectal varicie, rectal ulcer)
 Some of these are discussed in more detail below

Management
 Initial Steps – place 2 large-bore IVs; send labs (type & cross, CBC, H&H, CMP, PT/INR); start IV fluids
followed by packed RBCs as needed
 2nd step – place NG tube to rule out upper GI bleed depending on aspirate
o Blood/’coffee grounds’ – upper GI bleed confirmed
o Bile – upper GI bleed ruled out completely
o Clear fluid – upper stomach bleed ruled out, but NOT duodenal bleed
 If patient Unstable
o Admit to ICU for close monitoring and expedited work-up of bleed
o 1st line test – colonoscopy (bowel prep if possible, but do not delay if urgent)
o 2nd line test – if the colonoscopy fails to visualize the bleed, consider:
 Diagnostic arteriography – needs brisk bleeding (1mL/min); can be therapeutic/dx
 Tagged RBC scintigraphy – slower bleeding (0.1mL/min); only dx
o 3rd line test – at this point the bleeding may have stopped or not
 Stopped bleed/suspect small bowel – Meckel’s nuclear scan, capsule endoscopy, or
enteroscopy
 Stopped bleed/no clue of source – repeat 1st or 2nd line tests
 Continued bleeding – emergent laparotomy with total colectomy (save their life)
o Note that if embolization fails to stop a known bleed, partial bowel resection is the next step
 If patient Stable
o Age <40  anoscopy (basically a scope of the anus)
  Typically yields hemorrhoids, which will often resolve with symptomatic treatment or
minor surgery to remove them
 If no source sound, do a sigmoid or colonoscopy
o Age 40-49 without red flag signs  sigmoidoscopy/colonoscopy
o Age >50 or red flags colonoscopy
o Red flags include: recent bowel habit changes, abdominal pain, weight loss, anemia, or family
history of colon cancer

4086: Diverticulosis
 Outpouchings of inner colonic tissue through the outer layers of the colon due to weakened areas
encountering pressure, thus bulging out. The vasa recta are stretched out over the pouch, resulting in
an increased chance for bleeding
o Associated with constipation and oddly enough, may worsen existing constipation!
o Most diverticular occur in the sigmoid colon as stool is harder/dryer and the lumen decreases
in size (thus more pressure for damage to bowel!)
o May produce massive painless bleeding, especially with bowel movements
 Complications: diverticular hemorrhage, diverticulitis, perforation, abscess formation
o Adequate fruit/vegetable fiber in the diet and physical activity lower risk of complications
o Meat, aspirin/NSAIDs, obesity, advanced age, and smoking increase risk of complications
 While these often pose no problem, it’s important to take steps to limit the risk of complication in
those with diverticulitis with lifestyle changes

4389: Colorectal cancer: signs/symptoms

 An older man (>60) with abdominal pain, microcytic anemia, (+)fecal occult blood, and hepatomegaly
with a hard liver edge  prompt you to think infiltrative colon cancer
o Any old person with microcytic anemia (esp. men) or blood in stool  colon cancer
o Hepatomegaly with a hard liver edge  liver cancer (most often from metastatic colon cancer)
o Mildly elevated AST/ALT/Alk.phos in this setting  infiltrative/cholestatic disease (which
metastatic liver cancer would be a part of!)
 Dx: because this pt has signs of colon cancer and liver abnormalities without significant elevations in
LFTs, an abdominal CT should be sought as metastatic malignancy is suspected.

Ischemic Colitis (look in Surgery UWorld notes for better explainations)

 Lack of bloodflow to the typically blood-thirsty colon causing mucosal damage with prolonged ischemia
resulting in full-thickness damage
 Presentation: left sided abdominal pain, bloody diarrhea, especially those with volume depletion
(dehydration, heart failure, shock, trauma)
o Classically affects “watershed” areas first (splenic flexure poorly perfused by SMA/IMA)
o Can be due to any “low flow” state (low BP, low cardiac output, dehydration, heart failure,
extreme exercise, vascoconstrictive drugs, etc.)
o 80% will resolve spontaneously
 Dx: clinical presentation
 Tx: rehydration supportive therapy

Chapter 20: Right Lower Quadrant Abdominal Pain – Acute Appendicitis

Differential Diagnoses
 General Stuff: IBD, pancreatitis, cholecystitis, appendicitis, gastroenteritis, perforated duodenal ulcer,
pyelonephritis, nephrolithiasis, sigmoid/cecal/Meckel’s diverticulitis
  Women Stuff: PID, ovarian torsion, Mittelschmertz, ruptured ectopic
 Children Stuff: mesenteric lymphadentitis, Yersinia enterocolitica (pseudoappendicitis), gastroenteritis,
intussusception
Presentation
 Classic progression: anorexia  vague abdominal periumbilical pain  vomiting  pain shift to RLQ
 Other symptoms: paralytic ileus (absent bowel sounds from inflammation), Hamburger sign (pt would
not like to eat their favorite food), Rovsing’s sign (RLQ pain w/ palpation of LLQ), Psoas Sign (RLQ pain
w/ active flexion of hip or passive extension; often Pelvic Appendix), Obturator Sign (RLQ pain w/
internal rotation of hip), McBurney’s Point Tenderness (tenderness w/ palpation at McBurney’s point)
 Often children will initially present with viral URI, then the lymphoid hyperplasia resulting from fighting
the URI can cause obstruction and appendicitis
 Lumbar triangle palpation may be painful in those with retrocecal appendicitis. The cecum will shield
the appendix from many signs mentioned above, thus this can be an important test!
Pathophysiology
 Transition from vague pain  localized RLQ pain occurs due to diff. peritoneal layers getting affected
o Visceral peritoneum – innervated by autonomic nerves responding to stretch or distention;
sensation is poorly localized; this level is affected first as it’s more internal
o Parietal peritoneum – innervated by spinal nerve (somatic innervation of T10-T12); as
inflammation progresses, this level will be affected resulting in localized pain
 Where does pain occur based on gut level?
o Foregut – [mouth  ligament of Treitz (2nd part of duodenum)]  epigastric pain
o Midgut – [3rd part of duodenum  proximal 2/3 of transverse colon]  periumbilical pain
o Hindgut – [1/3 distal transverse colon  rectum]  hypogastric pain
 “Cutaneous hyperesthesia” – sensitivity to touch with peritoneal inflammation
 ‘Closed loop obstruction’ of the appendix – the appendix is a blind loop of bowel
o Obstruction  increased pressure  distention/inflammation/ growth of appendix bacteria
o Eventually pressure is so great that venous flow is compromised  backup of arterial flow
o Bloodflow congestion  ischemia/gangrene  weakening of the appendix wall
o Weakened wall + increased pressure  rupture!
 Important causes of appendix obstruction
o Fecalith – most common in adults; hard poop rock!
o Lymphoid hyperplasia – most common in children; often after viral URI
o Oral barium (bariolith) – occurs after radiologic studies with oral barium contrast
o Tumor – carcinoid tumor, adenocarcinoma of appendix, etc.
o Ingested seeds – aren’t digested well and get stuck in appendix
o Parasites – reproduce and grow in the GI tract; can get stuck in appendix
Workup
 Labs: CBC (leukocytosis with left shift), CRP (elevated), B-hCG pregnancy test (if of child-bearing age),
urinalysis (sterile pyuria)
 Imaging: used if H&P is equivocal or to rule out gynecologic problems/pregnancy in women
o CT a/p if non-pregnant female or adult man (periumbilical fat stranding and appendix >6mm
diameter, free abdominal fluid, phlegmon)
o Ultrasound if pregnant female or child (dilated, tubular structure in RLQ with thickened walls);
children have less abdominal fat making CT less valuable for visualization
o MRI may be used in pregnancy if pt is obese or ultrasound is unavailable
o Abdominal X-ray is not often useful; may show calcified fecalith, but not routinely ordered
Management
 Surgical appendectomy
 o Laprascopic approach – longer surgery, higher cost, high incidence of abscess; faster recovered,
lower overall complication/infection rate, smaller scar
o Open approach – shorter/cheaper/less abscess; slower recovery/higher complications/big scar
 If you get in there and you have a normal appendix
o Remove it anyway; this leads to effective ‘rule out’ in future presentations of RLQ pain
o Don’t remove it if cecal Crohn’s disease; high chance of fistula formation
o Also look for other causes of symptoms
 Non-operative approach with abx and supportive care only has been used but is controversial; not gold
standard; you won’t typically do this.
 Preoperative Abx are always recommended
 Postop Abx  non-perforated (24hr); perforated (till fever/leukocytosis resolve; usually 3-5 days)
Problems that can come up
 Pyuria does not necessarily mean cystitis! Don’t jump to that conclusion.
 If there’s pus in the abdomen…but the appendix is intact; diagnosis is peri-appendicitis and careful
abdominal exploration is needed to find source of infection/peritonitis
 If pt has pseudo-appendicitis (Yersinia Enterolitica); often will present with all the signs of appendicitis
but will also have bloody or watery diarrhea. Typically transmitted by contaminated water or pork.
Classically a child in day-care or a daycare worker.
o More common in pt with hereditary hemochromatosis (Y.entero loves iron)
o Self-limited; but Immunosuppressed patients may die from dissemination  sepsis
o Tx: doxycycline
 Ruptured appendix may be misdiagnosed as PID as both cause cervical motion tenderness and
adnexal tenderness. Often PID = bilateral pain since onset; pain lower in pelvis; additional signs of
vaginal infection, risk factors, or history of untreated STI
 Acute appendicitis is considered “urgent” not “emergent” as risk of rupture increases 5% every 12hr
 >5 day Hx of RLQ pain usually means the appendix is ruptured and often a local abscess has formed
o Small abscess – treatment with IV abx and admission  appendectomy
o Large abscess – percutaneous drainage, abx, and admission  appendectomy
Special Populations
 Pregnant Women: acute appendicitis is the most common surgical emergency in pregnancy! While
abdominal contents shift up…RLQ pain is still presented even in 3 rd trimester. Appendix rupture AND
appendectomy can cause significant morbidity and mortality to the fetus, thus diagnosis with imaging
(ultrasound or MRI) is critical before treatment
 Children <5yr: harder to get H&P and higher risk of early rupture (45% present with it)
 Elderly: more prone to rupture (50%) and microcytic anemia should prompt workup for perforated
colon cancer (can mimic appendicitis!)

Chapter 21: Pencil Thin Stools and Intermittent Constipation – Colorectal Cancer
Screening Guidelines for Colorectal Cancer
 Normal Risk:
o Age 50-75yr – colonoscopy every 10yr -OR- FOBT or Flexible Sigmoidoscopy every 3-5yr -OR-
annual FOBT (any (+) test that isn’t colonoscopy needs to be followed-up by colonoscopy)
o Age 76-85yr – if never screened or if clinically indicated, pt may benefit
 1st degree Family Member with Colorectal Cancer
o Age 40yr or 10 years prior to family member diagnosis (whichever comes first)
o Repeat colonoscopies every 5 years
 High Risk Patients:
 o Family Hx of polyps or CRC: colonoscopy every 2-3 years starting 10 years before first familial
diagnosis or age 40 (if the 10 years prior puts you lower than age 40)
o Inflammatory Bowel Disease (Crohn’s or UC): every 1-2 years starting 8 years post-diagnosis
 Can start 12-15yr post-diagnosis if disease restricted to left colon
o FAP: colonoscopy every year starting at age 10
o Lynch syndrome (HNPCC): colonoscopy every 1-2 years starting age 20
Risk Factors: older age (>50), African American, IBD, family Hx, low-fiber/high-fat diet, sedentary lifestyle,
obesity, smoking, EtOH, Type 2DM, Hx of radiation therapy to the abdomen
Epidemiology: 3rd most common and 3rd most fatal cancer in men & women
Presentation
 Common symptoms: Unintended weight loss (cachexia from TNF-a), anemia
 Left sided cancer: more common, at rectosigmoid junction, changes in bowel habits (constipation or
diarrhea), obstructive symptoms, pencil thin stools (circumfrential growth  narrowed lumen),
abdominal distention, colicky pain, hematochezia
 Right sided cancer: insidious iron deficiency anemia, melena, RLQ pain with mass (rare)
 Note that digital rectal exam is very important as you may be able to palpate a mass if it’s in the distal
ends of the colon. If palpable you may be able to assess the characteristics of the mass, allowing for
better surgical planning
Pathophysiology
 Three major types of colon polyps:
o Hyperplastic: most common non-neoplastic polyp; no need for further workup
o Hamartomatous: juvenile/Peutz-Jegher (hyperpigmentation of lips/genitals polyps…benign)
o Adenomatous: most common overall with potential malignancy  further workup, but less
than 1% of these will actually be malignant!
 Adenomatous polyps MUST be further assessed as this will determine its risk for malignancy:
o Morphology: sessile [more malignant] or pedunculated [more benign]
o Histology: [more benign] tubular < tubulovillous < villous [more malignant]
o Size: [low risk of invasion] (<1.5cm) < (1.5-2.5cm) < (>2.5cm) [high risk of invasion]
 Adenoma  Carcinoma sequence is the typical mechanism for developing colorectal cancer
o Step 1: APC tumor suppression gene loss  increased proliferation
o Step 2: KRAS mutation  unregulated intracellular signaling = growth  adenoma formation
o Step 3: p53 mutation  loss of genetic regulation, accumulation of mutations  carcinoma
o This sequence is thought to take about 10yr…thus the screening recommendations
 Common metastatic sites of colorectal cancer
o Regional lymph nodes & liver (distal mets from portal system) are most common
o Rectal cancer may disseminate via either portal or systemic veins thus lungs (internal iliac 
SVC), spine/brain (sacral veins), or iliac lymph nodes are common sites as well as liver &
peritoneum
Genetic Syndromes Associated with Colorectal Cancer
 Lynch Syndrome (Hereditary Non-polyposis colorectal cancer [HNPCC])
o Two major types:
 Lynch syndrome I: only colon cancer
 Lynch syndrome II: colon and extra-colonic cancer (endometrial carcinoma most
common)
o Dx: Modified Amsterdam Criteria (3-2-1-0 rule!)
 3 or more relatives with colon cancer (one must be first degree to the other two)
 2 or more generations affected
 1 familial case before age 50
  0 change of Familial Adenomatous Polyposis excluded (APC gene mutation excluded)
 Familial Adenomatous Polyposis (FAP)
o Familial deletion of one APC gene (chrom. 5), resulting in 100s-1000s of polyps
o 100% chance to progress to colonic adenocarcinoma before age
o Tx: prophylactic colon and rectum removal + increased CRC screening
 Gardner Syndrome
o FAP + fibromatosis + osteomas (often on forehead)
o May also have retinal pigment hypertrophy or impacted/supernumery teeth
 Turcot Syndrome “TURcot like a TURban on your head”
o FAP + CNS tumors (medulloblastoma or glial tumors) + café au lait spots
 Juvenile polyposis syndrome
o Benign hamertomatous polyp arising in children <5 y/o - rectal polyp can prolapse & bleed
o Commonly SMAD4 gene recognized mutation
o Dilated glands with mucin and surface erosion on histology
 Peutz-Jeghers Syndrome
o Auto dominant mutation in STK11 gene
o Benign hamertomatous polyps anywhere in GI tract
o Mucocutaneous hyperpigmentation (lips, oral mucosa, genital skin)
o Increased risk of colorectal, breast, and gynecological cancer
o ‘Arborizing’, pedunculated polyps with bands of smooth muscle
Workup
 FOBT – useless for the most part. If positive, you proceed with work-up, if negative you don’t have
enough negative predictive value to rule anything out…and proceed with workup
 Colonoscopy- the first step with clinical suspicion of CRC. Visualization and biopsy of any suspicious
lesions is key for diagnosis and treatment plan management
 Labs: CBC, Carcinoembryonic Antigen (CEA; post diagnosis, nice to help follow treatment response as
many things mal elevate CEA), LFTs (looking for liver mets)
 Imaging:
o Colon Cancer: CT c/a/p (check for mets; 20% of pts present with metastatic disease); PET scan
may be used but is not routinely needed
o Rectal Cancer: trans-rectal ultrasound & MRI a/p to better characterize/stage disease. The goal
is to preserve the sphincters surgically and assess the need for neoadjuvant chemotherapy
Staging
 0 – only involvement mucosa
 I – invades mucosa and submucosa
 II – invades through muscle layers and nearby tissues/organs
 III – lymph node involvement
 IV – distant metastatic spread
Management
 Bowel prep – oral polyethelene glycol +/- non-absorbable Abx to clear stool and decrease bacteria
from the gut. Helps with visualization and minimizes stool spillage in colon surgery
 Polyps – polypectomy or segmental resection with surveillance from 1-5 years
 Colonic Resection + Lymph Node dissection – depends on location of cancer
o Right-sided cancer – right colectomy + ligation of ileocolic artery
o Transverse colon – transverse colectomy or extended right colectomy + ileocolic/middle colic
artery ligation
o Left-sided colon – left colectomy with ligation of the IMA
o Sigmoid colon – left colectomy with ligation of the IMA
 o A minimum of 12 lymph nodes must be resected for accurate staging
 Neoadjuvant Chemotherapy – often used in rectal cancer in hopes of sphincter-sparing surgery as well
as later stage colon cancers (rarely in early stages)
 Radiation – used only in rectal cancer as it can be administered locally; colon cancer would require
whole pelvis radiation (which causes radiation enteritis and increased risk for further cancer!)
Complications of Colon Surgery
 Injury to the ureter/duodenum/spleen – often avoided with careful dissection
 Anastomotic leak – POD 1-7 with fever, abdominal pain/tenderness, ileus, and leukocytosis; if
confirmed, re-operation for resection/washout/ostomy diversion are required

Chapter 22: Chronic Constipation + Severe Abdominal Pain – Large Bowel Obstruction
Differential Diagnosis: colon cancer, diverticulitis, stricture, volvulus, fecal impaction, Ogilvie’s syndrome
(pseudo-obstruction), toxic megacolon
 Constipation – low frequency of stools (<3/week)
 Obstipation – complete lack of gas or stool per rectum (big suggestion of bowel obstruction)
Presentation
 Vital signs: fever/tachycardia (inflammation from bowel ischemia), & tachypnea (enlarged bowel
making it hard for diaphragmatic excursion)
 Abdominal Exam: little/no tenderness, distention, tympani; possible signs of irreducible hernia
 Rectal Exam: often empty, but may be with palpable mass (impacted stool, neoplasm, stricture)
 Often less or later onset vomiting (vs SBO) and decreased bowel sounds (vs SBO)
What causes abdominal distention? (5 Fs)
 Fat (big belly), feces (impaction), fetus (pregnancy belly), flatus (ileus/obstruction), and fluid (ascites)
Pathophysiology
 Most common causes – malignancy (CRC) is #1, then diverticulitis/stricture, then volvulus
 Left sided CRC is most likely to cause obstruction due to smaller diameter of the descending colon
 Ogilvie’s Syndrome – “pseudo obstruction” which will present nearly identical to LBO, but occurs in
debilitated hospitalized patients. Pt will often develop while in their hospital stay for something else
(most classically in the post-operative setting!)  neostigmine is Tx of choice
 Malrotation of the Gut – congenital condition where gut formation has not undergone proper rotation
during development. This puts the bowel and its mesentery out of normal position and often without
proper attachment.
 Volvulus – actual twisting of the gut to cause obstruction. It may be a result of malrotation!
o Cecal Volvulus – occurs due to congenital malrotation, cecum/right colon not properly attached
to peritoneal wall, thus allowing them to freely twist
o Sigmoid Volvulus – acquired condition where progressive stretching can cause twisting of the
sigmoid around it’s small mesentery. Risk factors all include things that can cause constipation
(anti-cholinergic drugs, stool retention, CF, Chagas’ disease, high fiber diet, etc.)
o Complicated volvulus – the result of volvulus causing ischemia and eventually gangrenous
bowel/sepsis! Severe abdominal pain, fever, tachycardia, altered mental status, and marked
tenderness (peritoneal signs) can all point to this
Work up
 Labs: CBC (leukocytosis), serum lactate (lactic acidosis), CMP (electrolyte imbalance/dehydration)
 Imaging:
o 1st imaging study = Abdominal (upright and supine) & chest (upright) X-rays
 Distended large bowel can be indicative of obstruction
 Mesentery twisted around the center (“coffee bean sign” or “bent inner tube sign”)
indicates large bowel volvulus as the cause
 o Additional imaging = CT with oral/IV contrast OR Contrast enema
 Can show “whirl sign” of volvulus
 Enema can be diagnostic and therapeutic as the enema may unblock the bowel
Management
 1st step: IV fluids + foley catheter placement + NG tube placement for decompression of gut
 Uncomplicated sigmoid volvulus: De-torsion via endoscopy (preferred) or barium enema
o If successful: semi-elective sigmoid resection after acute event is over. The recurrence rate is
high, so the best way to stop recurrence is to take out the damn thing. Poor surgical patients
have the option of medical management
o If unsuccessful: go to the OR for surgical de-torsion
 Complicated sigmoid volvulus: due to worry/evidence of bowel ischemia/perforation, colon resection
is mandated without attempts for de-torsion. Intraoperatively, the volvulus portion is removed without
de-torsion and the proximal end is brought out with a colostomy
 Cecal volvulus: surgery is 1st line due to high incidence of bowel necrosis and de-torsion failure
 Ogilvie’s Syndrome: neostigmine + colonic decompression
 Pregnancy + LBO: volvulus is the 2nd leading cause of LBO in pregnancy! Immediate de-torsion with
delayed resection until after birth (if possible)

Chapter 23: Left Lower Quadrant Pain – Diverticulitis

Risk Factors: obesity, low fiber diet, high fat/red meat diet, advanced age
Pathophysiology
 Diverticula
o Most common location for diverticula = sigmoid colon
o Most common site of infection of diverticula = left & sigmoid colon
o Rectal diverticula are very rare, as the tenia coli coalesce into a circumferential band of muscle
in the rectum, which is thought to eliminate weak points in this portion of bowel
o True diverticulum – all layers (mucosa, submucosa, muscularis) are involved
o False diverticulum – only mucosa/submucosa are involved
 Fistulas
o Main causes = diverticulitis (most common), colon cancer, IBD, bladder cancer, radiation injury,
trauma, foreign body
o Cause of failure to close (FRIEND) – Foreign body present, Radiation, Inflammation/Infection,
Epithelialization, Neoplasm, and Distal Obstruction
o Colovesicular fistula – feces/air in urine, recurrent/refractory/atypical UTI (multiple bugs or
anaerobes) due to recurrent seeding with stool
o Colovaginal fistula – feces in the vaginal vault
Presentation
 LLQ pain, nausea, anorexia, low-grade fever, absent bowel sounds
 RLQ pain may present if patient has especially redundant sigmoid colon, which can run into the RLQ
Diagnosis/Workup
 Largely clinical from presentation
 Imaging – CT scan showing diverticular outpouchings
 Note that barium enema and colonoscopy are CONTRAINDICATED as they may exacerbate
inflammation and result in perforation/fistula formation
 Staging (Hinchey Staging system)
o Hinchey I - localized abscess (para-colonic)
o Hinchey II - pelvic abscess
o Hinchey III - purulent peritonitis (pus in the abdominal cavity)
 o Hinchey IV - feculent peritonitis.
o Stage I-III can be managed surgically with laparoscopic approach and washout
Management
 First Step: determine if patient has evidence of SIRS (any two of the following)
o Temperature >100.4 or <96.8
o HR >90
o RR >20 or PaCO2 <32mmHg (hyperventillatory hypocapnea)
o WBC >12,000, <4000, or >10% band forms
 If no SIRS  send home with Abx/clear fluid diet; if SIRS  admit and give IV abx/fluids/analgesia
 Uncomplicated Diverticulitis: it’s only the diverticula and inflammation
o IV abx/fluids/analgesia/NPO; if failure to improve then CT scan for abscess search or movement
to the OR for colon resection!
o 6-8 weeks after resolution  colonoscopy is recommended to search for other disease
processes that might have caused presentation!
 Complicated Diverticulitis: abscess, obstruction, peritonitis or fistula makes for complication!
o Free perforation + diffuse peritonitis – emergent colectomy/colostomy (reversal in 12wk; distal
end of resection is rectum w/loss of taenia coli), proximal end is healthy bowel…not necessarily
parts free of diverticula)
o Large bowel obstruction – urgent colectomy/colostomy
o Large (>4cm) local abscess – CT-guided drainage with elective colectomy
o Small (<4cm) local abscess – IV abx with elective colectomy
o Colovesical fistula – IV abx with elective bladder repair/colectomy
 Note that non-emergent surgery can be repaired with primary anastomoses (you remove part of the
colon, then simply re-attach the two other portions and you’re done (no colostomy for later reversal!)
 Note that a bowel prep has not been shown to reduce infections in these surgeries
 Patients may be medically managed (without elective colectomy) as long as it remains effective.
Recurrences can occur, as long as they’re able to recover medically!

Chapter 24: Neck Pain and Paralysis Following Surgery – Anterior Spinal Artery Syndrome
Differential for Spinal Injury
 Complete spinal cord injury – complete loss of motor/sensory function below level of lesion
o Often penetrating trauma that transects the major tracts of the spinal cord
o Corticospinal tract (motor), posterior columns (proprioception, deep touch/pressure),
spinothalamic tracts (pain/temperature)
 Brown-Sequard syndrome (Cord Hemisection) – ipsilateral motor weakness, UMN signs, & loss of
touch/proprioception + contralateral loss of pain/temperature sensation starting 1-2 dermatomes
below the lesion
o Often penetrating injury to only part of the spinal cord
o Best prognosis for recovery of neurologic function, Bowel/Bladder function, and Ambulation
 Central Cord syndrome – weakness/sensory loss of upper extremity & proximal lower extremity. Distal
lower extremity unaffected (topographic layout of spine lays the lower extremity toward the lateral
portions & upper extremity in the central portions!)
o Classic is injury from severe extension injury (elderly with cervical subluxation)
 Anterior spinal artery (anterior cord) syndrome – paraplegia/loss of pain & temperature sensation;
preserved deep touch/pressure, vibration, and proprioception (posterior columns preserved)
o Classic is patient undergoing AAA repair with damage to the artery of Adamkiewicz; may also
occur with severe flexion injury
o Worst prognosis for recovery of ambulation (10%)
H&P
 Most common cervical spinal levels damaged in trauma  C2 (33%) > C6 > C7
 Most common cervical spinal level suffering subluxation damage  C5-C6 interspine (most mobility)
 Upper Motor Neuron Signs – weakness, increased tone, spasticity, hyperreflexia, clonus, (+)Babinski, &
(+)Hoffmann (no fasciculation, no atrophy)
 Lower Motor Neuron Signs – weakness, fasciculation, atrophy, decreased tone, loss of reflex,
diminished sensation along dermatomes (no clonus/special reflexes)
 Radiculopathy – damaged nerve root; burning/tingling pain radiating down the limb and LMN signs
 Myelopathy – damaged to spinal cord; radiating pain at level of lesion and UMN signs
 Some Classic Dermatomes – C4 (Shoulder), T4 (nipples), T10 (umbilicus), L4 (knees), S4-S5 (perianal)
o When examining the chest, note that dermatome levels will jump from C4  T1 with the other
cervical dermatomes covering the upper extremity
 Deep Tendon Reflexes
o Classics: C5/6 (biceps), C6 (brachioradialis), C7 (triceps), L4 (patella), S1 (achilles)
o Grading: 0 (none), +1 (sluggish), +2 (normal), +3 (brisk), +4 (clonus)
 Quick Facts
o Complete spinal cord lesion at or above C3 may cause diaphragmatic paralysis (thus death) and
paralysis of all four limbs
o Differentiating a complete vs incomplete spinal cord section is as simple is seeing if there is no
function (complete) or some residual function (incomplete)
o Babinski Sign is NORMAL in a child <2yr, but may occur in UMN lesions
Pathophysiology
 Spinal Shock – temporary syndrome resulting in flaccid paralysis, loss of all reflexes, and loss of
urinary/rectal tone below the level of the lesion
o Sacral sparing occurs when the sacral nerves (perianal sensation/anal sphincter tone) are
preserved and is a good sign of recovery in pts with spinal shock
 Neurogenic Shock – shock due to loss of sympathetic outflow from the spinal cord (vasodilation,
bradycardia, hypotension)
 Neck injury is commonly due to flexion, extension, axial loading (vertical compression), or rotation
o Thoracic spine is much more rarely injured; this is due to their better fixation of the thoracic
vertebrae from high facets/rib fixation as well as no anterior herniation of the T-spine
 Atlanto-Occipital Dislocation – dis-articulation of the atlas facets from the occipital condyles of the
head, causing severe instability in the cervical spine (quadraplegia, diaphragm paralysis)
o Kids with trisomy 21 have a heightened risk for this and should be screened prior to sports
participation (classic is before the special Olympics)
Work-Up
 Neurologic exam – elucidates deficits allowing for neurologic diagnosis
 X-ray/CT/MRI – used to correlate with neurologic exam findings to confirm suspicions
 NEXUS Criteria – criteria to clinically ‘clear’ patient of a C-spine fracture. If they have any of the
following criteria, the should have a 3-way cervical spine X-ray
o ‘NSAID’: Neurologic deficit (focal), Spinal Midline Tenderness, Altered Mental Status,
Intoxication, Distracting injury
o 3-way cervical spinal X-ray: anteroposterior (AP, lateral, and open mouth (odontoid)
 Cervical CT – used to investigate anything abnormal seen on X-ray; allows good evaluation of
fractures/hematomas/disc fragments & clearance for surgery in a comatose patient
 Cervical MRI – best used in assessing lesions to the spinal cord to better characterize neurologic
deficits & best for ant soft tissue damage
o Necessary to evaluate patients with SCIWORA
  Spinal Cord Injury Without Radiographic Abnormality (SCIWORA) – typically occurs due to contusion
or stretching of the spinal cord, so no overt injury has occurred.
o Most common in pt age <3yr & at the C2 level spinal column
o Can only be evaluated properly by MRI imaging
Management
 General Idea for Tx of Cervical Spinal Injury – immobilize patients with rigid cervical collar/spine board
o Maintain BP (fluids/pressors), insert Foley (monitor urine output, prevent bladder distention),
give stool softeners to prevent severe constipation, prevent DVT with compression/anticoag.
o External orthoses may be used to provide additional stability support
 Neurogenic shock is managed by IV fluids + pressors (for BP) + inotropes (for bradycardia)
 Complete/high spinal cord injury is managed by spinal stabilization, surgical decompression in still-
intact spinal cord, physical rehab, prevention of decubitus ulcers, bowel/bladder management, and
prevention of DVT and pneumonia
 Incomplete spinal cord injury is treated essentially the same as complete/high, but decompression is
typically more aggressive in as there is a higher chance for regain of function in the partially sectioned
spinal cord
 Emergent Surgery in Spinal Cord Injury is warranted with unstable vertebral fracture, non-reducible
spinal cord compression with deficits or ligamentous injury with facet instability
Complications
 When exposing the anterior cervical spine for decompression, the recurrent laryngeal nerve may be
inadvertently cut leading to hoarse voice (unilateral) or dyspnea/increased aspiration risk (bilateral)

Chapter 25: Loss of Consciousness Following Head Trauma – Traumatic Brain Injury
Differential Dx (Pt GCS <8 with TBI)
 Epidural Hematoma – MMA laceration by temporal bone fracture resulting in blood accumulation
between the dura mater and the skull
o Classically blunt head trauma causing a brief loss of consciousness (brainstem arousal center
disruption)/fracture  lucid interval  loss of consciousness with rapid decline (blood
accumulation/herniation from hematoma mass effect)
o “Lens-shaped” bleed on CT head
o Often rapidly expanding due to arterial source and may need emergent evaluation
 Subdural Hematoma – bridging vein rupture causing bleed between dura/subarachnoid layers
o Classically in old folks/alcoholics/anti-coagulated pt with mild trauma (fall from standing)
 Regular brain atrophy in elderly puts tension on bridging veins increasing risk!
o “Crescent-shaped” bleed on CT head
o Acute SDH – occurs within 72hr of insult, often in younger pt or very bad injuries
o Chronic ADH – often in the elderly with insidious onset of abnormal gait, decreased
consciousness, aphasia, cognitive dysfunction, memory loss, and personality changes
 Intraparenchymal Hematoma – bleeding within brain parenchyma often from aneurysm rupture or AV
malformation bleeding due to hypertensive hemorrhage. Rarely caused by primary brain contusion.
 Subarachnoid hemorrhage – bleeding into the normally CSF-filled subarachnoid spaces. Due to either
trauma or vascular rupture
o “Worst headache of my life” (“thunderclap headache”) is a classic complaint
 Diffuse Axonal Injury – acceleration/deceleration injury resulting in axonal stretching between grey &
white matter causing injury
o Pathology of “shaken baby syndrome” or other traumatic event without obvious bleed
H&P
  Traumatic Brain Injury (TBI) – injury to the brain that results in function (loss of consciousness, loss of
memory surrounding accident, altered mental status, or focal neurologic deficit)
 Glasgow Coma Scale (GCS) – exam designed to quickly evaluated head trauma patients and monitor
improvement or deterioration. Add up your three categories and that’s your number!
o Eye Opening – 1(none), 2(pain), 3(voice), 4(spontaneous)
o Verbal – 1(none), 2(nonsense), 3(inappropriate), 4(confusion), 5(oriented), T1(intubated)
o Motor – 1(none), 2(decerebrate), 3(decorticate), 4(pain withdraw), 5(local pain), 6(commands)
o GCS <8 is considered a ‘coma’ and should be intubated
o Note that GCS may be skewed by alcohol/drugs, sedative, hypoxia, shock, & hypothermia
 Signs of Basilar Skull fracture
o Battle’s Sign – retroauricular ecchymosis
o Raccoon eyes – bilateral periorbital ecchymosis
 Localizing the brain lesion on physical exam is as easy as looking for contralateral paralysis (disruption
of neural tracts) and ipsilateral abnormal pupillary findings (uncal herniation compressing CNIII). Thus
right side paralysis + left side abnormal pupil points to the TBI being on the right side
 Kernohan syndrome – paralysis and pupil abnormalities occur on the same side. This is due to an
abnormal herniation of the cerebral parenchyma making paralysis a “false localizing sign”
 Decorticate posturing - abnormal UL flexion with abnormal LL extension (loss of cortical input)
 Decerebrate posturing – abnormal extension of UL/LL (loss of cerebral input)
Pathophysiology
 Concussion – mild TBI causing problems with memory, balance, coordination, & concentration.
Headaches, dizziness, confusion, personality changes, and irritability may also occur
 Uncal Herniation – herniation of the uncus; results in compression of ipsilateral CNIII (ipsilateral blown
pupil) and ipsilateral cerebral peduncle (contralateral hemiparesis)
 Cerebral Perfusion Pressure = mean arterial pressure (MAP) – intracranial pressure (ICP)
o ICP is controlled by brain tissue, CSF, and blood within the cranial vault; to keep ICP constant
these three things will attempt to offset each other as a neural auto-regulatory response
o Knowing this, intracranial bleeds will increase ICP, subsequently decreasing cerebral perfusion
o Also, CO2 levels are the greatest drive of cerebral perfusion (more CO2 = more perfusion); thus
hyperventilation to blow off CO2 can have temporary benefit by decreasing ICP and allow for
longer time of effective cerebral perfusion
o Also note, that a patient will NOT spontaneously start breathing if they’ve been on high vent
settings (low CO2) as there is not enough CO2 drive for respiration on the brain. So don’t be
surprised if a patient is apneic if you try to take them off the vent after hyperventilating them
 Cushing’s Triad – hypertension, bradycardia, and irregular respiratory rate with increased ICP
o Hypertension – reflexive effort to maintain CPP with increased ICP (via vasoconstriction)
o Bradycardia – reflexive response to elevated BP from vasoconstriction set off by ICP
o Irregular respiratory rate – the combination of severe bradycardia and ICP not being offset by
BP results in medullary dysfunction (breathing center)
 Coup – direct brain injury sustained at the point of impact
 Countrecoup – brain injury sustained at the opposite side of the coup from the brain sloshing back and
striking the inside of the skull in response to the coup
Initial Management
 Assess and address the ABCs, neurologic exam, and assessment of injuries
 Intubation warranted with GCS <8
 Correction of any coagulopathy to aid in minimizing new/ongoing bleeding
 Imaging
 o Initial: Non-contrast CT of the head is warranted with anyone GCS <12 or with risk factors
(elderly, anti-coaglated, alcohol abuse)
o Repeat: new neurologic signs, continued vomiting, worsening headache, loss of >2 on GCS,
signs of increasing ICP
 Intracranial Pressure Monitoring is warranted when:
o TBI (GCS<8) with abnormal CT
o TBI (GCS<8) with normal CT + any of two of these (hypotension, abnormal posturing, age >40)
o Monitored via ventriculostomy tube (may also be used to drain CSF if pressure is too high)
 Increased ICP (>20mmHg) Treatment
o Intubate/paralyze – rocuronium/etomidate preferred as succinylcholine/ketamine increase ICP
o Mild hyperventilation – goal of PaCO2 30-35mmHg; <30 causes decreased cerebral bloodflow
o Elevate head of the bed (30-45o) – allow for better venous drainage
o Loosen cervical collar if restricting venous flow – buildup of venous pressure isn’t good!
o Mannitol – doesn’t cross BBB, allowing for shift of fluid from intracranial vault to peripheral
vessels, and diuresis. Avoid in patients with hypotension/hypovolemia (duresis will worsen this)
and pts with kidney failure (can’t handle the mannitol diuresis)
 Hypertonic saline may also be used for a similar effect
o Barbiturate coma may be induced if the above treatments are not working well enough
 Craniotomy Indications
o Drilling holes into the skull cranium to relieve pressure
o Epidural hematoma >30mL in volume OR causing >10mm midline shift
o Acute subdural hematoma >5mm thick or causing >10mm midline shift
 Decompressive craniotomy indications
o Removing parts of temporal skull to relieve even more pressure
o Failure of medical management
 Brain Death Criteria
o Testing warranted only if pt has GCS of 3; pt must be euthermic (>32.2C), PaO2 >90mmHg,
systolic BP >100mmHg, & cannot be paralyzed/sedated (proven with serum/blood testing)
o 1. Absence of Brainstem Reflexes (corneal, gag, oculocephalic, and oculovestibular)
o 2. No response to deep, central pain
o 3. Agreement of Two physicians
o 4. Apnea Test (no spontaneous respirations with PaCO2 >60mmHg

Chapter 26: Multiple Extremity Injuries After Motorcycle Accident – READ ONLY
Chapter 27: Immediate Swelling After Trauma to the Knee – READ ONLY
Chapter 28: Right Groin Pain/Limp – READ ONLY
Chapter 29: Chronic Right Hand Pain – READ ONLY

Chapter 30: Full Term Male Infant with Respiratory Distress – Congenital Diaphragmatic Hernia
Differential Dx:
 Transient Tachypnea of Newborn: most common cause of respiratory distress in term babies; residual
pulmonary fluid remains in lungs after birth
o Benign and should only last hours-days
o CXR: diffuse pulmonary infiltrates + “wet silhouette” around the heart
 Hyaline membrane disease (Respiratory distress syndrome): most common cause in premies
o Poor surfactant production in premature Type II alveolar cells
o CXR: homogenous pulmonary infiltrates + ‘air bronchograms’
 Meconium aspiration syndrome: meconium stained amniotic fluid will be noted at birth
  Persistent pulmonary HTN, bronchial atresia, pulmonary agenesis, pneumonia, and non-pulmonary
etiologies are less common but possible
Presentation
 Prenatal Screening: will be picked up at the latest around 24wk gestation on ultrasound (bowel loops
in thoracic cavity, contralateral displacement of heart/mediastinum)
 Displaced heartbeat: loops of bowel is moving the heart/mediastinum away from hernia
 Tachypnea/tachycardia/absent breath sounds/bowel sounds in chest: displacement/poor
development of lung tissue from infiltrating bowel causing respiratory distress/poor formed lung tissue
 Scaphoid abdomen/ Barrel shaped chest: loops of bowel moving out of abdomen and into the chest
 Supracostal retractions/grunting: sign of severe respiratory distress/impending cardiovascular
collapse. Baby should be intubated and placed on mechanical ventilation.
Pathophysiology
 Failure of the septum transversum to divide the pleural & coelomic cavities during development
(typically finished by week 12) allows for bowel herniation during critical lung development resulting in
lung hypoplasia.
 Mediastinal shifting also causes compression of the contralateral lung
 When the baby takes their first breath; normally pulmonary circuit pressure goes from high resistance
 low resistance, allowing for pressure changes in the heart to allow for adult circulation to be
established (closure of foramen ovale, ductus arteriosis, etc.)
 Lung hypoplasia + contralateral lung compression keeps pulmonary vasculature resistance high.
Resultant hypoxemia/acidosis/hypotension cause pulmonary vasoconstriction, further worsening flow
into the pulmonary circuit
 The poor pulmonary flow results in acute respiratory distress/hypoxemia/retention of CO2
Anatomy
 Side of defect: Left side most common (85%), right side (10%), and bilateral (5%) is most rare.
 Portion of diaphragm affected:
o Bochdalek hernia: posteriolateral defect (most common; cause classic symptoms)
o Morgagni hernia: parasternal or retrostenal (rare; often no pulmonary problems, but
symptoms of bowel obstruction)
o Diaphragmatic eventration: thinning of intact diaphragm due to poor muscularization (rare!)
o Diaphragmatic agenesis: no diaphragm; very severe
 Many children have additional accompanying anatomical defects (malrotation/non-rotation, ASD/VSD,
horseshoe kidney, polydactyly, NTDs, hydrocephalus, Trisomeies, etc.)
Workup
 Child unstable  immediate intubation
 Child stable or recently intubated  undergo NGT/OGT tube placement
 NGT tube placement where NGT fails to pass  Choanal atresia
 NGT/OGT passes past pharynx + CXR
o Tube won’t pass through esophagus + gas in abdomen  esophageal atresia + TEF
o Tube won’t pass through esophagus & no gas in abdomen  esophageal atresia & no TEF
o Tube in stomach but abdominal contents in thorax  CDH
o Tube in stomach with normal abdomen  cystic lung lesion or bronchopulmonary sequester
Prognosis
 Survival rate between 60-80% and directly correlates with degree of hypoplasia
Management
 First Step: intubate if in respiratory distress
o Best to intubate immediately without bag-mask oxygen delivery, as the air rush of the bag-mask
can cause significant barotrauma to the already poorly functioning lung tissue
  Second Step: placement of NGT/OGT with suction to decompress stomach (open up more space for
compressed lungs) & search for atresias
 Third step: admission to NICU with proper blood pressure/ventilator support
o FiO2 100%; PEEP at 3-5cmH2O; permissive hypercarbia (PCO2 <60mmHg) and O2 saturation
levels between 80-95% are acceptable to minimize barotrauma of aggressive ventillation
o Nitric oxide inhalation may be used to decreased pulmonary HTN
o Extracorporeal membrane oxygenation (ECMO) may be used if child is refractory to these things
 Surgical Repair of Defect: delayed until evidence of lung maturation in NICU (simply with time and
support). Whenever pt is being weened down on vent settings, surgery can be considered.
 Work-up for further congenital anomalies is also warranted

Chapter 31: Newborn with Bilious Emesis – Duodenal Atresia

Presentation
 Bilious Vomiting: yellow/green stained vomit proves that the GI tract is patient past the Ampulla of
Vater (rules out pyloric stenosis). Typically, this type of vomiting indicates a surgical problem
o Note that 20% of pts with duodenal atresia will have it before the Ampulla of Vater; this will
lead to non-bileous vomiting. Thus, just because it’s non-bileous, doesn’t mean it’s not
duodenal atresia.
 Polyhydraminos: too much amniotic fluid; can be an indicator impaired swallowing (which includes GI
obstruction) or urine overproduction (maternal diabetes, twin pregnancy)
 Passage of meconium: yes, even with bowel obstruction, the infant may still pass meconium. Lanugo,
amniotic fluid, bile will not be able to form it, but mucus is shed throughout the GI tract (even with an
obstruction) thus can form meconium
 “Double Bubble” sign on CXR: two pouches of gas (stomach and proximal duodenum) seen due to gas
filling the stomach, a stricture point at the pyloric sphincter, then gas filling duodenum proximal to the
atresia point.
Pathophysiology
 Bowel obstruction may in intrinsic (duodenal atresia) or extrinsic (annular pancreas, adhesive Ladd’s
bands); but gas throughout the bowel with signs of obstruction points to partial obstruction vs total
 Duodenal development involves lumen obliteration around week 8, with subsequent re-canalization
afterward. Failure of recanalization results in obstruction
 Jejunal/Ileal development does not undergo this obliteration/recanalization process and obstruction is
the result of poor bloodflow causing segmental ischemia  segmental obstruction
 There are several associated abnormalities with duodenal atresia with the top 4 being Down’s
syndrome, Annual pancreas, Malrotation of the gut, and congenital heart disease.
Workup
 First Step: IV access, fluid resuscitation, NGT placement for stomach decompression
 If unstable: suspect malrotation/volvulus  prophylactic ABX + exploratory laparotomy
 If stable: AP/lateral CXR
o No dilated loops of bowel (proximal obstruction) + Double bubble + no distal bowel gas =
duodenal atresia
o No dilated loops of bowel (proximal obstruction) + Double bubble + distal bowel gas  Upper
GI contrast study
o Dilated loops of bowel (distal obstruction)  contrast enema to assess Lower GI tract
Management
o Workup as indicated above
o Surgery should be delayed for thorough workup if patient is stable; but clinical instability warrants
emergent trip to the OR for exploratory laparotomy for repair of malformed gut
Areas to Get in Trouble
o Inadequate resuscitation before emergent surgery  hypovolemia can result in hypotension that’s
exacerbated by anesthesia, which may lead to shock!
o Not working up cardiac defects  nearly 20% of babies with duodenal atresia will have cardiac defects
due to comorbidity with Down’s Syndrome! These may take precedence over the GI problem and
should be addressed first.
o Damage to annular pancreas  this is another common co-malformation with duodenal atresia. In
surgery care must be taken to not damage the pancreas as it may lead to pancreatic enzyme leak!

Chapter 32: Infant with Bilious Emesis – Malrotation with Midgut Volvulus
Bilious Emesis Differential Based on Age
 Any age – Adhesions, Hirschprung’s disease, incarcerated inguinal hernia, malrotation w/volvulus
 Neonate (0-1mo) – annular pancreas, duodenal atresia, imperforate anus, jejunoileal/colonic atresia,
meconium ileus, meconium plug, necrotizing enterocolitis
 Infant (1-24mo) – intussusception
 Child (2-12hr) – ileus 2nd to appendicitis, intussusception
Presentation
 Bilious or nonbilious vomiting (depends on part that has undergone volvulus) should always prompt a
search for midgut volvulus, as it can be a life threatening condition!
 Basically any developmental defect (esp of the gut) puts a patient at risk for volvulus
Pathophysiology
 The midgut is defined by receiving blood from the superior mesenteric artery (starting at the Ligament
of Treitz) and includes the 2nd part of the duodenum through the proximal 2/3 of transverse colon
 Development of the midgut occurs in the 6th week of gestation with rapid elongation and herniation
into the umbilicus. Ultimately this section of bowel undergoes 270 o of counterclockwise rotation,
finally finding it’s final resting spot around week 12.
 Malrotation occurs when midgut starts to take it’s first 90o angle turn and return from it’s herniated
position back to the abdominal cavity. Improper fixation causes the remaining 180 o of turning to occur
around the midgut mesentery, giving the classic “corkscrew” appearance.
 Problems occur when this bowel becomes kinked, resulting in obstruction and strangulation  bowel
ischemia and eventually death/perforation
 While acute volvulus is an emergent surgical event, malrotation doesn’t necessarily cause volvulus AND
volvulus may “kink and un-kink” causing colicky symptoms chronically.
Workup
 If patient is hemodynamically unstable, skip imaging and go to the OR
 Abdominal X-ray: exclude perforation (free air under diaphragm)
 Upper GI series with contrast: show the course of the gut and will be diagnostic for volvulus
o Most commonly, this is a normal study
o Classically shows “corkscrew” gut from improper rotation around mesentery
Management
 If free air under diaphragm or hemodynamically unstable proceed to surgery without more imaging
 Surgical fixation is necessary for resolution of malrotation/volvulus
o IV fluid resuscitation + ABx + NGT for stomach decompression + emergent laparotomy
o If bowel is not infarcted  Ladd’s Procedure (un-twisting, division of Ladd’s bands, fixation +
prophylactic appendectomy to avoid confusing symptoms later in life should appendicitis occur)
o If bowel is infarcted  bowel resection with Ladd’s Procedure
 During surgery; large bore NGT should be passed through the end part of the duodenum to rule out
atresia or other malformations of the gut
  If pt is found to have asymptomatic malrotation, surgery the the earliest convenience should be done

Chapter 33: Infant with Non-Bilious Emesis – Hypertrophic Pyloric Stenosis

Differential Dx
 Surgically managed: antral web, pyoric atresia, pyloric stenosis, GERD from anatomic defect
 Medically managed: acute gastroenteritis, GERD, metabolic disorders, pylorospasm
Presentation
 Healthy baby with progressive non-bilious, projectile vomiting immediately following meals; baby will
always seem hungry despite vomiting (“hungry baby!”)
o Vomiting only food/mother’s milk directly after or during feeding sessions
o Olive shaped mass can be palpated and visible peristalsis can be seen in upper abdomen
o Sunken fontanelles from dehydration
 Risk factors: first-born child, erythromycin administration, formula feeding (late presentation at 3-5wk)
Pathophysiology
 Poorly understood; but histologic evidence points to immature/absent ganglia resulting in inability of
pylorus to relax, resulting in hypertrophy/hyperplasia and obstruction
 Stomach muscle hypertrophy/dilation occurs due to vigorous peristalsis in attempts to pass chyme
through the obstructing pylorus
 As stomach peristalsis strength grows, it becomes so intense that is overwhelms the lower esophageal
(cardiac) sphincter, resulting in projectile vomiting
Workup
 If palpable “olive” is appreciated  this is diagnostic, no further workup needed
 If no “olive” is appreciated  abdominal ultrasound showing pyloric thickness >3mm & length >15mm
are typically diagnostic (although this number can change with age!)
 If still uncertain or negative ultrasound with high suspicion  upper GI series with contrast showing
delayed emptying, retrograde peristalsis, and “string sign”/”tit sign” at the pylorus is diagnostic
o Major concern for aspiration of contrast fluid (as the child will surely vomit anything in it’s
stomach; thus this test should be done only if needed!)
 CMP may show a hypochloremic, hypokalemic metabolic alkalosis from protracted vomiting
o Hypochloremia – loss of Cl- ions from HCl in vomit
o Hypokalemia – dehydration from vomiting results in aldosterone activation to restore
intravascular volume with subsequent Na+ retention and K+ wasting
o Alkalosis – with decreasing K+, but still demand for Na+ resorption, the kidney is less able to
used the Na+/K+-antiporter. Na+ traveling more distally in the nephron results in more activation
of the Na+/H+ antiporter, wasting H+ to save Na+ resulting in paradoxical aciduria.
Management
 First Step: IV access with fluid resuscitation for protracted vomiting in this order:
o 1st - Isotonic normal saline bolus at 20mL/kg
o 2nd – D5 with ½NS at 1.5x normal infusion rate
o Once child urinates – add 20mEq/L KCl to the already running fluid
o Electrolyte abnormalities should be corrected before surgery
 Ramstedt pyloromyotomy – small incision into pylorus with spreading and fixation of the muscle to
relieve the obstruction; air or methylene blue are introduced via NGT to prove patency/lack of leak.
o Should be delayed until proper fluid resuscitation/electrolyte balancing has occurred
o Optimal fluid status shows normal urine output, serum bicarb <30mmol/L and normal K+
o Pt should be able to eat a few hours following surgery, although post-op vomiting isn’t
uncommon. Vomiting 3-4 days following surgery indicated complication
Areas of Trouble
  Inadequate fluid resuscitation may lead to anesthesia induced hypotension/death
 Leak – fever, tachycardia  feeding intolerance, leukocytosis  peritonitis, sepsis; must be re-
operated on to fix the leak

Chapter 34: Infant Born with Abdominal Wall Defect – Omphalocele/Gastroschisis

Differential Dx
 Gastroschisis – discussed below
 Omphalocele – midline abdominal wall defect with herniation of gut contents; amnioperitoneal
membrane covering gut contents, umbilical cord insertion into this membrane; heightened risk for
abnormal formation of other systems; liver herniation may allow for earlier detection
 Bladder/Cloacal Exstrophy – exstrophy of sac filled with hemi-bladder/urethra/kidney/intestine;
typically occurs inferior to umbilical stalk, often sac partially divides two hemi-bladders (inside and
outside), often extensive associated developmental defects
 Prune Belly Syndrome – abdominal wall hyposplasia, gut contents held within collagenous wall
(making it “pruned”), 95% males, associated with UG system underdevelopment (hypoplastic prostate,
bilateral undescended testes, infertility, bladder outlet obstruction)
 Urachal Abnormality – communication between bladder/anterior abdominal wall from poor/absent
ablation of the urachus. May be fistula/cystic sac/small outpouching. Associated with NTDs and
omphalocele
Gastroschisis
 Risk Factors: <20yr, white race, single pregnancy, low BMI, frequent UTIs, cigarette smoking, drug or
alcohol use
 Presentation: Paraumbilical (right sided), small (<5cm) abdominal wall defect with evisceration of gut
contents and sometimes associated evisceration of gonads, bladder, & stomach
o Lacks membrane covering cut contents (gut exposed to open air)
o Cord insertion is normal at the umbilicus
o Causes matting, dilation, and thickening of bowels; malrotation is common; Ileus is common
o Rarely associated with other developmental abnormalities; intestinal atresia rarely (10-25%)
o Maternal AFP may be mildly elevated
 Pathophysiology: not totally clear, but thought to be due to vascular accident in the umbilical ring
resulting in poor development and defect development. Right sided defect is thought to be more
common due to involution of the right umbilical vein
o Bowel abnormalities are due to extended exposure to amniotic fluid causing inflammation
 Workup: Covering/Peds Surgery consult, blood labs, IV fluids, urine output monitoring, Full body X-ray
for anatomic survey/implanted device location check
 Management:
o Initial: stabilize airway, Central/Peripheral IV access, IV fluids, cover with sterile plastic wrap,
warming lamp, OG-tube decompression, urinary catheter, broad spectrum Abx
o Place viscera in sterile dacron-silastic silo to allow for gradual reduction as inflammation slows
o Attempt reduction & schedule for surgical reduction when abdominal laxity will facilitate repair
o Ventilation/fluid & nutrition support with intra-abdominal monitoring for healing
Omphalocele
 Risk Factors: <20 or >40yr, high BMI, SSRI use/family Hx
 Presentation: Umbilical/epigastric/or hypogastric variable sized (but often large) abdominal wall defect
with herniation of gut and sometimes the liver into a membrane sac
o Covered in amnioperiotneal membrane (10-20% will rupture)
o Cord insertion is into the amnioperiotneal membrane
o Bowl is typically normal appearing; malrotation often present; bowel function normal
 o Commonly associated with other developmental disorders (Beckwith-Wiedemann, Trisomy
13/18, Pentology of Cantrell, various defects of the gut
o Maternal AFP severely elevated
 Pathophysiology: results from arrest of lateral-body fold migration and body wall closure during
organogenesis. When normal gut herniation occurs around week 5, development arrests, leaving the
herniated gut in place until birth. This is thought to be due to a failure of cell migration, thus the higher
association with concomitant developmental defects.
o Note that liver herniation (giant defect) is rarely associated with chromosomal abnormality!
 Workup: Peds Surgery consult, blood labs, IV fluids, urine output monitoring, Full body X-ray for
anatomic survey/implanted device location check
o Echocardiography for assessment of heart defects & genetic testing also recommended
 Management:
o Initial: stabilize airway, Central/Peripheral IV access, IV fluids, cover with sterile plastic wrap (if
sac is ruptured), warming lamp, OG-tube decompression, urinary catheter, broad spectrum Abx
o If ruptured – follow gastroschesis algorithm
o <2cm defect – immediate surgical reduction  support for healing
o 2-9cm defect – place viscera into sterile dacron-silastic silo for reduction  surgery/support
o >9cm defect – apply sclerosant to sac/cardiopulmonary stabilization  sterile dacron-silastic
silo for reduction  surgery/support
Which is More Urgent? Why?
 Short Term – Gastroschisis. The exposed, inflamed, nonfunctional bowel requires immediate
protection and surgical correction. The child also has increased insensible fluid losses which can also
cause problems
 Long Term – Omphalocele. The child has a protected, functional bowel. However, the high association
with other developmental defects makes the child’s future development very difficult and sometimes,
not viable.
Areas to Get in Trouble
 Remember to note respiratory distress and intubate as necessary
 Remember to carefully check for bowel ischemia/necrosis and address as needed
 Remember to wrap bowel in plastic wrap & warm with lamp immediately. Moist gauze is avoided as it
is not water-tight and will cause significant loss of insensible fluids
 TPN should be provided to patients with slow return of bowel function. Matted/inflamed bowels are
likely to be non-functioning.
 Post-reduction, abdominal compartment syndrome (low urine output, insufficient ventilation, positive
fluid balance) may occur. It should be monitored with intra-abdominal pressure monitoring.

Chapter 35: Excessive Drooling in a Newborn – Esophageal Atresia with Tracheo-Esophageal Fistula
Presentation
 Excessive drooling with white/frothy mucus buildup in mouth/nose
 Cannot tolerate feedings with immediate gagging/choking and vomiting of food
 Oxygen desaturation with feeding – often implies severe abnormality in tracheo-bronchial anatomy
(some of feedings go into the lungs!)
o May result in respiratory distress/pneumonia development
 EA may manifest via polyhydramnios (failure of swallow) on prenatal ultrasound
Pathophysiology
 Esophageal Atresia: Abnormal development of trachea-esophageal fold which normally separates the
caudal primitive foregut into the esophagus and trachea
  TEF: thought to be due to defective epithelial-mesenchymal interactions in a lung bud that fails to
develop. This lung bud wants to hang out with the esophagus and the fistula is formed.
Types of TEF
 Many types with different combinations of defect/TEF
 Type C (proximal esophageal pouch with distal TEF) is most common (85%) with Type A (pure EA
without TEF) being next most common (8%)
Associated Abnormalities
 VACTERL, CHARGE, or Trisomy syndromes are often diagnosed
 VACTERL = vertebral, anorectal, cardiovascular, tracheoesophageal, renal, and limb abnormalities
 CHARGE = coloboma, heart defect, atresia choane, retarded growth, genital defects, and ear defects
Workup
 First Step: Placement of NG-tube with CXR (AP and lateral)
o Gastric bubble presence = some connection between air and stomach (no EA or EA + TEF)
o EA = shows NG-tube coiled in the esophagus/mediastinum or going into the trachea
o Checks for abnormal lungs = pneumonia, primary lung lesions, congenital diaphragmatic hernia
 Contrast esophagram may be used in equivocal findings; however, the concern of aspiration
pneumonitis should reserve this test only if truly necessary
 Diagnosis can be made simply with history and radiologic findings consistent with disease
Management
 First Steps: intubate if signs of respiratory distress, place NG-tube into esophageal pouch/elevate
child’s head (minimize vomiting thus aspiration).
 If pneumonia: broad spectrum Abx & gastrotomy tube for decompression should be placed
 Surgical repair: able to undergo repair surgery as soon as patient is stable/able to tolerate surgery
o Physical exam, cardiac/renal ultrasound, ECG, and X-rays for anatomic survey must be done
prior to surgery to ensure anesthesia tolerance/find all defects for repair
 Complications:
o Esophageal anastamotic leak (15%) – often heal with stricture needing surgical revision
o Strictures (80%) – need esophagostomy and balloon dilation
o GERD (100%) with increased risk of Barrett’s esophagus
 Prognosis: 100% survival rates, but often with significant GI complications that will be addressed
Areas of Trouble
 Interrupted IVC (IVC drains into the azygous vein to get to heart) – the azygous vein is typically divided
during EA/TEF repair. If interrupted IVC is present, this will cause cutoff of lower extremity venous
drainage & death of the patient
 Right-sided aortic arch – rare, but possible (esp. with developmental defects!). Right thoracotomy is
the typical approach for repair, thus right-sided AA would result in disaster. If present, a left
thoracotomy is the proper approach.
 Avoid intubation/ventilation if possible as the abnormal connections between the trachea and GI
tract may result in pumping air into the GI tract  abdominal distention. This distention will compress
lung volumes, leading to worsening lung function (the opposite of what you want!)

Chapter 36: Recently Changed Skin Lesion – Cutaneous Cancers

Pathophys: UV light exposure (esp. UVB) resulting in DNA damage
Risk Factors:
 UV light exposure – ask about childhood blistering/peeling sunburns, use of tanning salons, & overall
sun exposure. All of these can result in double the risk for skin cancers.
 Immunosuppression – difficulty in repairing damage to DNA
 Fair-skinner/blue eyes – less pigmentation to protect from UV rays
  Certain occupations are predisposed to high sun exposure like farmers, lifeguards, construction
workers, gardener, field worker, etc.
 Chronic Skin inflammation (SCC only) – chronic venous ulcers, burns, long-standing infections,
hiradrenitis suppurativa, HPV, etc.

2762/2603: Basal Cell Carcinoma

 Most common, often an excellent prognosis. Correlates with cumulative sun exposure
o Worst subtype is morpheaform (characterized by collagenase production)
o Classically the upper lip will be this type of skin cancer
 Presentation: pearly/rolled edge nodule with keratinized or ulcerated center. Sometimes featuring
spider angiomata on the lesion, oozing or crusting
 Dx: clinical picture and biopsy
 Tx:
o Superficial – excision (3-5mm margin) or local destruction (cryotherapy/electrodessication)
o Deep – MOHS surgery

2604/4033/4319: Squamous Cell Carcinoma

 Intermediate incidence with intermediate prognosis, typically not metastatic when found, but will
invade if left untreated. Correlates with # of severe sun exposure events (burns, tanning beds, etc.)
 Presentation: rough scaly plaque/nodule with possible hyperkeratosis/ulceration/bleeding. Classically
can cause neurologic damage due to perineural invasion (numbness/parastheisa)
o Sunburns, radiation, immunosuppression, burns, scars, and warts are all risk factors
o Note that if you’ve a lesion on the lower lip (more sunlight exposure) is SCC
o Note that a Marjolin ulcer is an SCC arising from the site of a scar/burn/previous injury and has
an increased risk of metastases
o Bowen’s Disease is a SCC in-situ appearing as an erythematous plaque with adherent yellow
crust. While is may become SCC, it has no metastatic potential
 Dx: skin biopsy that includes the deep reticular dermis (assess depth of invasion) showing
dysplastic/anaplastic keratinocytes/keratin pearls
 Tx:
o Low risk: excision (5-10mm margin) or local destruction (cryotherapy/electrodessication)
o High risk or cosmetic areas: Mohs micrographic surgery

2767/2765/4312: Malignant Melanoma

 Arises from melanocytes (neural crest derivatives) either pre-existing or new-onset lesion
 Least common skin cancer, but most deadly
o Considered the most common malignancy of women age 25-29
o Women typically get it on the legs while men get it on the back
o Sites of Metastases: other parts of skin > lung > liver > brain > bone > small bowel
o Most common cancer to metastasize to the small bowel
o Digital melanoma is most commonly on the great toe
 Risk Factors:
o UV light exposure – ask about childhood blistering/peeling sunburns, use of tanning salons, &
overall sun exposure. All of these can result in double the risk for skin cancers.
o Immunosuppression – difficulty in repairing damage to DNA
o Fair-skinner/blue eyes – less pigmentation to protect from UV rays
o Certain occupations are predisposed to high sun exposure like farmers, lifeguards, construction
workers, gardener, field worker, etc.
  Subtypes:
o Superficial Spreading – most common & good prognosis due to long horizontal growth phase
occurring before a vertical growth phase
o Lentigo maligna – best prognosis; appears as a group of freckles growing as a unit
o Acral lentiginous – most common in dark-skinned individuals & poor prognosis likely due to
difficulty in detection. Often subungal, mucous membranes, or on palms/soles. NOT related to
UV light exposure
o Nodular – worst prognosis (rapid vertical growth), much more variable presentation that other
subtypes making it harder to catch in early stages
 Presentation: new or existing melanotic skin lesion demonstrating
o ABCDEs (Asymmetry, Raggy Border, verigated Color, Diameter >6mm, Enlargement or new
symptoms)
o Ugly Ducking Sign (suspected melanoma simply looks out of place next to other benign nevi on
the patient’s skin)
o Metastatic Disease may show palpable lymph nodes or other signs
 Dx: Incisional/punch or excisional biopsy down to dermis to show depth of invasion
o Shave biopsy is inappropriate
o Breslow Thickness will determine severity of disease
o Labs are taken to check for signs of metastatic disease
 If no palpable lymph nodes: CBC, LFTs, LDH, and CXR
 If palpable lymph nodes or signs of metastatic dx: CBC, LFTs, LDH, CT C/A/P & PET scan
 If signs of central neurologic Dx: MRI of brain
 Tx: surgical excision with wide margins (1-2cm)
o Margins will depend on Breslow Thickness
o Sentinel Lymph node biopsy is indicated in patients with depth >0.75mm
o Lymph node dissection indicated in patient with palpable
o Adjuvant therapy is of questionable benefit and isn’t always used
o MOHS surgery is considered a poor option for melanoma due to difficulty in obtaining stained
histologic slides during the surgery necessary for visualization
o If fingernail melanoma: amputation of finger at joint just proximal to the lesion
 Follow-up: every 3-6mo for the next 3yr; regional lymph node disease is most common recurrence

2764: Seborrheic Keratoses

 Benign lesion that tends to favor the face/trunk/old people and is often consider unsightly
o May be indicative of underlying GI malignancy as the Sign of Leser-Trélat where many of these
lesions appear rapidly.
 Presentation: waxy/greasy, “stuck-on”, well circumscribed lesion that may be flat or raised with normal
surrounding skin. Can vary from pink/white to pale to brown/black. Typically, slowly enlarging.
 Dx: clinical
 Tx: none needed except for cosmetic reasons

4410: Actinic Keratosis

 Presentation: hyperkeratosis causing “sand-paper like” papules in areas of sun exposure. Often begin
small/flat but may accumulate becoming “cutaneous horns”. Pre-malignant for SCC
 Dx: shave biopsy with light microscopy showing characteristic cell proliferation
 Tx: electrodessication or cryotherapy

Chapter 37: Right Leg Pain, Swelling, and Erythema for Two Days – Necrotizing Soft Tissue Infection (NSTI)
With a presentation like this, many infectious and cutaneous problems can be on the differential. It’s
important to know how to have some quick differentiators:
 NSTI – will be discussed in detail below
 Cellulitis – often redness and swelling of the skin, but without major tissue destruction
 Cutaneous anthrax – painless/itchy black eschar with edema/erythema
 DVT – unilateral (often leg) swelling/erythema/pain, with history of hypercoagulability, immobility, or
some inflammatory state
 Hypersensitivity – Redness/swelling with no fever/leukocytosis. Ask about plant/animal exposure.
 Stasis dermatitis – fibrosis and ‘brawny’ discoloration secondary to venous insufficiency. May become
inflamed/crusted with exudate. Hx of DVT and cardiovascular problems is common.
 Sweet’s Syndrome – acute eruption of plaques/vesicles with erythema, fever, and neutrophilia.
Associated with G-CSF administration, pregnancy, and malignancy.
Pathophysiology
 May involve skin (necrotizing cellulitis), fascia (necrotizing faciitis), or muscle (necrotizing myositis)
 Organisms responsible help organize the “typing” of infection: Type I (polymicrobial), Type II (Group A
Strep) and Type III (Clostridium perfringens or “gas gangrene”)
 Note that infection with Clostridium septicum is associated with occult malignancy, esp. colon cancer!
 Fournier’s gangrene is NSTI of the scrotum/perineum
Presentation
 Vitals: Fever, tachycardia, hypotension, leukocytosis, low serum sodium
 Skin: Acute painful area of erythema/swelling/bullae (tissue destruction and fluid accumulation/
violacous skin (ischemia to dermis/epidermis). Classically “pain out of proportion to appearance”
 Creptius and gas bubbles on X-ray indicate necrosis of tissue with gas-forming organisms (Clostridia sp)
Risk Factors
 Anything that may depress immunity or tissue perfusion (diabetes, IV drug use, alcohol abuse, obesity,
WBC cancers, chronic steroid use, renal failure, liver cirrhosis, etc.)
 Recent wound or surgery (introduction of bacteria into the area)
Diagnosis
 Often diagnosed clinically, but important to distinguish from cellulitis as management is total different
 Definitive diagnosis is based on surgical debridement pathologic examination (murky fluid, grey fascia,
lack of bleeding from fascia)
 If you are highly suspicious but not sure of diagnosis
o X-ray showing bubbles in soft tissue can help reassure the diagnosis
o Surgical debridement for definitive diagnosis can be undertaken on high suspicion alone
Management
 First Step – IV fluids, broad spectrum Abx, and aggressive surgical debridement
 When debriding, you go until you find viable soft tissue without evidence of infection.
o Typically, dead tissue is liquefied (grey, “dishwater” fluid). Fascia can appear grey with little
bleeding and may separate from muscle too easily on digital exploration
o It is unacceptable to leave borderline-looking tissue, thus you must go until obviously healthy
tissue is visualized
 If extensive muscle necrosis is present, amputation may be the best option to save patient’s life
 A second-look operation should be scheduled for 24hr post-initial debridement to ensure that more
tissue has not become infected. Further debridement is necessary if dead tissue is found.
 Hyperbaric oxygen may be used adjectively along standard fluid/Abx/debridement care
 Sadly, mortality is around 25% for these patients
Chapter 38: Post-Operative Bleeding – Congenital & Acquired Bleeding Disorders
Pre-Op History
 Important to ask about history of excessive bleeding from gums, epistaxis, bleeding into
muscles/joints, excessive menstrual bleeding, & bleeding after minor procedures (tooth extraction,
skin biopsy, etc.)
 Ask about family history of bleeding (hints at congenital bleeding disorders)
 Ask about liver/kidney disease and malabsorption syndrome (short gut syndrome, cystic fibrosis) which
may potentially limit production of clotting factors (either directly or via Vit.K malabsorbtion)
 Ask about heart disease (pt may be in anti-platelet or anti-coagulant medication)

Pathophysiology
 Primary Hemostatic Disorder – disorder of platelet function (quantitative or qualitative), thus the
initial clot cannot be formed properly (primary hemostasis)
 Secondary Hemostatic Disorder – disorder of coagulation cascade (locking up the platelet plug with
conversion of fibrinogen  fibrin by factor VIII)
 Coagulopathy – anything impairing the body’s ability to clot blood. Note that hypothermia and
metabolic acidosis can exacerbate coagulopathies!
 Medical post-op bleed – diffused bleeding caused by underlying coagulopathy. Because it’s diffuse,
these bleeds will not benefit from re-operation, but rather medical management/support
 Surgical post-op bleed – focal bleeding from an artery or vein that was not properly ligated during
surgery. Re-operation and proper ligation of bleed is the best treatment
 Fibrinolysis – normal process which limits coagulation to only the area of damage. Plasmin binds to
fibrin, and breaks it up, breaking up the cross-linked platelets
 Hyper-Fibrinolysis – excess plasmin production that counteracts clotting and leads to bleeding
o Primary – increase in circulating tPA (poor clearance, loss of anti-tPA mechs)
o Secondary – systemic hypercoagulable state, leading to physiology tPA increase (DIC, etc.)
 Thrombocytopenia – <150,000 platelets causing in primary hemostatic disorder
o Symptoms are based on how low the count is
 >100,000 – asymptomatic
 50,000-100,000 – occasional petechiae
 10,000-50,000 – purpura after minor trauma  Plt infusion if invasive procedure
 <10,000 – spontaneous bruising/bleeding gums  everyone gets Plt transfusion
o Many causes (below), but most common cause is alcohol abuse
 Vitamin K dependent clotting factors are factors II, VII, IX, X, protein C, and protein S
 INR – measures extrinsic (VII, X)/common pathways (I, II, V); monitors Warfarin
 PTT – intrinsic (VIII, XI, X, XI, XII)/common pathways (I, II, V); monitors Heparin

Specific Disease Processes

[Congenital Coagulopathies]-------------------------------------------------------------------------------------------------------------
2256/4412: Anti-phospholipid syndrome
 Presentation: typically, a woman with recurrent fetal loss or arterial/venous clots. Elevated PTT
despite hypercoagulable state is due to the responsible antibodies interfering with lipid components
of the PTT test itself. PTT will not correct with 1:1 dilution of normal plasma.
o Diluted Russel viper venom test OR kaolin clotting time tests may also be used
o Occurs in approx. 30% of women with SLE
o Will have a (+)VRDL/(-)FTA-ABS
 Dx: must meet 1 clinical criterion and 1 lab criterion
o Clinical:
  Arterial/venous thrombosis
 >3 unexpected fetal losses before the 10th week gestation
 >1 unexpected fetal loss after the 10th week gestation
 >1 premature, normal birth before 34 weeks due to pre-eclampsia, eclampsia, or
placental insufficiency
o Lab:
 Lupus anticoagulant (pro-coag in-vivo and anti-coag in-vitro)
 Anti-cardiolipin antibody (IgG or IgM with medium to high titer)
 Anti-b2GP1 antibody (IgG or IgM with high titer)
 Tx: immediate anticoagulation with LMWH (even before testing)
o Note that corticosteroids are not the current standard of care

4861: Hemophilia
 X-linked recessive disorder causing lack of clotting factors (A = factor VIII def; B = factor IX def)
 Presentation: delayed/prolonged bleeding after minor trauma/procedure
o Hemarthroses (bleed into joint), intramuscular hematomas, GI bleeding, hematuria (without
kidney damage), and spontaneous bruising are all common signs
o Labs: Prolonged aPTT with normal platelet count, bleed time, and PT
 Dx: decreased amount of either factor VIII or factor XI
 Tx: Administration of missing factor through injection
o Desmopressin can promote Factor VIII production and be used in mild Hemophilia A

Von Willebrand Disease

 Presentation: often pts unaware, as symptoms are mild. Hx of prolonged bleeding after minor
procedures (tooth extraction/skin biopsy) or excessive menses with eventual clotting is classic.
o Intra-op: diffused oozing of blood within operated on tissue
o Post-op: continued bleeding or post-op hematoma formation
 Pathophysiology: von Willebrand Factor (vWF) is a protein that binds sub-endothelial collagen when
it’s exposed after damage to tissue. vWF provides a link between the collagen and the GP1b receptor
on platelets, allowing for primary hemostasis of be achieved.
o A lack of vWF causes difficulty in primary hemostasis due to poor platelet plug formation
o vWF is also a co-factor for factor VIII, thus low wVF can decrease factor VIII levels
 Labs: normal to prolonged PTT (decreased factor VIII), normal INR (coagulation cascade intact)
increased bleed time (BT; poor platelet plug formation)
 Subtypes:
o Type 1 (AD): quantitative decrease in vWF levels; mild symptoms
o Type 2 (AD): quantitative decrease and qualitative dysfunction; 4 subtypes with 2A being the
most common; all cause moderate symptoms
o Type 3 (AR): severe quantitative decrease, rare, most severe symptoms
 Dx: ???
 Tx: ???

[Acquired Coagulopathies]---------------------------------------------------------------------------------------------------------------
Liver Failure
 Coagulation factor production is a job of the liver, thus dysfunction of the liver results in poor factor
production  coagulopathy (increase PT/INR)
 Note that Factor VIII is not exclusively produced in the liver…thus all other coagulation factors will
drop, but Factor VII will be at normal or elevated levels!
  Tx: FFP, cryoprecipitate, coagulation factor infusion, platelet transfusion

Renal Failure
 Failure to eliminate uremic toxins from the blood results in uremia  platelet dysfunction
 Will likely cause an anion-gap metabolic acidosis and can be initially managed with emergent dialysis
(definitive) & administration of desmopressin (symptomatic)

Malnutrition
4112: Vitamin K Deficiency
 Vit K is a critical co-factor for enzymatic carboxylation of clotting factors II, VII, IX, X. Typically vitamin K
stores can last 30 days but in sick folks only last about 1 week!
 Presentation: bleeding diathesis with evidence of pathologic anticoagulation
o Classically lack of supplementation at birth, malabsorption for any reason, or liver disease will
lead to Vit.K deficiency
 Dx: clinical presentation
 Tx: Fresh Frozen Plasma administration with vitamin K injection

Acquired FVIIII (Factor XIII) inhibitors

 Some funky autoimmune destruction of factor VIII either post-partum, in rheumatic disease, or in
malignancy presenting with new purpura/soft tissue bleeding

[Thombocytopenia]------------------------------------------------------------------------------------------------------------------------
Impaired Production of Platelets
 Occurs due to medications/infection/alcohol (most common)/nutritional deficiency
 Decreased megakaryocytes in bone marrow biopsy is diagnostic
 Treatment is based on underlying disorder (treat disease, stop medication, etc)
Platelet Pooling
 Sequestration in the spleen; can happen for various reasons
 Tx: splenectomy if symptomatic

4316/4859/4616/2250: Heparin-Induced Thrombocytopenia (HIT)

 Type 1 – mild thrombocytopenia (<100,000) usually within 2 days of starting Heparin
o Does not cause any ill effects, nor warrants intervention.
o Not immune mediated and will resolve within a few days after stopping heparin
 Type 2 – immune mediated platelet activation by HIT antibody (IgG against PF4, which is exposed with
platelet exposure to heparin)
o Presentation: worsening thrombosis in response to heparin (usually 5-10 days, may be earlier if
prior exposure to heparin), skin necrosis in injection site (belly, periumbilical) or gangrene
distally (blue/darkening toe can be a confusing, but classic symptom!)
 Thrombocytopenia – destruction of platelet-HIT complexes by spleen and on-going
thrombus formation
 Thrombus formation – HIT antibodies activate platelets with promote aggregation and
activation of coagulation cascade, promoting arterial/venous thrombus formation
o Dx: serotonin release assay (gold standard) or immunoassay (only high titers)
o Tx: immediate cessation of heparin with initiation direct thrombin inhibitor (fondiparinux or
argatroban) – start treatment immediately before confirmatory testing

4338/4339: Thrombotic Thrombocytopenic Purpura (TTP)

  Autoimmune or hereditary decrease in ADAMTS13 enzyme (cleaves vWF multimers) resulting in extra-
long vWF which promotes intravascular platelet thrombus formation, which can shear passing RBCs
 Presentation: Thombocytopenia, Microangiopathic hemolytic anemia, renal insufficiency, neurologic
changes (headache, confusion, stroke, coma), and fever. Sometimes scleral icterus.
o Labs: normal PT/PTT (no activation of coagulation cascade!), anemia/thrombocytopenia,
elevated creatinine (kidney damage from clots),
o Smear: fragmented RBCs (schistocytes)
 Dx: presentation with labs/smear
 Tx: emergent plasmapheresis (replenishes ADAMTS13/removes possible autoantibody),
corticosteroids, FFP for support, +/- splenectomy

4383/4860: Immune Thrombocytopenia (ITP)

 Platelet destruction/inhibition of megakaryocyte production by IgG anti-platelet membrane
glycoprotein antibodies
 Presentation: asymptomatic petechiae/ecchymosis, mucutaneous bleeding, possible recent viral inf.
o Labs: isolated thrombocytopenia (<100,000)
o Smear: megakaryocytes wit no other abnormalities
 Dx: clinical presentation, CBC, Labs with HIV/HCV testing (may be cause of disease)
 Tx:
o Kids: Skin only = observe | bleeding = IVIG or glucocorticoids
o Adults: Plt >30k + no bleed = observe | Plt <30k or bleed = Glucocorticoids  IVIG, dapsone, or
danazol  splenectomy (in that order of escalation)

DIC
 Presentation: severe deterioration in the setting of some other disease process; often diffused
bleeding/evidence of clotting, diffuse end-organ dysfunction, and shock are present
 Etiology:
o Delivery (of a baby): amniotic fluid enters the blood, activating the coagulation cascade (tissue
thromboplastin present in fluid)
o Infection: sepsis causing wide-spread endothelial cell production of tissue factor OR gram(-) rod
sepsis results in widespread TNF-a production
o Cancer: Auer rods in AML active the coagulation cascade; mucin with adenocarcinoma
activating the coagulation cascade
 Pathophysiology: initial coagulopathy that leads to widespread clotting/consumption of platelets &
clotting factors causing clotting and bleeding diffusely throughout the body
 Labs: increased INR, increased PTT, decreased fibrinogen, increased fibrinogen split productions/D-
dimer, decrease hemoblobin, deceased hematocrit
 Dx: presentation/labs
 Tx: treatment of underlying problem; platelet/FFP/cryoprecipitate infusion may be used as support

4796: HELLP syndrome

 Presentation: pre-eclampsia, nausea/vomiting, RUQ pain;
 Labs: Hemolysis (low hemoglobin, low haptoglobin, schistocytes), Elevated LFTs, and Low Platelets
 Pathophysiology: Unclear, may have to do with aberrant placental development
 Dx: clinical presentation with agreeing labs
 Tx: stabilization with IV fluids/MgSO4, Methyldopa to reduce BP, corticosteroids to speed fetal lung
development with immediate delivery of the fetus (best if >34wk gestation)
Common Anti-platelet/Anti-coagulant Medications
  Aspirin (non-rev) – COX-inhibitor decreasing PGE2/TXA2 formation to inhibit platelet activation
 Clopidogrel (non-rev) – blocks ADP receptors stopping platelet-fibrinogen binding
 GPIIb/IIIa (abciximab; non-rev) – stops GPIIb/IIIa receptors on platlets to stop plt-plt aggregation
 Heparin (protamine sulfate) – activates AT-III  inactivates thrombin/factor Xa
 LMWH (enoxaparin; protamine sulfate) – binds factor Xa to inactivate
 Direct thombin inhibitor (agatroban; hemodialysis) – inhibits thrombin to stop clot cross-linking
 Warfarin (FFP or Vit.K) – inhibits Vit.K-epoxide reductase  stops II,VII,IX,X production

Work-up
 Clinical history, PTT/INR are the best way to workup a bleeding disorder of any kind post-op

Management
 First Step: ABCs, adequate IV access, assess H&P for bleeding disorder, order a type-and-cross, CBC,
INR, and PTT
 Re-exploration surgery should only be done if medical bleed has been effectively ruled out and the
patient fails to stop bleeding/becomes hemodynamically unstable

Complications of Blood Transfusion

4160/4671/4672: Transfusion Reactions and Special Situations with Blood Transfusion
 There are several adverse reactions that can occur with blood transfusion, however more common
ones have fairly specific time frames where they’ll appear, giving you a clue to the problem
o Seconds-Minutes – anaphylactic reaction
o Within 1hr – acute hemolytic reaction (poor type matching)
o 1-6 hrs – Transfusion-related acute lung injury (TRALI) or Febrile Non-hemolytic reactions
o 2-10 days – delayed hemolytic reaction
 Anaphylactic reaction
o Rapid shock, angioedema/urticaria, and respiratory distress within minutes of transfusion
o Caused by Anti-IgA antibodies in recipient reacting to IgA in the donor blood (occurs classically
in patients with select IgA-deficiency)
o Tx: stop transfusion; epinephrine, intubation, fluid resuscitation
 Acute Hemolytic Reaction
o Occurs due to poor type matching (clerical error) within the 1st hour of infusion
o Presentation: fever, chill, flank pain, hemoglobinuria  DIC/renal failure
o Dx: (+)direct Coombs test or pink plasma (due to hemolysis)
o Tx: immediate cessation of transfusion and fluids for supportive therapy
 Febrile Non-Hemolytic Transfusion reaction
o Most common adverse reaction to a blood transfusion
o Because small bits of leukocytes/plasma cells are present even in packed RBC transfusions,
WBCs can release cytokines in storage that will trigger transient fever, chills, and malaise
without hemolysis in response
o Leukoreduction is necessary to limit these reactions – reduces number of WBCs via various
methods, decreasing released cytokines AND decreasing cytomegalovirus transmission (often
resides in WBCs)
o Tx: Stop transfusion, administer anti-pyretics, and only use leukoreduced products for future
transfusions
 Premedication with anti-pyretics/anti-histmaines NOT EFFECTIVE
 Transfusion Related Acute Lung Injury (TRALI)
o Respiratory distress/non-cardiogenic pulmonary edema 6 hours after transfusion
 o Anti-leukocyte antibodies in the donor’s serum cause this reaction; Antibody-WBC complex
aggregates in the lung vasculature causing inflammation and pulmonary edema
o Tx: fluid resuscitation, vasopressors, aggressive respiratory support
 Delayed hemolytic reaction
o Mild fever/hemolytic anemia 2-10 days post transfusion caused by amnestic antibody response
(antibody was previously formed, but only in low titers. The transfusion jacked those titers up)
o Dx: (+)direct Coombs or (+)new antibody screen
o Tx: supportive care
Areas to Get in Trouble
 Not stopping blood thinners early enough before surgery: Aspirin (4 days), clopidogrel (7-10 days),
warfarin (2-3 days for INR<2.0, and 4-6 days for INR at 1.0…below 1.5 is safe for surgery!)

Chapter 39: Post-operative Decreased Urine Output – Post-op AKI

Differential Dx
 Pre-renal – poor perfusion of a normal kidney (hypovolemia for any reason, or CHF)
 Intra-renal – kidney damage causing poor function (ischemia, toxic damage from drugs, etc.)
 Post-renal – obstruction in the ureter/bladder/urethra causing backup pressure and nephron damage
Presentation
 Rarely physical signs of AKI; signs may be of underlying cause resulting in AKI (oliguria with
concentrated urine, signs low volume, etc.)
 Labs: BUN/Creatinine (>20:1 = pre-renal azotemia, thus poor perfusion!)
 Urine output
o Normal Adult is 0.5mL/kg/hr
o Normal Child is 1.0mL/kg/hr
o Oliguria – less than normal urine output for 2 consecutive hours…but not absence of output
o Anuria – lack of urine output…typically defined at 50-100mL urine over 24hr period. There
should never be 0mL urine output (this is a technical error if you see it)
 Common nephrotoxic medications – contrast agents, aminoglycosides, amphotericin B, cisplatin,
cyclosporine and NSAIDs
 Contrast induced nephropathy – absolute increase in Cr >0.5mg/dL or relative increase of 25% from
baseline 48-72hr following contrast administration
o Prehydration with normal saline – helps ward this off by helping flush out the contrast media
o N-acetylcystine, bicarbonate, and normal saline hydration with contrast media help prevent
renal damage as well
Pathophysiology
 Kidney filtration is driven by high filtration pressure in glomerular capillaries pushing fluid into
Bowmann’s space.
o Pre-renal – not much fluid passing through overall…thus less urine
o Intra-renal – glomeruli not working properly, may not be able to accept filtrate at all
o Post-renal – pressure buildup in Bowmann’s space stops filtrate from the capillaries
 Non-renal of increased BUN/Cr ratio
o Upper GI bleed – breakdown and absorption of RBC nitrogenous components raises BUN, but
creatinine is left unchanged leading to ratio changes
o Increased urea production – often due to steroids (similar mech to Upper GI bleed)
o Low muscle mass – poor creatinine production from regular muscle breakdown
 Unilateral kidney obstruction will NOT lead to renal failure, as the other kidney should normally
compensate for the poor-functioning kidney (unless there’s only 1 kidney present)
  Post-Op Oliguria is a common thing as the HPA axis under acute stress/blood loss will release
Aldosterone/ADH to replete intravascular fluid
o Poor urine output is expected within 24hr post-op; any longer than 24hr should be assessed for
renal injury/hypovolemia
o Post-op bleeding may also present as oliguria (even with a normal H&H). The blood loss causes
hypovolemia, and fluids have yet to redistribute into the intravascular space, meaning that
blood total volume is low, but concentration is normal (normal H&H with oliguria). H&H will
drop over the next 8-10 hrs, revealing the bleeding
 Prolonged pre-renal AKI can result in intra-renal AKI due to poor perfusion of kidney parenchyma,
which may eventually result in Acute Tubular Necrosis  prolonged oliguria with proper resuscitation!
 General anesthesia effect causes loss of sympathetic tone
o Cardiovascular function – slowed heart rate, vasodilation, drop in BP  poor organ perfusion
o Renal function – lack of perfusion  acute insult  kidney damage in pt with pre-existing renal
problems (healthy folks can likely tolerate it!)
Work-Up
 Examine for signs of hypovolemia/hypoperfusion
 Labs:
o BUN/Cr (allows for some identification of renal dysfunction and may clue a pre-renal azotemia)
o Fractional Excretion of Sodium (FENa)  FENa = (UNa/PNa)/(UCr/PCr)
 Pre-renal – FENa (<1%); UOsm (>500); UCr/PCr (>40); UNa (<20) – sodium/water being
retained because of low volume resulting in very concentrated urine (kidney works well)
 Intra-renal – FENa (>1%); UOsm (<350); UCr/PCr (<20); UNa (>40) – intravascular volume is
fine, but glomeruli are being damaged, leading to wasting of Na/water
 Post-renal – FENa (>4%); UOsm (<50); UCr/PCr (<20); UNa (>40); intravascular volume is fine,
but kidney is quickly being damaged by back-up of urine causing more severe features
 Note that diuretics will alter these levels, making FENa useless
o FEurea may be a more useful measure to delineate different levels of renal damage when a
diuretic is in use
o Urinalysis – allows for microscopic evaluation of urine for clues to renal damage
 High specific gravity – volume depletion
 Hematuria – renal stones/damage to renal collecting system
 Muddy Brown cast – acute tubular necrosis
 RBC cast – glomerulonephritis
 WBC casts – interstitial nephritis or pyelonephritis (inflammation in the kidney)
 Fatty casts – nephrotic syndrome
 Broad casts or waxy casts – chronic renal failure
 Imaging – ultrasound of bladder/ureter/kidney (hydronephrosis) or Doppler ultrasonography to assess
renal perfusion are both worthwhile studies for assessment
 RIFLE criteria – grading system of renal dysfunction based on Serum Cr, GFR, and urine output
o Risk of Injury – Cr (1.5x inc.), GFR (25% dec.), Urine (<0.5mL/kg/hr for 6h)
o Renal Injury – Cr (2.0x inc.), GFR (50% dec.), Urine (<0.5mL/kg/hr for 12h)
o Renal Failure – Cr (3.0x inc.), GFR (75% dec.), Urine (<0.5mL/kg/hr for 24h or anuria)
o Loss of Renal Function – total loss of renal function for >1mo
o End-Stage Renal Function – total loss of renal function for >3mo
Management
 First Step: rule out is obstructed urinary catheter (easy to assess and fix just by flushing the catheter)
 Next Step: order labs, review nephrotoxic medications, dose-adjust all renal-excreted drugs
 Fluid Challenge: infusion of 500mL saline over 30min to see if oliguria resolves
 o Pre-renal AKI from hypovolemia should resolve with fluid challenges
o If no response  obtain CVP  if low, continue challenges, if normal consider renal pathology
 Post-renal obstruction: always check he catheter first; then undergo further evaluation
 10776: Indications for Immediate Dialysis
o Acidosis – if metabolic acidosis with pH <7.1 refractory to therapy
o Electrolyte Abnormalities – symptomatic or severe (>6.5) hyperkalemia
o Ingestion – methanol, ethylene glycol, salicylate, lithium, valproic acid, or carbamazepine
o Overload – if volume overload is refractory to diuretics
o Uremia – typically if its symptomatic (encephalopathy, pericarditis, or bleeding)
 Diuretics in oliguria will only be beneficial if decompensating heart failure is the cause (less overfilling
of the heart to help improved cardiac output, thus perfusion to kidney)
 Dopamine in oliguria theoretically would work (helps increase cardiac output and promote naturesis)
but actually causes worsening of AKI insult  don’t use it.
Remember to NEVER order anything with contrast (MRI, CT with con, etc.) on a patient with AKI unless you
want to kill their kidneys

Chapter 40: Shortness of Breath 5 Days Post-op – Pulmonary Embolism

Risk Factors for DVT/PE (Virchow’s Triad)
 Stasis – immobilization
 Endothelial injury – surgery, trauma, central line within past 3mo, or Hx of DVT/PE
 Hypercoagulability – smoking, OCPs, Hx DVT/PE, cancer, congenital thrombophilias
 Note if pt with DVT/PE lacks these risk factors, even with careful history, workup for underlying
malignancy or hereditary hypercoagulable state should be undertaken
Presentation
 Recent history of at least one of Virchow’s Triad
 Symptoms: Acute onset SOB, unilateral pleuritic chest pain worsening with inspiration, hemoptysis,
tachycardia, tachypnea/hypocapnea/respiratory alkalosis (pH>7.4), hypoxemia (poor perfusion)
 Massive Pulmonary Embolus (saddle embolus) will present with additional hypotension, elevated
JVP/central venous pressure, right ventricular heart failure, elevated BNP/troponins, new onset
arrhythmia (RBBB), more centralized chest pain, and sometimes instant death
 Signs of DVT (unilateral leg swelling, calf pain, leg warmth/erythema/tenderness/Homan’s sign) should
be assessed as this may be the underlying cause for the PE
o May-Thurner syndrome – syndrome of left iliac vein compression due to anatomy of the left
iliac artery. Causes a 2x increase in DVT of the left leg vs the right
Anatomy
 Area of occasion is Peripheral Artery (10%), Proximal Artery (90%), Pulmonary artery (rare)
Pathophysiology
 Hereditary Thrombophilias - Any patient with young age of PE/DVT (<45 y/o), recurrent PE/DVT, or
unusual sites of PE/DVT (cerebral artery, mesenteric artery, portal veins) should be tested
o Factor V Leiden – a classic of white women and the most common overall. Autosomal dominant
mutation of the gene for Factor V in coagulation cascade, making it resistant to Protein C
cleavage/inactivation. Thus it induces a hypercoagulable state.
o Prothrombin 20210A – 2nd most common causing increased prothrombin levels
o Anti-thrombin III deficiency – decreased anti-thrombin III levels, often acquired during DIC,
cirrhosis, or nephrotic syndrome (peeing out all you’re anti-coagulation proteins)
o Protein C/Protein S deficiency. – if one isn’t present, there’s decreased inactivation of Factors
V/VIII. Protein C deficiency classically causes Warfarin induced skin necrosis.
 o Homocysteinemia – not well understood; pts benefit from B6 (pyridoxine) and B12 (cobalamin)
supplementation to aid conversion of homocysteine  methionine or cysteine
 Acquired Thrombophilias – advanced age, pregnancy, cancer, OCPs, HRT, smoking, obesity, nephrotic
syndrome, and HIT are all ones to consider
Workup
 Wells criteria – help determine what the pre-test probability of PE is present
o +3 – signs of DVT
o +1.5 – previous PE/DVT | Heart Rate +100 | recent surgery/immobilization
o +1 – hemoptysis | cancer
o Interpretation: <2 low risk | 2-7 moderate risk | >7 high risk
 First Step
o If low risk – obtain a D-dimer assay (<500 ng/mL is negative and PE is ruled out; >500ng/mL is
positive and workup should continue as PE has not been ruled out)
o If intermediate risk – you can go either way…but the safe side the to bet on high risk
o If high risk or (+)D-dimer – immediately start heparin & order CT angiogram of chest
(remember Heparin halts propagation of clot, allowing intrinsic fibrinolytic system to start
working slowly on breaking up the clot)
 Labs
o ABG – acute respiratory alkalosis, hypoxemia, increased A-a gradient
 Normal A-a gradient is calculated via [(Age/4) + 4]
o ECG – sinus tachycardia; sometimes arrhythmias if saddle PE
 SI/QIII/TIII (20%) – sign of right ventricular strain; S-wave in Lead I is huge; Q wave in
Lead III is huge, and T-wave is inverted in Lead III
o V/Q scan – multiple areas of perfusion deficit with normal ventilation
 Reported as High, Intermediate, Low, Very low probability of PE
 Not the best test (not readily available, not great predictive value), but a ‘Very Low’
score has a high negative predictive value
 Imaging
o CTa chest – will show a filling defect in the pulmonary arterial system & sometimes will show
peripheral infarction of tissue (Hampton’s hump!)
o CXR – typically normal, but sometimes with unusual features:
 Westermark’s sign – area of hyper-lucency representing collapse of distal blood vessels
where the PE is lodged
 Hampton’s hump – wedge-shaped hyperdense region at peripheral lung representing
area of ischemia/infarction
 Fleischer’s sign – prominent central pulmonary artery (only seen in saddle embolus)
o Echocardiogram – may be used to quickly assess for right heart strain (indirect sign of PE)
o Lower Extremity Doppler ultrasound – may be used to quickly assess for evidence of DVT (may
show signs of embolic disease, thus raising chance of PE)
Management
 Anticoagulation
o Normal renal function: any anticoagulant will be fine, factor Xa inhibitors preferred
o Poor renal function (GFR <30): limited to un-fractioned heparin (until PTT 1.5x normal)
followed by warfarin. Any inhibition of renal function can cause accumulation of the really
cleared factor Xa inhibitors  uncontrolled anticoagulation.
o If Hx of HIT: direct thrombin inhibitor should be used (argartroban, lepirudin, or bivalirudin)
o If ongoing bleeding/contraindication to anticoag: placement of IVC filter and stabilization
 Subsequent Treatments
 o Low risk (no sign of R. heart strain) – heparin alone (body will dissolve clot)
o Sub-massive (evidence of R.heart strain but not hypotension) – consider tPA
o Massive (R.heart strain and sustained hypotension) – tPA or pulmonary embolectomy (if pt is
not candidate for tPA)
 Long Term Treatment
o First PE – 3 months anticoagulation & minimize risk factors
o Subsequent PE – 6 months anticoagulation & minimize risk factors
o If malignancy  LMWH is preferred over warfarin these pts
o If pregnant  unfractioned or LMWH cannot cross placenta (warfarin is a teratogen!)

Chapter 41: Abdominal Pain Following MVA – Traumatic Bleeding and Hemorrhagic Shock
Shock defined as ‘inadequate perfusion for aerobic metabolism, leading to hemodynamic instability, and end-
organ dysfunction’

Types of Shock typical for trauma settings

 Hypovolemic/Hemorrhagic – trauma causing hemorrhage or burns typically cause decreased
blood/plasma volume leading to this type of shock
 Cardiogenic – blunt heart trauma (arrhythmia, tamponade, contusion) or tension pneumothorax result
systolic (pump doesn’t work) or diastolic (blood can’t fill the heart) failure
 Neurogenic – high-cervical spinal trauma results in loss of sympathetic tone  peripheral vasodilation
and leakage of blood plasma. Differs from classic presentation of shock featuring warm extremities and
normal-low heart rates
 Anaphylactic shock and septic shock typically aren’t part of acute traumatic settings

Presentation: tachycardia, hypotension, pale/cool extremities, weak pulses, prolonged capillary refill, low
urinary output, and altered mental status; often signs of trauma and internal bleeding present
 Note that young patients often can maintain blood pressures due to strong vascular tone, despite
significant blood loss from trauma
Pathophysiology: the 5 main ‘cavities’ for hemorrhage are the chest, abdomen, pelvis/retroperitoneum, long
bones, and the ‘floor’ (outside the body)
 Blood loss is classified based on % of blood lost and accompanying signs/symptoms
o Class I (0-750mL; <15%) – all vitals normal
o Class II (750-1500mL; 15-30%) – normal BP; tachycardia, decreased pulse pressure, tachypnea
o Class III (1500-2000mL; 30-40%) – decreased BP/tachycardia/dec. pulse pressure/tachypnea
o Class IV (>2000mL; >40%) – same as III with severely decreased pulse pressure (<25mmHg)
 Common hemorrhagic injuries based on ‘cavity’ injured
o Chest – lung laceration, rib fracture/intercostal artery tear; rarely aortic transection (distal to
ligamentum arteriosum) from deceleration injury
o Abdomen – liver laceration (most common organ injured) or spleen laceration (most common
cause of bleeding)
o Pelvis/retroperitoneum – pelvic fracture (internal iliac artery or pelvic veins), renal trauma;
very rarely aortic or IVC rupture
o Long bones – bilateral femur fractures
o “Floor” – any major trauma communicating with outside the body can have this; although large
scalp lacerations are often an overlooked cause of massive bleeding
 Closed head injury and bleeding into the cranial vault will NEVER cause hemorrhagic shock (not enough
space to bleed into!)
 o Cushing reflex – increased ICP (from intracranial bleed)  vasoconstriction to maintain brain
perfusion  baroreceptor sensation of intense BP  profound bradycardia
Initial Management
 ABCDE’s of Trauma (“Primary Survey”)
o Airway (with C-spine precaution) – is the patient breathing spontaneously? Is the airway
patient? If not, check for C-spine injury/disease. Intubate with C-spine in mind.
o Breathing – after establishing the airway; look for symmetric chest wall expansion, auscultate
both lung fields for breath sounds, palpate the chest for crepitus/deformity
o Circulation – check peripheral pulses (radial pulse = at least 80mmHg systolic; femoral/carotid
pulse = at least 60mmHg systolic); place two large bore (16 gauge or higher) needles/start fluids
o Disability (neurologic evaluation) – GCS with focused neurologic exam based on complaint
o Exposure/Environmental Control – cut away clothes for full exposure for survey. After survey,
cover in warm blankets to minimize temperature changes
 AMPLE Secondary Survey
o If patient is able to speak/respond to questions, the AMPLE survey can get more info
o Allergy, Medications, Past Medical history, Last Meal, Events Preceding the Injury
o Careful head-to-toe physical exam if time
Basics of Trauma Airway Management (the A & B in ABCDE)
 Remember that establishing the airway is the 1st task of any trauma setting
 Rapid Sequence Intubation (RSI) – two man technique where 1someone sedates the pt using weight-
based calculated doses of sedative (etomidate)/NMJ blocking agents  performs orotracheal
intubation & 2someone holds the C-spine neutral as spinal injury is there until proven otherwise in
trauma
o Nasotracheal intubation is NOT recommended in acute trauma as basilar skull fractures may be
present. The tube may pass into and damage the intracranial space/contents!
 Surgical Airways result in surgical creation of an airway to bypass damaged normal airways
o Cricothyrotomy – airway of choice in acute trauma (fast/few complications); incision through
cricothyroid membrane (between thyroid cartilage/cricoid cartilage). Works well for short term,
but sub-glottic stenosis makes this a poor long-term option
o Tracheostomy – less preferred in acute setting (longer time/more difficult); incision is made
through tracheal rings; good for long-term airway management
 Proper intubation is confirmed clinically (misting of tube, auscultation of breath sounds), CO 2 detection
strip test in exhaled air, CXR confirming placement of tube
Basics of Trauma Circulatory Management (the C in ABCDE)
 After placement of large bore needles (16 gauge or greater)  draw blood for labs & type/cross
 Placement of IV lines are preferred in the antecubital fossa; but access in other places is fine if this is
not available (like with significant arm trauma)
o Note that interosseous IV access may be needed in children <6yr due to small vessels
 Central Line placement is indicated if peripheral lines cannot be obtained or if patient is
hemodynamically unstable and close BP monitoring is required. Femoral access is preferred during
acute event due to ease of placement.
Fluid Resuscitation in Acute Trauma
 Crystaloids – standard fluids featuring only osmotic ions (normal saline, lactated ringers, etc.)
 Colloids – standard fluids that have additional large molecules (like albumin) in them to, theoretically,
help retain intravascular volume by bolstering plasma oncotic pressure. They’re not really used, as
they’re more expensive & studies have not shown clear benefit vs normal fluids
 First Step: Rapid infusion of 2 liters normal saline or lactated Ringers
o Normal Saline – 154meq/L Na, 154meq/L Cl
 o Lactated Ringers – 130meq/L Na, 109meq/L Cl, 28meq/L lactate, 4meq/L K, 3meq/L Ca2+
 Lactate is converted to bicarb in the liver; helps with buffering with academia
 Hypotonic in regards to sodium; infusion may cause hyponatremia (cerebral swelling)
 Name is from the presence of lactate & original inventor, Dr. Sydney Ringer
o 5% Dextrose (D5W) – 278mmol/L glucose; usually added to normal saline to add some
nutrition; not typically indicated in traumatic setting
o Large amounts of K+ are NOT given as decreased renal perfusion in shock decreases K+ excretion
& traumatic injury may release K+ into the serum from intracellular space
 Next Step (if 2 Liter fluid challenge fails): Massive Transfusion Protocol
o [1:1] ratio of [Packed RBCs:Fresh Frozen Plasma (FFP)]
 1:1 – PRBCs  FFP  PRBCs  FFP  (up to 10 units PRBCs every 24hr)
 Start with O-type blood and convert to specific blood with cross/type
o [1:1:1] ratio of [PRBCs:FFP:Platelets] has come into recent favor and may be used
 After Starting Fluid resuscitation: identify the bleed and try to stop it
o Determine bleeding compartment (Chest/Abdomen/Pelvis/Retroperitoneum/Long Bone/Floor)
with a FAST scan/CXR/Pelvic X-ray
o Chest – insertion of chest tube for drainage
o Abdomen – immediate exploratory laparotomy
o Pelvis – assess need for pelvic stabilization & plan for embolization of bleeding artery
 Diagnostic Peritoneal Lavage – local anesthesia with small abdominal incision with placement of
catheter. Withdrawal of more than 20cc blood is confirmatory. Lavage with 1L NS yielding 100,000
RBCs/mm3 is confirmatory. Often done if FAST is equivocal.
Subsequent Management
 Liver Injury – most commonly injured organ after blunt abdominal trauma
o Hemodymanically stable = medical management + selective liver embolization
o Unstable = exploratory laparotomy (Ex-Lap) to stop bleeding (usually perihepatic packing with
laparotomy pads, cauterization, & suturing with pad removal 48hr after bleeding control)
o Note the pringle maneuver may be used to temporarily control bleeds intra-op. If this fails to
control bleed, it’s concluded that bleeding if from hepatic veins
 Splenic Injury – the most common cause of abdominal bleeding after blunt abdominal trauma
o Hemodymanically stable with clean FAST = selective splenic embolization to control injury
o Henodynamically unstable or FAST(+) = splenectomy or spleen repair + immunization against
encapsulated organisms 2wk later (H.flu, N.meningititis, S.pneumoniae, etc.)
o Kehr’s Sign – referred left-shoulder pain due to splenic injury irritation of the diaphragm
 Pelvic Fracture – stabilization of fractures and placement of pelvic binders across the femoral greater
trochanters is best to control ongoing bleeding.
o If ruled out other sites of bleeding, Selective embolization of bleeding pelvic vessels should be
done to control the bleeding
Areas of Trouble
 Free fluid in the peritoneum without solid organ damage is NOT a sign that everything is OK. It means
that some occult leak (intestinal leak, intestinal bleed, bladder rupture, etc.) has occurred.
 Using vasopressors in hypovolemic shock will only lead to worsening end organ damage. The
peripheral arteries are already constricting to maintain BP, thus further alpha-adrenergic stimulation
will only worsen end organ ischemia and have limited effect on blood pressure
 Hypotension definition varies with age
o Age 20-49  systolic <100 mmHg
o Age 50-69  systolic <120 mmHg
o Age 70+  systolic <140 mmHg
Chapter 42: Penetrating Abdominal Trauma
Presentation
 Pre-hospital report (from EMTs/etc.) is Mechanism, Injuries, Vitals, Treatment (MIVT)
 Two most common penetrating abdominal traumas:
o Stab wound = low velocity/kinetic energy, damage only to area of penetration
o Gun shot = high velocity/kinetic energy, remote damage from fragmentation/blast can occur
 Two most common organs injured in penetrating abdominal trauma: small intestine and liver
 Three physical exam findings mandating immediate surgical intervention in PAT:
o Hypotension, peritonitis, & evisceration  2 out of 3 mandate surgery
o Often X-rays are taken to help quickly characterize the path/extent of injury
 Tangential gunshot wound – PAT where path of the bullet has clear entry and exit wounds &
penetrated no internal organs/deeper structures
o Don’t forget that blast injury and fragmentation can still occur
o X-ray and CT assessment should be done to assess for internal injuries
Anatomy
 Border Definitions of Body areas
o Anterior abdomen – xiphoid/costal margins, anterior mid-axillary lines, and inguinal
ligaments/public symphysis
o Flank – anterior/posterior mid-axillary lines from 6th intercostal space to iliac crest
o Back – tips of the scapula, posterior axillary lines, and iliac crests
 Three Distinct regions of the internal abdomen – peritoneal cavity, pelvis, & retroperitoneum
 Retroperitoneum
o Organs – 2nd-4th parts of duodenum, ascending/descending colon (posterior wall), rectum
(distal), pancreas, kidney, ureter, bladder
o Retroperitoneal hemorrhage is difficult to diagnose as normal signs of peritonitis are not there,
FAST exam, and peritoneal lavage will not show hemorrhage.
o Retroperitoneal hematomas are divided into Zones, which aids in remembering what organs
are present in each zone and directs surgical intervention
o Zone 1: upper midline/central (ICV, SMV, aorta & branches)  always explore surgically
o Zone 2: upper lateral (renal artery/vein)  BAT (selective), PAT (explore surgically)
o Zone 3: lower midline/pelvic (common/internal/external iliac A & V)  BAT (DO NOT explore),
PAT (explore surgically)
 Transpelvic gunshot wound is concerning for damage to ureters, bladder, iliac vessels, rectum, &
vagina. CT scan of abdomen & pelvis with rectal/vaginal exam (if woman) should be done.
Workup
 Immediate Surgery indicated with hypotension, peritonitis, or evisceration
 In absence on Immediate Surgical indication  CT chest/abdomen/pelvis
o FAST exam and DPL are of limited utility due to poor assessment of retroperitoneal structures
o Local wound exploration should only be attempted by an experienced physician; allows for
assessment of anterior fascia (penetrated or not)  if penetrated, surgery indicated; if not
penetrated, no surgery needed
Initial Management
 1st step: ABCDEs with careful survey for injuries (make sure to check axilla & perenium)
 2nd step: draw labs, fluid/blood product resuscitation/any steps to address specific problems
 Permissive hypotension: less aggressive fluid resuscitation to avoid “popping the clot” and creating a
dilution coagulopathy. Used in the setting of penetrating torso trauma only (not blunt/head trauma)
  ABx/Analgesia: not recommended unless pt has indication for immediate surgery (may mask
signs/symptoms needed for assessment if not going to surgery!)
 Tetanus prophylaxis: no if up to date with tetanus shot; if immunization status unknown, then only
tetanus-prone injuries should get prophylaxis (soil contaminated, >6hr old wound, rusty nail, etc.)
 Impalement: same trauma assessment WITHOUT attempt to remove penetrating object until 1proper
imaging can be done to assess anatomic effects, 2pt can be taken to the OR for removal.

Subsequent Management
 Trauma patients are draped from chin to knees in the OR for immediate access to any portion of the
chest/abdomen/pelvis if needed during surgery
 Exploratory laparotomy is the mainstay of surgical management for PAT
 Laparoscopic approach may be used if surgical assessment of peritoneal penetration is needed, but
immediate laparotomy is not indicated (no peritonitis, hypotension, or evisceration).
 Lethal Triad – Acidosis/Hypothermia/Coagulopathy
o These are three major killers seen in trauma patients which, if not corrected, will lead to death
o Should be watched and corrected immediately should they pop up
 Damage control surgery – due to concern intra-op of the “lethal triad”, this approach takes patients
for a limited time in the OR to correct life-threatening hemorrhage, limit bowel contamination, and
temporary closure with prompt ICU transport for resuscitation
o After adequate resuscitation, pt may return to the OR for further work
 Non-operative management – appropriate in patients who are hemodynamically stable, without
peritonitis, with normal mental status, and CT scan showing no intra-abdominal injury
 Prophylactic Abx should be given for 24hr post-trauma admission; even with evidence of bowel
perforation, increased duration does NOT provide benefit
Complications
 Abdominal Compartment Syndrome – clinical deterioration due to heightened intra-abdominal
pressure; often decreased urine output, increasing peak pressures on ventilator, and increasing
vasopressor support will be symptoms
o Bladder pressure measurement increase may help make Dx
o Tx: decompressive laparotomy w/ re-opening of abdominal fascia and leaving it open to allow
for pressure relief

Chapter 43: Pedestrian Struck by Motor Vehicle – Traumatic Extremity Injury

Presentation
 6Ps of Ischemic Limb Injury – pain, pallor, polar, pulselessness, paresthsias, paralysis (the final two are
signs of critical ischemic injury and require emergent intervention if present!)
 Signs of vascular injury to limb
o “Hard Signs” of limb damage – bleeding, expanding pulsatile hematoma, palpable thrill, audible
bruit, absent pulse
o “Soft signs” of limb damage – Hx of hemorrhage, small/stable hematoma, unexplained
hypotension, penetrating wounds without hitting major vessels, nerve deficit, abnormal pulses
 Examination of Injured Limb
o Vascular – pulses, perfusion (temp, color, capillary refill), hard/soft signs of injury
o Neurologic – sensation, strength, reflexes
o MSK – fracture/gross deformity, joint exam (active/passive range, instability, effusions)
o Soft tissue – intact, degree of contamination
Pathophysiology
  Popliteal Artery – due to it’s course (tethered above/below the knee with anastomotic network as it
passes behind the knee), forceful traction (posterior knee dislocation)/transection (medial tibial
plateau fracture) injuries are most damaging. Typically presents with popliteal artery thrombosis &
distal limb ischemia.
 Axillary artery – most commonly from anterior dislocation of shoulder girdle. Posterior dislocation
more often injures the axillary nerve
 Subclavian artery – classically from clavicle fracture (subclavian runs just between the clavicle and 1st
rib). May present with associated pneumothorax/hemothorax
 Brachial artery – supracondylar fractures; most common in children because of their thinner humeral
supracondylar region. Lack of treatment may result in Volkmann’s contracture (hand flexure)
 Superior Gluteal (posterior)/Inferior Pudendal (anterior) (internal iliac branches) – pelvic fractures
(depending on posterior/anterior) could damage either one. Often major blood loss!
 Femoral artery – anterior hip dislocations (external rotation/abduction) more often injure the artery;
posterior dislocation (internal rotation/adduction) more likely sciatic nerve. Always concern with
avascular necrosis if femoral head fracture is also present.
Workup
 If “hard signs” present – no further workup, go to OR for hemorrhage control/injury repair
 If no “hard signs” present
o Ankle-Brachial Index (ABI) – allows for possible identification of vascular injury
o If ABI is <0.9 (abnormal; evidence of injury), vascular imaging must be done to assess injury
 CT angiography (rapid/non–invasive, requires contrast) – test of choice
 Duplex ultrasonography (accurate/noninvasive, not quickly available, operator dep.)
 Contrast arteriography (very sensitive/specific, but invasive/expensive)
o If penetrating trauma is close to an artery, but not causing symptoms/normal ABI, no further
workup is needed
 Posterior knee dislocations should also have:
o Pre-reduction a plain film X-ray (assess damage to surrounding structures)
o Post-reduction plain film X-ray (assess for fractures and success of reduction)
o Post-reduction clinical assessment (check for neuro/vascular damage & joint function)
 Mangled Extremity Severity Score (MESS) – scoring system used to evaluate whether a severely
injured limb should be attempted to be salvaged or not.
o Ischemia >6hr, older patients, severe shock, high-energy wounds, and presence of
arterial/nerve injury are all criteria that would point to amputation rather than salvage
o Even if a limb is technically salvageable, if function is completely lost & leads to a worse quality
of life, it may be better to amputate
Management
 First Step – Primary survey (ABCDEs) and secondary survey (H&P) with aggressive control of bleeding
 Tourniquets – early application and proper placement with limb exsanguination have been shown to
result in better outcomes. Make sure to minimize application time to as little as possible.
 Posterior Knee Dislocation
o Immediate reduction (good to have X-ray beforehand) with exam focused on restoring
circulation and assessing neurologic function/ligamentous injury/open fractures
o After reduction, re-check vascular status (ABI  CTa if ABI is still <0.9  if abnormal go to OR)
o If ABI is normal, resume medical management and close watch
 Surgical management is best achieved within 6hr with goal of restoring distal perfusion
o Typically resection  anastomosis/grafting is basis for restoring bloodflow
 o If autologous vein graft is needed for popliteal artery repair the greater saphenous vein from
uninjured leg is the best choice (preserves collateral flow; remember to reverse orientation so
venous valves don’t impede bloodflow)
o If popliteal vein also injured – every attempt should be made to repair the vein, but if it is not
salvageable, the ipsilateral saphenous vein flow should be ensured (collateral bypass).
o If orthopedic repair also needed – if ischemia is severe, vascular intervention takes
precedence, and often a temporary shunt is placed. Orthopedic manipulation in surgery may
cause damage to an arterial repair, so the shunt is helpful here. After ortho is done, definitive
vascular repair can be achieved.
o Heparin – helps reduce rate of amputation in the affected limb as long as patient isn’t
contraindicated to it’s use
o Post-op complications – thrombosis/compartment syndrome following re-establishment of
flow are the two biggest concerns
Areas of Trouble
 Just because the patient has a palpable pulse does NOT mean there is not arterial injury! Retrograde
flow from collateral arteries and inherent unreliability of physical vascular exam make a palpable pulse
less conclusive. ABI + pulse exam is always the best course!

Chapter 44: Gunshot Wound to the Left Neck

Important Signs to Look for in Pt with Neck Injury
 Stridor – compression of the upper airway; often intubation or surgical airway will be needed
 Odynophagia – pain with swallowing; oropharyngeal/esophageal injury likely causes this
 Horner’s Syndrome – ptosis/myosis/anhydrosis; damage to cervical sympathetic chain nerve fibers,
which travel along the internal/external carotids. May indicate injury to these vessels
 Bruit – arterial damage (carotid/subclavian) may result in fistula formation with adjacent veins
resulting in a bruit (result of venous vibration from arterial pressure flow)
 Crepitus – air under the soft tissue; indicates damage to lungs/airways with release of air
 Hoarse voice – vocal cord dysfunction due to vagus nerve or recurrent laryngeal nerve damage
Anatomy
 Neck Zone 1 [clavicles/sternal notch  cricoid cartilage] – great vessels, common carotids, vertebral
arteries, lung apicies, thymus, thoracic duct, distal trachea, esophagus, cervical spine, brachial plexus
 Neck Zone 2 [cricoid cartilage  angle of the mandible] – mid-carotids/vertebral arteries, jugular
veins, esophagus, vagus/recurrent laryngeal nerves, phrenic nerve, cervical spine, larynx, trachea
 Neck Zone 3 [angle of the mandible  base of skull] – proximal internal/external carotids, vertebral
arteries, proximal jugular veins, oropharynx, cervical spine
Pathophysiology
 Penetration of the Platysma is how a penetrating neck injury is defined. If it has not been penetrated,
then no further workup for neck trauma is needed.
 Pseudoaneurysm – may develop when an artery has a focal full-thickness injury that gets tamponaded
by local soft tissue. The vessel is not exsanguinating, but the space is filled with blood, generating an
enclosed pulsatile mass
o Classically a pulsatile mass following trauma is either A-V fistula, aneurysm, or pseudoaneurysm
 Arterial intimal injury – concussion/blast damage may injure only the arterial intima. If small, this may
be insignificant. If large, it may occlude the lumen or generate a false lumen for dissection.
o Larger intimal injuries will likely need surgical correction
o If large intima injury extends high into intracranial carotid, you may be forced to manage
medically, due to lack of access
 Two major nerve lesions from neck trauma:
 o Recurrent laryngeal nerve – vocalis paralysis = hoarse voice (unilateral)
o Phrenic nerve – hemidiaphragm paralysis = difficulty breathing, elevation of diaphragm on
affected side
Workup/Management
 Algorithm
o Standard Primary & Secondary Survey of Trauma (intubate, transfuse, etc. as necessary)
o If hard signs of vascular injury present  prep for OR
o If hard signs absent  helical CT angiography (characterize extent/location/nature of injury)
 No concern for injury  observation
 Zone 1 or 3 injury  catheter angiography (arterial damage) or triple endoscopy
(aerodigestive tract damage)
 Zone 2 injury (most common)  surgical exploration (arterio-venous damage) or triple
endoscopy (aerodigestive tract damage)
 Zone 1 Injuries should always be assessed for pneumothorax
 Zone 2 surgical threshold is lower as this zone is easily accessible via incision anterior to the
sternocleidomastoid muscle
 Management of Vascular injuries
o First gain proximal, then distal control of the injured artery (cut off bleed at it’s source!)
o If arterial bleeding that cannot be controlled by direct pressure  passage of Foley catheter
into wound with balloon inflation to tamponade the vessel may be done!
o Carotid Injury – gain proximal/distal control & start heparin. Resect any portions of damaged
carotid. If <2cm resected do primary anastomosis; if >2cm, then take greater saphenous vein to
use as an autologous graft anastomosis
 Always prep drape both thighs with vascular injury, just in case you need the greater
saphenous vein for autologous graft!
o Internal Jugular Injury – primary repair (venorrhaphy) or end-to-end repair should be
attempted. If not possible, ligation of proximal/distal vein is accepted/well-tolerated
o Pseudoanaeurysm – surgical resection/repair; unstable and may enlarge/rupture
o AV fistula – stable, but rarely closes. Needs surgical resection
o Intimal injury – stable, with either medical management (small) or repair (large or complex)
Areas of Trouble
 Because bullets (and bullet fragments!) may cross multiple zones of the neck, it’s important to evaluate
with helical CT to make sure of damage, instead of simply using entry/exit wounds
 Not addressing airway first can be a costly mistake. There is NOT much space for an expanding
hematoma, thus tissue displacement may easily impede the airway, esp in a patient who started with a
normal patent airway.
 Blunt Carotid Injury – often hard to diagnose and clinically occult; high index of suspicion needed.
o Presentation: MVA with focal neurologic deficit not obvious on CT head.
o Pathophys: stretching of the vessel or direct trauma causing dysfunction/damage
o Dx: CTa of the neck to assess vessels
o Tx: anticoagulation only (prevent clot formation)

Chapter 45: Stab Wound to the Chest – Thoracic Trauma

“Lethal Six” Thoracic Trauma Injuries
 Airway obstruction – stridor/gurgling following trauma/foreign body aspiration/expanding hematoma
 Tension pneumothorax – one-way valve to an injured lung
o Presentation: Hypotension, dyspnea, tachypnea, JVD, unilateral absent breath sounds
(damaged side), deviation of trachea to unaffected side
 o Pathophysiology: trauma generates a one way valve (tissue being the valve) which causes
buildup of air within the chest cavity. As this increases, compression of the heart/IVC/SVC result
in poor preload filling and eventually loss of cardiac output due to diminished preload.
o Imaging: enlarged “water-bottle” heart; may be normal in acute settings
 Open pneumothorax – open chest all injury with air entry into pleura from outside world
 Massive hemothorax – total whiteout of lung field & muffled lung sounds, typically from lung
parynchymal injury or intercostal artery injury
 Flail Chest – paradoxical motion of chest wall, often with underlying lung contusion. Result of trauma
fracturing two or more consecutive ribs  free wall that stays in place during respiration
 Cardiac tamponade – fluid filling the pericardium (trauma often causes hemopericardium)
o Presentation: Beck’s triad (hypotension, JVD, muffled heart sounds), narrowed stroke volume,
hepatojugular reflex, pulsus paradoxus, & electrical alterans
 Trauma to the cardiac box (clavicles superior, nipples lateral, and subcostal margin
inferior) can cause this
o Pathophys: pericardial pressure begins to exceed left ventricular diastolic pressure, resulting in
septum infiltration of the left ventricle. This reduces preload, thus causing hypotension and
narrowed stroke volume (<30mmHg)
 Rapid accumulation of pericardial fluid is the most important factor in tamponade; at
rapid pace, only 200-300mL of fluid can result in full manifestation
 Slowly evolving tamponade may allow for up to 1000-2000mL because it gives time for
the pericardium to stretch/adjust to the new pressures
o Dx: made with FAST scan in trauma setting (fluid surrounding the heart!)
“Hidden Six” Thoracic Trauma Injuries
 Blunt aortic injury – deceleration injury; widened mediastinum/tracheal deviation to the right
 Esophageal injury – subcutaneous air surrounding esophagus; typically penetrating trauma
 Tracheobronchial injury – massive subQ emphysema; either deceleration or penetrating injury
 Diaphragmatic rupture – sudden rise in intra-abdominal pressure or penetrating injury to the
diaphragm itself; may be asymptomatic (delayed Dx); herniation of stomach/colon may occur
 Blunt cardiac injury – spectrum from unexplained tachycardia, BBB, cardiac rupture, to cardiogenic
shock; typically has accompanying sternal fracture
 Pulmonary contusion – rarely seen initially on CXR, but develops within 24hr of injury
H&P/Pathophysiology
 Combative trauma patients may have ‘air-hunger’ (hypoxia), hypovolemia, cardiogenic shock,
hypoglycemia, EtOH intoxication, drug intoxication. (acting funny doesn’t always mean high/drunk!)
 Penetrating injury above the nipple = likely thoracic injury
 Penetrating injury below the nipple = may be thoracic, diaphragmatic, or abdominal injury (due to
diaphragmatic excursion during respiration cycle!)
 Type of weapon causing injury should be noted, as ballistic course may be predictable (knife) or may
change upon entry (bullet). Bullets have even been seen entering an artery and embolizing!
 Narrowed pulse pressure (systolic – diastolic = <30mmHg) – indicates some form of systolic
dysfunction (tamponade, hypovolemic shock, or cardiogenic shock)
 Rolling the patient over and checking axilla/perineum are very important for checking entire body for
trauma wounds. Done only in situations where neck/spinal damage is very unlikely.
 “Sucking Chest Wound” – air bubbling from a chest wound due to open pneumothorax large enough
that inspired air takes the path of least resistance into the chest cavity… through the wound (>2/3
diameter of the trachea), not the trachea! Bubbling is “expiration” during diaphragm relaxation.
 Subcutaneous emphysema = pneumothorax until proven otherwise. Typically causes crepitus!
 Air embolism – entry of large amounts of air into the bloodflow, significantly disrupting it
 o Presentation: cardio (chest pain, arrhythmia, right heart failure), pulm (dyspnea, hypoxemia,
hypercarbia), CNS (confusion, paradoxical cerebral embolism)
o Pathophysiology: most commonly from damage around the lung hilum, causing a fistula
between a bronchus & the pulmonary vein
 Air will disrupt normal bloodflow long enough to cause ischemic damage
 Note that a normal abdominal exam does NOT rule out abdominal injury. Peritonitis may more slowly
develop, only to show a smaller injury that’s been there the whole time.
Initial Management
 First Step: Primary and Secondary survey
o If cardiac tamponade is suspected, DO NOT INTUBATE a patient, as positive pressure ventilation
will increase pulmonary pressure, further decreasing preload and worsening cardiac output
 Airway/Breathing (Concern for pneumothorax was in this patient)
o Breath sounds/Obtain CXR to rule in/out pneumothorax
o Needle Thoracostomy – immediate decompression of thoracic cavity with pneumothorax.
Needle is placed in 2nd or 3rd midclavicular intercostal space on affected side (minimal risk to
heart and collapsed lung tissue) above the rib (minimial risk to intercostal neurovascular
bundle). Needle is advanced till a rush of air is noted
o Tube Thoracostomy (chest tube) – definitive management of pneumothorax/hemothorax;
placement of a hollow plastic tube between the 4th/5th intercostal space to allow drainage.
o Thoracotomy – indicated for massive hemothorax (>1.5L immediately or >150-200mL/h for 3hr)
in order to gain acute hemorrhage control.
 Allows for hemorrhage control, decompression of tamponade, cross-clamping of
descending aorta, cardiac massage, prevention of air embolism, and repair of cardio-
pulmonary injury
 Indications: penetrating trauma with <15min pre-hospital CPR; blunt trauma with <5min
of pre-hospital CPR; persistent post-penetrating trauma hypotension (SBP <60mmHg)
 Contraindications: pt has no signs of life
 Circulation (concern for hemorrhage/tamponade)
o Palpate pulses, start 1L fluid bolus, send type/cross, apply pressure to external injury
o FAST scan should be able to show fluid surrounding the pericardium
o Continue IV fluids (increases pre-load to maintain cardiac output)
o Do NOT use pressors (increases afterload, decreasing cardiac output)
o Subxiphoid (pericardial) window: surgical procedure that opens a small portion of the chest to
view the pericardium for blood. Only used in stable pts with equivocal FAST suspected of
tamponade. If negative, you’ve avoided a median sternotomy; if positive, undergo sternotomy
for definitive treatment.
o Definitive Tx: go to the OR for median sternotomy for release of tamponade & repair of injury;
note that pericardiocentesis is NOT recommended in trauma patients (likely clotting blood, less
effective with the needle; may be used in situations where surgical intervention is not readily
available to buy time until OR can be reached)
Subsequent Management
 Combative Pt: order blood glucose finger-stick, pulse Ox, and vitals (altered mentation may be due to
non-intoxicant reasons!)
 Chest Tube Management: must be monitored for eventual removal
o Collection – collects fluid/blood/pus & measures amounts; connects water seal to chest tube
o Water seal – one-way valve allowing air to be removed from pleural space but doesn’t allow air
to enter pleural cavity; connects suction-control chamber to collection chamber
 If air bubbles are passing through, then a large pneumothorax is decompressing
  If no air bubbles, disconnect suction and ask pt to cough or kink the chest tube for a bit
then release. If bubbles, then the pneumothorax has not healed. If nothing, then chest
tube may be removed.
o Suction control – controls the amount of suction; connects wall suction and water seal
o [Wall suction  water seal  collection chamber  chest tube  pleural cavity]
 100% oxygen (vs normal 21% oxygen room air) has been shown to speed pneumothorax healing. This
is because more O2 enters the vasculature and increases the pressure within them, somehow leading
to increase rate of resorption of the damaged tissue.
 Sucking chest wound management – initially placement of occlusive dressing to stop airflow; definitive
treatment is occlusive dressing + tube thoracostomy (chest tube) placement
 Flail Chest management – give analgesia to maximize comfort with respiration (allowing for breath =
atelectasis not happening) & oxygenation/PEEP if ventilation is compromised. The role of Rib fixation
apparently has yet to be established.
Complications
 Laceration of a coronary vessel may occur with pericardiocentesis; worsening tamponade!
 The Left phrenic nerve passes over the posterior left ventricular pericardium and is at risk when
opening the pericardium.
 If chest tube fails to drain a hemothorax properly; thoracotomy/drainage (if unstable) or VATS
procedure (if stable) are recommended
 If a chest tube fails to fix a pneumothorax, first check to see the tube isn’t occluded or kinked. If it’s
proper, major airway damage has occurred and the patient requires immediate intubation,
bronchocscopy to assess injury, and immediate thoracotomy for repair.

Chapter 46: Burns to the Face, Trunk, and Extremities – Acute Burns
Presentation
 Risk factors for burn injury: extremes of age, alcohol/drub abuse, smoking, violence, low SES
o Children and elderly = highest morbidity risk for burns
 Degrees of Burns
o 1st degree (superficial) – epidermis only; like sunburn (painful, dry, blanching, red, NO blisters)
o 2nd degree (superficial partial thickness) – epidermis and part of dermis (painful, swollen, warm,
mottled areas, YES blisters)
o 2nd degree (deep partial thickness) – epidermis and part of dermis (painless, warm, white,
mottled areas, YES blisters often with weeping surfaces)
o 3rd degree (full thickness) – epidermis and dermis (painless, white, dry, leathery, no blanch)
o 4th degree (oh shit) – skin, underlying bone, tendon, adipose, or muscle (bad news and
disfiguring. If the burn has gone through more than the
skin, you’re at this level)
 Estimating Total Body Surface Area (TBSA) affected by burn:
o Rule of 9s: the body can be divided into sections that are
easily divisible by 9 as an estimate for surface area 
Head (9 a/p), Each arm (9 a/p), Anterior torso (18),
posterior torso (18), each leg (9 a/p), genitals (1)
o Handprint estimate – adult size palm estimates about 1%
of body surface area burned. Best when estimating patchy
areas of burn
o Non-superficial burns >40% of TBSA = higher mortality
 When to transfer to a burn center
o 2nd/3rd degree >10% TBSA (<10yr or >50yr)
 o 2nd/3rd degree >20% TBSA (any age)
o 2nd/3rd degree involving hands, face, feet, genitals, perineum, or skin on major joints
o Electrical or chemical burns (additional associated problems to be addressed with these)
o Concomitant inhalational injury (classic for people in building fires)
o Significant pre-existing medical conditions
o Suspected child abuse/neglect
 Inhalational Injury – smoke/heat causing damage to oropharynx/lungs
o High concern in patients with burn injuries occurring in enclosed areas/facial burns
o Upper airway edema – stridor or failure of upper respiratory system. Often burn of the
oropharynx will swell while in the hospital; best to prophylactically intubate if concerned.
o Acute respiratory failure (chemical pneumonitis) – low pO2 with high pCO2, chest pain,
respiratory acidosis, tachypnea w/ shallow breathing
o CO poisoning (house fires/gas heaters/car exhaust) – headache, nausea/vomiting, cherry-red
skin, deceptively high pO2  seizure, coma, death (anoxia)
o Cyanide (CN) poisoning – may be considered in any patient with burn injury (discussed below)
o Carbonaceous Sputum – dark sputum from inhalation of smoke; indicator of inhalational injury
o Changes in voice quality & singed nasal hairs (signs of burns to face)
 Burn Wound Sepsis – 2nd degree  3rd degree burn while in the hospital (skin necrosis), discolored
burn, eschar with green hue, black/necrotic skin, skin separation, signs of sepsis
o Fever isn’t accurate here as the skin (the body’s primary temp regulator) is compromised
o Dx: finding >105 bacteria/g of tissue on quantitative analysis
 Circumferential, Full Thickness Burns – concerning as the forming eschar can compromise venous, but
not arterial bloodflow via circumferential swelling (acts as tourniquet).
o Extremity – compartment syndrome from high pressure blood pooling
o Chest – difficulty with chest wall expansion/respiration
o Tx: escharotomy (remove the restricting band of tissue)
Pathophysiology
 Thermal Burns – caused by extreme heat, most common is scalding from boiling water
 Chemical Burns – caused by caustic substances; alkali burns (basic) are often more severe due to the
substances to penetrate tissues & cause liquefactive necrosis; acidic burns are less damaging and cause
coagulation necrosis
 Electrical Burns – external burn may be deceivingly small, as electrical current can run through
underling tissue causing damage (muscle necrosis, shoulder dislocations, myoglobinuria/renal failure
o Arrhythmias are an immediate life-threatening cause of death due to disruption of the hearts
electrical conduction system. Direct current (DC) = asystole & Alternating current (AC) = V-fib
o Cataracts are (somehow) a long term complication of electrical injury
 First 24hr – elevated glucose (catecholamine release), Decrease in cardiac output 50% (decreased
plasma volume via dehydration & increased vascular resistance from vasoconstriction), decreased CVP
(dehydration), decreased in #circulating erythrocytes from direct damage in injured tissue.
 Dehydration – because the skin plays a large role in maintaining a fluid barrier (keeps water in)
disruption with burn can quickly lead to evaporative losses  hypovolemic “burn” shock
o GI (Curling) ulcers – loss of fluid leading to decreased GI perfusion can cause GI mucosal
ischemic necrosis  ulceration (classically in duodenum)
 Burn Wound Infections – delay healing, encourage scarring, and may result in wound infection/sepsis.
Systemic Abx are NOT recommended for burn infection prevention but topicals are.
o Bacterial most common [Pseudomonas (Gram -) >> S.aureus > Strep. pyogenes]
o Fungal infections (C. albicans) typically occurs later in course as topical Abx eliminate all
bacteria from the wound, allowing fro real-estate to be taken over by fungus
 o Viral infections are less common but most common is Herpes Simplex Virus if occurring
Workup
 1st step – primary & secondary survey; if signs of inhalation injury present, then immediate intubation
is essential as worsening edema may make later intubation impossible.
 Inhalational Injury
o Clinical signs (mentioned about) should prompt immediate intubation and further workup
o Fiberoptic bronchoscopy (gold stnrd) - visualize carbon deposition & damage/necrosis of tissue
o High probability V/Q scan – can show low V/Q ratio noting impaired ventilation
o Labs – >10% carboxyhemoglobin, <90% oxygen saturation
o CXR – rarely positive early in injury; little value in diagnosis
 Carbon monoxide poisoning
o Carbon monoxide pulse oximetry – will show elevated CO presence in blood
o Standard ABGs – show normal pO2 with decreased SaO2 (CO bound to Hb causing elevated
partial pressure, but tissue saturation will be low)
Management
 Inhalational Injury – early intubation to prevent loss of airway from worsening edema
 Fluid Management
o Parkland Formula [Total Fluid Volume = (4cc/kg)(weight in kg)(%TBSA burned)]
 Used with 2nd degree burns or worse with >20% TBSA covered
 Infuse half of total fluid in 1st 8hr from time of injury (thus if you got them 7hr after
injury, you need to haul ass to get it all in within 1 hr!)
 2nd half of fluid infused over next 16hr following 1st half
 Some concerns due to lack of account/adjustment for compartmental fluid shifts; may
lead to electrolyte abnormalities if not monitored
o Urine Output can be used; titrate fluid infusion to 0.5mL/hg/hr (adults) or 3mL/kg/hr (children)
o Lactated Ringer’s is preferred as it’s closer to physiologic ion concentrations and may aid with
resolving possible metabolic acidosis from hypovolemia
 Colloid solutions are more expensive and linked with pulmonary complications in burns
 Normal saline (due to high Cl- content) can lead to hyperchloremic metabolic acidosis
(wasting of HCO3-) due to high amounts of fluid needed to resuscitate burn pts
 Wound management – regular cleansing and debridement with application of topical antimicrobial
ointments & dressing.
o Prophylactic IV abx – contraindicated; no benefit and selection for resistance organisms
o Topical Agents
 Silver sulfadiazine – antimicrobial; may result in neutropenia or thrombocytopenia,
poor deep penetration, ineffective against Pseudomonas
 Silver nitrate – antimicrobial; poor deep penetration, ineffective against Pseudomonas,
may stain skin brown, and rarely causes methemoglobinemia
 Sulfamylon (madenide acetate) – antimicrobial; good deep penetration and kills
Pseudomonas; carbonic anhydrase inhibitor (metabolic acidosis can occur) and painful
to apply to burns
o Skin graft – used if wound bed is deemed “clean”; do not do if signs of infection
 CO poisoning – 100% O2 via non-rebreather face mask
 Circumferential Chest burn – chest escharotomy should be done, as the restricting band of tissue can
lead to respiratory decline
 Circumferential extremity burn – escharotomy (concern for compartment syndrome)
 Curling Ulcer prevention – PPI or H2 blocker should be given prophylactically
  Nutrition – enteral route is preferred but TPN may be used if pt cannot tolerate these. Oral feedings
are not recommended due to likely damage/swelling to the oropharynx
 Chemical Burn considerations – copious irrigation/removal of caustic substance is extremely
important; also protection of others/removal of patient from area of exposure are critical
 Electrical Burn considerations – cardiac monitoring for 12-24hr (concern for arrhythmias)
Areas of Trouble
 Child Abuse – may be represented by burn injury (cigarette burn is classic) with inconsistent/conflicting
histories by parents. All child abuse is reported to proper authorities by mandate.
 Chronic non-healing burn wounds are concerning Marjolin’s Ulcer (SCC arising from the site of a
scar/burn/previous injury and has an increased risk of metastases)
Tips from UWorld
4446: Carbon Monoxide Poisoning
 Carbon monoxide has better steric interactions with heme as a molecule. Thus is tightly binds heme,
shifting the oxygen dissociation curve to the left  holds on to oxygen and won’t deliver
 Presentation: headache, confusion, malaise/dizziness, red cheeks  syncope, seizure, coma,
arythmia/myocardial ischemia. May be intermittent if patient exposure is intermittent (like works at a
traffic stop)
o Labs: secondary polycythemia (reactive EPO production from tissue hypoxia)
o Smokers are more sensitive to external CO as they have a low level (3%) of carboxyhemoglobin
at any given time
 Dx: elevated carboxyhemoglobin level on arterial blood gas
o Note that pulse oximetry does NOT differentiate between normal/carboxyhemoglobin
 Tx: 100% oxygen until labs normalize

11566: Cyanide Toxicity

 Presentation: CNS (headache, altered mental status, seizure, coma), cardio (arrhythmias), respiratory
(tachypnea turning into respiratory depression), GI (abdominal pain, nausea, vomiting), renal
(metabolic acidosis from lactic acid, and renal failure)
o Etiology: prolonged sodium nitroprusside infusion (metabolized to CN-), combustion of
wool/silk (contain CN-), or industrial exposures
 Dx: clinical presentation
 Tx: sodium thiosulfate or hydroxycobalamine infusion to remove CN- from blood

Chapter 47: Severe Right Leg Pain following Tibia Fracture – Compartment Syndrome
Presentation
 5Ps – early (pain on passive motion/out of proportion to exam), nerve compression (paresthesia,
paralysis), vascular compromise (pallor, polar, pulselessness, increased capillary refill time)
o Similar to acute limb ischemia, but vascular compromise is a LATE symptom (vs as an early sign)
o Failure to recognize (like assuming pain is from fracture) may lead to ischemic necrosis!
Anatomy
 Thigh compartments (3) – anterior, medial, posterior
 Lower leg compartments (4) – anterior, lateral, superficial posterior, deep posterior
o Anterior compartment most susceptible to compartment syndrome; the deep peroneal nerve
runs through this compartment and compression can cause 1st web interspace foot numbness
(sensory fibers) & foot drop (extensor digitorum brevis & extensor halluces brevis)
 Upper arm (2) – anterior, posterior
 Forearm (3) – dorsal, volar, mobile wad
Etiologies
  Decreased compartment size – plaster cast, circumferential 3rd degree burn, external compression,
splints, or anti-shock garments
 Increased compartment volume – vascular/blast/crush injury, fracture, electrical burn, hematoma,
ischemia reperfusion syndrome, SIRS/sepsis
Pathophysiology
 Compression syndrome occurs when limb compartment pressure begins to rise due to any etiology.
Normal compartment pressure is 5-10mmHg. When pressures rise upwards of 20mmHg, veins/venules
are compressed and venous outflow is impaired. Increased pressure backs up into the capillaries,
resulting is halt of capillary flow, loss of O2 delivery to tissue, and ischemic necrosis!
o Circumferential burn – eschar forms contraction band, blocking venous outflow. Capillary
pressure increase causes leakage and edema
o Ischemia/reperfusion – inflammation from reperfusion injury causes capillary leak
o Large-volume resuscitation – in situations where this is necessary, often extensive damage or
infection/shock are occurring. High volume + elevated capillary leak = edema.
o Severe exertion – muscle breakdown causes inflammation  capillary leak
o Prolonged surgery/immobilization – may result in a crush injury (constant pressure on one
area) resulting in inflammation/edema
 Acute extremity compartment syndrome – classic syndrome that was described in “presentation”
 Chronic extremity compartment syndrome – less common syndrome where syndromes occur
chronically with muscle exertion. Transient tissue edema with activity causes pain/swelling, that is
relieved with cessation and rest. Dx made with clinical history & presentation. NOT an emergency.
 Abdominal compartment syndrome – occurs with increased intra-abdominal pressures causing
compression and dysfunction/damage of internal organs of the abdominal/thoracic cavities
o Impaired respiration – compression of diaphragm/thoracic cavity  hypoxemia/hypercarbia
o Compressed IVC – decreased preload  decreased cardiac output/stroke volume  ischemia
o Compressed kidney – impaired renal perfusion/diminished urine output and AKI
o Often can lead to multi-organ failure and high risk of mortality
 Pulselessness – only occurs in extremely high compartment pressures; sign of serious damage and
concern for irreversible ischemic damage should be raised
 Volkmann’s Contracture – fixed, intense wrist/hand flexion due to fibrosis of
damaged forearm muscles following forearm compartment syndrome
o Classically occurs in children following supracondylar fracture; brachial
artery injury results in ischemic inflammation in forearm  muscle
damage  fibrosis/contracture
Workup
 Clinical Dx: tense, swollen compartment with pain on passive motion + clinical Hx suggestion
 Compartment pressure measurement: contraindicated strong clinical suspicion (delay in treatment &
risk of false negative); best used as a rule-out or if clinical exam cannot be performed
o 5-10mmHg (normal) with >20mmHg diagnostic
 Bladder pressure measurement: used to diagnose abdominal compartment syndrome. Physical exam
isn’t reliable for diagnosis; thus measurement is necessary every time. >20mmHg is diagnostic
Management
 Extremity compartment syndrome: Immediate decompressive fasciotomy of all compartments of
affected limb section. It’s hard to rule out specific compartments, thus the risk is not worth reward.
o Fasciotomy should be generous, as swelling can continue to increase. Open that thing up!
o The deep posterior compartment is the most difficult to decompress (lower leg); but vital as it
contains both the posterior tibial nerve, tibial nerve, and peroneal arteries (foot function!)
  Abdominal compartment syndrome: urgent decompressive laparotomy with maintenance of open
abdomen wound + wound vac. Closure can be done with decreased edema/intra-abdominal pressure.

Chapter 48: Bloody Emesis – Upper GI Bleed

Differential Dx: Gastritis (pernicious anemia, H.pylori), PUD (gastric or duodenal), erosive esophagitis, Mallory-
weiss tear, Esophageal varicies, gastric cancer, Curling/Cushing ulcers (Stress ulcer), Aortoenteric fistula, Osler-
Weber-Rendu syndrome

Characteristics of Emesis or Stools can give insight to upper/lower GI bleeding

 Upper GI – bright-red bloody or coffee-ground emesis
 Upper > Lower – melena or maroon stools (digestive enzymes  oxidation  RBC darkening)
 Lower > Upper – hematochezia (less digestive enzymes, thus blood is red; massive upper GI bleed can
overwhelm the GI enzymes action, resulting in this presentation, although this is more rare)
Pathophysiology
 Esophageal Varices
o Proximal 2/3 of esophagus mucosa is drained by the esophageal veins  SVC
o Distal 1/3 of esophagus mucosa is drained by the left gastric vein (coronary vein)  portal vein
o When liver cirrhosis occurs, the portal venous drainage is backed up, resulting in portal venous
high pressure/distention, thus distention of all the veins feeding it
o The distal esophagus is then prone to bleeding with these torturous veins (risk of upper GI)
 Acute Gastritis
o Erosive, superficial inflammation of the gastric mucosa due to impaired defenses allowing
damage by normally produced HCl
o Normal defenses include prostaglandins (minimize inflammation from HCl), bicarbonate
(neutralize HCl), and somatostatin (turn off hormonal stimulation of HCl production)
o Impairment can occur from small amounts of alcohol (increase HCl secretion), chronic NSAID
use (limit COX-1/COX-2 prostaglandins), or consuming corrosive materials
 Chronic Gastritis
o Non-erosive inflammation of the gastric mucosa due to various inflammatory states
o Type A – fundus-dominant, associated with pernicious anemia
o Type B – antrum-dominant, associated with H.pylori infection (most common)
 Dieulafoy’s Lesion
o Rare vascular malformation where a large, torturous artery runs along the gastric sub-mucosa
(typically along the lesser curvature of the stomach), which can be damaged and bleed
o Endoscopy – pin-point defect in gastric mucosae with
active bleeding, with subsequent identification of
arterial malformation NOT associated with ulceration
Anatomy
 Remember that the stomach has a fairly extensive blood
supply, and bleeding at different areas will result in different
involvement of gastric blood supplies
o Gastric ulcers (posterior stomach wall)  splenic artery
o Gastric ulcers (lesser curvature)  left gastric artery
o Duodenal ulcer  gastroduodenal artery
 The “upper GI tract” is considered from the [oropharynx 
distal duodenum at the Ligament of Treitz] as this spot is the transition from retro to intraperiotoneal

Work-up
  “Occult GI bleed” – bleed isn’t known to the patient (no obvious bleed) but signs (FOBT or anemia)
point to a bleed occurring. These tend to be lower GI bleeds.
 “Obscure GI bleed” – bleed is known (often obvious bleeding) but the source cannot be identified on
endoscopy. These tend to be upper GI bleeds.
 Fluid resuscitation – (two large-bore needles) restores blood volume and will reveal extent of bleeding
 Placement of NG tube – suction out blood for better GI tract visualization, using this for lavage is great
way to confirm bleeds (use only room temp fluid; cold fluid may cause increased Vagus stimulation)
o Bloody/coffee grounds suctioned  confirmed upper GI bleed
o Clear fluid suctioned  no stomach bleed, but cannot rule out duodenal bleed
o Bilious fluid suctioned  confirmed no upper GI bleed
 Coagulation studies – may show evidence for bleed & need for transfusion
 Blood type/cross – get some blood ready just in case infusion is needed
o Type & screen  just get pt blood characteristics, likely won’t need the blood
o Type & cross  blood is suspected to be necessary; actually crosses pt with donor blood
o Immediate transfusion  give O negative blood as it won’t cause a reaction
 Hemoglobin/Hematocrit – may be totally normal early on, and may not even change until patient has
lost 30-40% of their blood volume! Remember that whole blood is being lost (thus the proportions are
all the same!). H&H only begins to change once the kidneys start conserving sodium/H20 (12-24hr) or
IV fluids are administered. Hypovolemic shock (tachycardia, decreased urine output, drop in BP) may
be an earlier sign than changes on H&H!
 BUN/Creatinine - RBC proteins will be broken down increasing intestinal urea production/absorption
(>20 is considered increased). If the kidneys are hypoperfused due to bleeding, they may reabsorb
more urea to increase blood volume. The increased absorption in both the intestines/kidney raises the
BUN increasing the BUN:Creatinine ratio!
 Endoscopic study – either upper or lower depending on suspected etiology; the only time you won’t
have an endoscopy is with massive GI bleed making endoscopy unable to visualize anything. This done
after pt is stabilized and best done within 12hr of admission

Treatment
 If endoscopy is negative – further studies to figure out problem
o Capsule endoscopy/Further endoscopic studies/Tagged RBCs – for less energetic bleeds
o Angiography – typically used in brisk bleeds (1cc/min) & may allow for therapeutic embolization
 If endoscopy is positive – found etiology must be treated accordingly
 If pt actively vomiting blood, they should be upright at 30 o unless contraindicated
 Conservative management should be done if pt is stable
o Mallory-weiss  observe (spontaneous resolution occurs often)
o Gastritis  H2/PPI + d/c EtOH + H.pylori workup
o Esophageal Varices  octreotide (venoconstriction) + endoscopy/banding
o Peptic ulcer  gastric level + H2/PPI + H.pylori workup
o Dieulafoy’s lesion  endoscopic banding
 Surgical management is reserved for unstable patients, those who fail conservative therapy, or to
exclude esophageal varicies
Further Information on Etiologies
2596: MALT lymphoma (MALToma)
 Gastric cancer often the result of H.pylori infection; looks like a heaped up ulcer
 Dx: endoscopy with biopsy showing MALT-lymphoma
 Tx:
 o Eradication of H.pylori ([omeprazole, clarithromycin, amoxicillin] or [bismuth, omeprazole, a
tetracycline, an aminoglycoside]
o Chemotherapy ([CHOP] or [CHOP + bleomycin]) can still play a role should H.pylori eradication
fail to cure the cancer

Chapter 49: Severe Epigastric Pain – Peptic Ulcer Disease/Perforated Viscus

PUD Presentation
 ‘Burning’, non-radiating epigastric pain with onset depending on region of damage
o Gastric ulcer – pain with eating (HCl production = further erosion) & weight loss (avoid eating)
o Duodenal ulcer – relief with eating (Bicarb from pancreatic juices) & weight gain (yay eating!),
but pain re-starts 2-3hr post-prandially
 Nausea, vomiting, abdominal distention, melena, tenderness to palpation of epigastrum
 History of GERD, chronic NSAID use, smoking, Family Hx of ulcers

Perforated PUD Presentation

 Presentation: chronic epigastric pain that suddenly worsens with an initial sharp pain which quickly
radiates; rebound tenderness/guarding (peritonitis due to gastric contents in peritoneal cavity), & air
under the diaphragm on CXR (indicates perforation)
o Pt often lays very still because of abdominal pain with movement; exquisite pain with palpation
with guarding/rigidity.
o Shoulder pain may be present (diaphragm irritation, referred pain via phrenic nerve)
o Septic shock & hypovolemia may be initial presentation depending on duration of condition
 Dx: immediate CXR, as diagnosis and prompt treatment (<12hr) is critical to limit mortality
o Serum amylase/lipase should be ordered to rule out acute pancreatitis
o Labs will often be normal outside an elevated WBC with left shift
 Tx: immediate surgical repair

Pathophysiology
 Remember that ulceration results from either acid hyper-secretion or decreased mucosal barriers
(NSAIDs, lack of somatostatin, lack of bicarb)
 H. pylori infection (90% of duodenal ulcers & 80% of gastric ulcers) result in ulceration by provoking
gastrin hypersecretion  HCl hypersecretion  antral gastritis  ulceration
 Chronic NSAID use (including aspirin) inhibits COX-1/COX-2  inhibits prostaglandin/thromboxane
production. These typically regulate inflammation & HCl secretion, thus their absence causes damage!
 Cigarette smoking (x2 risk of PUD) results in decreased prostaglandins and mucus proliferation as well
as throwing off he apoptosis/proliferation balance in the stomach.
 Cushing Ulcer – increased intracranial pressure resulting in Vagal hyperstimulation  HCl
hypersecretion  mucosal damage; high perforation risk
 Curling ulcer – severe burns cause hypovolemia  mucosal ischemia  mucosal damage  ulceration

Classification of Peptic Ulcers

 Type I – lesser curvature at the incisura (most common type) – mucosal barrier disruption etiology
 Type II – lesser curvature/duodenum – HCl hypersecretion
 Type III – prepyloric antrum – HCl hypersecretion
 Type IV – cardia of the stomach near gastroduodenal junction (very painful!) – barrier disruption
 Type V – Anywhere, but associated with NSAID use – barrier disruption
Work-Up
 Making the diagnosis is largely clinical (no lab tests are really going to help you here; remember that
most of your labs are going to be normal!)
 Labs: CBC (is there bleeding?), CMP (contraction alkalosis? Loss of HCl?), amylase/lipase (rule out acute
pancreatitis), LFTs (help rule out choledocolithaisis/cholecystitis)
 Imaging: abdominal series OR upright CXR (look for pneumoperitoneum; absence doesn’t rule out
perforation); thickened viscera may also be seen
o If perforation is suspected barium UGI series (causes barium peritonitis) and upper endoscopy
(insufflation can make perforation worse!) are contraindicated
o CT abdomen with gastrografin contrast may be used to confirm diagnosis; may also show that
perforation has sealed itself, allowing for non-operative management

Management of Perforated PUD

 ICU admission with close observation
 Volume resuscitation – likely inflammation, leakage of fluid, and vomiting need replacement
 NG tube placement – stomach decompression (decrease leakage into abdominal cavity)
 Broad spectrum IV ABx – only if sepsis if noted
 Initiation of PPI + Testing for H.pylori  triple therapy for H.pylori if (+)

Surgical Management of Perforated PUD

 Excision of perforated ulcer with patching + PPI therapy
 Laprascopic approach is preferred and outcome are similar in surgeons with experience
 Surgery is ALWAYS indicated unless the ulcer has spontaneously healed (40-80% of perforations).
Consider a conservative approach if: (1) It’s been <12hr since onset of symptoms, (2) Pt is
hemodynamically stable, (3) Pt is <70yr old, (4) Pt doesn’t have any history of peptic ulcer treatment
failure, (5) Pt is high risk for surgery due to co-morbidities, (6) Radiologic evidence points to
spontaneous sealing of the perforation

Chapter 50: Chest Pain and Early Satiety – Gastric Cancer

Epidemiology
 4th most common cancer in the world; more common in the Far East, less common in USA
 Typically occurs in 70-80 y/o patients
 Rate in USA is very low due to H.pylori treatment & widespread use of refrigerators (less salting,
pickling, etc. for food storage)
Risk Factors
 Typically, several risk factors come together for gastric cancer
 Common ones: Family Hx, Diet high in nitrates/salt/fat, H.pylori infection, tobacco use
 Genetic: BRCA1/2, HER2 overexpression, Peutz-Jegher syn., HNPCC, Type A blood
Screening
 Most common type is gastric adenocarcinoma (90%), typically with metastatic spread at time of dx
 Typically, only 50% have local disease at dx with only 50% of local disease being resectable!
o Though to be due to vague, non-specific symptoms associated with these diseases
 Because it’s much rarer in the US, screening is not routinely recommended
Anatomy
 Blood supply to the stomach
o Celiac Trunk  left gastric artery
o Celiac Trunk  common hepatic  right gastric artery
o Celiac Trunk  common hepatic or right gastric  right gastroepiploic artery
 o Celiac Trunk  splenic  left gastroepiploic artery
o Celiac Trunk  splenic  short gastric artery
History & Physical
 Common Symptoms: Vague abdominal pain, weight loss, fatigue, dyspepsia, melena/anemia
 Specific Symptoms: Virchow’s nodes, Sister Mary Joseph nodule, Irish’s node (left axillary node)
 Less Common Symptoms: Dysphagia/early satiety (cardia involvement), acute upper GI bleed, palpable
mass, obstructive jaundice/elevated LFTs (growth into hepaticoduodenal ligament)
Pathophysiology
 Intestinal Type Gastric Adenocarcinoma: well-differentiated type arising from gastric mucosa, typically
occurring due to chronic inflammation in the stomach (H.pylori, poor diet, smoking, etc.). Most
commonly found in the distal stomach (where all that ingested crap lies!)
 Diffuse Type Gastric Adenocarcinoma: poorly-differentiated tumor asiring from lamina propria; grows
in a diffuse, sub-mucosal pattern resulting in gastric thickening (not a discreet mass); typically occurs
due to congenital disorders (younger pts); Most commonly found in the proximal stomach.
o Linitis Plastica: formation of the gastric wall into a thickened “plastic” wall due to thickening
 GI Stromal Tumors (GIST; 1%): mesenchymal tumors arising from the interstitial cells of Cajal (GI
pacemaker cells) appearing as smooth masses with regular borders. Express c-KIT & CD117 universially.
o Neoadjuvant/maintainence therapy with Imatinib (Tyr-kinase inhibitor)
o Resection of mass through wedge resection (gastrectomies are only rarely needed)
 Gastric Carcinoid Tumors (1%): rare to arise in the stomach; often small and treated endoscopically or
only observed unless functional)
 Gastric Lymphoma: typically occur as a MALT-oma (H.pylori infection; treatment of bacterium causes
regression of tumor) or as a diffuse B-cell lymphoma (CHOP chemotherapy followed by radiation)
o CHOP  cyclophosphamide, doxorubicin, vincristine, & prednisone
Workup
 Diagnosis  Upper endoscopy allows for visualization and biopsy. Multiple biopsies have a sensitivity
around 98% (gold standard)
 Staging  endoscopic ultrasound (assess size, depth, and local lymph nodes) + CT CAP (identify distant
metastatic disease. PET scan also very good at assessing lymph node involvement
o At least 15 nodes must be resected and analyzed for proper staging of gastric adenocarcinoma
o D1 dissection – perigastric lymph node dissection for staging
o D2 dissection – hepatic, left gastric, celiac, and splenic lymph node dissection for staging
(preferred for completeness but higher rate of morbidity)
Management
 No invasion of mucosa/lamina propria – mucosal resection with 5mm margins (met. risk is LOW!)
 Distal invasive cancers – subtotal gastrectomy with Bilroth II or Roux-en-Y reconstruction
 Proximal invasive cancers – proximal gastrectomy or total gastrectomy with reconstruction
 With proper staging of gastric adenocarcinoma:
o Operable T1N0 – limited resection is good
o Operable >T1N0 – Neoadjuvant chemo  surgical resection  post-op
 Neoadjuvant care MAY be skipped, but not preferred
o Inoperable or metastatic disease  palliative chemo with re-assessment following treatment
 HER-2 (-)  classic chemo drugs
 HER-2 (+)  trastuzumab + classic chemo drugs
 If not a candidate for chemo (can’t handle it) then just initiate palliative care
Complications
  Dumping Syndrome – syndrome of high-osmolar food entry into the small intestine (loss of pyloric
sphincter due to gastrectomy) resulting in diarrhea, stomach cramps, & hypotension 20-30 minutes
following eating
 Anastomotic Leak – leakage of the abdominal tract due to incomplete healing. Often presents with
abdominal pain, peritonitis, fever/tachycardia/leukocytosis  sepsis if untreated.
o Upper GI CT with gastrografin – use if unsure about diagnosis – (+)if showing a leak!
o First line: source control with operation to fix leak with subsequent bowel wash-out; keep pt
NPO and place on TPN post-op with NG tube placement to minimize gastric contents
o 2nd line: complete resection of leaking area

Chapter 51: Chest Pain After Vomiting – Boerhaave Syndrome (Spontaneous Esophageal Rupture)
Risk Factors
 Alcoholism/overeating/bulemia (all can cause forceful vomiting/wretching)
 Most common in pts 50-70yr
Presentation
 Mackler’s Triad: vomiting, thoracic pain (radiation to back/flank/abdomen, aggravated by swallowing),
subcutaneous emphysema (crepitus on sternal palpation; pathognomonic for syndrome)
o Dyspnea & dysphagia are often common signs as well
 Note that early Dx is critical! Boerhaave’s has high mortality (40%) which increases higher after 24hr
Pathophysiology
 Esophageal perforation is not typically spontaneous. 60% are iatrogenic (upper endoscopy). Trauma,
foreign body ingestion, or malignancy are all more common causes. Only about 10% are spontaneous.
 Forceful vomiting causes intense intragastric pressure. This pressure is transmitted through the
esophagus, which normally propels vomitus out the mouth. If the cricopharyngeus muscle fails to relax
the upper GI tract to allow passage of vomitus, the pressure is retained in the esophagus  rupture!
 Sepsis occurs due to contamination of the mediastinum by GI bacteria
o Pleural effusions may also occur due to erosion of the pleural membrane from gastric contents
in the mediastinum. This may also lead to pleuritis  sepsis
 The most common place for rupture is the left, posterolateral aspect of the esophagus, 2-3cm proximal
to the GE-junction  this is why left-sided pleural effusion/atelectasis is most often seen
Work up
 First step: chest X-ray
o Look for pneumomediastinum (air in mediastinum) and left-sided pleural effusion/atelectasis
o Up to 1/3 of pts will have normal CXR and air in mediastinum is best seen 1hr post-perforation
 If X-ray is questionable: CT with water-soluble oral contrast
o High sensitivity for diagnosis & allows for evaluation of surrounding structures (a huge
advantage over an esophagram with contrast) aiding surgical planning/approach
o Also, it allows for assessment of other diagnoses if Boerhaave’s isn’t what’s going on
o Water-soluble oral contrast is critical…barium can cause a huge inflammatory rxn if it leaks into
mediastinum/surrounding structures
 Endoscopy is NOT used as insufflation runs the risk of enlarging the perforation
Management
 Initial: Aggressive IV fluids (2 large-bores; if septic, monitor with central venous catheter), NPO, broad
spectrum Abx for mouth/gut bacteria, anti-fungal, H2 blocker or PPI, if hemodynamically unstable
place arterial line and start vasopressors
 Conservative: accepted in pts with low co-morbidities, no sepsis/shock, and a small perforation that’s
<24hr old or healed already
o All initial treatments + nasogastric suction + parenteral nutrition
 o Repeat imaging at hospital day 7
o If perforation seems to be healed, resume oral intake and continue Abx for 6-8wk
 Surgical: preferred treatment for everyone else
o Perforation closure: preferred in pts with smaller perfs
o Esophageal resection: preferred for larger perfs. Often resected, then re-constructed with
colon or jejunum at a later date (after they recover!)
o Both procedures require debridement of de-vitalized tissue in the esophagus, mediastinum,
and pleura (pleural decortication)

Chapter 52: Scrotal Pain – Testicular Torsion

Presentation
 Classic symptoms: nausea/vomiting, sudden onset testicular pain >24hr, superiorly displaced testicle,
absent cremaster reflex
o Cremaster reflex: ipsilateral testicular elevation due to cremaster muscle contraction with
stroking of the inner thigh (genitofemoral nerve; L1-L2)
 Other causes of acute unilateral testicular pain & some differentiating signs
o Trauma – 85% blunt, often due to sporting injury; this should be in the history
 May cause rupture & hematocele
o Torsion of epididymal appendage (appendix testis) – gradual onset unilateral pain (most
common reason in child), cremaster reflex present
 Blue dot sign: palpation of small, firm tender nodule on epididymal head, that has a blue
discoloration on examination
 Tx: NSAIDs, ice packs, and scrotal support; surgical excision for refractory symptoms
o Epididymitis – scrotal pain relieved with support (Prehn’s sign), fever, dysuria, induration
Pathophysiology
 Bell-Clapper deformity – congenital defect of the processus vaginalis resulting in failure of the
gubernaculum/testis/epididymis posterior anchoring to the inner scrotum. Both testes are allowed to
swing freely (like the ball inside a bell), predisposing to torsion later in life!
 Most common age 12-18yr
 Prior torsion puts the other testicle at risk for torsion!
Work-Up
 Scrotal exam should ALWAYS be performed in adolescent male with nausea/vomiting
 Labs:
o If high clinical suspicion, none are needed. This would delay surgical intervention.
o If low clinical suspicion: urinanalysis/CBC (rule out infectious causes)
 Imaging: Doppler ultrasound of testes (high sensitivity/specificity for torsion & rule in/out other things)
o Confirm adequate bloodflow, look for blood in testis (new = hyperechoic; old = hypoechoic)
o Trauma and torsion often occur in sporting events, which can muddy the waters here!
Management
 Torsion <6hr (100% viability): attempt at ED manual de-torsion (lateral rotation of testis) with elective
bilateral orchiopexy. If manual de-torsion not possible, surgical de-torsion/orchiopexy is needed
 Torsion >6hr: immediate surgical de-torsion/orchiopexy is needed
o If testicle is necrotic, orchiectomy is warranted
 Minor trauma (no significant swelling/pain/breaks in scrotum): scrotal support, ice packs, NSAIDs, rest
 Major trauma (penetrating, lack of bloodflow, rapidly expanding hematoma, avulsion, scrotal de-
gloving, or violation of tunica albuginea): go to OR for exploration and repair
Prognosis
 Torsion timing: <6hr (100% viability), 12hr (20% viability), 24hr (0-10% viability)
  Fertility is often not affected significantly with unilateral loss of a testicle. However, risk of anti-sperm
antibodies (loss of immunologically privileged site) may occur with trauma/necrosis of testicle
decreasing sperm count

Chapter 53: Scrotal Mass – Testicular Cancer

Differential Based on Anatomic Location of Mass
 Scrotal Skin: epidermoid/pilar cyst, squamous cell carcinoma
 Spermatic cord: indirect inguinal hernia, hydrocele, varicocele
 Epididymis: epididymitits, spermatocele, torsion of testicular epididymal appendate (appendix testis)
 Testis: orchitis, testicular torsion, testicular cancer
Risk Factors – cryptorchidism (biggest), personal/family Hx of testicular cancer, Klinefelter’s Synndrome, white
race, male 20-35yr (most common age range)
Presentation
 Painless mass within the testicle (cancer until proven otherwise!)
 Constitutional signs suggest metastatic disease
o Retroperitoneal lymph nodes: back/abdominal pain, weight loss, nausea
o Pulmonary mets: cough, SOB
 Gynecomastia: may be present in hormonally active tumors secreting B-hCG (choriocarcinoma)
 Hyperthyroidism symptoms: alpha unit of B-hCG similar to TSH; thus choriocarcinoma may cause this
Pathophysiology
 When Cryptorchidism results in testicular cancer, the distribution is undescended testicle (75%) and
descended testicle (25%); thus an underlying problem with the tissue may be present, not just the
problem of lack of descent
 Seminomatous germ cell tumors (35%)
o Seminoma – most common in adults; high response to radiation; rarely metastasizes with good
prognosis, rarely B-hCG production
 Nonseminomatous germ cell tumors (65%)
o Embryonal carcinoma – malignant/aggressive hematogenous spread, often necrosis, B-hCG or
AFP production is common
o Yolk sac tumor – most common children, malignant, AFP production
o Choriocarcinoma – malignant, early hematogenous spread, B-hCG production common
o Teratoma – derived from >2 embryonic layers, may be benign or malignant, AFP or B-hCG
o Mixed germ cell tumor – multiple components of the above
 Sex-Cord stroma tumors
o Leydig cell – benign, paraneoplastic syndromes due to testosterone production
o Sertoli cell – benign, often clinically silent
 Other
o Lymphoma – older men, diffuse large B-cell, often bilateral/malignant
Workup
 Labs: B-hCG, AFP, LDH (used for staging/response tracking/prognosis)
 Imaging:
o Ultrasound: solid mass within the testicle (cystic/fluid mass is less likely)
o CT abdomen/pelvis: used to assess lymph nodes for staging
o CXR: used to assess lungs for staging
o CT chest: done only if signs of metastatic disease is found on CT a/p or CXR
o CT head or MRI brain: done only if neurologic symptoms present
 Biopsy is contraindicated due to high risk of seeding
Management
  Radical inguinal orchiectomy: allows for removal of testicle and spermatic cord up to internal ring
o Approach preferred as it allows for removal of more spermatic cord = less local recurrence
 Post-surgical treatments may be utilized based on tumor type/clinical situation
o Radiation: often used in seminomas
o Chemotherapy: may be used in most testicular cancers
o Retroperitoneal lymph node dissection: often used in non-seminomas
 Complications
o Unilateral orchiectomy will NOT lead to infertility or erectile dysfunction
o RPLND may injure nerves leading to erectile dysfunction

Chapter 54: Blood in Urine

Differential Diagnosis: Acute cystitis, bladder cancer, nephrolithiasis, prostatitis, renal cancer, pyelonephritis,
PKD, prostate cancer, BPH, trauma, urethral stricture, vigorous exercise, IgA nephropathy, intense exercise
Differential By Age:
 <20yr – Acute (UTI, Foley trauma, exercise); Chronic (IgA nephropathy)
 20-50yr – Acute (UTI, Foley trauma, nephrolithiasis); Chronic (PKD, prostate/bladder/kidney cancer)
 >50yr – Acute (UTI, Foley, nephrolithiasis); Chronic (BPH, PDK, prostate/bladder/kidney cancer)
Presentation
 Gross Hematuria – visible urine color change to pink (mild active bleed), red (moderate-severe active
bleed), brown (old blood/glomerular bleed), or passage of clots
 Microscopic Hematuria – grossly normal urine with RBCs or heme seen on urinanalysis
o >3RBCs/HPF on only one urine specimen warrants complete hematuria workup
 Pseudohematuria – pink/orange/red/brown discoloration not due to RBCs in urine
o Foods (beets/rhubarb/artificial dyes)
o Drugs (rifampin, sulfonimides, phenazopyridine, nitrofurantoin, phenytoin, levodopa,
methyldopa, quinine, choloquine, Adriamycin, metronidazole)
o Rhabdomyolysis (huge amount of myoglobin)
o Conjugated bilirubinemia (conj. bili is water soluble)
 Pain + Hematuria – likely indicates infection/urinary obstruction/urinary trauma
 Nephrolithiasis – colicky flank/groin pain, pt will move/shift body weight relieving pain due to shifting
of stone (as opposed to peritonitis where pts stay very still)
o Risk Factors - Hx, fHx, high protein diet, male, low fluid intake, dehydration, recurrent UTI,
diabetes, gout, RTA, hypercalcemia, some medications
 Renal Cancer – incidental discovery of mass on imaging most common; may have flank pain, abdominal
mass, and hematuria triad (10-15% all three)
o Risk factors – smoking, male, older, obesity, fHx, heavy metal/chemical exposure
 Bladder Cancer – painless gross hematuria, rarely with urinary symptoms
 Prostate Cancer – incidental discovery with PSA or DRE most common; may have urinary obstruction
symptoms similar to BPH
o Metastatic disease can present as bone pain, obstructive renal failure, weight loss
Anatomy
 Upper UG tract – kidney  end of ureter
 Lower UG tract – bladder  exit of urethra
Pathophysiology
 Kidney Stones – typically form in the kidney/renal pelvis and often pass freely through the UG tract iif
<5mm. Obstruction commonly occurs ureteropelvic junction, pelvic brim, or ureterovesical junction.
o Calcium oxalate stones – most common stones; radiopaque; HyperCa2+/Chrohn’s risk factors
 o Struvite (magnesium ammonium phosphate) stones – classically occur secondary to urease(+)
UTI bugs (Proteus, Klebsiella), staghorn calculi, radioopaque
o Calcium phosphate stones – form well in alkaline urine, radiopaque; RTA/hyperaparthroidism
o Uric acid stones – form poorly in alkaline urine, so best to alkalinze urine to treat; radiolucent;
risk factors (low urine pH, gout, chemotherapy, ileostomy patients, high protein diet)
 Renal Cancer
o Renal Cell carcinoma (most common) arises from renal tubular cells
o Histologic Subtypes – Clear Cell (70%), papillary (15%), and chromophobe (5%)
o 33% metastatic at Dx – most commonly to lungs, but may go many places
o Genetic syndromes associated with RCC are von Hippel-Lindau (AD; chrom 3p), tuberous
sclerosis (AD, chrom 9), or Birt-Hogg-Dube (AD, chrom 17)
o Paraneoplastic syndromes associated – polycythemia (EPO production), hypercalcemia (PTHrP
production), hypertension (renin production), Cushing’s syndrome (cortisol production), or
Stauffer’s syndrome (liver dysfunction/hepatosplenomegaly, unknown mechanism)
 Bladder Cancer
o Urothelial cell carcinoma (transitional cell carcinoma; most common type)
o Graded low or high + staged based on local invasion depth
 Prostate Cancer
o Prostatic adenocarcinoma (most common)
Workup
 First Step: urine dipstick (beware of false positives with myoglobinuria, or iodine solution cross-rx)
o Even if negative, pt should probably have a urinanlysis
 Second step: urinalysis with urine microscopy (RBCs/HPF, WBCs, bacteria, crystals, dysmorphic RBCs,
casts) to further determine presence/source of bleeding
o Casts, proteinuria, dysmorphic RBCs, brown urine  glomerular source and should be referred
to nephrologist for further workup
 Labs: CBC (anemia, infection, thrombocytopenia), CMP (BUN/Cr), PT/PTT/INR (rule out coagulopathy),
PSA (prostate screening, some false positives with instrumentation/infection), urine culture (infection),
urine cytology (malignancy)
o Negative cytology does NOT rule out malignancy; low-grade tumors sensitivity of 50% and large
amount of urine RBCs can result in false-negative
 Concern for nephrolithiasis: non-contrast helical CT (CT-KUB) is most sensitive for imaging; ultrasound
should be used in pregnancy women/women of childbearing age
o In HIV patients, anti-retroviral drugs can crystalize in the UG tract forming small radiolucent
stones. CT-KUB will not show anything! So this is the one situation where contrast CT is useful
for stones to show a filling defect
 Typically, any further workup will be based on suspected etiology
Management
 Remember that the 1st thing to do is to find and address the underlying cause. The below are common
causes and should be easily recalled.
 Renal Stones – based on estimated size of stone and likelihood of passing spontaneously
o <5mm – likely to pass; supportive care + tamsulosin (alpha blocker, relax ureteral wall) unless
septic/solitary kidney/uncontrolled pain
o 5-9mm – intermediate; clinical judgement should be your guide
o >9mm – unlikely to pass, invasive treatment (shock wave lithotripsy, percutaneous
nephrostomy, or nephrolithotomy)
o Emergent Surgery – urosepsis, intractable pain, progressive renal damage, or solitary kidney.
Need to relieve obstruction with ureteral stent or nephrostomy tube placement.
  Renal Masses – depend on size and health of patient
o Surveillance + thermal/cryoablation – small masses or poor surgical candidates
o Partial/Radial nephrectomy – recommended for masses with any concern of RCC
o Radical nephrectomy removes kidney/perinephric fat/Gerota Fascia/ureter/lymph nodes and
sometimes the ipsilateral adrenal gland
 Bladder Cancer
o Dx/Staging – transurethral resection
o Small/superficial mass – complete transurethral resection + intravesicluar mitomycin
(chemotherapy) or bCG infusion (immunotherapy) + close monitoring
o Invasive to detrussor/non-metastatic - Radical cystectomy with urinary diversion
o Radical cystectomy removes entire bladder, pelvic lymph nodes, [prostate, seminal vesicles] for
male and [cervix, uterus, fallopian tubes, and part of vagina] for women
 Prostate Cancer
o Disease contained in prostate + >10yr life expectancy – removal of prostate/seminal vesicles
o Poor surgical candidate/reduced life expectancy – noninvasive therapy (external beam,
brachytherapy, or androgen deprivation) + surveillance
Special Situations
 Persistent bleeding despite Foley/Manual Irrigation
o 3-way catheter placement for continuous irrigation – allows for drainage alongside stopping
urokinase exposure (stops regular coagulation cascade)
o If continued bleeding – go to OR for cystoscopy for clot evacuation, pathologic assessment and
fulguration (cauterization of bleeding sites)
 Admission for gross hematuria is warranted by (1) bleeding despite adequate bladder irrigation or (2)
symptomatic anemia
Areas to Get You in Trouble
 Assuming hematuria is due to UTI and not doing a full workup (don’t be a dumbass)
 Not placing a Foley in the setting for significant gross hematuria (you need to irrigate clots out)
 Placing a Foley with trauma/blood at the urethra (worry of urethral transection) may lead to a full
transection and worsening damage

Chapter 55: Transient Loss of Vision in the Right Eye – Carotid Artery Embolization
Differential Dx:
 Circulatory – embolus to ophthalmic artery; central retinal artery occlusion (cherry red spot), retinal
vein occlusion (“cloudy vision” with cotton wool spots, edema, retinal hemorrhage); giant cell arteritis
(jaw claudication, headaches, ^ESR), or severe orthostatic hypotension
 Ocular – retinal detachment (floaters), or open angle glaucoma (peripheral  central vision loss)
 Neurologic – papilledema, optic neuritis, retinal migraine
Risk Factors
 Older age, male gender, HTN, smoking, hypercholesterolemia, diabetes, obesity
Presentation
 Amaurosis Fugax (Greek – ‘darkness’; Latin ‘fleeting’) – transient vision loss (“shade coming down”)
resulting from atherosclerotic debris breaking from a plaque in the internal carotid, and transiently
lodging in the ophthalmic artery (1st branch of ICA)
 Hollenhorst Plaques – bright yellow, refractory spots seen on ophthalmic indicative of cholesterol
microemboli breaking off and lodging into the eye arteries
 Carotid Bruit – indicative of a carotid plaque. Must rule out heart murmur (can be transmitted up
carotids), external carotid bruit (benign), and subclavian bruit (possibly subclavian steal syndrome!)
Signs of Other Problems Mimicking Carotid Embolization
  Motor weakness/paralysis & Sensory loss – indicative of a TIA or stroke! While a patient may have
transient vision loss, additional symptoms suggesting brain involvement are not ok!
o ACA stroke – leg weakness, hemiplegia, urinary incontinence (contralateral; lower > upper) –
medial surface of frontal/parietal lobes
o MCA stroke – aphasia, hemi-neglect, hemiparesis, gaze preference (contralateral; most
common form of anterior circulation stroke) – lateral surface of frontal/parietal lobes
o PCA stroke – homonymous hemianopia; note that posterior circulation strokes are NOT from
carotid embolism; thus a carotid endarterectomy is NOT useful
 Dizziness, Syncope, Headaches – most commonly due to vertebral artery disease, but rarely may be
caused by bilateral carotid stenosis
Anatomy
 Internal Carotid branches – no branches in the neck (easy to identify on scans!)
o Intracranially, the Ophthalmic Artery is the 1st branch of the internal carotid
 External Carotid branches – Superior Thyroid, Ascending Pharyngeal, Lingual, Facial, Occipital,
Posterior Auricular, Maxillary, and Superficial temporal (“some attendings like freaking out potential
medial students”)
Pathophysiology
 Stroke stuff – consult neuro block notes
o Typically, the size of the embolus is the critical factor in determining stroke vs TIA. Larger
emboli (like from the left atrium) are harder to dissolve via the fibrinolytic system, thus making
for longer interruptions in bloodflow
o Recurrent TIAs are likely from carotid artery plaques (consistent course when breaking off)
o Multiple TIAs/strokes in different parts of more likely from atrial plaques (longer distance
allows for greater variability when breaking off)
 Atherosclerotic Plaque Formation – endothelial damage  thrombin/ADP/cytokine release  platelet
migration/fatty streak formation  ultimately smooth muscle infiltration/calcification/fibrosis
 Carotid artery bifurcation is a classic place for atherosclerotic plaque formation due to alteration of
shear stresses on the intimal walls of the artery
o High shear stress – good for the intima, kind of like how mechanical stress promotes bones to
grow. The Inner wall of the bifurcation is blasted with blood and rarely has plaque buildup.
o Low shear stress – makes favorable conditions for plaque formation (blood isn’t blowing away
the atherosclerotic plaques). The outer walls have transient reversal of blood flow due to the
diverting flow of medial blood (hitting the bifurcation) getting blasted out toward the outer
walls. These slower flow states favor formation of plaques.
 Typically, carotid stenosis symptoms are due to cholesterol emboli (NOT significant stenosis).
Collateral blood flow to the circle of Willis will provide adequate bloodflow.
o This is also why amarosis fugax is typically NOT accompanied by stroke symptoms
o Larger plaques are more unstable, thus more likely for cholesterol emboli to break off
Workup
 Auscultation for bruits: not bad but not the most sensitive/specific test. May be helpful as a nice
correlate but won’t make or break the diagnosis
 First diagnostic test: carotid duplex scan – ultrasound scan that shows the plaque and estimates
degree of stenosis based off of post-plaque bloodflow velocity (higher velocity = more stenosis; 0-49%,
50-69%, 70-99%, or occluded)
 Confirmatory tests: either CTa or MRa (allows for actual measurement of stenosis
Treatment
 Distinguishing degree of stenosis is critical for treatment decision making
 In symptomatic patients:
 o <49% - aspirin + statin +/- clopidogrel
o 50-69% - carotid endarterectomy (CEA) is considered (men/brain symptoms/ Increasing %
stenosis more benefit; women/amaurosis fugax/lower & stenosis less beneficial)
 Risk reduction at 5 years – 22%  16%
o 70-99% - CEA for both men and women (within 2 weeks; stops risk of further embolization)
 Risk reduction at 2 years – 26%  9%
o 100% - aspirin + statin +/- clopidogrel (control risk factors; no risk of embolization due to no
bloodflow in the artery!)
 In asymptomatic patients
o <59% - aspirin + statin +/- clopidogrel
o 60-99% - CEA for men; aspirin + statin +/- clopidogrel for women
 Risk reduction at 2 years  11% - 5%
o 100% - aspirin + statin +/- clopidogrel
 CEA is always followed by medical initiation of aspirin and a statin
 CEA has no benefit in a person with previous stroke causing severe neurologic deficit; the point of CEA
is to stop any further embolization to protect perfused tissue. If that tissue is dead, then there’s no
benefit to the risks of the procedure.
 Women are treated more conservatively due to data showing worse post-op outcomes. Smaller caliber
vessels are thought to be the culprit (more likely for recurrent stenosis!)
 Blood pressure control prior to CEA is critical. Concern of perioperative cerebral hyperperfusion
syndrome (severe headache, neurologic deficits, seizure, or cerebral hemorrhage) due to carotid body
manipulation. Pts with high BP have a higher incidence of this syndrome.
 Acceptable stroke/death rate after CEA is <3% (asymptomatic) and <6% (symptomatic)
 Cranial Nerves that are at risk with CEA
o CN VII (marginal mandibular branch) – drooping at the corner of the mouth
o CN IX (glossopharnyngeal nerve) – difficulty swallowing
o CN X (recurrent laryngeal nerve branch) – hoarseness
o CN XI (spinal accessory nerve) – sternocleidomastoid/trapezius muscle weakness
o CN XII (hypoglossal nerve) – tongue deviation toward injured side
 Note that carotid artery stenting (CAS) may be considered in symptomatic patients with high
perioperative risk (previous surgery, neck irradiation, lesion high in the neck)

Chapter 56: Right Calf Pain with Walking – Peripheral Artery Disease/Claudication
Risk Factors
 Smoking, diabetes, hypertension, hypercholesterolemia, old age, male gender, obesity, sedentary
lifestyle, family Hx of vascular disease, heart attack, or stroke
Presentation
 Claudication: triad of 1pain in the leg with walking, 2relief with a few minutes of rest, 3reproduction of
the pain with walking the same distance each time
 Peripheral Artery Disease: buildup of atherosclerotic plaques which limit arterial flow, resulting in
ischemia to leg muscles and pain with use
o Severity is based on the Rutherford rating scale (0 – asymptomatic; 1 – mild claudication; 2 –
moderate; 3 – severe; 4 – ischemic rest pain; 5 – minor tissue loss; 6 – major tissue loss)
o Ischemic Rest Pain (Rutherford 4) – classically occurs at the toes (hardest to get blood to) and
at night (bloodflow is gravity dependent); pt will describe pain in the feet that wakes him up at
night, where he must get up or dangle his legs till it passes. This sign is considered limb
threatening ischemia
  Buerger’s Sign (dependent rubor) – elevation of the foot (1-2min) causes them to become pale. When
putting the feet back down, they become very red like lobsters (arteriolar vasodilation!). If this sign is
absent, it’s very unlikely to have ischemic rest pain.
 Pulse deficit – can give a clue as to level of atherosclerotic stenosis
o When examining pulses, which ones do you check? (17 total!)
 Bilateral: superficial temporal, carotid, brachial, radial, femoral, popliteal, posterior
tibial, dorsalis pedis
 Unilateral: abdominal aorta (just above umbilicus)
o Calf muscle atrophy, hair loss (follicle death), dry scaly skin (sweat glands death), shiny skin
(thinning skin), ulceration, and increased capillary refill time (<2 sec is normal)
Anatomy
 Which muscle groups are commonly noticed with PAD/claudication?
o Calf muscles (superficial femoral artery) – travels through the Hunter/Adductor canal; it’s the
most common site for atherosclerotic plaques, thus the most commonly affected!
o Buttock (internal iliac artery) – the aorta/common iliacs provide flow the to internal iliac, thus
compromise of either of these palpable sites will affect the butt!
o Hamstrings are NOT often affected – they are not utilized heavily in normal walking, thus pain
here is more likely to be some some other pathology
o Feet muscles (rare; tibial artery) – usually from some isolated disease process!
 Hunter/Adductor Canal – lies within the femoral triangle (inguinal ligament, adductor longus, and
Sartorius) and allows passage of the SFA down the leg.
 Note! That while the SFA is the most common site of atherosclerosis, the common femoral artery is
the most common site of arterial emboli!
Pathophysiology
 Dependent Rubor – the distal arterioles are so poorly perfused that they are constantly vasodilated,
allowing for intense pooling of arterial blood in the feet when gravity is allowed to pull it down.
 Pain onset – often occurs at a consistent distance (fixed deficit of blood flow), but this distance may
shorten with increased effort in walking (walking up a hill, etc.)
 Claudication of certain muscles – shows the level at which claudication is occurs (referenced above)
Named Syndromes
 Subclavian Steal Syndrome – atherosclerotic disease of one subclavian artery proximal to the vertebral
artery. In higher demand situations, the diseased subclavian cannot provide perfusion…thus the
vertebral artery reverses flow from the vertebral to perfuse the arm.
o Transient vertigo, dizziness, & syncope during upper body exercise
 Buerger’s Disease (thromboangiitis obliterans) – classically occurs in young, male, heavy smokers;
smoking through to cause inflammatory occlusion of distal arteries in the hands/below the knees.
Smoking cessation is the only effective treatment!
 Leriche Syndrome – occlusion of the intrarenal aorta, often seen in smokers.
o Triad: buttock/thigh claudication, absent femoral pulses, erectile dysfunction
o E.D. from [aorta  internal iliacs  internal pudendal arteries]
o Often slow developing, thus collaterals enlarge and allow for only claudication, not ischemia
Workup
 Ankle-Brachial Index – blood pressure is measured in the ankles (dorsalis pedis & posterior tibial) and
the arms (brachial arteries); the highest ankle & highest arm systolic pressures are used.
o Normal – 1.2 – 1.0
o Mild PAD – 0.9 – 0.7 (claudication)
o Moderate PAD – 0.7 – 0.4 (claudication)
o Severe PAD - <0.4 (ischemic rest pain)
  Arterial Duplex scan – Doppler ultrasound is used to search for evidence of atherosclerosis and
estimates % stenosis based on flow velocity after the plaque
 If interventions are being planned, better visualization of the plaques should be gotten via CTa or MRa
 Screening of asymptomatic PAD patients does not provide any benefit; thus is not indicated!
Prognosis
 Risk of limb loss with only claudication is 5% at 5 years
 Risk of limb loss with ischemic rest pain is 50% at 1 year
 Ischemic rest pain, non-healing ulcer, and gangrene are poor prognostic signs and warrant more
aggressive interventional planning
Management
 First Step: smoking cessation, diet change, supervised exercise program, control chronic diseases (HTN,
dyslipidemia, diabetes, etc.)
 Symptomatic management:
o Cilostazol – vasodilator, thrombin inhibitor, inc. HDL, dec. TAGs; useful for symptom control but
contraindicated in patients with heart failure
o Pentoxifylline – FDA approved but no better than placebo (decreases blood viscosity)
 Drugs for medical management
o Statins – typically given to PAD patients, even with normal cholesterol levels (stabilize plaques).
Goal is an LDL <100, or <70 if cardiovascular risk factors. Doesn’t increase walking distance.
o Aspirin – indicated (less platelet aggregation), but doesn’t increase walking distances.
o Clopidogrel –indicated (irreversible platelet inhibitor); doesn’t increase walking distances.
o Heparin/Warfarin – no role; the problem is atherosclerosis, not blood clots/emboli
 Invasive Management
o Endovascular angioplasty/stenting or open endarterectomy/bypass are options
o Rutherford Class 0 or 1 – not indicated
o Rutherford class 2 or 3 – indicated if 1pt is a good candidate for surgery and 2claudication
significantly interferes with lifestyle
o Rutherford class 4, 5 or 6 – indicated as limb loss is distinct possibility
Areas of Trouble/Controversy
 Note that diabetic patients may have falsely normal ABIs due to Monckeberg’s arteriosclerosis
(intense medial layer calcification of the artery; often in vessels below the knee) making arteries
incompressible by your blood pressure cuff. The ABI cannot adequately assess these arteries!
 If a patient refuses to quit smoking it’s your call whether or not to do an invasive procedure. It
typically has worse outcomes, thus they’re often refused.
 Endovascular and open approaches have similar outcomes in class 5/6 disease.

Chapter 57: Sudden Onset Severe Abdominal Pain – Ruptured AAA

Risk Factors
 Classics: Smoking (strongest risk factor!), age >60yr, white race, male sex
 Others: Hx of extra-abdominal aneurysm/ coronary artery disease/atherosclerosis/HTN, family Hx AAA
 Note that diabetes is NOT a risk factor…and is actually protective against AAA
Presentation
 Un-Ruptured AAA – often asymptomatic and often undetected…only revealing itself when it ruptures.
o Abdominal/lower back pain (interface with surrounding tissue) or thrombus formation with
distal embolization causing symptoms can, but rarely, occur
 Ruptured AAA – acute abdominal pain radiating to the left flank, palpable pulsatile abdominal mass,
hemorrhagic shock (hypovolemia, tachycardia, pallor, diaphoresis), weakened LE pulses
Screening
  Physical exam – deep palpation of the abdomen for aortic pulse with diameter estimation
 Duplex Ultrasound – one-time screen for men 65-75yr with (+)smoking history
o If relative with AAA  screen at age 60
o If found to have AAA between 3-4cm  annual ultrasound monitoring
o If found to have AAA between 4-4.5cm  biannual ultrasound monitoring
Pathophysiology
 Normal AA size – 1.8cm (women) to 2.0 (men)
o By definition, aneurysm is 1.5x larger in diameter than average size
o Thus an infrarenal aortic aneurysm would have to be >3cm at minimum
o Aneurysm expansion is typically 2-4mm/year; but can grow >5mm/6month (rapid expanding)
 Medial layer breakdown through elastin & collagen degradation of the AA results in aneurysm
o Thought to be driven by matrix metalloproteinase (MMP) activity (increased in AAA pts)
o Note that statin drugs and having diabetes have been shown to DECREASE MMP activity!
 Rupture risk increases with increasing size
o Typically rupture occurs into the retro-peritoneum to the left (vena cava is on the right!)
o While rare, peritoneal rupture would like cause instant death, as there’s no ability to compress
this rupture point
Work-up
 First step: ABC management (intubation if unstable; two large bore needles with limited fluids)
o IV fluids are limited as permissive hypotension (goal of 70mmHg systolic) as aggressive
resuscitation tends to exacerbate bleeding (increased BP/dilution of coagulation factors)
o <1L of crystalloids, then packed blood products are recommended
 If hemodynamically stable: get CT angiogram w/ contrast of abdomen (confirms Dx, area of rupture,
and if endovascular approach can be used)
 If hemodynamically unstable: imaging is NOT needed with confirmatory exam findings. Bedside
abdominal ultrasound may be used to confirm large AAA presence (likely won’t show hemorrhage as
bleeding is typically retroperitoneal)
Management
 Non-ruptured Asymptomatic AAA
o < 5.5cm diameter - you simply watched it based on guidelines. The risk of surgical repair
outweighs the risk of rupture in this size aneurysm
o > 5.5cm diameter or Enlarging >1cm/year – elective repair (either approach)
 Ruptured AAA
o Emergent repair (open preferred)
 AAA elective repair
o Open repair – cheaper, faster, lower rate of re-operation; higher risk and longer recover
o Endovascular aneurysm repair (EVAR) – (opposite characteristics than open repair)
 AAAs with short ‘aortic neck’ (length between renal artery branch and aneurysm) are
not suitable for this repair
 Concern of persistent ‘endoleak’ due to incomplete resolution of aneurysm sac
 Requires lifetime follow-up for endoleak surveillance (CTa at 1month  yearly)
o Most common cause of post-op death is heart attack
 Endoleak – persistent high pressure flow into aneurysm sac following surgery
o Type 1 – most worrisome; persistent high-pressure aortic/ iliac vessel flow
o Type 2 – most common; persistent low-pressure retrograde flow from visceral branches
o Type 3 – flow between junctions of multiple stents at aortic/iliac vessels
o Type 4 – flow through stent pores
Pearls of Wisdom
  AAAs can rupture and temporarily seal, leading to no contrast leakage on CTa. However, these CTa
scans can also retroperitoneal fluid adjacent to the AAA. This is considered ruptured AAA until proven
otherwise and should be treated as such!
 Early onset diarrhea after AAA repair is high sign of post-op ischemic colitis, classically due to ligation
of the inferior mesenteric artery. Proper medical or surgical management is warranted!
 GI bleed after AAA repair could be several things however, aortoenteric fistula is a CLASSIC reason
why this might happen months to years following repair.
o Typically occurs at the 4th part of duodenum (rests next to the aorta)
o Upper endoscopy is typically NEGATIVE, but fluid/air around the graft can be seen on CT
o Management – excision of graft + bypass surgical repair + long-term abx

Chapter 58: Cold, Painful, Right Lower Extremity – Acute Limb Ischemia
Presentation
 “6 Ps” – pain (typically calf), pallor, pulselessness (defining feature), paresthesia, paralysis, and
poikilothermia (cold limb)
o Acute – sudden decrease in perfusion lasting <2 weeks
o Chronic – lasts >2 weeks
 A good cardiac history is essential as 80% of emboli causing ALI come from the heart (Atrial fibrillation
(most common, hypomobility); recent MI (hypomobility), valvular disease (vegetation), left atrial
myxoma (tumor breaks off and embolizes)
 Palpation of the abdominal aorta, femoral artery, or popliteal artery may revel a stiff mass present
 Always examine the contralateral limb to compare for polkiothermia/pallor/etc.; if the other leg is
totally normal, embolic may be more likely vs systemic signs of atherosclerosis (ischemic)
 Past interventions for PAD are a common cause (grafts or iatrogenic trauma are classics!)
Etiology
 Thrombotic (50% of cases)– arterial thrombosis, hypercoagulable disorder, arterial trauma
 Embolic (40% of cases)– cardioembolic (a-fib, CHF, recent MI, myxoma), popliteal/aortic aneurysm
embolism, paradoxical embolism (signs of DVT)
 Other (10% of cases) – acute aortic dissection, systemic shock (late manifestation)
Pathophysiology
 Thrombotic ALI is the result of two mechanisms:
o Plaque buildup – progressive narrowing of the arterial lumen resulting in low-flow to limbs
o Intraplaque rupture – local hemorrhage/clot formation can seal off an already narrowed artery
resulting in an acute manifestation and total limb ischemia
 The most common place for an embolus to lodge is at arterial bifurcations (the sudden decrease in
diameter from supplying artery  two smaller arteries means the embolus will stop as soon as it hits a
new artery that’s too small for it to pass through)
o Aortic bifurcation – bilateral femoral pulses (and below), 5Ps distal to the umbilicus bilaterally
o Common femoral bifurcation – unilateral symptoms of affected limb
o Popliteal bifurcation – pedal +/- popliteal pulses absent, 5Ps of foot +/- calf
 Muscle shows irreversible cell damage after 3 hr with total cell death occurring after 6hr
Some Imaging Modalities Used to Assess Arterial Bloowflow
 Ultrasound Doppler – measures bloodflow based on ultrasound waves bouncing off moving blood;
often more sensitive than palpating for pulses; reported in several different ways
o Triphasic – normal flow; [initial high flow systolic phase  brief retrograde diastolic phase 
final diastolic low flow phase] – ALI may be present but other processes should be considered
o Biphasic – often normal, but may represent early disease – ALI maybe present, consider others
o Monophasic – abnormal, severe reduction in flow – ALI likely present
 o Absent – typical of affected vasculature in acute limb ischemia – ALI likely present
 Duplex Ultrasound – combined Traditional + Doppler ultrasound (the ‘duplex’), with display
superimposed on each other to allow for structure identification and bloodflow assessment
o Often used to locate area disease and characterize the lesions; very useful in planning for
surgical intervention
 Ankle-Brachial Index – compares systolic pressure of ankle arteries and brachial arteries; with chronic
limb ischemia (like intermittent claudication) this is essential. However, as lower extremity flow is
often severely reduced in ALI it’s less valuable in that situation.
Work-up
 Good history/physical exam/vital signs can never be replaced, always start with these.
 Determining severity of ALI is CLINICAL
o Stage I (viable) – no sensory or muscle weakness – good prognosis
o Stage IIa (marginal threat) – minimal sensory weakness (restricted to the toes), no muscle
weakness – salvageable with prompt treatment
o Stage IIb (immediate threat) – sensory loss more than the toes with mild-moderate muscle loss
– salvageable with immediate re-vascularization
o Stage III (irreversible) – profound sensory loss with paralysis/rigor – permanent irreversible
damage has been done
 Imaging
o Duplex ultrasonography – good initial assessment to rule out ALI. Can show problems in the
affected limb but not the proximal arterial tree, limiting it’s use to a degree
o CTa – gold standard; allows for full visualization of arterial tree (proximal disease as well as
distal disease causing symptoms) allowing for surgical planning
o Femoral contrast angiography – former gold standard; invasive and contrast expose has led it
to be replaced by CTa
 Still can be used intra-operatively in emergent situations where immediate re-
vascularization is necessary (like presentation after a few hours of symptoms)
o Transthoracic Echocardiography
 May be used to assess the heart if cardioembolic disease is suspected
 May be use used to assess for atrial septal defect with a bubble study in suspected
paradoxical embolus (bubbles passing from RA  LA isn’t OK!)
o Venous duplex ultrasonography – if paradoxical embolus is suspected; use to assess venous
thrombosis as source of embolus
Management
 Initial Steps:
o Immediate anti-coagulation – clinical suspicion is only thing necessary; stops propagation of clot
so the body can work on dissolving it with the fibrinolytic system)
o Placement of limb in dependent position – increase bloodflow to area of ischemia)
o IV fluids – optimize fluids to allow for optimal perfusion in collateral vessels
 2nd step: Doppler/Duplex ultrasound – used as a ‘rule out’
 Treatment is Based on Stage
o Stage I – imaging (CTa)  thrombolysis or surgery if proximal embolus suspected
o Stage IIa – imaging (CTa)  thrombolysis or surgery if proximal embolus suspected
o Stage IIb – immediate surgical intervention (femoral contrast angiography used intra-op)
o Stage III – amputation to save healthy tissue
 Surgical Modalities of Tx
o Endovascular approaches (catheter tPA thrombolysis, percutaneous aspiration thrombectomy,
or percutaneous mechanical thrombectomy)
 o Surgical approaches (embolectomy, endarterectomy, distal bypass)
 Often patients with cardioemblolic disease should be on systemic anticoagulation
 Reperfusion syndrome – systemization of toxic metabolites released by dead cells during ischemia
o Check CPK/myoglobinuria (rhamdomyolysis can occur from ischemia and systemization can
result in acute kidney injury due to heme pigments precipitating in high-solute parts of the
renal tubules resulting in toxic injury from cast formation in proximal tubules!)
 50% of pts with CPK >5000 will have AKI
o Monitor electrolytes – hyperkalemia (K+ high intracellularly) may result (discussed below)
Monitoring should be done with ANY re-vascularization procedure (not just Stage II or III!)
o Prevent it from happening with with IV fluids (more fluid for dissolving) & bicarbonate infusion
(alkaline urine for dissolving)
Areas To Get You in Trouble
 Diagnosing ALI as a neurologic condition – parestethsias and weakness are common in nerve problems,
but the key is checking pulses/proper imaging. If these are normal, then ALI is much less likely!
Extra info from UWorld
3648/2167/4760/4422/4288/8331: Hyperkalemia
 Presentation: confusion, lethargy
o EKG changes: peaked T-waves, QRS widening, bradycardia, and ventricular arrhythmias with
sine wave pattern
 Etiologies:
o Recent stroke (high neuronal activity means lots of K+ getting into the blood)
o Drugs (non-selective B-blockers, ACE inhibitors, ARBs, K-sparing diuretics
[spirononlactone/eplerenone/amiloride/triamterene], digoxin, NSAIDs, TMP-SMX as it can
block aldostone, apparently)
 Dx: high K+ (>5.0) on basic metabolic panel or fast rise in K level
 Tx:
o Emergent treatment – Ca2+ carbonate or Ca2+ gluconate infusion (stabilize cardiac myocyte)
o Fast-acting treatments – IV insulin + glucose AND/OR albuterol inhalation (activate Na/K+
ATPases and pull K+ into the cells, lowing blood concentration)
o Long-term treatments – aim to reduce total body potassium after stabilization by other tx
 IV fluids – dilute blood and promote diuresis for K removal
 Diuretics – promote diuresis to promote K removal
 Exchange resins (sodium polystyrene sulfonate) – pull K from the body via the GI tract
(takes hours for effect)
 Hemodialysis – remove K directly via hemodialysis
 Note that any of these treatments (esp. albuterol for bronchodilation) may result in hypokalemia