Surgery de Virgilio

What are the lethal six injuries to of thoracic trauma?
1) Airway obstruction
2) Tension pneumothorax
3) open pneumothorax
4) Massive hemothorax
5) flail chest
6) cardiac tamponade
Characteristics of airway obstruction?
Laryngeal trauma; foreign body aspiration; stridor; expanding neck hematoma; gurgling
Characteristics of massive hemothorax?
Lung parenchymal or intercostal artery injury;
Total whiteout of lung field
Characteristics of flail chest?
>2 fractures in consecutive ribs leading to parodoxical motion of chest wall; underlying lung contusion
Characteristics of cardiac tamponade?
Beck’s triad = hypotension, distended neck veins, muffled heart sounds
What is the most common cause of airway obstruction?
Patients w/ diminished airway reflexes in which a relaxed tongue falls back against the rear of the pharynx
What are the hidden 6 injuries of thoracic trauma?
1) blunt aortic injury
2) esophageal injury
3) tracheobronchial injury
4) diaphragmatic injury
5) blunt cardiac injury
6) pulmonary contusion
Characteristics of blunt aortic injury?
High energy rapid deceleration;
Widened mediastinum;
Deviation of trachea to the right on CXR
Combative nature in a trauma patient may represent what?
Cardiac tamponade;
Hypovolemic/cardiogenic shock
Signs of tension pneumothorax?
Hypotension, dyspnea, tachypnea, jugular venous distention, unilaterally absent breath sounds, deviated trachea to the unaffected side
How can cardiac tamponade be confirmed?
FAST scan which demonstrates fluid in pericardial sac;
Pulsus paradoxus is seen
What area defines the cardiac box?
Area on anterior chest wall bounded by:
Sternal notch and clavicles superiorly;
Nipples laterally;
Subcostal margin inferiorly
Ddx for absent breath sounds on the left?
Massive hemothorax
Injury BELOW the nipple line is important because?
May result damage to either thoracic structures, abdominal contents, or the diaphragm itself
What does a narrow pulse pressure indicate?
Compromised stroke volume. DDx: pericardial tamponade, hypovolemic shock, cardiogenic shock
Significance of air bubbling from a penetrating chest wound?
Open pneumothorax. Means that air enters into the chest cavity through the wound instead of through the trachea
Mechanism of sponteneous pneumothorax?
Rupture of apical alveolar blebs. Seen in young, tall, thin, male smokers
What do you need to order following a central line placement?
CXR to ensure you did not cause an iatrogenic pneumothorax
In trauma setting, what causes subQ emphysema?
Pneumothorax until proven otherwise
What does a tension (one-way) valve pneumothorax lead to?
Air leaks out of lung into the pleural cavity with each breath. Compresses the superior/inferior venae cavae; decreases preload; reduces cardiac output; hemodynamic instability
Next step when suspecting tension pneumo?
Decompress w/ chest tube PRIOR to starting positive ventilation
What do distended jugular veins indicate in trauma setting?
Cardiac tamponade or tension pneumo
Why does cardiac tamponade lead to hypotension?

The septum in the heart is shifted to the left ventricle, which reduces preload and cardiac output.

More blood pumped into pericardial sac, and the pressure in the sac eventually outstrengthens the heart, leading to reduced cardac output and hypotension

Where would an injury be more likely to lead to air emboli?
Stab wound or gunshot to hilum because the bronchus and pulmonary veins are in such close proximity there
How would air emboli present in CV, CNS, reps systms?
CV: chest pain, arrhythmia, right sided heart failure
CNS: confusion, AMS, cerebral embolism
Resp: dyspnea, hypoxemia, hypercarbia
Should you intubate/positive ventilate cardiac tamponade patient?
NO. Will make it worse
Next step in hemodynamically unstable patient w/ suspected tension pneumo?
needle decompression (needle thoracostomy)
Where is a needle thoracostomy done?
2nd or 3rd intercostal space just above the rib at the midclavicular line. Advance until air is aspirated into the syringe
After you do immediate needle decompression in tension pneumo, what is definitive management?
Tube thoracostomy
What is tube thoracostomy?

Place tube between 4th/5th intercostal space at midaxillary line to decompress

*if massive hemothorax is encountered, transport to OR for thoracotomy

What does emergent thoracotomy involve?
Hemorrhage control, decompression of cardiac tamponade, cross-clamping of descending thoracic aorta, facilitation of cardiac massage, prevention of air emboli
Indications for emergent thoracotomy?
*penetrating trauma with <15 mins of prehospital CPR
*blunt trauma with <5 min of prehospital CPR
*persistent severe hypotension
Next step after suspected cardiac tamponade?
IV fluids to increases preload;
definitive management involves median sternotomy, release of tamponade, repair of underlying cardiac injury
Why is pericardiocentesis not recommended in trauma setting?
Bc in this setting, the blood is likely coagulated; would be ineffective to remove w/ needle
What does the subxiphoid window tell you to do if find NO blood when opening the pericardium?
Full median sternotomy can be avoided
What needs to be ordered in patients w/ combative behavior?
Rapid serum glucose measurement;
pulse ox;
complete set of vitals
CXR description of cardiac tamponade?
Enlarged water-bottle shaped cardiac silhouette
How does 100% O2 help in pneumothorax?
It causes alveolar partial pressure of nitrogen to fall and increases oxygen uptake into the vascular system. Accelerated rate of absoprtion from the pleural space
How to manage an open pneumo?
Cover the chest wall defect w/ an occlusive dressing that is taped on 3 sides. Then can do a tube thoracostomy in the ER
Management of flail chest?
Analgesics for pain and preventing splinting
Most dangerous complication following pericardiocentesis?
Laceration of coronary vessel. Can lead to worsening of cardiac tamponade
What nerve is at risk when opening the pericardium?
Left phrenic nerve
Why is a diaphragm injury on the right less significant than left?
The liver prevents herniation of bowel into chest
Classic presentation of long term missed diaphragmatic injury?

Chest pain and SOB in patient w/ remote history of trauma

CXR will demonstrate bowel gas and air-fluid levels in left chest

What can FAST be used for in penetrating trauma setting?
Cardiac tamponade and pneumo; it is more used for BLUNT trauma
Singed nasal hairs and carbonaceous sputum is concerning for?
Inhalation injuries which need to be addressed by securing the airway via intubation and administration of 100% O2
Significance of cherry red skin, confusion, disorientation?
Carbon monoxide poisoning
At what level do burns become painless?
2nd degree, deep partial thickness w/ blisters that appear to have open weeping surfaces
What is the rule of nines for burns?
Head = 9
Each arm = 9
Anterior torso = 18
Posterior torso = 18
Each leg = 18
Adult palm = 1%
What are the 3 components of inhalation injury?
Upper airway edema; acute respiratory failure; carbon monoxide poisoning
How does a 2nd degree burn progress to 3rd degree burn?

Via burn wound sepsis. Finding >10^5 bacteria/g of tissue is highly suggestive of this.

May see discolored burn, eschar w/ green pigment, black necrotic skin, skin separation, signs of sepsis

What do circumferential burns increase risk of?
Developing compartment syndrome. They should undergo escharotomy
What are the different chemical burns?

Acidic lead to coagulation necrosis

Alkali lead to liquefactive necrosis

Two electrical burns and their effects?
Direct current = asystole
Alternating current = ventricular fibrillationLong term complication = cataracts

What changes are seen in burns in the first 24 hours?
*release of catecholamines
*glucose concentration increase
*cardiac output decreases to 40-60%
*decrease in plasma volume
*decrease in central venous pressure
*decrease in circulating erythrocyte volume
What is a curling ulcer?
Ulcer in duodenum in patients w/ severe burns
Organisms involved in burn wound infections?
*pseudomonas aeruginosa = most common
*S aureaus, Strep pyogenes
*Candida is the most common fungal
*most common viral is HSV
How is inhalation injury definitively diagnosed?

Fiberoptic bronchoscopy

carboxyhemoglobin >10%
Ox sat <90

Best way to evaluate for CO poisoning?
Carbon monoxide pulse ox
Parkland formula for fluid resuscitation?
Total fluid volume = 4cc/kg x weight x TBSA
What should urine output be to establish/guide fluid management?
0.5mL/kg/h in adults
2-4mL/kg/h in kids
What type of fluid should be used acutely in burn patients?
Lactated Ringers; normal saline will lead to hyperchloremic metabolic acidosis
What electrolyte abnl must be monitored in burn patients?
Sodium. Hyponatremia can lead to seizures.
Potassium. Hyperkalemia can lead to destruction of cells and tissues and can lead to cardiac conduction abnl.
Indications for escartotomy?
Circumferential deep burns
Neurovascular compromise of extremity (weak pulse, decreased cap refill, motor weakness, decreased sensation)
What other topical burn agents are used in burn patients?
Silver sulfadizine;
Sulfamylon or mafenide acetate;
Silver nitrateOnly the second is effective against pseudomonas

What meds will prevent curling ulcers?
PPI or H2 blockers
What is the most important principle in the management of chemical burns?
Copious irrigation
What are patients w/ chronic nonhealing wounds at risk for?
Squamous cell carcinoma of the skin (Marjolin’s ulcer). Evaluate w/ skin biopsy
Features of leg compartment syndrome?
Severe pain in the calf w/ passive motion of the ankle; tense leg edema; recent trauma; PULSE Present.
Features of necrotizing soft tissue infection?
Crepitus, bullae, necrosis of subQ tissue; mixed flora
Features of cellulitis?
Infection of deep dermis and subQ fat prsenting w/ redness and erythema without tissue distruction like NSTI
DVT triad?
Prolonged stasis, hypercoagulable state, endothelial injury.
Acute limb ischemia?
The 6Ps. Hx of claudication or atrial fibrillation
Pathophys of compartment syndrome?

Elevation in compartment pressure results in diminsihed capillary filling pressure that leads to the P’s symptoms

*in compartment syndrome, PULSELESSNESS is a LATE sign

Early signs of compartment syndrome?

Pain, esp during passive ROM. Then nerve ischemia, sensory deficit

*typically, physical exam and clinical situation may be deceptively benign

Both etiologies of compartment syndrome lead to what?
Decreased capillary perfusion and tissue ischemia
What etiologies of comparment syndrome are due to decrease in comparmtent size?
Plaster casts; circumferential third-degree burn; external compression; military anti-shock garments; splints
What etiologies of comparment syndrome result from increased compartment volume?
Vascular injury, blast injury; bone fracture; crush injury; electrical burns; hematoma/bleeding; ischemia/reperfusion; SIRS
Describe change in pressure in compartment syndrome?
Normal pressure 5-10mmHg. As pressure elevates, venules collapse and venous hypertension results
How can compartment syndrome lead to end-organ damage?
Hyperkalemia, acidosis, myoglobinuria lead to kidney failure most commonly
Treatment for compartment syndrome?
First web space numbness?
Deep peroneal nerve courses through ANTERIOR compartment. Motor to extensor digitorum brevis and extensor hallucis brevis. Sensation to first web space
What is volkmann’s ischemic contracture?
Sequela of untreated compartment syndrome. Clawlike hand w/ flexion of the hand at the wrist as well as damaged and insensate nerves. Muscle becomes ischemic and fibroses.
RF for abdominal compartment syndrome?
Trauma patients that receive massive fluid resuscitation
Presentation of abdominal compartment syndrome?

Can impair respiration. Decreased airway compliance, decreased TLC and RV –> hypoxemia and hypercabia

Can compress inferior vena cava and decrease venous return –> decreased CO and decreased SV.

Compression of kidney –> diminished urine output

How is abd comparment syndrome diagnosed?
A bladder pressure >25-30
Which compartment in leg is most often missed during fasciotomy?
Deep posterior. Contains posterior tibial and peroneal arteries + tibial nerve.
Tx of abd compartment syndrome?
Urgent decompressive laparotomy w/ maintenance of an open abd and coverage with vaccum-assisted suction device
Complications of lower leg fasciotomy?
1) Wound infection (most common)
2) superficial peroneal nerve injury = results in foot drop
3) incomplete fasciotomy
4) chronic swelling = diminished limb function
What meds must be inquired about in bleeding in the post-op setting?
Aspirin, clopidogrel, heparin, warfarin; any other antiplatelet or anticoagulant
Spontaneous hemorrhage into joints in childhood?
Hemophilia A and B
Ddx for post op bleeding?
Liver disease; renal failure; DIC (sepsis, malignancy, childbirth complications); surgical bleeding; meds; inherited coag disorders
Ddx for prolonged PTT?
Acquired F9 deficiency; SLE; Hemophilia A and B; Heparin; von Willebrand disease
History of acquired factor 9 deficiency?
Occurs in postpartum, rheumatic disease, malignancy.
Presents w/ purpura and soft tissue bleeding
History of von Willebrand dz?
young woman w/ bleeding after minor surgery;
history of excessive menses
What can you ask regarding bleeding history?
Menses; epistaxis; bleeding into muscle/joints; excessive bleeding after dental procedures
What med conditions are RF for bleeding?

Liver and renal disease; nutritional deficiency (this one due to vitamin K deficiency)

Short bowel syndrome and Cystic fibrosis may lead to low vitamin K too

Cardiac disease bc of antiplatelets prescribed

Primary vs secondary hemostasis disorders?

Primary = due to platelet abnormalities

Secondary = factor abnormalities

*ultimately, fibrin is cross-linked w/ factor 8 to form platelet-fibrin thrombus

Function of vWF?

Platelets bind to vWF using the GPIb receptor to ultimately form platelet plug of primary hemostasis

Also cofactor for Factor 8 –> can lead to abnormally prolonged PTT

Most common type of wWD?
Type 1. AD. mild symptoms.
How does renal failure cause coagulopathy?

ESRD leads to uremic toxins in the blood –> platelet dysfunction.

Can manage w/ desmopression and/or hemodialysis

Manifestations of liver disease and coagulopathy?

Prolonged PT and increased INR. Can’t make the factors.

Will see Thrombocytopenia, factor deficits

*Factor 8 the only one not exclusively made here

Pathology of heparin induced thrombocytopenia?

Heparin forms complex w/ platelet factor 4 –> produces IgG ab that destroy platelets; remnants activate remaining platelets –> thrombus.

Labs = sudden decrease in platelet count >50%

Tx: stop heparin

Immune thrombocytopenic purpura?

Autoimmune prod of IgG leading to platelet destruction

platelets common ly <50K

Management of ITP in adults?
Corticosteroids, IVIG, dapsone, danazol, splenectomy
Thrombotic thrombocytopenic purpura?
Platelets consumed in formation of microthomrbi in small vessels, deficiency in ADAMSTS13 that normally cleaves vWF multimers.
Initial coagulopathy w/ widespread clot formation taht quickly evolves to a state of pathologic consumption of platelets and coag factors
Vitamin K dependent factors
2,7,9,10, C, S
Most frequently encountered etiology for thrombocytopenia?
Alcohol abuse
Etiology for DIC in delivery?
Tissue thromboplastin in amniotic fluid activaes the coagulation cascade
When does physiological fibrinolysis begin?
When plasmin binds to fibrin. Starts clot breakdown
When does primary hyperfibrinolysis occur?
Results from increase in circulating tPA activity. Should normally have low plasminogen activating capability that increases when it is bound to fibrin.
What are conditions of excess amount of circulating tPA?
Decreased hepatic clearance, loss of antiplasmin mechanisms
When can secondary fibrinolysis occur?
Systemic hypercoagulable state and increased amounts of fibrin
What factors does INR measure?

Extrinsic. I, II, V, VII, X.

They monitor Warfarin therapy

PTT measures?

Intrinsic. 1, 2, 5, 8, 9, 10, 11, 12.

Monitors heparin

Aspirin blocks?
COX enzymes. Decreased PGE2 and Thromboxane A2
Clopidogrel MOA?
Blocks ADP receptors to suppress fibrinogen binding to platelets –> inhibits platelet adhesion
Heparin MOA?
Activates antithrombin III –> inactivates thrombin and Xa

Binds to factor Xa to prevent clot formation

Reversible w/ protamine sulfate

Warfarin MOA?
Inhibits vitamin K epoxide reductase
How to manage bleeding secondary to liver disease?
FFP, cryo, coag factors, platelet transfusion
Threshold for platelet transfusion?

If <50K, may do prophylactic one

If <10K, need it to prevent spontaneous intracranial bleeding

What reverses warfarin?
Which transfusion reaction occurs within minutes to hours?

1) febrile nonhemolytic. Most common, caused by cytokines from donor leukocytes. Self limited, acetaminophen can help

2) allergic/urticarial. From plasma present in donor blood. Tx: diphenhydramine

3) anaphylactic. Rapid and sudden. Tx: stop transfusion, epinephrine, intubation, fluid resuscitation.

When does acute hemolytic reaction happen?
Within 24 hours. ABO incompatability leads to severe destruction of donor RBCs by preformed host antibodies
Delayed hemolytic reaction?
1-14 days after transfusion. Rh antibodies leading to destruction of donor RBCs
What is TRALI?

Transufion related acute lung injury. Non-cardiogenic pulmonary edema. Leading cause of transusion-related fatalities

MOA: donor ab attacking the recipients WBC. These complexes aggregate in vasculature of the lungs –> release of inflammatory mediators which increase permeability of lung capillaries –> pulmonary edema

Causes of prerenal AKI?
Hypovolemia (bleeding, dehydration)
Decreased cardiac output (heart failure)Mech: inadequate perfusion of normal functioning kidney

Causes of intrinsic/renal AKI?

Acute tubular necrosis; interstitial nephritis

Mech: prolonged ischemia of the kidney or toxins leading to parenchymal injury

Causes of postrenal AKI?

Obstruction of urine benign prostate hypertrophy, prostate cancer, nephrolithiasis, bilateral ureteral ligation, urethral stricture

Mech: increased nephron tubular pressure

What is consistent w/ prerenal AKI?
Orthostatic hypotension, hypovelemia; increased BUN and creatinine (>20:1)
What is azotemia?

Elevated BUN and creatinine

Earliest sign of AKI is oligoruia

Normal urine output?
Normal urine output in adult = 0.5-1.0 mL/kg/hr
Normal children = 1-2 mL/kg/hr
Oligouria vs. anuria?

Oligo = <0.5 mL/kg/hr for 2 consecutive hours

When <50-100 mL over 24 hours = anuria

Most common nephrotoxic meds?
IV contrast, aminoglycosides (gentamycin), amphotericin, cisplatin, cyclosporine, NSAIDs
How do you identify contrast-induced acute kidney injury?

Increase in creatinine of 0.5mg/dL OR a relative increase of 25% from baseline value;

This is assessed 48-72 hours following IV admin

What may prevent contrast-induced renal failure?
N-acetylcysteine, bicarb, normal saline hydration
What conditions may give increased BUN/Creatinine ratio?
1) Upper GI bleed (high protein abs)
2) increased urea production (steroid therapy)
3) low muscle mass (decreased serum creatinine creation)
Mechanism for oligouria following major surgery?

In response to stress of surgery, body releases aldo and ADH = salt and water retention

If >24 hours of oligouria, warrants investigation

Prolonged periods of poor renal perfusion will cause what?
What is the effect of general anesthesia on heart and kidney?

Myocardial depression and systemic vasodilation.

–> Decrease cardiac output & end-organ perfusion

When can you not use FEna?

When patient is on diuretics.

Use Fe urea instead.

How does FEna help in diagnosing the different types of AKI?

<1% = Prerenal >1 % = intrinsic

>4% = postrenal

High specific gravity on UA?
Volume depletion
Red cell casts on UA?
Glomerular disease
Hematuria on UA?
Renal emboli or stones
WBC casts on UA?
Infection or inflammation
Granular casts on UA?
Acute tubular necrosis
What is the Rifle criteria?
Allows grading of kidney dysfunction based on creatinine, GFR and urine output
What needs to be ruled out first when patient presents w/ low urine output?
Obstructed urinary catheter. Look for kinking in the tubing and flush the catheter to make sure it is not clogged
What is fluid challenge?
Giving patient a bolus of NS .5-1L and this should increase urine output if it is due to prerenal, hypovolemia
How can a central line help you gauge volume status?

Measure central venous pressure (CVP)

Normal 8-12

What is next step if suspect postrenal obstruction?
Insert foley catheter to relieve obstruction
Indications for emergent hemodialysis?
Electrolyte imbalance (hyperkalemia)
Intoxication (ethylene glycol)
Overload (fluid)
When can diuretics help in treatment of oligouria?
In the setting of cardiogenic oligouria
Is dopamine recommended for treatment of oligouria?

NO. Because it actually further decreases the blood flow to the kidney and worsens the insult.

This is bc it increases renovascular resistance in oligoruic patients

What can happen if a patient w/ renal failure gets an MRI?
Nephrogenic systemic fibrosis: thickening and hardening of skin; fibrosis of muscle, fascia, lungs, heart
DDx for post-op SOB?
1) pna
2) pulmonary emolism
3) Myocardial infarction
4) pneumothorax
5) cardiogenic pulmonary edema
6) noncardiogenic pulmonary edema
7) anxiety
8) bleeding
H&P consistent w/ pna?

Fever, dyspnea, dullness to percussion, prolonged intubation, aspiration, PPI use

most common cause of nosocomial mortality

Where will aspirate go if patient is upright?
Right lower lobe
Where will aspirate go if patient is supine?
Right upper lobe
H&P consistent w/ PE?

recent travel (long airplane/car ride), immobilization, recent surgery, trauma or central line, hx of DVT/PE, moking

Usually from DVT in pelvic or leg veins

H&P consistent w/ MI?
Hx MI, DM, CHF. Surgery creates proinflammatory state and leads to plaque rupture and thrombosis of coronary artery
H&P consistent w/ cardiogenic pulmonary edema?

Rales, JVD, S3, bilateral leg swelling

PCWP >18mmHg

Labs consistent w/ PE?
Hypoxia, resp alkalosis, tachycardia, wide A-a gradient
What is virchow’s triad?
Stasis, endothelial injury, hypercoagulable state
RF for venous thromboembolic event?
1) Stasis: immobilization
2) endothelial injury: surgery, trauma, central line, history of DVT/PE
3) hypercoagulability: smoking, OCP, inherited disorders
What is the wells score?
>4 = likely PE
Clinical findings in DVT?
Leg swelling, calf pain, warmth of leg, mild redness of calf, calf tenderness
What is may-thurner syndrome?
Left leg is 2x more commonly affected by DVT bc left iliac vein is often compressed by the right iliac artery
What is homan’s sign?

Physical exam finding that was classically associated w/ DVT. Positive when calf pain elicited w/ dorsiflexion of foot.

No longer used bc sensitivity of 30%

What are the 5 Ws?
Wonder drugs
Most commonly inherited causes of hypercoagulability?

Factor V leiden, prothrombin mutations.

Then protein C def, Protein S def, antithrombin def, and homocysteinemia

What are patients w/ protein C or S deficiency at risk for?
Warfarin induced skin necrosis
Most common acquired causes of hypercoagulability?
Advanced age, pregnancy, malignancy, OCP, HRT, smoking, obesity, nephrotic syndrome
When do you suspect heparin-induced thrombocytopenia?
Acute drop in platelet levels (<50% of baseline); LMWH began in last 4-10 days
What is pulmonary edema?
Excess fluid in the alveoli
What is noncardiogenic edema?

Caused by inflammation that leads to increased pulmonary capillary permeability secondary to cytokine signaling

Ie = pna, ARDS, pulmonary contusion, fat embolism

What is cardiogenic edema?
Arises from increase in hydrostatic pressure within capillaries of the lungs as a result of increased pulmonary venous pressure
Exam of cardiogenic edema?

Evidence of acute heart failure, low flow state, S3, JVD, crackles on auscultation, cool/pale extremities. PCWP >18

Tx: reduction of preload, reduction of afterload

Routes to developing post-op pna?

Inhalation, aspiration, heme.

After surgery, cough reflex suppressed; mucociliary transport may be inhibited by endotracheal intubation

DDx of wide A-a gradient?
Atelectasis, pna, pulmonary embolism
What is an A-a gradient?
Difference in partial pressure of oxygen between alveoli and arterial blood.
When suspect venous thromboembolic event, next step?

Start heparin ASAP. It is an anticoagulant. Prevents the clot from progressing/propagating

Then do CT angio of pulm arteries

If suspicion of VTE is low, next step?
D dimer. High negative predictive value. If <500, can rule out PE in low-risk patients. If elevated, CT angiogram.
Workup findings in pulmonary embolism?
ABG: acute resp alkalosis, hypoxemia, increased A-a gradient
ECG: sinus tachy
CXR: normal. Classic sign is westermark’s sign; also Hamptons’ hump
Classic ECG findings in pulmonary embolism?
Large S wave in lead 1, large Q wave in lead III, inverted T wave in lead III
A saddle embolus in pulmonary artery can result in?
Death secondary to right heart failure
If patient cant get transported for imaging in setting of PE, what can they get for indirect diagnosis?
1) echo = right heart strain
2) venous duplex doppler US for legs to show thrombus
Massive PE vs. submassive?
Massive adds sustained hypotension, in addition to RV dysfunction or myocardial necrosis
Initial management of PE?
Therapeutic anticoagulation w/ subQ LMWH or IV unfractionated heparin
What if patient has history of heparin-induced thrombocytopenia in setting of PE?
Start lepirudin, argotroban, or bivalidudin. These are direct thrombin inhibitors.
What if patient has contraindication to anticoagulation?
Can place inferior vena cava filter once the presence of PE has been confirmed
4 options for subsequent treatment of PE?
1) heparin alone
2) tPA
3) endovascular clot aspiration
4) open pulmonary embolectomy
When is tPA indicated?
Massive PE. NOT indicated in low-risk PE
When should open pulmonary embolectomy be considered?
Massive PE who are not candidates for tPA therapy
Long term anticoag after first-time VTE?

Heparin or LMWH for the first 5 days after VTE

Warfarin should be started on first or 2nd day.

Both should overlap 4-5 days

Goal INR 2-3

Should receive anticoag for at least 3 months after VTE. For recurrent, do 6 months

Anticoagulant of choice in patients w/ malignancy?
Anticoagulation during pregnancy?

LMWH or unfractionated heparin.

WARFARIN is teratogen!!

Ddx for lower GI bleed?
1) diverticulosis 30-50%
2) neoplastic 10-20%
3) iatrogenic
4) colitis 10-20%
5) angiodysplasia 5-10%
6) anorectal 5-10%
What do you need to do in workup of lower GI bleed?
Rule out large upper GI bleed by placing nasogastric tube to aspirate for blood/coffee grounds; confirm bile is obtained to know you have assessed duodenal bleeding
Most common cause of lower GI bleed?
Watery diarrhea progresing to bloody diarrhea w/o fever?
EHEC evaluation
H-DRAIN mnemonic?
Diverticular bleed
Radiation colitis
Lower GI bleed in >50yo is likely?
Diverticulosis, angiodysplasia, malignancy
Lower GI bleed in <50yo?
infectious, hemorrhoids, anal fissures, IBD
Diverticular vs. angiodyplasia and neoplastic bleeding?

Diverticular is arterial, presents acutely and large amounts

The others are chronic, anemia, dark stools

Dark maroon, mixed w/ stool bleed?
Upper GI, small intestine, right colon
Hematochezia likely from?
Right colon (diverticulum), rectum, anus, massive upper GI
Spots of blood on toilet paper?
Rectum, anal source
Scant, dark red blood?
What does occult blood raise suspicion for in younger vs. older patients?

1) younger = IBD or familial cancer syndromes

2) older = malignancy, esp colorectal cancer

What is tenesmus (sense of incomplete evacuation of stool) associated with?
Ulcerative colitis and infectious etiologies
Recurrent painless bleeding may indicate?
Angiodysplasia. Not many large acute bleeds as seen in diverticulosis
In lower GI bleeding, why ask about alcohol history and liver cirrhosis?
Varices can occur in rectal veins of lower GI
In lower Gi bleeding, what does abd tenderness tell you?

May point to IBD, ischemic colitis, infectious diarrhea

Not usual w/ diverticulosis and angiodysplasia

Significance of iron-def anemia in association w/ lower GI bleed?
Colorectal cancer may manifest as larger, acute bleed when cancer causes erosion through or ulceration of the bowel wall
Presentation of ischemic colitis?
Left sided abd pain, bloody diarrhea in elderly patients w/ low-flow states (severe dehydration, heart failure, shock, trauma)
RF for diverticulosis?
Older people
Low fiber diets
High fat diets
High red meat diet
Connective tissue disorders
What is a diverticulum?

Saclike protrusion through the colonic wall

Presence of these = diverticulosis

What causes a diverticulum?
High intraluminal pressures in the colon can cause mucosa and submucosa to herniate through the muscular layer of the intestinal wall
Most common site of diverticula?
90% in sigmoid colon bc harder stool passes through here and diameter of the lumen is decreased
What is diverticulitis?
Microperforation or macroperforation of a diverticulum
Is there bleeding in diverticulitis?
Not associated
What is angiodysplasia?

Focal submucosal areas of thin, weak, dilated vessels in the GI tract (most commonly cecum and right colon) in >60yo.

Most common vascular abnormality of Gi tract.

Bleeding is small/occult. Venous bleeding.

What is angiodysplasia associated with?
von Willebrand disease, aortic stenosis, chronic kidney disease
Where does ischemic colitis tend to happen?
Watershed areas. Splenic flexure
Ischemic colitis vs. acute mesenteric ischemia?

AMI is caused by arterial embolus or thrombosis; often transmural; leads to bowel necrosis requiring resection; high mortality

Territory = ligament of Treitz area to transverse colon

Initial steps in lower GI bleed?

2 large bore IVs and send type&cross, CBC, chemistry, INR/PTT

Next step = placement of nasogastric tube recommended in all patients w/ large-volume hematochezia

How do you rule out upper Gi bleed w/ nasogastric tube?
If tube returns w/ bile but without blood
What diagnostic test of choice indicated for lower GI bleed pt that is unstable?

Colonoscopy. (cannot visualize the small bowel, though)

If patient continues to bleed? Diagnostic arteriography or a tagged red blood cell scan (nuclear scintigraphy) using technetium-99.

If still bleeding? emergent laparotomy w/ recommended total colectomy

Ddx for acute appendicitis in adult?
IBD, pancreatitis, cholecystitis, appendicitis, gastroenteritis, nephrolithiasis, pyelonephritis, sigmoid diverticulitis
What is the first symptom of appendicitis?
Usually anorexia. Then vague periumbilcal abd pain, vomiting, then RLQ pain
Absent bowel sounds in appendicits?
Indicates paralytic ileus; secondary to inflammation/infected bowel
Hamburger sign?
Patient w/ true anorexia will deny their favorite food (ie hamburger) if they are asked about it
Rovsing’s sign?
RLQ pain w/ palpation of LLQ
Psoas sign?
RLQ pain on passive extension of the right hip or active flexion of the right hip
Obturator sign?
RLQ pain on internal rotation of the hip, typical of a pelvic appendix
McBurney’s sign?
Tenderness to palpation on McBurney’s point
What happens when visceral peritoneum senses pain?

It is innervated by autonomic nerves. –> poorly localized pain + n/v.

Usually early in appendicitis, visceral peritoneum senses it

How does appendicitis pain localize in RLQ?
As inflammation progresses, parietal peritoneum, innervated by spinal nerves, is affected and results in sharp, severe RLQ pain
Where is pain of midgut perceived?
Pain in foregut is perceived?
In epigastrum
Pain in hindgut perceived?
Hypogastrium/suprapubic pain
Why is cutaneous hyperesthesia seen in acute appendicitis?
Bc the peritoneum is supplied by spinal nerves and this irritates the dermatomes very much
How does closed-loop obstruction pertain to acute appendicitis?
It is a commonly accepted etiology. Obstruction of proximal appendiceal lumen by fecalith or lymphoid hyperplasia. The appendix is a closed loop, and it can be obstructed.
How may children present differently from adults in acute appendicitis?
Sx of viral URI followed by true onset of acute appendicitis
What is the inferior lumbar (petit) triangle?
Floor = internal abd oblique muscle
Inferior = iliac crest
Margins = latissimus dorsi and external obliquePain is elicited on palpation in RETROCECAL appendicitis

What should women of childbearing age be screened for if present with sx of abd pain?
beta-hCG to rule out ectopic pregnancy
What critical lab values should be used to workup acute appendicits?
Leukocytosis w/ left shift
elevated CRP
Can pyuria be present in appendicitis?
Yes. Don’t be misled to think cystitis!
What imaging for appendicitis is useful in women & children?

Ultrasound. can rule out ovarian torsion, tubo-ovarian abscess, ectopic pregnancy.

Children are not readily visualied on CT

What may be seen on Xray that is highly suggestive of appendicitis?
Calcified fecalith
Definitive treatment of appendicitis?
When should abx be given pre-operatively for appendicitis?
In acute non-perforated and perforated appendicitis
Management of perforated/gangrenous appendicitis?
IV abx until fever and leukocytosis resolves in 3-5 days
What should NOT be present in urine of appendicitis patient?
What infection presents just like appendicitis?

Yersenia enterocolitica infection. RLQ pain, fever, vomiting, bloody diarrhea

Tx: doxy

How can appendicitis be misdiagnosed as PID in women?

Both cause cervical motion tenderness and right adnexal tenderness

Ask RF for PID: young age sex, unprotected sex, history of PID and STDs, multiple sex partners

How can you misdiagnose acute appendicits during pregnancy?
Because its been thought that the appendix shifts upwards with pregnancy and so may mistake pain site. Majority STILL present with RLQ pain in all 3 trimesters
What do you need to consider in patient w/ >5 day history of RLQ pain?
Rupture –> abscess
Ddx for change in bowel habits
1) colorectal cancer = constipation, Fe def anemia, diarrhea
2) IBS = diarrhea alternating w/ constipation; no blood
3) IBD = diarrhea +/- blood
4) Celiac = pale, loose greasy stools
5) instestinal pseudo-obstruction = constipation
6) thyroid = diarrhea or constipation
7) drugs = diarrhea or constipation
8) infectious = diarrhea
Pencil thin stools, constipation is suggestive of?
Left-sided colon cancer
Screening for colorectal cancer?
>50yo until age 75
What screening is recommended for colorectal cancer in pts w/ first-degree family member w/ colorectal cancer?
Begin at age 40 or 10 years prior to onset of first degree cancer. Screen every 5 years
What diet can result in false-positive FOBT?
Red meat
Frequency for colonoscopy?
10 years
Frequency for flexible sigmoidoscopy?
5 years + FOBT every 3 years
FOBT frequency screen?
Frequency for barium enema w/ sigmoidoscopy?
5 years
How does cancer-related cachexia work?
TNF-alpha seems to play a central role and has a direct catabolic effect on skeletal muscle
RF for colon cancer?
older age, AA, IBD, FHx, low fiber diet, sedentary lifestyle, obesity, smoking, alcohol, T2DM
Where do majority of colon cancers occur?
Left sided near the rectosigmoid junction
How do left sided colon cancers present?
Change in bowel habits, obstruction. Pencil-thin stools, tinged with blood. Lower abd colicky pain
How do right sided colon cancers present?
Insidious onset of Fe def anemia secondary to chronic GI blood loss; melena is more common here
How can nonneaplastic polyps arise?
From abnormal mucosal maturation, inflammation, colonic architecture
Features of hyperplastic polyps?
Small <5mm; most common; isolated ones are typically benign
Features of juvenile polyps?
Rounded, smooth, sometimes have stalk; <2cm; most commonly in chldren <5yo
What is the step-wise adenoma to carcinoma progression?
1) loss of APC tumor suppressor gene = decreased IC adhesion, increased proliferation
2) KRAS mutation = unregulated IC signaling and transduction
3) loss of P53 = carcinoma
What is Peutz-Jeghers syndrome?
Multiple hamartomatous polyps + mucocutaneous hyperpigmentation on the lips and genitala
Which adenoma is the most common?
Tubular. In rectosigmoid usually, but can be found anywhere
Which adenomas have high malignant potential?

Villous. Larger and in older people; typically in rectum. More commonly sessile, cauliflower-like projections

Also, sessile serrated. Sawtooth appearance under microscope

Most common metastatic sites for colorectal cancer?
Liver, due to venous drainage of colon to liver via mesenteric veins draining to the portal system
Where may rectal cancers metastasize first?
Lungs bc of inferior rectal veins drain into inferior vena cava via internal iliac veins
What heritable condition is assoc w/ colon cancer?

HNPCC or Lynch syndrome. Commonly has colorectal and endometrial

FAP = AD, develop hundreds to thousands of polyps in colon. If untreated –> cancer.

What is the mutation in FAP?
APC gene
Tx for FAP?
colectomy recommended to prevent development of cancer
What age should individuals w/ first degree family members w/ FAP be screened?
By 10yo
What characaterizes Gardner’s syndrome?
Osteomas and colonic poyps
What is Turcot syndrome?
Cafe au lait spots, malignant CNS tumors, neoplastic colon polyps that progress to cancer
Modifieed amsterdam criteria for HNPCC?
3 or more relatives w/ histologically verified cancers
2 or more successive generations affected
1 or more relative dx prior to 50yo
1 should be first degree relative of the other two
What is a synchronous tumor?
Second primary cancer (nonmetastatic) that is present at the initial diagnosis
What is a metachronous tumor?
Primary cancers that develop elsewhere in the colon at least 6 months after the primary resection
Once you establish colon cancer, what labs are recommended?

CEA levels and liver enzymes (alk phos).

Elevated alk phos is suggestive of possible liver mets

What do high levels of CEA at diagnosis suggest?
Metastatic disease
What are CEA levels used for?
Treatment success and recurrence detection
What other conditions can elevate CEA levels?
Gastritis, PUD, hepatic dz, COPD, DM, IBD, chronic inflammatory conditions, smoking
What imaging is recommended at diagnosis of colon cancer?

CT scans of chest, abd, pelvis to detect metastasis

nearly 20% present w/ mets.

What imaging is obtained w/ rectal cancer?

Transrectal ultrasound (TRUS) and MRI = improve staging ability compared to CT and physical exam

Locally advanced tumors undergo chemo + radiation prior to surgery. Increases the chance for sphincter preservation and decreases recurrence rates

What is neoadjuvant therapy?
Administered prior to surgery and often done to shrink or debulk tumors to make resection more amenable
What operation is done for right sided colon cancer?
Right colectomy with ligation of ileocolic artery
What operation is done for transverse colon cancer?
Transverse colectomy or extended right colectomy with ligation of the ileocolic and middle colic artery
Descending colon cancer operation?

Left colectomy with ligation of IMA

*also done for sigmoid colon

What is used for bowel prep?
Ingested polyethylene glycol
What charaacterizes the colon?

Taenia coli (longitudinal white line) and taenia epiploica (fat appendages)

Small bowel has smoother features

If tumor is more than 3 cm from dentate line, what operation is done?
Low anterior resection = remove part of rectum through the abdomen and reconnect proximal colon w/ distal rectum
If tumor is within 3 cm of dentate line, what operation is performed?
Abdominoperineal resection = remove entire distal rectum, anus, sphincters, leaving a permanent colostomy
How many lymph nodes should be resected in colon cancer?
minimum 12
Presentation for acute radiation enteritis?
Persistent nausea, vomiting, abdominal cramping, fecal urgency, watery diarrhea
How should CEA levels be followed after surgery?
Check every 3 months for the first 3 years following surgery
Radiologic finding of “coffee bean” or bent-inner tube?
sigmoid volvulus
Massive, slowly progressive abd distenstion, obstipcation?
Large bowel obstruction
DDx for large bowel obstruction?
1) Colon cancer
2) Volvulus = sigmoid in elderly, debiliated; + chronic constipation
3) diverticulitis = LLQ tenderness
4) stricture
5) fecal impaction = firm stool in rectal vault on exam
6) ogilvie’s syndrome = marked colonic distention without mechanical cause can lead to perforation
7) small bowel obstruction
8) toxic megacoon = transmural inflammation of a markedly dilated colon associated w/ UC, pseudomembranous colitis.
What signs are seen in toxic megacolon?
High fever, tachycardia, abd tenderness, acidosis, leukocytosis
What is obstipation?

Complete absence of gas or stool per rectum. Highly suggestive of bowel obstruction.

Vs. constipation = <3 per week

Classic physical exam findings in bowel obstruction?

Fever, tachycardia, tachypnea (diaphragm excursion is impaired), distended abdomen that may be tympanitic.

Perform rectal exam to r/o fecal impaction, rectal neoplasm, stricture.

SBO vs. LBO?

SBO = more pronounced vomiting. Hyperactive sounds.

LBO = pronounced distention, less vomiting, decreased bowel sounds.

What drugs can predispose to chronic constipation, elongation of sigmoid, and volvulus?
neurologic/psych drugs
Presentation of ogilvie’s syndrome?

Progressive massive abd distention over several days, nausea, vomiiting

**Someone who is already hospitalized and often in post-op setting

5 Fs of abd distention? Causes of it
Fat (obesity)
Feces (fecal impaction)
Fetus (prego)
Flatus (ileus/obstruction)
Fluid (ascites)
Most common causes of LBO
malignancies, then diverticulitis and then volvulus
Where in colon is cancer most likely to cause an LBO?
Left-sided colon
What is cecal volvulus?

Due to congenital partial malrotation.

Vs. sigmoid volvulus = acquired condition caused by progressive stretching and redundancy of the sigmoid colon

RF for sigmoid volvulus?
Anticholinergic drugs (impair mobility)
Neurologic and psych diseases
Chagas dz
High fiber diet
What is complicated volvulus?

Indicates presence of bowel ischemia and its sequela such as gangrenous bowel and sepsis

= diffuse abd pain, fever, tachy, AMS, marked tenderness

Labs in suspeted LBO?

CBC, serum lactate, chemistries to determine dehydration

Leukocytosis and lactic acidosis are concerning for ischemia or complicated volvulus

Imaging for suspected LBO/

Plain abd and upright chest XR. Distinguish SBO vs LBO

Can also see coffe bean sign for sigmoid volvulus

If unclear = CT w/ oral and IV contrast.

Or contrast enema to show birds beak or ace of spades sign of narrowing at the point of obstruction

Initial steps in managing LBO?

IV fluid resuscitation and placement of foley catheter to monitor urine output

Nasogastric tube may help the vomiting patient

Subsequent treatment for sigmoid volvulus?

In incomplicated = attempt untwisting via endoscopy

If this fails = undergo urgent surgery

Next step after successful detorsion of uncomplicated sigmoid volvulus?
Schedule semi-elective sigmoid resection with or without primary anastomosis. This prevents need for colostomy
Management of complicated sigmoid volvulus?
Treatment for cecal volvulus?

Attempted endoscopic detorsion is not recommended.

SURGERY! Bc of high rates of bowel necrosis, failure of endoscopy, and its recurrence

In pregnancy, what causes intestinal obstruction?
1) SBO due to adhesions
2) colonic vulvulusDetorsion is indicated; but resection may be delayed until after delivery

Management of ogilvie’s sydnrome?
Neostigmine and/or colonic decompression
What is an emerging treatment for LBO?
Percutaneous endoscopic colostomy tubes. May provide adequate fixation to prevent recurrence until abdominal-colonic adhesions have time to form.
DDx of LLQ pain and fever?
1) acute gastroenteritis
2) acute diverticulitis = most commonly in sigmoid colon
3) PID = Cervical motion tenderness, foul smelling vaginal discharge
4) acute appendicitis
5) sigmoid volvulus = more common in elderly, presents as large bowel obstruction
6) ischemic colitis = bloody diarrhea; hypoperfusion
7) acute mesenteric ischemia
8) IBD = abd cramps, bloody diarrhea, acute abd pain
9) colon cancer
LLQ pain, tenderness, fever, leukocytosis?
Acute diverticulitis
RF for diverticulitis?
Obesity, low fiber diet, red meat diet, age
Where do diverticula occur most frequently?

In the sigmoid colon. These here are more likely to become infected.

On the right side, they are more likely to bleed

Do diverticula occur in the rectum?
very RARE bc the taenia coli coalesce into a circumferential band around the rectum, thereby eliminating points of weakness that precede a diverticulum
True diverticula?
All 3 layers outpouch
Complications of diverticulitis?
1) abscess = fever, localized pain, ileus, leukocytosis
2) perforation = can progress to purulent peritonitis
3) fistula = colovesical (UTI, pneumaturia, fecaluria); colovaginal (feculent vaginal discharge)
4) stricture
5) LBO = feculent comiting, abd distention, obstipation
Main etiologies for colovesical fistula?
Colon cancer
bladder cancer
radiation injury
foreign body
Presentation of colovesical fistula?
Fecaluria, pneumaturia, recurrent UTIs refractory to treatment. Or UTI caused by multiple enteric anaerobes
What is complicated diverticulitis?
Occurs w/ abscess formation, colonic obstruction, diffuse peritonitis, fistulization
How is diverticulitis graded?
Hinchey staging system
How can sigmoid diverticulitis present w/ RLQ pain?
Because some people’s sigmoid may be long and elongated and redundant and lie in this plane
What imaging is recommended in diverticulitis?
CT scan
What is contraindicated in diverticulitis?
Barium enema
First step in management of acute divefticulitis?
Determine if its ocmplicated or uncomplicated; and then assess SIRS criteria
What is SIRS criteria?
2 of the following:
1) T >100.4 or <96.8 2) HR >90
3) RR >20 or PaCO2 <32 4) WBC >12K or <4K or >10% band
Management in patient w/ uncomplicated diverticulitis w/o SIRS?

Oral abx and clear liqueds

If meet SIRS, then admit to hospital, NPO, IV abx, fluids, analgesia

Management of uncomplicated diverticulitis?
Majority will resolve w/o surgery. If fail, do repeat CT to look for abscess or take patient to OR for colon resection
After resolution of diverticulitis, what is needed 6-8 weeks after discharge?
Colonoscopy to rule out other diagnoses like IBD or colon cancer
Tx for diverticulitis complicated by localized abscess?
Pericolic abscess <4cm w/o peritoneal signs = bowel rest and broad-spectrum abx >4cm = CT guided percutaneous drainage, which may allow for one-stage surgical resection of affected bowel at a later date
Tx for diverticulitis w/ colovesical fistula?
Resect affected segment of colon; repair the bladder
How may you treat patient w/ diverticulitis w/ free air on CT?
Supportively and possible percutaneous abscess drainage; may do elective sigmoid colectomy at a later date
Tx for diverticulitis free perforation with diffuse peritonitis?
Emergent colectomy w/ end colostomy
Tx for diverticulitis c/b LBO?
Urgent colectomy w/ end colostomy
What operation is performed electively for sigmoid diverticulitis?

One step primary anastomosis = colon is resected and proximal and distal segments are connected to each other

Different bc in urgent setting, it is done without anastomosis

Can patients w/ diverticulitis be managed medically?
Yes, as long as it remains effective. If it doesnt, then consider elective surgery at that point
DDx for postprandial RUQ pain?
1) symptomatic cholelithiasis = RUQ pain radiating around right back after fatty meals, resolves
2) acute cholangitis = RUQ pain, fever, jaundice (charcot triad)
3) acute cholecystitis = >4h, murphys sign
4) acute pancreatitis
5) acute gastritis
6) PUD = if duodenal, improves w/ eating; gastric ulcer worsens w/ eating
7) malignancy
8) fitz-hugh-curtis syndrome
9) MI
10) acute hepatitis
11) hepatic abscess
Positive murphy sign, fever, tachy, elevated WBC count?

Acute cholecystitis

Normal total bili and alk phos make acute cholangitis LESS likely

What is biliary colic?
Colicky pain that waxes and wanes
RF for cholesterol gallstones?
Females, prego, OCPs (excess estrogen), obesity (decereases bile salts), high fat diet (increases bile cholesterol), hereditary, chrohns disease (loss of bile salts), rapid weight loss after gastric surgery (impaired gallbladder emptying)
What are the 4 Fs?
Female, fat, forty, fertile. RF for cholesterol gallstones/biliary disease
Symptomatic cholelithiasis vs. acute cholecystitis?
The former you can manage outpatient. The latter requires hospital admission, IV abx, and urgent cholecystectomy
Sx of symptomatic cholelithiasis?
RUQ pain resolves within 3-4 hours; mild RUQ tenderness, normal vitals, normal WBC
Sx of acute cholecystitis?
RUQ >6h; n/v; murphy’s sign; fever, tachy; elevated WBC; see gallstones, gallbladder thickening, sonographic Murhy’s sign
Abd pain after eating fatty foods?
Suggests biliary origin of pain. Fat triggers release of CCK –> contracts gallbladder –> if stones present, will feel the pain
RUQ pain + scapular pain?
Gallbladder and scapula share same cutaneous dermatome. Gallbladder distention/inflammation triggers scapular pain via phrenic nerve
Phys of murphys sign?
When patient inspires, diaphragm moves caudally and so does the gallbladder. Palpating deep in RUQ causes gallbladder to come into contact w/ parietal peritoneum –> further irritates inflamed peritoneum –> cessation of inspiration secondary to pain
Does symptomatic cholelithiasis present w/ systemic sx?
What is chronic cholecystitis?
Recurrent bouts of symptomatic cholelithiasis –> chronic inflammation of gallbladder w/ fibrotic changes
Cause of acute cholecystitis?
Sustained contraction (impaction) of the cystic duct most often by a gallstone –> inflammation and edema of gallbladder wall and eventually bacterial overgrowth and invasion of the gallbladder wall –> ischemia and necrosis and perforation could ensue as complications
Organisms in bile?
E coli, Bacteriodes fragilis, Klebsiella, Enterobacter, Enterococcus, Pseudomonas
What makes up bile?
Bile salts
Lecithin (phospholipid)
Cholesterol+ water, electrolytes, proteins, bile pigments

Main types of gallstones?
Cholesterol 70-80%
Pigment 20-30%
How do cholesterol gallstones form?

concentration of cholesterol exceeds solubility –> precipitation.

Happens in low concentrations of bile salts or lecithin; and high levels of cholesterol

How do pigmented gallstones form?

Black stones assoc w/ hemolytic disease such as hereditary spherocytosis or sickle cell disease

Brown stones form within the bile ducts; larger and softer than black stones and assoc w/ bacterial infection and parasites

What gives pigment stones its dark coloration?
Presence of calcium bilirubinate within the stones
Diagnostic test of choice for cholecystitis?
How do gallstones appear in US?
Highly echogenic areas w/ acoustic shadows. Note gallbladder thickness and any fluid.
How is acute cholecystitis diagnosed on US?
Gallbladder thickening >4mm + pericholecystic fluid
Normal common bile duct diameter?
4-5cm. If dilated –> suggests obstruction from either a gallstone or a tumor
Is US useful for detecting gallstones in common bile duct?
Very poor for this bc bowel gas interferes w/ US waves
Gas bubbles in gallbladder wall?
Emphysematous cholecystitis. Infection w/ gas forming organisms (clostridium). Common in older men often w/ diabetes. Progresses to perforation, intraabd abscess, sepsis, death
What is pneumobilia?
Air in the biliary tree secondary to gallstone ileus, due to fistula between gallbladder and duodenum
What can significantly elevated alk phos and GGT in proportion to AST/ALT suggest?
Cholestasis or biliary obstruction
Why send amylase and lipase in setting of cholelythiasis?

R/o gallstone pancreatitis

Lipase has much higher specificity than amylase

What are better tests to assess liver function?
serum albumin, PT, INR
How can acalculous cholecystitis happen?

Most often in critically ill patients. Secondary to biliary stasis and gallbladder ischemia in the presence of systemic illness

Can also be caused by long-term total parenteral nutrition

What do you do when biliary disease is suspected but see no gallstones on US?
HIDA scan. If obstruction secondary to gallstones, no cntrast will be seen within the gallbladder and HIDA is positive
When should laparoscopic cholecystectomy be performed?
Within 48 hours
What abx would you give in acute cholecystitis?

Second gen cephalosporins (cefoxitin) are first line

Alternative = pip/tazobactam or amp/sulfbactam

Is there benefit for cholecystectomy for asymptomatic gallstones?
Complication of laparoscopic cholecystectomy?
common bile duct injury. More common in men
Blood supply to the common duct?
Right hepatic artery
Proper hepatic artery
If injury to common duct is <50% of circumference, what is done?
Primarily repaired (over a T tube which acts as a temporary stent)
If common duct is >50% damaged?
Loop of jejunum has to be brought up and anastomosed to the proximal end of the bile duct (roux-en-Y hepaticojejunostomy)
How does CBD injury present if not caught intra-op?

Abd pain, bloating, anorexia, elevated LFTs

Work up = US/CT to look for large fluid collection

What is postcholecystectomy syndrome?
1) residual stone in CBD = lead to pancreatitis, cholangitis, biliary obstruction
2) gallstone in cystic duct stump = pts at risk for retained gallstones
3) dysfunction of biliary tree = impaired function of biliary tree
How do you manage CBD injury?
Endoscopic retrograde cholangiopancreatrophy (ERCP) to determine whether a major ductal injury exists
DDx for RUQ pain several weeks after cholecystectomy?
Postcholecystectomy syndrome. If ongoing pathology in the biliary tree is suspected, an ERCP is next test of choice
When should you suspect gangrenous cholecystitis?

Severe unrelenting abd pain, high fever, presistent tachy, markedly elevated WBC, hyponatremia

More common in men and DM

If suspected = urgent laparoscopic cholecystectomy

When does cholangitis occur?
Setting of obstruction of CBD leading to ascending infection of the biliary tract. Occurs secondary to choledocholilithiasis
What is assoc w/ cholangitis?
Charcot triad = RUQ pain, jaundice, fever
Pentad = + hypotension and AMS
Tx of cholangitis?
Immediate decompression of the biliary tract, most often w/ ERCP; although percutaneous transhepatic cholangiography w/ drainage is an option if ERCP is not available.
1 day history of RUQ pain, nausea, AMS, jaundice, fever, leukocytosis, hypotension, elevated bilirubin, elevated LFTs?
Acute cholangitis secondary to gallstone impaction
Diagnostic criteria for cholangitis?
1) evidence of systemic inflammation
2) cholestasis (jaundice, abnl liver enzymes)
3) biliary obstruction (dilated bile ducts on ultrasound)
Causes of obstructive jaundice that lead to cholangitis?
1) gallstones
2) bile duct strictures
3) parasites (ascaris, chinese liver fluke, clonorchis sinesis)
4) instrumentation of biliary system like ERCP
5) indwelling biliary stents
What level bili is jaundice first visible?
Consequences of unrecognized acute cholangitis?
Severe sepsis, hepatic microabscesses (AST and ALT markedly increased), death
AST vs. ALT. Which is more specific to liver?
ALT is more specific. AST is found in muscle and in other cells
What liver enzyme values are indicative of hepatocellular damage?
When AST and ALT are in the thousands, out of proportion to alk phos
What would be more indicative of posthepatic pathology?

Significant rise in ALP, since this is released from cells in the bile duct.

A conomitant increase in GGT is helpful and more specific to liver disease

When SIRS is recognized, what is the next step?

1) Targeted aggressive IV fluid resuscitation w/ normal saline or lactated ringers. Acquire central venous access to guide this

2) broad-spectrum abx should be started within 1 hour!

3) send 2 sets of blood cultures

Once initial management for cholangitis has been given, what is next step?
Biliary decompression (drain the infected bile) via ERCP
How is ERCP done?

Scope inserted through mouth to ampulla of vater. Extract the stone, cut the sphincter of Oddi to allow drainage of bile into duodenum, and place a stent.

If unsuccessful, do percutaneous transhepatic drainage

What is next step after successful ERCP?
laparoscopic cholecystectomy to prevent future episodes
What does a history of diarrhea in patient who presents w/ cholangitis suggest?
Inflammatory bowel disease w/ primary sclerosing cholangitis
What characterizes primary sclerosing cholangitis?
inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts
Ddx for epigastric abd pain?
1) gastroenteritis = n, extensive vomiting, diarrhea, fever
2) acute gastritis = burning/gnawing pain, NSAID use
3) acute cholecystitis
4) PUD = H pylori
5) peforated ulcer
6) pancreatitis = radiates to back, alcohol use, anorexia
7) appendicitis
8) SBO
9) mesenteric ischemia
10) ruptured AA
11) MI
Classic presentation of acute pancreatitis?

Epigastric abd pain radiating to the back; nausea and vomiting; prior episodes after eating HEAVY meals = symptomatic gallstones; sx that worsen with food; anorexia

Elevated amylase and lipase levels

What is the atlanta criteria for acute pancreatitis?
1) sudden, severe persistent epigastric pain radiating to the back
2) elevated lipase or amylase 3x greater than the upper limit of normal
3) characteristic findings on imaging (enlarged pancreas, sentinel loops, colon cutoff sign)
What nonsurgical conditions can mimic an acute abdomen?
Gastroenteritis, acute adrenal insufficiency, sickle cell crisis, DKA, acute porphyria, PID, kidney stones, pyelonephritis
What is the blue-black discoloration of the flanks and what does it mean?
Grey Turner’s sign. Indicates retroperitoneal hemorrhage due to acute pancreatitis
What is blue-red discoloration of the umbilicus and what does it mean?
Cullen’s sign. Results from digested blood products in the retroperitoneum, forming methemalbumin that then travels to the anterior abd wall
First step in the eval of gallstones?
Abd ultrasound
What physical exam findings suggest acute pancreatitis?
Fever, tachycardia, tenderness w/ localized guarding, hypoactive bowel sounds secondary to reactive ileus
What structures are in the retroperitoneum?
Descending colon
Duodenum (2nd and 3rd)
Ascending colon
How does pancreatitis happen physiologically?

Inappropriate activation of pancreatic enzymes –> peripancreatic inflammation.

Enzymes extravasate intraparenchymally –> autodigestion of pancreatic parenchyma –> damages peirpancreatic tissues and vasculature.

Inflammatory response is out of proportion –> fluid sequestration, fat necrosis, vasculitis, hemorrhage

Etiologies for pancreatitis?
Gallstones 40%
Ethanol 30%
Scorpion stings
Mycoplasma or mumps
Embolic or ischemic
4 Fs for gallbladder disease?
Female, fat, forty, fertile
What meds can cause pancreatitis?
*Furosemide and thiazides
*sulfasalazine, 5-ASA for IBD
*azathioprine for immunosuppression
*valproic acid for seizures
*exenatide for DM
*didanosine, pentamidine for HIV
How do gallstones cause acute pancreatitis?

Gallstone passes from gallbladder into the common bile duct, which leads to transient impaction of at the ampula that causes increased pancreatic duct pressure and results in reflux of dudenal juices and bile into the pancreatic duct

= opie’s common channel theory

Is ERCP usually needed for gallstone pancreatitis?
No, because the stone is usually small and usually passes into the duodenum. Vs. cholangitis which is usually caused by a large stone that requires ERCP for removal
How does alcohol cause pancreatitis?
Intra-acinar activation of proteolytic enzymes seems to be central requirement. Products of ethanol metabolism result in pancreatic hypoxia and oxidative damage –> excessive increase in calcium ion concentration in pancreatic cells
Acute vs. chronic pancreatitis?
1) Acute is severe and sudden; chronic sees recurrent episodes
2) acute is caused by gallstones and alcohol most likely; chronic caused by alcohol 90% and anatomic defects
3) chronic has recurrent epigastric pain, wt loss, DM, steatorrhea
4) chronic has low fecal elastase levels
Radiology for acute vs. chronic pancreatitis?

Acute = dilated loops of bowel near pancreas (sentinel loop)

Chronic = pancreatic calcifications

What are the 3 phases in acute pancreatitis?
1) premature activation of trypsin within pancreatic acinar cells
2) intrapancreatic inflammation
3) extrapancreatic inflammation (affecting multiple organ systems)
What defines severe pancreatitis?
development of systemic complications and/or local complications such as pancreatic pseudocyst, abscess, necrosis (worst prognosis)
What organ systems can be affected by acute pancreatitis?
Cardiac, pulmonary, renal, GI
How is organ failure defined?
1) shock = systolic pressure <90
2) PaO2 <60 3) creatinine >2 after rehydration
4) GI bleeding >500cc/24hr
How is hypotension caused in pancreatitis?

Inflammation and cytokine storm cause endothelial injury and increased permeability in the peripancreatic vasculature –> extravasation of fluid –> hypotension.

Cytokines also cause massive vasodilation –> hypotension

What are the main pulmonary complications of acute pancreatitis?
1) pleural effusions on the left side
Mechanism for lung involvement in acute pancreatitis?

Severe inflammation can obstruct lymph drainage around the diaphragm –> collection of lymph fluid which travels across the diaphragm pores into the ipsilateral base of the lung

Inflammation can also contribute to fistula formation between pancreas and thoracic cavity, permitting free flow of pancreatic enzymes into the lungs

What are the majority of acute pancreatitis histopathologically?
>80% have acute interstitial edematous pancreatitis = enlargment of the pancreas due to inflammatory edema. No inflammation or destruction of pancreatic cells
What is necrotizing pancreatitis?
<20% of patients. Necrotic pancreatic parenchyma that can lead to sepsis in over half of the cases
What is central gland necrosis in pancreatitis?
Subtype of necrotizing pancreatitis characterized by necrosis within the body of the pancreas
Do levels of amylase and lipase correlate w/ severity of acute pancreatitis?
NO. do not use for management
How is the BISAP score determined for acute pancreatitis?
1 point for each:
*BUN >25
*impaired mental status
*pleural effusion
Ranson criteria on admission? GA LAW
Glucose >200
Age >55
LDH >350
AST >250
WBC >16K
C Hobbs Ranson criteria after 48 hrs?
Calcium <8 Htc decrease >10%
Oxygen PaO2 <60 BUN increase by 5 Base deficit >4
Sequestration of fluids >6L
Drawback of the ranson criteria?
Takes 48 hours to get all the variables measured, and by then the patient has already declared themselves as to their course
How do you get hypocalcemia with severe pancreatitis?
Free fatty acids are generated by the action of pancreatic lipase; they chelate calcium salts and lead to saponification (deposition of calcium soaps in the retroperitoneum) –> hypocalcemia
Natural course of acute pancreatitis?
Most recover in less than 5 days without any complications. 20% have complications
Most common cause of mortaility in the first week of acute pancreatitis?

Multiorgan failure as a result of SIRS

After the first week, most commonly due to pancreatic necrosis and peripancreatic abscess

What lab tests do you need to order when suspecting acute pancreatitis?
Serum amylase, lipase, LFTs, electrolytes, CBC, lipid panel
In patients w/ no hx of alcohol abuse, what does an elevated ALT greater than 3x normal suggest?
Gallstone pancreatitis
What is the lipid panel used for in acute pancreatitis?
Rule out hyperlipidemic pancreatitis, usually due to hypertriglyceridemia
What lab test is most specific to acute pancreatitis?
Diagnositic imaging of choice for acute pancreatitis?
What can cause elevated levels of amylase?
Pancreatic disease; salivary disease, GI disease, Gyn disease, neoplasms
Classic abx x ray findings of acute pancreatitis?
1) sentinel loop = dilated loops of proximal small bowel in LUQ near pancreas
2) colon cutoff sign = distended proximal colon with abrupt collapse in the LUQ at splenic flexure
Classic Chest X Ray finding in acute pancreatitis?
Pleural effusion, classically on the left side
Role of abd CT scan on admission in pancreatitis?
Only ordered when the diagnosis of acute pancreatitis is in doubt
When can CT be useful in pancreatitis?
Beyond the first week, when patient develops worsening symptoms, it may demonstrate pseudocyst or pancreatic abscess
When do yo uuse ERCP in gallstone pancreatitis?
Never really; only with concomittant aute cholangitis
How can you identify concomitant acute cholangitis and acute pancreatitis?
Look for evidence of infection, biliary obstruction (total bili >4) and alk phosphatase, dilated CBD on US
Initial treatment for acute pancreatitis?

Vigorous IV hydration, NPO, analgesics, nasogastric decompression if vomiting

Majority of sx resolve within 3-5 days

What pain control is preferred in acute pancreatitis?

Meperidine because it does not cause contraction of the spincter of Oddi, whereas morphine does. Allows for quicker resolution of sx.

Meperidine does increase risk of seizures, though.

If gallstones are found in pancreatitis, what is next step?
Cholecystectomy should be performed bc recurrence is high
Management for pancreatitis w/o gallstones?
Management for pancreatitis WITH gallstones and suspected cholangitis?
ERCP urgently
Management for pancreatitis WITH gallstones WITHOUT cholangitis?
Rank as mild or severe. If mild, do cholecystectomy within 48-72 hours. If severe, cholecystectomy weeks later
What should you suspect if patient has severe acute pancreatitis, develops fever and leukocytosis 3 weeks into hospitalization?
pancreatic abscess. First step? CT w/ contrast to look for necrotic tissue (areas that do not enhance) or a pancreatic abscess. If find either –> CT or US guided aspiration and cultures sent. If infection present –> abx. Do surgical debridement
What do you suspect if patient w/ recent pancreatitis comes in 4 weeks later w/ persistent abd pain and palpable epigastric mass and elevated serum amylase?
Pancreatic pseudocyst. Dx w/ CT scan
Most common cause of death from pancreatic pseudocyst?
Excessive hemorrhaging into pseudocyst due to erosion into adjacent artery
Complications from chronic pancreatitis?
DM secondary to destruction of beta-islet cells; steatorrhea due to poor abs of digestive tract; chronic pain
Most common indication of surgical mangement in chronic pancreatitis?

Persistent and severe pain. Thought to be due to nerve injury in the pancreatic head. Can place a stent in pancreatic duct, allowing for improved anterograde flow of pancreatic juices

Definitive treatment includes the puestow procedure (lateral pancreaticojejunostomy)

Should prophylactic abx be administered for severe acute pancreatitis?
No as the disease is due to inflammation, not infection
What etiology for pancreatitis must you consider in patient w/ hypertension controlled w/ hydrochlorothiazide?
Hypercalcemia. It leads to secretory block in the pancreatic duct
What are sodium levels like in pancreatitis
What type of nutrition is preferred in pancreatitis?
ENTERAL, with the feeding tube placed past the ligament of Treitz to avoid activation of the pancreas
Prehapatic causes of jaundice?
Hemolytic anemia = pallor, fatigue, SOB
Gilbert syndrome = triggered by overexertion, dehydration, menstruation, illness
Hepatic causes of jaundice?
Ischemic liver injury = 2/2 hypotension and hypoxia or in transplanted donor liver
Toxic ingestion
Primary biliary cirrhosis = skin xanthomas, rheumatoid arthritis or Sjogren’s syndrome
Primary slerosing cholangitis = UC, fatigue, pruritus
Wilsons disease
Posthepatic causes of jaundice?
*acute cholangitis
*chronic pancreatitis
*mirizzi syndrome
*pancreatic carcinoma = painless jaundice arising from head of pancreas, new onset diabetes if in body of pancreas; poor prognosis
*apullary carcinoma
New onset of T2DM in older patient is associated w/?
Tumor of the pancreatic body
What is courvoisier’s sign?
Presence of palpable RUQ mass = non-tender, enlarged gallbladder. Signifies obstruction of the distal CBD. Seen with malignancy (pancreatic, ampullary, bile duct)
Painful vs. painless jaundice?

Painful implies acute biliary obstruction usually due to gallstone

Painless suggests more insidious obstruction as seen with malignancy; absence of pain suggests absence of infection. Cancers may be accompanied by mild, vague RUQ or epigastric pain.

RF for pancreatic cancer?
chronic pancreatitis (strongest RF), tobaco, high fat diet, male gender, family history
What patients are at increased risk for developing bile duct malignancy?
Those w/ ulcerative colitis, especially w/ primary sclerosing cholangitis. Also choledocholilithiasis
What is associated w/ gallbladder cancer?
Long-standing gallstone disease
What is a sister mary joseph nodule?

Periumbulical mass or nodule signifying possible metastatic abdominal or pelvic malignancy.

Most often seen w/ GI malignancies

What is a blumer’s shelf?

Steo-off felt during rectal exam suggesting metastatic disease to the pouch of douglas

Usually site of metastiasis of lung, pancreas, stomach

When does jaundice become apparent?
How is bilirubin metabolized?

Bilirubin is product of heme degradation. Breakdown of RBC occurs in spleen, liver, intravascular space.

Initially, bili is unconjugated, not water soluble, and bound to albumin. It is conjugated in the liver, becoming water soluble and excreted into intestine. Intestinal bacteria convert conjugated bili to UROBILINOGEN which can be reabs into systemic circulation and excreted into urine. Gives pee yellow color. Remaining urobilinogen is converted to stercobilin and excreted in stool.

Why does clay colored stools happen?
Decrease in bilirubin due to obstruction –> decreasing amounts of stercobilin
What can help identify hepatic causes of jaundice?

AST and ALT in the thousands and rise out of proportion to the alk phosphate level

Marked rise in alk phos (present in cells that line the bile ducts) out of proportion to AST/ALT is more indicative of posthepatic pathology such as choledocholilithiasis or cholangitis

With increase in alk phos, what can help establish it is from the liver?
Concomitant and proportionate rise in GGT
Imaging for painful jaundice?
RUQ US to detect gallstones and dilation of the biliary tree consistent w/ obstruction
Imaging for painless jaundice?
Triple phase abd CT scan bc US cannot rule out pancreatic lesions
What is a triple phase CT?
captures images during 3 phases of contrast
1) arterial
2) early venous
3) late venousCan detect pancreatic and periampulary masses and provide vital information regarding the resectability of the mass

Indirect jaundice w/ positive hemolysis?
Workup of hemolytic anemia
Indirect jaundice without hemolysis labs?
Gilbert syndrome
Role of CA 19-9?
Can be used for prognostication and for monitoring therapy; NOT for screening purposes
When is pancreatic cancer unresectable?

Tumor invasion into the superior mesenteric, celiac, or hepatic arteries.

Also if there is metastatic disease.

Resectabiility is primarily determined by the triple phase CT scan.

Role of neoadjuvant therapy for pancreatic adenocarcinoma?
Can make as many as 1/3 of them resectable
What is the surgical management for pancreatic cancer?
Whipple procedure = pancreaticoduodenectomy. Removes the head of pancreas, duodenum, and proximal jejunum, distal stomach, gallbladder, and common bile duct.
When is the whipple also used?
Cancers of duodenum, cholangiocarcinoma, ampullary carcinoma IN ADDITION to pancreatic cancer
What conditions may warrant palliative procedures in patients w/ nonresectable pancreatic cancer?
Chronic abd mass, gastric outlet obstruction, symptomatic biliary obstruction
Complicaton to pancreatectomy whiopple?

Delayed gastric emptying (gastroparesis). Treat w/ metoclorpramide

Others: leak/fistula, hemorrhage, malabsorption, weight loss, marginal ulceration

Is there a risk for DM after whipple procedure?
Not if only the pancreatic head is removed. Assess preoperative DM status and glucose levels
How do the different colors of fluid leaks in drains after pancreatic head removal suggest different things?

Normal drainage = serosanguinous or straw yellow-red

High outputs of serosanguinous suggests hemorrhage

Green suggests biliary leak

Gray-white milky suggests pancreatic leak

What will any process that leads to prolonged biliary obstruction lead to?
Vitamin K deficiency and a prolonged INR. Can treat w/ parenteral vitamin K (if not actively bleeding) or fresh frozen plasma (if pt is actively bleeding)
Ddx for upper GI bleed?
1) gastritis = h pylori, NSAID, dyspepsia, alcohol
2) gastric ulcer = pain after eating
3) duodenal ulcer = pain relieved after eating
4) erosive esophagitis = infections like HSV, CMV, candida; drug ingestion
5) mallory-weiss tear = alcohol; partial tear into mucosa/submucosa
6) esophageal varices = stigmata of liver disease
7) gastric cancer
8) stress-related mucosal damage = curling ulcer, cushing ulcer
9) andiodysplasia = degeneration of previously healthy small vessels, assoc w/ renal failure, valvular heart disease, CHF
10) isolated gastric varices
11) aortoenteric fistula
12) osler-weber-rendu disease
What characterizes osler-weber-rendu disease?
epistasix, red nodules, starry telangiectasias on lips, nodular angiomas/telangiectasias in the small bowel
Most likely cause of hematemesis in absence of cirrhosis/portal HTN, absence of alcohol abuse, no history of retching, with + NSAID abuse?
Acute gastritis, or an ulcer; NSAIDs may mask the symptoms of dyspepsia
What gives coffee-ground appearance?
Iron in RBC when exposed to gastric acid becomes oxidized. This can also be excreted in stool which gives melena
What color is likely Upper GI bleed?
Bright red bloody emesis, coffee ground, melena
What variables adversely affect prognosis in patient w/ UGI bleed?
*increasing age >60
*comorbid conditions
*variceal bleed
*shock on presentation
*need for transfusions
*active bleeding during endoscopy
*bleeding from large >2cm ulcer
*recurrent bleeding
*need for emergency surgery
What are esophageal varices?
Dilated tortuous veins located in submucosa of the DISTAL THIRD of esophagus that form as a result of portal hypertension
What is primary venous drainage of esophagus?

Esophageal veins that empty into SVC

Distal veins in the submucosa empty into the left gastric vein, which drains into portal vein

How does cirrhosis lead to esophageal varices?
Portal vein has much more difficulty draining its blood into the scarred liver –> blood forced to flow retrograde –> leads to esophageal varices
What is acute gastritis?

Erosive, superficial inflammation in the lining of the stomach secondary to dysfunction of mucosal defenses (which include prostaglandins, bicarb, somatostatin).

*NSAIDS reduce prostaglandins, so reduce protective mechanisms.
*Corrosive materials (household cleaners, pesiticides, gas, cosmetics) damage the mucosa

What is chronic gastritis?
Nonerosive inflammation of the gastric mucosa
What is type A chronic gastritis?

Fundus-dominant chronic gastritis. Assoc w/ pernicious anemia.

Mech: body produces autoantibodies to parietal cells leading to megaloblastic anemia and vitamin B12 def

What is type B chronic gastritis?
antral-dominant. Most common form. Caused by H pylori leading to peptic ulcer disease
What is a dieulafoy’s lesion?
rare cause of acute upper Gi bleed. Vascular malformation in which a large tortuous artery in the submucosa is eroded by gastric acid
Endoscopy finding of dieulafoy’s lesion?
small, pinpoint defect in the gastric mucosa
Why might Hb/Hct be normal in spite of major GI bleed?
Because patient is losing whole blood, plasma and red cell volume decrease in the same proportion –> and thus no change initially
What percent blood volume is lost before a patient may present w/ hypotension?
What happens to the BUN/Cr ratio during UGI bleed?

Increases as a result of absorption of degraded blood products during intestinal transit and prerenal azotemia secondary to hypovolemia.

*Decreased Hb/hct and increased Bun:cr = UGI bleed

What part of GI tract is considered upper GI bleed?
oropharynx down to the distal duodenum (ligament of teritz)
If patient presents with both bloody emesis and BRBPR, is it most likely upper or lower?
Probably a massive upper w/ rapid transit of blood through GI tract
First step in evaluation of upper GI bleed?
Fluid resuscitation. 2 large-bore IV lines and nasogastric tubes; send blood for type & cross
Why place NG tube in UGI bleed?

NG tube lavage is used to help differentiate upper and lower Gi bleed. If tube returns blood or coffee grounds –> upper GI.

If tube returns clear, nonbilious fluid –> unlikely to be proximal to the pylorus of the stomach

If bilious w/ no blood –> very unlikely that it is UGI, and thus likely LGI

What fluid is used during NGT lavage?
Room-temp NS. Iced used to be used to promote vasoconstriction in nearby vessels but no longer recommended
Type & screen vs. cross?

Screen is when transfusion is not likely, ie elective surgery.

Cross is when prob of transfusion is high. Repicipent blood is tested against donor packed cells to determine if there is a significant response

Management for mallory-weiss tear?

Observe if minimal bleeding.

Endoscopic band/clip if heavy bleeding

Mangament for esophageal varices?
TIPS vs. shunt
Management for ulcer and dieulafoy’s lesion?
What blood do you give if needed immediately?
O negative
Next step after fluid resuscitation in UGI bleed?
Correct any coagulopathy w/ blood products. Reverse any anticoagulatnts
After the patient is stabilized, next step in UGI bleed?
Upper endoscopy, ideally within 12 hours
If upper endoscopy fails to show source of bleed, what can be done?

angiography if bleeding is brisk.

if bleeding is minor, capsule vidoe endoscopy and push enteroscopy is recommended.

technetium-99m-labeled RBC scan is more helpful in lower GI bleed

Indications for surgery in patient w/ UGI bleed?
1) failure of endoscopic therapy after 2 attempts
2) persistent hemodynamic instability despite resuscitations
3) CV dz
4) hemorrhagic shock
5) excludes varices
Optimal treatment for gastric ulcer that fails medical management?
Excise part of the stomach to include the ulcer, as there is a higher risk of underlying malignancy with gastric ulcers
What do you do if duodenal ulcer fails medical management?
Truncal vagotomy to reduce recurrence. Reduces stimulation of parietal cells and secretion of gastric acid
Most common reason for surgical intervention in benign gastric ulcers?
Failure of the ulcer to completely heal after 6-month trial of medical or endoscopic therapy
If ulcer or gastritis is found on endoscopy, what must you test for?
H pylori. Untreated may lead to perforation
What does H pylori increase risk of?
Lymphoma = MALToma and gastric adenocarcinoma
What is the triple therapy for H pylori?
PPI, clarithromycin, amox. Tx for 1 week
How do you test for H pylori eradication?
Urea breath test. Dont give PPI before testing bc can be falsely negative.
How is esophageal varices managed?

Short term abx prophylaxis. Endoscopic band ligation is recommended as FIRST LINE bc causes less injury to the esophagus.

Repeat endoscopy in 48 hours to band any remaining vessels.

Somatostatin and vasopressin are given to reduce portal blood flow

If this fails –> TIPS

Best way to prevent recurrent UGI bleed from esophageal varices?
long term B blocker
How are mallory weiss tears managed?
caused by vomiitng, retching, straining at stool, lifting, coughing. Bleeding is almost always self limited. Surgery rarely indicated
Best management for stress ulcers/stress gastritis?
maintaining gastric pH grater than 5 using IV PPI
What Hb level necessitates transfusion?
When should you abandon medical management and proceed to surgery for UGI bleed?
Typically once you’ve gone through 4 units of PRBC over initial 24 hours or 10 units of PRBC in total
Ddx of severe epigastric pain
1) acute cholecystitis
2) acute pancreatitis
3) acute cholangitis
4) perforated gastric or duodenal ulcer
5) diverticulitis
6) small bowel obstruction
Most common sx in a patient w/ peptic ulcer dz?

Abd pain that is burning in epigastric region and does NOT radiate.

Gastric = pain during consumption. Duodenal = pain 2-3h after eating.

Presentation of perforated peptic ulcer?
Acute onset of sharp abd pain within the epigastric region that rapidly becomes diffuse. May complain of shoulder pain secondary to diaphragm irritation. Abd guarding, rigidity. Abd usually NOT distended. Labs may be benign aside from a left shift leukocytosis.
How do NSAIDs lead to peptic ulcers?
Inhibit COX1 and COX2 –> inhibit production of prostaglandis and thromboaxanes, which are protective to the gastric mucosa
Other factors that lead to formation of peptic ulcers?

smoking, alcohol, high stress environments

Smoking reulsts in imbalance between mucosa apoptosis and proliferation. It also has inhibitory effect on prostaglandins and mucus proliferation –> decrease in defense mechanisms

What are the most common type of ulcers?
Type 1 located on lesser curvature of the stomach near the incisura. NO acid hypersecretion
Type 2 ulcers?
in 2 locations: stomach and duodenum. YES acid hypersercretion
Type 3 ulcers?
Located in prepyloric antrum. YES acid hypersecretion
Type 4 ulcers?

Within the cardia of the stomach near the GE junction and tend to be PAINFUL.

NO acid hypersecretion

Type 5 ulcers?
assoc w/ NSAID and can occur anywhere on the stomach. NO hypersecretion.
Vomiting results in what acid/base disruption?
Metabolic alkalosis. If vomiting continues, lose sodium as well and leads to activation of RAAS –> contraction alkalosis which is reabs of sodium and water
What labs should be sent in suspected PUD?
CBC, chemistries, CRP, albumin, BUN:creatinine, amylase, lipase
Classic CXR for PUD?

Pneumoperitoneum = hyper-lucent area under one or both hemidiphragms = perforation

*in elderly, free air is absent in 40% of perforations

What is contraindicated if suspect perforated peptic ulcer?

Barium UGI series bc it causes barium peritonitis

Upper endoscopy bc may exacerbate it

role of CT scan in PUD?
Can diagnose pneumoperitoneum and confirm perforation
Basic principles of management of peptic ulcers?
1) adequate volume resuscitation for organ perfusion
2) ICU setting
3) NG tube
4) broad spectrum abx within an hour of shock recognition
How is a perforated ulcer repaired?
Through and through sutures aka a Graham patch
In how many patients does spontaneous sealing occurs for perforated ulcers?
40-80%. Can treat supportively and this can be an alterantive to surgery
What criteria are met in order to consider a conservative approach for PUD treatment?
1) less than 12 h since onset of sx
2) patient is hemodynamically stable
3) <70yo
4) does not have hx of failed medical therapy for peptic ulcer
5) comorbidities that make surgery high risk
6) radiologic documentation that perforation is sealed
Elderly patient w/ wt loss, positive FOBT?
cancer until proven otherwise. Gastric cancer patricularly common in asians
RF for gastric cancer?
FHx; diet high in nitrates salt and fat; FAp; gastric adenomas; H pylori; tobacco; Type A blood; BRCA1/2; HER2 overexpression
Is gastric cancer screening recommended in US?
Why is mortality so high of gastric cancer?
Bc usually found to be metastatic in 50% of patients at time of diagnosis
Common sx of patient w/ gastric cancer?

Weight loss and abd pain. + dysphagia, nausea, EARLY SATIETY, rarely a palpable mass

Abd pain tends to be vague, epigastric, and persistent

Tumor needs to be large before experience pain and early satiety

What may you find on physical exam in gastric cancer?

Palpable left supraclavicular nodes (virchows) in advanced stages

Periumbilical LAD and left axillary nodes

2 histologic types of gastric adenocarcinoma?

1) intestinal-type = well differentiated, in the distal stomach. Poor diet, smoking, alcohol, other environment RF. Decreasing bc of eradiation of H pylori

2) diffuse-type = poorly differentiated, originates from lamina propria of the stomach and grows in infiltrative, submucosal pattern. Proximal stomach near the cardia

What is linitis plastica?
When diffufse type gastric cancer infiltrates the entire gastric wall. It is stiff, undistensible, infiltrated w/ tumor
Vascular supply to the stomach?

Lesser curvature: left and right gastric arteries

Greater curvature: left and right gastroepiploic arteries

All vessels are derived from the celiac artery

Where does the right gastric most commonly branch from?
common hepatic artery
Why do patients w/ gastric cancer get iron def anemia?
Due to slow intermittent bleeding of the tumor
Best way to diagnose a patient w/ suspected gastric cancer?
Upper endoscopy is standard of care.
What work up is recommended after dx of gastric cancer is established?

Endoscopic ultrasound (EUS) to assist w/ TNM staging

CT scan to confirm that the patient is a surgical candidate. Will also rule out liver metastasis as well as distant suspicious lymph nodes

What can you use in locally advanced gastric cancer?
Chemo prior to surgery
How many lymph nodes must be removed to stage gastric adenocarcinoma?
At least 15
What 2 types of lymph node dissections are there?
1) D1 = perigastric lymph node dissectoin
2) D2 = hepatic, left gastric, celiac, splenic artery dissectionCurrently D2 are recommneded over D1

What stage of gastric cancer and beyond should multi-therapeutic approach be considered?
Stage IB. Chemotherapy can work pre- and postoperatively. When used together, improves survivial by 33%
Role of HER2 gene amplification and chemo in gastric cancer?
HER2 overexpression has been recognized as a moleulcar abnl that increases the aggressive nature of breast cancer. Also implicated in gastric cancer. Responds to trastuzumab!!! So test for HER2 in your patients prior to induction of chemo
Gastric adenocarcinoma accounts for what percent of gastric cancers?
90%. The others = GI stromal tumors, gastric carcinoids, gastric lymphomas
What are GI stromal tumors?

Mesenchymal tumors of variable malignant potential that originate from interstitial cells of Cajal within Gi tract. These are pacemaker cells of GI tract.

Near universal expression of c-KIT and CD117 by GISTs.

Wedge resection can be performed allowing for anastomosis-free procedure.

Rarely spread through lymphatics (unlike adenocarcinomas)

Imatinib is proven 70-80% effective in GISTs

Waht are gastric adenocarcinoids?
1% of all gastric cancers. Treat either endoscopically or with close observation
What is dumping syndrome following gastric resection?

Caused by rapid distribution of food within the small intestine in the absence of regulartory effect of pyloric sphincter.

Leads to hyperosmolar state –> increased water secretion into intestinal lumen –> diarrhea and occasionally hypotension

Common complications after gastric resection?
Diarrhea, early satiety, dumping syndrome, afferent limb syndrome, internal hernia, small bowel obstruction
How are anastomotic leaks identified and treated following gastric resection?

Present w/ abd pain and varying degrees of peritonitis, fevers, tachycardia, leukocytosis, sepsis if not treated rapidly

Confirm w/ upper GI gastrografin that shows contrast extravasation

First line treatment = source control, involves re-operation

*FIRST CONTROL THE LEAK and often can salvage the initial operation

Ddx for chest pain after vomiting?
1) MI
2) pericarditis = substernal, pleuritic chest pain worse when supine, better leaning forward
3) pneumothorax
4) pna
5) aortic dissection
6) PUD
7) acute pancreatitis
8) mallory weiss tear
9) boerhaave’s syndrome = forceful vomiting and retching followed by chest pain and sepsis typically in an alcoholic or a bulimic patient. See crepitus with palpation around the sternum
What is boerhaave’s syndrome?
A type of spontaneous esophageal rupture
RF for boerhaave’s syndrome?

ALCOHOL! binge drinking places at risk of foreceful vomiting/retching.

Also pateints who overeat. Common in 50-70yo males.

What is mackler’s triad?
1) vomiting 84%
2) thoracic pain 79%
3) subcutaneous emphysemaSuggestive of boerhaave’s syndrome

Most specific sign of esophageal rupture?
Subcuteanous emphysema after foreceful retching is PATHOGNOMONIC for esophageal rupture. ID by crepitus with palpation around sternum. Seen in 27% of patients
Boerhaave’s vs. mallory weiss?
*both have same population: alcoholics/bulimics after forceful vomiting
*pathophys: boerhaaves is full thickness rupture; MW is partial rupture
*presentation: B = thoracic pain radiates to back, left sided pleural effusion, signs of sepsis. MW = UGI bleed
*course: B = sepsis and death; MW = most will resolve spontaneously
Most common causes of esophageal perforation?

60% are result of iatrogenic injury w/ upper endoscopy perforation being the most common cause

Others: blunt/penetrating trauma.

10-20% are sponteanous ruptures AKA boerhaave’s syndrome

How does esophageal rupture happen in boerhaave’s?
Forceful vomiting causes dramatic rise in intragastric pressure –> transmitted to esophagus in presence of relaxed lower esophageal sphincter. Tremendous pressure is transmitted to esophageal wall –> perforation
Sepsis in boerhaave’s?
Perforation leads to gross contamination of the mediastinum. Leads to rupture of the pleura as well commonly. This all leads to sepsis and can lead to death
First step in workup for suspected boerhaave’s syndrome?


Findings: left sided pleural effusion and atelectasis

*normal CXR in 12-33% patients.
*takes at least 1 hour post-perforation to see on imaging

What do you do if CXR is questionable in boerhaave’s?
Do an oral contrast study to confirm the diagnosis. CT w/ oral contrast. Allows to ID extent of perforation into surrounding structures
What kind of contrast should you use if suspect perforation?
Water-soluble bc barium can cause SIRS in mediastinum and pleura
Should you perform endoscopy in boerhaave’s?
Initial step in managing boerhaave’s?

Aggressive IV resuscitation, NPO, broad-spectrum abx and antifungals. Start H2 blocker or PPI to reduce gastric acid secretions

If hemo unstable = arterial line should be placed

What time window is optimum in detecting and treating boerhaave’s?
24 hours. Delays greater than this doubles mortality
What do you do in boerhaave’s if uncontained leak in less than 24 hours?

Transthoracic/transhiatal repair; decompression; feeding jejunostomy

*if >24h? Closure over T-tube or exlclusion + diversion

When do you do conservative managemnet for spontaneous perforation of esophagus?
minimal comorbidities, no signs of sepsis or shock, perforation that has been present for less than 24 hours, leak that is small or contained or has healed itself
Surgical management of boerhaave’s syndrome?

Priamry closure of the perforation and esophageal resection are two options. Primary closure is preferred if small. Must debride all tissue for closure to be successful.

Pleural decortication must occur = debridement of mediastinum and pleura

If there is a large hole, or prolonged ddelay, successful closure is unlikely and will require esophagectomy

Ddx of a benign palpable breast mass?
1) fibrocystic change = vague irregularity, upper quadrants. Most common breast mass in women; normal variant, though some assoc w/ increased cancer risk
2) fibroadenoma = most common benign tumor; <30yo; estrogen sensitive causes it to grow during pregnancy
3) intraductal papilloma = unilateral bloody nipple discharge in premenopausal women; usually does not show up on mammogram
4) fat necrosis = abnl calcification on mammogram 2/2 saponification; follows trauma or recent breast surgery
5) abscess = PAINFUL, typically in lactating breast; postpartum mastitis
6) galactocele = painful or painless aseptic mass in lactating breast that is not warm or erythematous; usually on cessation of lactation
Ddx of malignant palpable breast mass?
1) ductal carcinoma in situ = incidental calcifications on mammogram; good prognosis
2) invasive ductal carcinoma = firm, immobile, discrete mass, nipple retraction, painless. prognosis depends on stage
3) invasive lobular carcinoma = painless, frequently bilateral
4) mucinous carcinoma = gelatinous well circumscribed mass, slow growing, more common in elderly. poor prognosis
5) inflammatory carcinoma = inflammed, peau d’oarange. poor prognosis
6) phyllodes tumor = mobile, slow growing, rubbery. patients often transient or immigrants; poor prog
What do you need to do on physical exam in evaluating breast mass?
1) look for asymmetry, skin changes, nipple discharge
2) bimanual in supine position. Note hard, immobile, irregular borders
3) palpate cervical, supraclavicular, infraclavicular, axillary nodes
Low relative risk factors for breast cancer?
Menarche <12 Menopause >55
Moderate relative risk factors for breast cancer?
Age at first birth >30
Mother or sister w/ breast cancer
Previous breast cancer
Radiation exposure
High RR for breast cancer?
BRCA1/2 mutation
Age >70
Describe benign nipple discharge
clear, bilateral, multiductal
Describe pathologic nipple discharge
*can be due to prolactinoma, hypothyroidism, cushings disease, meds
*tends to be unilateral
*bloody, spont, uniductal is suggestive of breast cancer
What features of fibrocystic changes are assoc w/ increased risk for cancer?

Ductal hyperplasia or slcerosing adenosis doubles risk. Atypical hyperplasia has the highest risk.

Apocrine metaplasia has NO increased risk.

Pea d’orange seen commonly in?

Inflammatory carcinoma. Requires a full-thickness, punch biopsy of the dermis for definitive diagnosis.

Mech: lymph drainage of breast is compromised –> edema expanding the interfollicular dermis –> dimpling, pitting

How does nipple retraction happen?
When breast tumor infiltrates suspensory ligaments of breast (coopers), it will retract the skin, often around the nipples
Triple test for new breast mass?
physical exam, imaging, tissue sample
Why is mammography not useful in younger women?
Bc breasts consist of dense, fibrous tissue and it cannot detect abnl well. And most masses <30yo are benign.
First line imaging for woman <30 yo w/ breast findings?

US. If cyst is found, simple = observe, painful or enlarging = aspirated. If the fluid is bloody, send to pathology.

If mass is solid = CORE NEEDLE BIOPSY

What imaging for woman >30yo?
Diagnostic mammogram. Suggestive features of malignancy = =asymmetry, clustered pleomorphic calcification, increasing density, irregular borders or spiculation
Where would you look for metastases if concerned?
Liver, bone, lungs
Are tumor markers used for breast cancer?

Not routinely used for all patients.

Include: CA-15-3, CA 27.29, CEA

What is a triple negative breast cancer?
Negative for estrogen receptor, progesterone receptor, and HER2 receptor. Difficult to treat w/ conventional therapy. The most common subtype in BRCA1 carriers
What are the 2 types of surgeries for breast cancers?

1) breast-conserving therapy = lumpectomy (partial mastectomy) and sentinel lymph node biopsy (SLNB) followed by radiation therapy to decrease risk of local recurrence

2) simple mastectomy w/ SLNB only

When would you typically do a breast conserving therapy surgery?

Stage 1 and 2. Same survival rates as simple mastectomy while cosmetically appealing.

*carries increased risk of local recurrence despite radiation

Contraindicatons to BCT?
*multiple primary tumors in >2 quadrants
*diffuse malignant appearing microcalcifications throughout breast
*hx of previous chest wall radiation
*early prego
What are characteristics of stage 3 breast cancers?
*large >5cm
*invaded skin
*presence of large matted clinically positive axillary lymph nodes
When do you perform axillary lymph node dissection?
When more than 2 positive sentinel lymph nodes are present or in patients who underwent mastectomy
Boundaries of the axilla?
Superior = axillary vein
Posterior = floor of the axilla
Lateral = latissimus dorsi
Medial = pectoral minor muscle
Purpose of axillary lymph node dissection?
For staging. Removing them does not necessarily improve survival
What study must be done prior to starting trastazumab?
Echocardiogram or MUGA scan to determine ejection fraction. Because of risk of cardiomyopathy
How does aromatase inhibitor work?
Inhibit aromatase enzyme in fat tissue that makes small amounts of estrogen in postmenopausal women. So only work in post-menopausal women since this is their primary source of estrogen
Mech of tamoxifen?
*blocks estrogen receptors
*acts like estrogen in some tissues (endometrial)
*antiestrogen in others (SERM)
*increases risk for endometrial cancer and blood clots
Raloxifene mech
*blocks estrogen receptors
When would you use fulvestrant?
Postmenopausal women that have failed therapy w/ tamoxifen.
*severe osteoporosis risk
Mech of anastrozole?
aromatase inhibitor
Mech of trastazumab?
*risk of cardiomyopathy
Features of anthracyclines?
*doxorubicin, epirubicin, idarubicin
*inhibits DNA/RNA synthesis
*hair loss, vomiting, cardiomyopathy
Features of alkylating agents?
*promotes DNA damage by alkylating guanine bases
*risk of leukemia, cystitis, bladder cancer
Features of antimetabolites
*MTX and 5FU
*interfere w/ DNA synthesis
*hair loss, vomiting, bone marrow suppression
AE of paclitaxel and docetaxel?
What patients would you not use chemotherapy in?

Noninvasive breast cancers (carcinoma in situ)

Very small invasive cancers <1cm w/ favorable tumor markers and negative SLNB

Deficit if long thoracic is damaged?
Upward rotation, abduction, and weak elevation of scapula = WINGED SCAPULA
Deficit if thoracodorsal nerve is damaged?
Weak extension, adduction, and internal rotation of the shoulder joint
Deficit if medial pectoral nerve is damaged?
Weak internal rotation of humerus
Deficit if lateral pectoral nerve is damaged?
Weak flexion, adduction, and internal rotation of the humerus
Which lymph node dissection has greatest risk for lymphedema?
ALND over SLNB. Chronic patients can develop lymphangiosarcoma
Why can you miss breast mass in prego?
*breasts are denser, makes it harder to visualize on mammogram
*hormonal changes in prego may mask sx
*women can be given chemo during second trimester
*never do radiation or hormonal therapy during prego
Ddx benign calcifications on abnl mammogram in absence of mass?
1) skin calcifications 2/2 dermatitis or hygiene products
2) vascular calcifications
3) popcorn like = underlying fibroadenoma
4) round or punctate = fibrocystic changes
5) eggshell = deposited on the surface of a sphere; can be seen as fat necrosis
6) dystrophic = coarse, irregular shaped seen w/ trauma
What calcifications would be suspicious on mammogram?
1) amorphous
2) coarse
What calcifications are high probablity of malignancy on mammogram?
1) fine pleomorphic = BI-RADS5 assoc w/ DCIS
2) fine linear/linear branching = assoc w/ intraductal carcinoma or necrosis
Why are mammograms not as useful in ages <30?
Bc breasts are denser due to decreased level of fat, and may not pick it up on imaging
What is the Breast Cancer Risk Assessment Tool?
age, age at menarche, reproductive history, family history in first degree relatives, prior biopsies
Difference between large and small calcifications?
Larger ones are almost always benign
Describe ductal carcinoma in situ (DCIS)
Malignant epithelial cells within the mammary ductal system, without invasion into stroma
*patterns: comedo w/ prominent central necrosis; cribriform w/ back to back glands; and papillary
*comedo is typically high grade and has worse prognosis
*often multifocal and assoc w/ concurrent invasive carcinoma
*high risk of invasive carcinoma
Describe LCIS?
*malignant epithelial cells that arise form the lobules and terminal ducts of the breast
*nor a premalignant lesion
*marker for dev of future ipislateral and contralateral invasive breast cancer
*incidentally found usually
*classic form and pleomorphic form w/ larger cells
*lower risk of dev invasive carcioma
Treatment for DCIS vs. LCIS?

DCIS = lumpectomy to negative margin; consider SLNB

LCIS = if incidentally found, observe. If on core needle biopsy, excise and rule out adjacent cancer

Which BIRADS are probably malignant?
4 and 5; consider biopsies for these
What if you ID invasive ductal carcioma?

Perform lumpectomy w/ SLNB followed by radiation therapy to the remainder of the breast



What is acute cornary syndrome?

Includes STEMI, NSTEMI, unstable angina. Chest pain described as elephant on chest.

SOB, sweating, nausea, vomiting, tachy, hypotension

Features of coronary vasospasm?
*younger pts, cocaine users, comen
*coronary narrowing caused by autonomic dysfunction and mimics typical angina assoc w/ true MI
Features of diffuse esophageal spasm?
Esophageal motility disorder presenting w/ chest pain, dysphagia, food regurg
*may be triggered by reflux, caffeine, spicy foods
What murmur might we expect to see in aortic dissection?
Diastolic from aortic regurg
What makes an MI less likely on H&P?
*no CV RF
*pain reproducible by palpation (MSK)
*localized pain that is sharp
*assoc w/ foods/eating
Classic H&P findings of MI?
CP, diaphoresis, anxiety, tachycardia, tachypnea, n/v
*may present w/ HF w/ bilateral rales, JVD, new S3 or S4 heart sounds, new murmurs and hemodynamic instability 2/2 large ischemic damage
Why are postmenopausal women at higher risk of MI?
Decline in estrogen levels contribute to increased risk bc estrogen promotes growth and maintenance of intimal layer of arterial wall, maintaining its ability to expand and accomodate blood flow
occluvie thrombosis eliminates perfusion to only partial thickness of the myocardial wall and causes MYONECROSIS leading to elevation in cardiac enzymes and ECG findings suggestive of ischemia
Eliminates perfusion to full thickness of the myocardial wall and causes myonecrosis, leads to elevationin enzymes and ST segement elevation on ECG
Series of events that take place during an acute MI?
Thrombus formation –> plaque rupture –> coronary vessel obstruction –> ischemia –> myocyte necrosis and tissue death
Which coronary vessel is most often affected?
What other mechanisms of MI are there?
*decreased oxygen supply = hypoxia, hypotension, anemia
*increased myocardial oxygen demand = sepsis, tachyarrhythmias
Episodic chest pain unrelated to exertion in young person?
*prinzmetal angina
*coronary artery vasospasms are responsible -> reversible injury to myocytes
*ST elevation secondary to transmural ischemia, similar to unstable angina
*not due to coranary artery disease
Initial steps for suspected MI?
ECG, blood test for enzymes, CXR
Trend of cardiac enzymes in MI?
*CKMB is first to rise, peaks 12-40 hours, decreases after 2-3d; low specificity
*Troponin I increases in 3 hours, peaks in 6, decreases over 7 days; highest sensitivty
Which enzyme can you use to dx second MI on top of recent MI?
CKMB bc it will rise again
What can lead to persistently increased levels of cardiac enzymes?
Kidney dz bc they are cleared by kidney
Changes in V2, V3, V4?
LAD. Supplies the anterior wall of left ventricle, anterior 2/3 of intraventricular septum
ECG changes in aVL, V5, V6?
Circumflex branch. Supplies lateral and posterior wall of left ventricle, left atrium
ECG changes in II, III, aVF?
Posterior descending artery. Supplies inferior wall of left ventricle, posterior 1/3 of IV septum
How does heparin work in management of STEMI?
prevent clot formation; given before PCI or fibrinolysis
How does B blocker help in management of STEMI?
Alleviates chest pain by HR and contractability (reduces oxygen demand); prevent reinfacrion and v fib
How does nitroglycerin help in management of STEMI?
Alleviates chest pain by vasodilation –> reducing preload and afterload and improving myocardial perfusion
*may cause hypotension
Preferred treatment for STEMI reperfusion?

Clot removal and stenting in the cath lab via Percutaneous coronary intervention (PCI) within 90 mins of sx onset

If cannot go to cath lab, do systemic thrombolysis via IV tPA

What if PCI is unsuccessful in STEMI?
Emergency coronary artery bypass grafting
Initial mangement of NSTEMI?

aspirin, b blocker, nitroglycerin, heparin, platelet glycoprotein IIb/IIIa receptor antagonist, supplemental oxygen, morphine, and ACE inhibitor

*same w/ STEMI

What is the long-term outcome determinant for STEMI?
*Speed at which blood flow is restored to ischemic myocardium
*CABG is recommended in patients w/ cardiogenic shock, recurrent ischemia secondary to failed PCI, mechanical complications, or those presenting >12 hours of the initial insult
Indications for CABG in elective setting?
>50% stenosis of L main coronary artery
>70% stenosis of all other arteries
Stenosis of proximal LAD and one other artery
Stenosis of 3 coronary arteries
Obstructions not amenable to stenting (bifurcations)
What is the best conduit for CABG?
Internal mammary artery coming off the subclavian artery
What medical interventions are assoc w/ improved CABG outcomes?
Aspirin, beta blockers, statin, antibacterial prophylaxis
What are predictors of mortality following CABG?
Preoperative cardiogenic shock
emergent surgery
age >65yo
depressed LVEF
Management of prinzmetal angina?
Ca channel blockers to treat underlying vasospasm
Nitroglycerin to rapidly decrease chest pain
Immediate complications of MI?
1) cardiogenic shock = large ischemic areas and necrosis compromise contractability and cardiac output
2) CHF = decreased ejection fraction, can progress to cardiogenic shock
Post MI complications within 2-3 days?
1) Arrhythmia. 90% develop it
2) pericarditis
3) cardiac tamponade
Which patients can present w/ silent/atypical MIs?
Women, elderly, diabetic patients
Crescendo-decrescendo murmur loudest at the upper right sternal border?
Aortic stenosis
What does S4 suggest?
Left ventricular hypertrophy. Common in aortic stenosis too and HCM as these also cause LV hypertrophy and decreased LV distensibility
What other valvar disease can be mistaken for aortic stenosis?

Pulmonic stenosis; Hypertrophic obstructive cardiomyopathy

*diff from aortic stenosis by valsalva –> increases HOCM but decreases aortic stenosis murmur

Three classic sx of aortic stenosis?
Angina, syncope, CHF
Most concerning sx for aortic stenosis?
Dyspnea since they will succumb to CHF within 2 years w/o surgical valve replacement
Review the various cardiac murmurs
What is pulsus alterans?
Amplitude of peripheral pulse changes from beat to beat assoc w/ changing systolic blood pressure
What is pulsus bisferiens?
AKA biphasic pulse. 2 strong systolic pulses w/ a midsystolic dip. 2 pulses during systole. Seen in aortic regurgitation
Classic physical findings associated w/ endocarditis?
1) petechia = septic emboli or vasculitic proccess
2) splinter hemorrhage = microscopic blood clots under the nail
3) osler nodes = septic emboli to microvessels in the skin causing tender microabscesses
4) janeway lesions
5) roth spots = retinal hemorrhages
When are abx for endocaridits prophylaxis NOT indicated?
Aortic stenosis or sclerosis = both of these caused by calcification of the aortic valve
What is aortic sclerosis?

Calcification of aortic valve w/ minimal restriction of motion of the aortic valve leaflets = asymptomatic. may progress to stenosis

Vs. stenosis = sig restriction of the motion = symptomatic

3 etiologies for aortic stenosis?
Senile after 6th decade
Congenital present in middle aged
Rheumatic valvular disease
How does AS cause sudden death?
Ventricular arrhythmias or abnormal baroreceptor reflex contribute to it
What labs are recommended in workup for a patient w/ acute chest pain?
Serum electrolytes, coag panel, cardiac biomarkers, ECG
BNP is marker for?
Released by ventricular myocytes in response to increased stretch, as in CHF
What can echo reveal in MI workup?
Ventricular dysfunction. Sequelae of ACS = papillary muscle rupture, pericardial effusion, ventricular dilation
When do you do CT angio?
If PE or aortic dissection is suspected
Tx for mild aortic stenosis
*medical tx of HTN and other cardiac risk factors is appropriate
*aortic valve replacement if they need to undergo heart surgery for another reason
*echo every 3-5 years to monitor
Tx for aortic stenosis w/ HF?
*may benefic from aortic valve replacement, as it immediately reduces the afterload. Over tie, LVH may reverse
Indications for surgery for aortic stenosis?
*asymptomatic if they are to undergo cardiac surgery for another reason or if LVEF <50%
Do statins slow progression of AS?
No. reduce risk of ischemic cardiac events yes.
What meds should you use w/ caution in aortic stenosis?
Diuretics, B blockers, vasodilatros bc cause hypotension
What do patients w/ mechanical valves require for the rest of their lives?
Anticoagulation –> increased risk of bleeding
What is Ross procedure?
Replace aortic valve w/ pulmonary valve. Replace pulmonary w/ homograft (decreased individual)
What is option for patients w/ aortic stenosis that are poor surgical candidates?
Percutaneous balloon valvuloplasty. Transient effects
What are possible complications secondary to aortic dissection?
1) acute aortic insufficiency = early diastolic murmur and increased pulse pressure
2) pericardial effusion = muffled heart sounds
RF for aortic dissection?
Connective tissue dz
Advanced age
Cocaine use
Aortic injury (trauma, cardiac cath)
Aortic coarctation
Bicuspid aortic valve
How does location of dissection depend on the upper vs. lower extremity pulse discrepancies?
Upper = aortic arch
Lower = descending aorta all the way down the iliac arteries
Increased pulse pressure?
Aortic insufficiency. Diastolic pressure decreases due to regurgitation; Systolic pressure increases secondary to increased stroke volume
Pathologic progression of aortic dissection?

Tear in intima –> media –> splits aorta into inner layer of intima and inner media and OUTER layer of outer media and adventitia –> produces 2 lumens (true and false) –> blood flows into false lumen –> tear propagates and false lumen enlarges

true lumen is where blood usually flows; false lumen is blind sac formed between intimal flap and outer media

What causes the aortic tear?
Aortic wall shear stress; most often in areas exposed to high mechanical forces (aortic arch, proximal descending aorta just distal to the left subclavian artery)
Why are Marfans pts at increased risk for aortic dissection?
Misfolding of fibrillin –> cystic medial necrosis of large vessels such as aorta –> weak wall susceptible to dissection
Standford type A vs. B dissections?
A is ascending aorta/aortic arch
B is descending aorta, distal to take-off of left subclavian artery
What is malperfusion syndrome?
Expanding false lumen interferes w/ blood flow into the true lumen –> compromises perfusion to vessels supplying vital organs
What complications are specific to type A aortic dissection?
1) compromised flow to coronary arteries = MI
2) compromised flow to carotid arteries = ischemic stroke
3) pericardial sac dissection = acute tamponade
4) dissect aortic valve = aortic insufficiency
Complications of Type B aortic dissection?
Kidney failure, limb ischemia, mesenteric ischemia, paraplegia if involves the spinal cord
Lab tests to order immediately in aortic dissection?
Blood type and crossmatch; cardiac biomarkers; ECG (ACS can be a sequela)
Imaging for aortic dissection?

CXR first line.

CT w/ IV contrast if doubt. or MRA if available.

What is TEE?
Transesophageal echocardiography = performed if patient is hemodynamically unstable and aortic dissecton is highly suspected in the OR
First step in management of aortic dissection?
Maintain low blood pressure w/ IV beta blockers. Decreases change in pressure over change in time
Next step after antihypertensives for type A?
Urgent repair in OR via median sternotomy
Next step after antihypertensives for type B?
Admitted to ICU and BP closely monitored
When do you do surgery for type B dissection?
When they develop complications (malperfusion, limb ischemia, visceral ischemia) or expanding aortic diameter or ongoing pain despite medical therapy
Surgical options for type B dissection?

Open repair vs. thoracotomy and endovascular repair w/ placement of stent graft

complication = spinal cord ischemia (artery of adamkiewics compromised)

Management for type B dissection?

Medical therapy ONLY. B blocker first line.

+ nitroprusside, Ca channel blocker, morphine for analgesia

When do you not administer b blockers in aortic dissection?
If its complicated by cardiac tamponade or severe aortic regurgitation as it may precipitate cardiac arrest
Ddx for hoarseness
1) viral laryngitis = acute onset of fever, sore throat, cough, URI sx
2) vocal cord paralysis = breathy voice, injury to recurrent laryngeal nerve
3) vocal cord nodules, polyps, cysts, granulomas = unilateral or bilateral lesions resulting from trauma to vocal cord (voice abuse, endotracheal intubation)
4) recurrent resp papillomatosis = benign, growths of HPV
5) spasmodic dysphonia, parkinsons dz, or other neuro = vocal tremors
6) laryngeal cancer = subacute to chronic onset, possible cervical LAD; SMOKING is greatest risk factor
How do vocal cords move to produce sound and breathe?
Sound = move and oppose at the midline (adduction)
Breathe = must open (abduction)
Different natures of hoarseness?
Breathy = incomplete closure as seen with unilateral vocal cord paralysis
Aphonia = inability to create any sound, can be due to mucosal swelling
Strained = narrowing at level of the vocal cords as with massess/cancer
Tremulous = neuro disorder
When should you consult otolaryngologist?

When hoarseness persists longer than 3 or 4 weeks

Viral laryngitis is self limited after 1-2 weeks*

Tobacco use is greatest risk factor for what in terms of hoarseness?
SCC of upper aerodigestive tract. Alcohol has a compounded effect
What does bloody sputum/hemoptysis suggest w/ hoarseness?
Malignancy in upper airway or lungs
Most common type of laryngeal cancer?
SCC related to chronic inflammation and increased cellular turnover causing metaplasia, dysplasia, and eventual carcinoma
Most common site of malignant lesions of the larynx?
What does the superior laryngeal nerve innervate?
Sensory = supraglottis
Motor = inferior constrictior, cricothyroid muscles
Recurrent laryngeal nerve innervations?
Sensory = glottis and subglottis
Motor = all laryngeal muscles except cricothyroid
Do laryngeal papillomas cause cancer?
Rarely. HPV 6 and 11. Adults tend to have singles, children multiples
What are ways to evaluate vocal cords?

1) indirect laryngoscopy = via mirror or flexible fiberoptic laryngoscopy. assess massess, motion of vocal cords

2) direct via metal laryngoscope. Can perform biopsies during this procedure.

If laryngeal cancer is suspected, what additional tests are warranted?
CXR bc most common location for metastasis of SCC
What is early stage laryngeal cancer?
TNM I and II
Tx for early stage laryngeal cancer?
Single modality therapy – either surgery or radiation.
Tx for late-stage laryngeal cancer?
Combined-modality therapy (surgery and radiation, chemo and radiation, or all three). Neck dissection of metastasis to cervical lymph nodes may be required
Narrowest segment of human airway?
Neck mass K in KITTENS mnemonic?
1) thyroglossal duct cyst = midline mass, moves w/ tongue protrusion
2) branchial cleft cyst = lateral to midline, at risk for infection
3) dermoid cyst = entrapment of epithelium during fetal midline closure
4) laryngocele = intermittent lateral neck swelling cuased by herniation of laryngeal diverticulum through the thyrohyoid membrane
5) sebaceous cyst = obstruction of sebaceous gland duct
6) lymphangioma
7) thymic cyst = may occasionally be ectopic parathyroid tissue
I in KITTENS mnemonic?
1) lymphadenitis
2) TB = lymph nodes may be matted together and form draining sinus tract. AKA SCROFULA
3) Toxo = may cause lymphadenitis
4) cat scratch dz = same as toxo
5) actinomycosis = suppurative lymph nodes form sinuses w/ bright red color
6) deep neck abscess

Toxin = metal drugs

Trauma = hematoma, foreign body, aneurysm

1) thyroid hyperplasia
2) Ectopic thyroid gland
1) benign growths = lipoma, neuroma, fibroma
2) malignant growths = thyroid carcinoma, lymhoma, carotid body
3) metastatic
2) Kawasaki dz
RF w/ head/neck cancer?
Age >40
Poor dental hygiene
Radiation exposure
HPV assoc w/?
Oropharyngeal cancer
EBV assoc w/?
Nasopharyngeal cancer; Burkitt lymphoma
Chinese are susceptible to what specific head/neck cancer?
GERD assoc w/?
Laryngeal cancer
Sx of plummer-vinson syndrome?
Glossitis, cervical dysphagia, iron deficiency anemia, esophageal webs
How is otalgia assoc w/ head/neck cancer?
Pain referred to ear from CN IX via Jacobsons nerve and CN X via Arnolds nerve
How is dysphagia assoc w/ head/neck cancer?
Mass effect of tumor obstructing the path of food bolus vs. interference with swallowing mechanism
How is odynophagia assoc w/ head/neck cancer?
tumor-related inflammation can cause pain
How is dysphonia assoc w/ head/neck cancer?
lesion on vocal cords blocking efficient phonation or vocal cord paralysis from neural involvement
How is dyspnea assoc w/ head/neck cancer?
upper airway obstruction
How is trismus assoc w/ head/neck cancer?
tumor invasion into pterygoid muscles
What is the most common benign salivary gland tumor?

Pleomorphic adenomas

2nd most = papillary cystadenoma

What is the most common malignant salivary gland tumor?

Mucoepidermoid carcinoma

2nd most = adenoid cystic carcinoma

Hx of peritonsillar abscess?

Older children, fever, odynophagia, trismus

Tx: aspirate and drain through tonsillar bed

Hx of retropharyngeal abscess?

Younger children, drooling, can lead to airway obstruction.

Tx: intubate, drain through posterior pharyngeal wall

Hx of parapharyngeal abscess?

All age groups, assoc w/ dental infections and tonsillitis

Tx: drain through lateral neck

Salivary gland massess?
large ones = benign likely
smaller ones = likely malignant
parotid glands (largest) are most frequent site of malignant tumor
What are the salivary glands?
parotid, submandibular, sublingual, minor salivary
What is virchows node?

Enlarged left supraclavicular node. It occurs on the left, where cisterna chyli empties into the subclavian vein

Suggests metastatic lung or GI malignancy

Most common sites of head/neck cancer?
Oral cacity 44%
Larynx 31%
Pharynx 25%
What does a newly discovered malignant neck mass most likely represent?

Spread of cancer via lymphatic system until proven otherwise

<15% chance that a malignancy found in the neck represents a primary neck tumor

When is observation acceptable for newly discovered, isolated, enlarged cervical lymph node?
If no red-flag sx present and if present for <3 weeks
What procedure is performed in office when metastatic neck lymphn ode is suspected?
Flexible nasopharyngoscopy to evaluate nasal cavities, nasopharynx, oropharynx, hypopharynx, and glottis for primary tumor
What labs should be obtained in neck mass eval?
Coag profile
Liver enzymes
Chemistry panel
What imaging is first line to search for primary head/neck tumor?

CT w/ contrast

CXR also recommended

What is first line way to get tissue sample of neck mass?
If FNA confirms neck mass is metastasis, what is next step?
Panendoscopy in the OR under general anesthesia
What is panendoscopy?
AKA triple endoscopy of the upper aerodigestive track = includes laryngoscopy, esophagoscopy, and bronchoscopy
What signs should prompt immediate evaluation of the airway by an otolaryngologist?
Dyspnea or stridorous breathing. Any bleeding from mouth
Ddx for hearing loss in a child?
1) AOM = otalgia, fever, bulging and red tympanic membrane w/ decreased mobility, poor light reflex. <3 weeks
2) OME = without signs of acute infection. commonly follows AOM
3) chronic otitis media = recurrent or chronic eaer infections that result in perforations of TM +/- otorrhea
4) cholesteatoma = preceded by eustachian tube dysfunction and COM; expansile collection of keratinized, desquamated epithelium in middle ear
5) labyrinthitis = preceded by viral infection; acute onset of vertigo, gait instability, nausea, vomiting, hearing loss. NYSTAGMUS
6) otitis externa/swimmers ears = warm water contact; tender, swollen pinna
7) congenital = TORCH
8) cerumen impaction, foreign body, trauma
What is cholesteatoma?
secondary to desquamated keratinized epithelium
What other diagnoses need to be considered in adult w/ hearing loss?
1) exposure = work, loud noises, concerts
2) drugs = aminoglucosides, aspirin, loop diuretics, cisplastin
3) tumor = vestibular schwanomma most common
4) menieres disease = hearing loss, episodic vertigo, tinnitus
Predominant sx in OME?

Hearing loss.

See: immobile TM and air-fluid levels w/ partial opacification. Should NOT have any signs of acute infection.

PE: CONDUCTIVE hearing loss

Peak age of OME?
2 and declines after age 6
RF for OME?
Cigarette smoke exposure
Younger maternal age
Shorter/absent breastfeeding
Supine feeding position
Implication of regression in language?
Need to be evaluated for hearing loss
Otalgia implication?

Along with other acute signs or sx of infection is more consistent w/ AOM and less so w/ OME.

Pain of outer ear = otitis externa

Otorrhea is consistent w/?
Middle ear disease w/ TM perforation.
Most common sx of otitis externa?
Otalgia upon manipulation of external ear, pruritus, hearing loss. Edematous and erythematous external ear canal
What ear condition do you see air-fluid level in?
OME; rarely in AOM
What ear condition will you see bulging/fullness and redness?
Main sx seen w/ OME?

Conductive hearing loss 2/2 fluid bulidup within middle ear space

May also have sleep disturbances, ear fullness, tinnitus, even balance problems

Majority of OME cases resolve within what period of time?
50% by 3 months
Most likely etiology for sudden deafness?

Viral infections leading to sensorinueural hearing loss

HSV, herpes zoster. Majority of pts regain hearing in 2 weeks.

Mainstay treatment of viral induced hearing loss?
High-dose empiric steroids coupled w/ antiviral therapy
2 main causes of OME?
1) AOM. Residual fluid results in chronic inflammation triggered by bacteria already present in middle ear
2) isolated eustachian tube dysfunction. anatomic blockage form inflammation secondary to allergies, URI, trauma
What should OME in audults be considered?
cancer obstructing eustachian tube until proven otherwise and should prompt consultation w/ otolaryngologist
Roles of the eustachian tube?
1) maintain gas pressure homeostasis within middle ear by equalizing the pressure across the TM
2) helps prevent infection of middle ear and reflux of contents form nasopharynx
3) clears middle ear secretions
How is the eustachian tube different in children <6yo?
Shorter, more horizontal tube lined by flappy elastic cartilage. Also its adjacent to adenoid tissue, which is larger in childhood and predisposes child to obstruction of the ET and reflux of nasopharyngeal contents
Pathogens most common in OME?
Strep pneumo
nontypable H influenza
Moraxella catarrhalis
Most sig complication from OME?
Conductive hearing loss. Frequent infections leads to TM scarring and damage (tympanosclerosis) –> erosion of middle ear ossicles, TM perforation, cholesteatoma formation
What is tympanosclerosis?
hyaline and calcium deposition within the TM and middle ear mucosa 2/2 infection or trauma
What is the use of myringotomy?
Surgical creation of a small hole in the TM to assess OME. Pneumatic otoscopy is preferred now.
Weber and Rinne test

Weber = unilateral SNHL lateralazies to the unaffected ear. CHL lateralizes to the affected ear

Rinne = positive = air greater than bone. Negative is bone greater than air as seen w/ CHL.

Management for majority of OME cases?
Observe for 3 months
What is autoinflation?

Method to raise pressure within the nose in order to reopen the ET and may be useful in cases of ETD. Holding nose and mouth closed while forcibly exhaling

Can be trialed for ETD while awaiting spont resolution

Is there a use for antihistamines, decongestants in OME in children?
NO. Oral steroids may accelerate short term resolution, however.
Indications for tympanostomy tube insertion?
Placed through a myringotomy. Indicated in:
1) bilateral OME w/ hearing impairment
2) OME w/ sx such as vestibular probs, poor school performance, otalgia
3) recurrent AOM w/ OME
4) at risk children w/ OME
Long term consequences from untreated OM?
Permanent hearing loss, ruptured TM, mastoiditis, tempoeral bone osteomyelitis, meningitis, sigmoid sinus thrombosis, brain abscess
Ddx of cervical spine injury?
1) complete spinal cord injury = complete loss of motor and sensory function below level of lesion including perineal and anal regions
2) brown-sequard syndome = ipsilateral motor weakness; contralateral loss of pain and temperature
3) central cord syndrome = weakness and loss of sensory function in upper extremity and proximal leg muscles; distal lower extremities are typically spared
4) anterior spinal artery syndrome = paraplegia and loss of pain and temperature sensation
What is consistent with an anterior cord syndrome?

Bilateral loss of motor function = paraplegia

Loss of pain and temperature = spinothalamic tract loss

Preserved deep touch, pressure throuhgout the body

What would be signs of spinal shock?
Flaccid paralysis in extremities and absent reflexes. + loss of urinary and rectal tone
Most common level of cervical vertebrae fracture?
C2, w/ 1/3 of them being odontoid fractures. Followed by C6 and C7
Most common level of subluxation injury?
C5-6 = the area of greatest flexion and extension in the cervical spine
What dermatome level supplies the shoulders?
Nipple dermatome?
Belly bottom dermatome?
Knee dermatome?
Perianal dermatome?
Biceps reflex nerve root?
Brachioradialis reflex nerve root?
Triceps reflex nerve root?
Patellar reflex nerve root?
Achilles tendon reflex nerve root?
How can DTRs change in acute vs. later phase of spinal cord injuries?
Acute may be completely blunted but then progress to hyperactive and brisk reflexes as the inhibitory forces from UMNs are lifted
Complete spinal cord injuries at or above C3 would result in?
Inability to breathe and paralysis of all four limbs
What is radiculopathy?

Sensory or motor dysfunction caused by pathology of nerve root.

Sx: burning, tingling pain that radiates down the limb. LMN signs = loss of reflexes, weakness, diminished sensation along dermatomal distributions

Signs of myelopathy?
intermittent neck pain that radiates into shoulders or head. Will see UMN signs = hyper-reflexia, weakness and numbness in extremities, babinski
What does sacral sparing suggest about prognosis?
Better compared to when the sacral roots are affected. These govern anal sphincter, perianal sensation
What can atlanto-occipital dislocation lead to?
Quadriparesis and diaphragm paralysis
Who should be screened for atlanto-occipital dislocation?
Trisomy 21. Consider when special olympics
Pathophys of brown-sequard syndrome?

Mech: hemisection of spinal cord.

Injuriess: corticospinal = motor. Posterior = proprioception, deep touch/pressure. Spinothalamic = pain and temp

Pathophys of anterior cord?

Mech: damage to anterior 2/3 of spinal cord CLASSICALLY DUE TO SEVERE FLEXION INJURY.

Injuries = corticospinal and lateral spinothalamic bilaterally

Pathophys of central cord syndrome?

Mech: damage to central part assoc w/ SEVERE EXTENSION INJURY.

patients usually elderly and have pre-existing cervical stenosis

In the spinal cord, the central motor fibers control what part of body?
Upper extremity. Lateral aspect = lower extremity motor function
What is the NSAID mnemonic to disqualify patients from getting a c-spine radiograph?
Neuro deficit
Spinal tenderness
Distracting injury
What 3 views should be obtained w/ c-spine?
Open-mouth (odontoid)
Indications for CT scan spine?

Detect vertebral fractures and identifying hematomas or disk fragments within the spinal canal;

Also for clearance of c-spine in comatose or obtunded patients

Indication for MRI of cervical spine?
Detect injury to the spinal cord itself in pts w/ neuro deficits. And it is the only imaging modality to detect abnormality in patients w/ “Spinal cord injury without radiographic abnormalities”
What is SCIWORA?

Spinal cord injury without radiographic abnormalities.

15-25% of peds c-spine injuries. C2 most common level injured. most common age <3yo

Treatment principles for patients w/ c-spine injuries?
1) rigid cervical collar for immobilization
2) early closed reduction w/ tongs or halo traction devices
3) maintain BP w/ phenylephrine or dopamine
4) foley to monitor urinary output and prevent bladder distention in case of neurogenic urinary retention
5) venous thromboembolism prophylaxis
How do you treat neurogenic shock?

rapid infusion of crystalloid normal saline (0.9%NaCl)

bradycardia treated w/ atropine or dopamine

Findings of neurogenic shock?
Sympathetic outflow of spinal cord is disrupted = vasodilation, bradycardia, hypotension
Indications for emergent surgery w/ spinal cord injury?
Unstable vertebral fracture
Non-reducible spinal cord compression w/ deficit
Ligamentous injury w/ facet instability
Should steroids be used for acute spinal cord injury?
Most common complication of exposing anterior cervical spine for decompression surgery?
Recurrent laryngeal nerve injury = paralyzes vocal cords –> hoarseness and risk of dyspnea if bilateral
DDx for severe (GCS<8) TBI?
1) epidural hematoma = middle meningeal artery = lucid interval, rapid decline in level of consciousness
2) subdural hematoma = bridging veins, accumulates b/t dura and arachnoid membrane. Acute and chronic forms
3) intraparenchymal hematoma = in assoc w/ hypertensive hemorrhage or AVMs
4) diffuse axonal injury = accel and decel injury results in stretching of axons between the gray and white matter. Shaken baby syndrome
5) subarachnoid hemorrhage = accumulation of blood in CSF-filled subarachnoid spaces = worst headache of my life
What are signs of intracranial hypertension and uncal herniation?
Dilated nonresponsive pupils and left-sided hemiplagia (if on right side)
Criteria for TBI?
1) loss of consciousness
2) loss of memory for events immediately before or after incident
3) AMS
4) focal neuro deficits
What GCS mandates intubation?
What are signs of basilar skull fracture?
Racoon eyes = bilateral periorbital ecchymosis
Battle’s sign = retroauricular ecchymosis
GCS calculation?
Motor 6
Verbal 5
Eye 4
How does PE help you localize site of intracranial bleeding?
Paralysis will be contralateral side
Abnormal pupillary findings are ipsilateral to lesion (dot marks the spot)
What is kernohan syndrome?
when paralysis occurs on the same side as the intracranial bleed. In this case, pupil is more reliable in localizing the bleed
Which is better prognosis? Decorticate or decerebrate?
What is a concussion?

Mild TBI. Altered brain function w/ problems in memory, balance, coordination, concentration.

+/- h/a, dizziness, confusion, personality changes, irritability

What is seen in uncal herniation?
Blown ipsilateral pupil and contralateral paralysis
What is the lucid interval classically seen in EDH?
Initial LOC due 2/2 brainstem arousal centers (RAS)
Second LOC 2/2 expanding hematoma and mass effectInterval may last minutes to hours

What is cerebral perfusion pressure?
Difference between MAP and ICP
What factors affect cerebral perfusion pressure?
3 components of ICP = brain tissue, CSF, blood
Most powerful intracranial vasodilator?
CO2 level. Low Co2 via mild hyperventilation provides tempeorary therapeutic benefit for elevated ICP
Is hypotension ever caused by TBI?
No. Look for other sources
Cushings triad?

Tri: HTN, bradycardia, irregular resp rate in response to increased ICP

W/ increased ICP, HTN increases to maintain cerebral perfusion pressure –> negative feedback at carotid sinus –> bradycardia

Indications for head CT w/ TBI?
*GCS 9-12 and 3-8 = non contrast CT
*mild brain injury w/ risk factors
What inducing/paralyzing agents are CI in TBI?

Succinylcholine and ketamine = they can increase ICP

Rocuronium and etomidate are better options

Normal ICP?
5-15mmHg. Treatment indicated for pressures >20mmHg in adult patients and lower levels for children
Preferred method of ICP monitoring in setting of trauma?
What do you need to follow in patients w/ severe TBI?
DIC. Follow coag labs and platelet counts
Role of hyperventilation in increased ICP?

Goal of PaCO2 = 30-35. This can reduce ICP through cerebral vasoconstriction.

Do not reduce <30 as it may decrease cerebral blood flow. This method should only be used mildly and sparingly until other ICP methods are found

Medical treatments for intracranial HTN?
1) elevate head of bed 30-45 degrees
2) loosen cervical collar
3) hyperthermia should be treated if present
5) can paralyze patient and induce hypothermia
How does mannitol work?

Increases tonicity of extracellular space –> shift of water from IC space to EC space

Also reduces hematocrit and blood viscocity which increases cerebral blood flow and reduces ICP

in what patients do you want to avoid mannitol in?
Hypotension and hypovolemia
How do tumors produce edema?
Inflammation (cytotoxic edema) and will respond to corticosteroids
How does trauma cause edema?
Triggers abnormal vasoregulation and causes brain capillaries to beocme abnormally leaky (vasogenic edema). NOT RESPONSIVE TO CORTICOSTEROIDS
When is craniotomy indicated?
Acute subdural and epidural hematoma that are asociated w/ midline shift >10mm, hematoma thickness >5mm, or ICP >20mmHg
Criteria for brain death?
GCS <3. 1) euthermic >32.2C
2) PaO2 >90mmHg
3) SBP >100
4) pt cannot be sedated or paralyzed
5) absence of brainstem reflexes
6) no response to deep central pain
7) agreement of two physicians
8) no spont resp w/ a PaCO2 >60 when discontinued from ventilator
Indications for head CT in children?
1) GCS <14
2) suspected basilar skull fracture
3) palpable skull fracture
4) AMS
What fracture most likely will give you radial nerve injury?

Middle and distal third humerus fractures, where it can be stretched from bony disconnection or become entrapped between bone ends

Spares the triceps at this point bc radial nerve gives off triceps branch proximal to this site

What presentation with radial nerve injury 2/2 humerus fracture?
Wrist drop = weakness in extension
Loss of MP joint extension
Sensory loss over the dorsum of the hand
Presentation of fat embolism syndrome?

24-72hrs following trauma.

Triad = resp sx (hypoxemia, dyspena, tachypnea are early manifestations), neuro changes (confusion, AMS, seizures, paralysis), reddish-brown petechial rash (in 50-60% of cases)

What causes the rash in fat emnbolism syndrome?
Extravasation of erythrocytes secondary to occlusion of dermal capillaries by fat emboli
Dangerous sequela for a tibia fracture?
Compartment syndrome. Remember 6 P’s. POOP, pressure, paresthesia, pulselessness, poikilothermia, paralysis
What fracture must you rule out in all femur fractures?
Concomitant femoral neck fracture. Missing it = avascular necrosis if not treated
What is neuropraxia?

Mnimal injury (myelin) but not axon or nerve sheath.

Temporary nerve conduction block; loss of motor and sensory function, but not autonomic. Full recovery expected hours to months

What is axonotmesis?

Myelin plus axon is disrupted, nerve sheath is intact.

Recovery often incomplete, weeks to months, axon sprouts within nerve sheath

What is neurotmesis?
Myelin, axon, nerve sheath damaged. Recovery requires surgery or results in permanent paralysis
How fast does injured axon regenerate?
What nerve injury does wallerian degeneration occur with?
Axonotmesis, neurotmesis. NOT neuropraxia
What nerve is classically injured w/ humeral head/proximal humerus fracture?
Axillary. Will see impaired arm ABduction
What nerve is classicially injured w/ fracture to mid-shaft of humerus?
Radial. Will see impaired extension of elbow, wrist
What nerve is injured in supracondylar (humerus) fracture?
Anterior interosseus nerve (branch of median). Will see impaired handgrip
What nerve is injured w/ distal radius fracture?
Median. Will see impaired thumb opposition
What nerve is injured w/ hip fracture dislocation?
Sciatic (peroneal division). Will see impaired knee flexion
What nerve is injured w/ fracture to fibular head?
Fibular/peroneal. Will see foot drop, impaired eversion/dorsiflexion
Increased grade of open fracture correlates w/?
Increased risk of infection, nonuion, and amputation
What patients w/ open fracutres should be given abx?

All open fractures.

Grade I and II main risk for G+ = 1st gen cephalosporin
Grade III = add aminoglycoside

What abx for open fractures in farm accidents or soil-contaminated wounds?


Also consider tetanus immune globulin and tetanus toxoid

What is open vs. closed reduction?

Reduction = putting displaced bones back to normal anatomic positions.

Open = direct manipulation of bone through surgical incisioin

Closed = external manipulation of limb manually or with fracture table

What fracture is at greatest risk for hemorrhagic shock?
Pelvic fractures
Optimal timing of femur fracture repair?

2-12 hours of injury w/ polytrauma that are heme stable.

Definitive management in adult = intramedullary nailing

Do all femur fractures require fixation?
No. Children 3-5yo can be managed w/ spica casting
Management for fat embolism syndrome?
Suportive care, ventilatory support, early stabilization of fractures
Ddx of acute knee pain following trauma?
1) hemarthrosis, bone infarct = hx of hemophilia or SCD
2) septic arthritis = fever, unwillingness to bear weight or range a knee held constantly around 30degrees flexion. N gonorrhea in sex active
3) acute osteo = fever, constitutional sx; IVDU, children, immunocomp
4) neoplastic = constitutional, more insidious onset
5) inflammatory = RA; bursitis, tendinitis
6) traumatic = onset of pain at time of acute sporting or vehicular injury; unwillingness to bear weight
7) iatrogenic = recent knee injection
Ligamentous injury vs. meniscal tears?
Ligamentous has IMMEDIATE swelling;
Meniscal develops swelling the next day
If patient is able to bear weight following trauma to knee, what is less likely?
What does anterior knee laxity on physical exam suggest?
ACL disruption. What is associated w/ it commonly? meniscal tear
How can you test for meniscal tear?
McMurray sign = pain, palpable/audible snap w/ compression and axial rotation maneuver of the knee while extending it from a fully flexed position
What can test for ACL tears?
Anterior drawer or Lachmans test
What tests for PCL tears?
Posterior drawer test;
tibial sag on 90 degrees felxion
McMurray test tests for?
Meniscal cartilage tears
What suggests LCL tear?
Varus instability = knee pressed laterally, foot pressed medially, significant laxity here = LCL tear
What suggests MCL tear?
Valgus instability. Opposite of varus
A posterior blow to the lateral knee is history for?
ACL tear
Lateral blow to knee is history for?
MCL tear
Locking or catching w/ range of motion of the knee signifies?
Meniscal tears, especially mobile flaps
What vessels can be affected in knee dislocations?
Popliteal vessels -> dysvascular limb –> amputation
What is the most common neurologic finding in trauma to knee?
Foot drop w/ damage to peroneal nerve
What must be considered w/ recurrent fractures?
Neoplastic leasions weaking bones.
Red vs. white zone of menisci?
The menisci receive blood supply from the lateral side (outside in) to cover about 20-30% of their diameter. So injuries on the outer rim are more likely to heal (red zone) than the inner central part which are called the white zone
Popping noise s/p traumatic injury in knee most likely to be?
ACL rupture
A dashboard knee injury in MVC would result in?
The anterior force would create a PCL tear and a positive posterior drawer test
If patient is unwilling to bear weight and you see no trauma or fracture on xray, what do you do?
Suspect septic arthitis and perform arthrocentesis
If patient cant actively extend knee but examiner can do so passively, what does this suggest?
Disruption of the quadriceps or patllar tendon; or fracture of the patella or tibial tubercle
Pain along the patellar tendon near its attachment to the patella with INTACT extensor mechanism of the knee suggests?
Patellar tendinitis
What radiographic sign is pathognomonic for ACL injury?
Segond fracure or small fleck of bone avulsed from the lateral tibial plateau
Radiographic features of osteoarthritis? Why consider after ACL injury?
*consistent w/ degenerative arthritis of knee = joint narrowhing, osteophytes (bone spurs), subchondral sclerosis, subcondral cysts
*must recognize these as ACL surgery is NOT appropriate in these settings
Pseudogout vs. gout crystals?

Pseudogout = calcium pyrophosphate = positively birefringent

Gout = monosodium urate = negatively birefringent

WBC counts in synovial fluid?
<200 = normal.
Inflammatory = 200-50,000
Above 50,000 = infectious
What can you use to CONFIRM suspected ACL tear
MRI. Also used for menisci
How do you nonsurgically manage ALC tears?
How does reconstruction of ACL work?
Use of a tendon graft placed into bone tunnels across the knee in the femur and the tibia approximating the normal position of the ACL
Long term goal of ALC resoncstruction?
Slow the wear and tear breakdown of knee cartilage occuring w/ abnl knee motion w/ ACL dysfunction
Lyme disease presentation?

Early: chills, fatigue, erythema chronicum migrans (bullseye)

Late: chronic synovitis, monoarthtirtis or oligoarthritis, aseptic meningitis

Psoas abscess H&P?
Fever, patient holds thigh in sligh hip flexion and internal rotation;
passive hip extension which stretches the psoas muscle is met w/ sig pain;
assoc w/ osteo of spine or PID
Juvenile idiopathic arthritis H&P?
Nonmigratory arthropathy affecting one or more joints for >3mo;
morning stiffness, fevers
Transient synovitis H&P?
Hx of URI in presence of hip pain;
most common cause of hip pain during childhood;
usually worse upon awakening and improves throughout the day;
Slipped capital femoral epiphysis H&P?
Obsese, adolescent male aged 10-16yo presenting w/ grown pain, painful limp, externally roated hip, not irritable
Which tumors metastasize to bone?
“BLT and Kosher Pickle”
Breast, lung, thyroid, kidney, prostate
RF for SCFE?
Age 10-16;
AA and polynesian ethnicities
Antalgic gait = painful limp
Groin pain that radiates to thigh/knee
Decreased internal rotation; internal rotation maneuvers re-create pain
What if patient holds thigh in slight hip FLEXION and INTERNAL rotation?
Along w/ fevers and signs of infection = psoas abscess w/ reflexive contracture of the psoas muscle due to spasm
What is a psoas abscess usually a sign of?
Osteomyelitis of spine, PID
What is a hip held in flexion and internal rotation after a traumatic event, without signs of infection?
Hip dislocation until proven otherwise and is a surgical emergency. Real risk of avascular necrosis
What endocrine disorders are assoc w/ SCFE?

Hypothyroid, growth hormone abnl, renal osteodystrophy, hypopituitarism, hyper/hypoparathyroid

These weaken the physis leading to slippage

Who to work up: young <10yo and thin <50% weight

What may cause pain to radiate to the groin?
Hernias, testicular disease, ectopic pregnancies
In clarifying hip pain, where should true hip joint pain present?
Medially, felt in the groin region
In clarifying hip pain, what does pain at the lateral aspect of thigh or buttock suggest?
Trochanteric bursitis, neurogenic claudication, sciatica, or sacroiliac joint pathology
Most common cause of hip pain during childhood?

Transient synovitis. Most commonly <5yo

Tx: observation as it is self-limiting

what can corticosteroids predispose pediatric population to?
Avascular necrosis of femoral head AKA osteonecrosis
RF for secondary ostenecrosis of the hip?

SCD and Gaucher Dz

Aduts: alcoholism, dysbarism, trauma, corticosteroid use

Child w/ longstanding leg legnth discrepancy can develop?
Compensatory scoliosis
What test would suggest sacroiliac joint pathology?
FABER = flexion, abduction, external rotation while patient is supine
What is the trendelenburg test?
Patient standing is asked to lif one leg. Pelvis should remain level, but if it falls or dips inferiorly on the side of the raised leg –> abductor muscle weakness on side of standing leg
Legg-Clave-Perthes disease?
Idopathic osteonecrosis of femoral head. Typically ages 4-8
What is the Kocher criteria for septic arthritis?
Fever >38.5C
Inability to bear weight
ESR >20
WBC >12K3% with 1. 40% with 2. 93% with 3. 99% with 4

Management for Dev dysplasia hip if 0-6mo?
Pavlik Harness
Management of dev dysplasia of hip if 6-18mo?
Surgical closed v.s open reduction w/ spica casting
Complications of SCFE surgery?
If screw too short = further slippage and dysfunction may occur
If screw too long = destroys cartilage aka chondrolysis
Avascular necrosis
Thoracic outlet H&P?
Positive adson’s or wright’s test; ulnar-sided symptoms most likely
Medial neuropathy H&P?
often diffuse and bilateral; hx of cancer or its treatment, DM, HIV, nutritional deficiency
History of carpal tunnel?

Nighttime dysestehsias in the median nerve distribuition to only one hand without prior injury or congenital defect + isolated thenar muscle wasting

Usually bilateral, rarely in median nerve distribution exactly, occurs in association w/ overlapping aches, pains, medical conditions like diabetes

What is Durkan’s median nerve compression test?
Direct compression over the median nerve at the wrist using the thumb. Positive test if patient reports new or worsening numbness or tingling in some portion of the median nerve distribution on the hand within 30-60 seconds.
Most sensitive test for carpal tunnel?
Durkan’s median nerve compression test
How do you tell difference between proximal median nerve compression at elbow from compression at carpal tunnel?

Palmar cutaneous branch of median nerve branches before the carpal ligament. It innervates the thenar eminence.

CT will NOT show sensory dysesthesias here, whereas pronator syndrome will

If presentation suggests thoracic outlet syndrome, what are you gonna look for on CXR?
Pancoast tumor of the lung
How does myelopathy present in upper extremitiy?
Hand pains and dysestheisas, but NOT neck pain
Thumb is which finger number?
Origin of median nerve from cervical spine roots?
Boundaries of the carpal tunnel?
Carpus dorsally
Transverse carpal ligament volarly = roof
What structures course through the carpal tunnel?
9 tendons and 1 nerve:
4 flexor digitorum superficialis
4 flexor digitorum profundus
1 flexor pollicis longus
1 median nerve
RF for carpal tunnel?
Age 40-60
Obesity, pregnancy, smoking, repetitive activitis, RA, hypothyroid, alcoholism, CKD
What innervates thenar muscles?
Recurrent motor branch of median nerve. Check this; if wasting = long standing or severe carpal tunnel disease leading to denervation of the thenar muscles
3 stages of median nerve compression?
1) sensory sx (numbness, pain, tingling) at night
2) sx during day
3) motor sx of weakness and/or muslce wasting
What does a median nerve laceration at the elbow result in?
Hand of benediction when trying to form a fist
What is happening in an ulnar claw?
All intrinsic muscles are denervated except the radial two lumbricals.
What is froment’s sign?
Positive when the examiner can easily pull a flat piece of paper from the hand of the patient who uses thumb IP flexion via the FPL tendon of the median nerve to grasp the paper
What systemic condition is often assoc w/ CTS?
What test do you order if patient cannot have MRI in evaluating carpal tunnel?
CT myelogram. Involves dural puncture and injection of contrast into the thecal sac to outline spinal cord and nerve roots
Initial treatment of carpal tunnel?
Splinting of the wrist in a neutral position. NSAIDS and activity modifications
Second line treatment for CTS?
Injection w/ local anesthetic and corticosteroid medication. Response is good prognostic indicator for improvement w/ surgery if later needed
Indications for surgical intervention for CTS?
Failure to respond adequately to conservative nonoperative management or thenar motor involvment
Gold standard treatment for CTS?
carpal tunnel release which is surgical cutting of the transverse carpal ligament, the roof of the carpal tunnel. Performed through a small open incision or endoscopically
Complications to carpal tunnel release?

Injuries to median nerve; recurrent motor branch or palmar cutaneous branch;

chronic pain including neuroma, scar;

infection, hematoma, inadequate release


RF for cancer common to SCC, BCC, and melanoma?
Excessive UV light, particularly UVB.
Melanoma = blistering subnurns and overal sun exposure
Fair colored skin, hair, and blue eyes
Genetic conditions assoc w/ increased risk of skin cancer?
Xeroderma pigmentosum leads to photosensitivity due to deficient repair of DNA damaged by UV radiation. High rate of melanoma, BCC, SCC at early age
Is hair growth on lesion consistent w/ melanoma?
No. suggests a benign nevus. Melanomas destroy hair follicles
Chronic skin inflammation is a known risk factor for what cancer?
On what areas of skin are melanomas most likely to present in NONWHITES?
Nonexposed skin w/ less pigment = palms, soles, mucous membranes, nail regions
Most common site of melanoma in men vs. women?
Back. Legs in women.
Most common site of digital melanoma?
Great toe. Amputation and sentinel lymph node is preferred treatment
Melanocytes are derivatives of?
Neural crest cells
Most common skin cancer?


Melanoma accounts for most deaths.

Most common precancerous skin lesion?
Actinic keratosis
What is Bowen’s disease?
SCC in situ. No potential for metastasis
Breslow’s thickness 5 year survival
<0.75mm = 95-100% 0.75-1.5mm = 80-96% 1.5-4.0mm = 60-75% >4.0mm = 50%
Metastatic risk of BCC?
Locally destructive; mets are rare
Most common site for melanoma to metastasize?
Other areas of skin, lung, liver, brain, bone
Most common metastasis to the small bowel?
LDH in melanoma?
It is a prognostic indicator in melanoma and has been found to be a sign of liver mets
Poor prognostic indicators w/ melanoma?
Thicker lesions, ulceration, location on trunk, male gender
Primary therapy for BCC/SCC? Margins?
Excisional bipsyy.
BCC 3-5mm
SCC 5-10mm
Which BCC has the worst prognosis?
Morpheaform and is characterized by collagenase production
What is Mohs surgery?
Tangential excisoins of lesion till margins are negative. Excellen cure rates, accurate margins, tissue-sparing procedure
Ddx of swelling and erythema on leg x3d?
1) necrotizing soft tissue infection = acute infection of the deep fascia, with crepitus, bullae, necrosis of subQ tissue, mixed flora
2) cellulitis = infx of deep dermis and subQ fat presenting w/ redness and erythema w/o tissue distruction characteristic of NSTI
3) cuteneous anthrax = painless or pruritic eschar surrounded by edema
4) hypersens reaction = no fever or leukocytosis. Look for history o fexposure to platns or animals
5) DVT = leg. look for hypercoag, immobility, inflammatory state
6) sweet’s syndrome = acute eruption of tnder erythematous plaques with vesicles, fever, neutrophilia. Caused by treatment w/ G-CSF
7) pyoderma gangernosum = neutrophilic infiltration of skin, exquisitely painful lesions
8) erythema multiforme = erythematous or purpuric plaques and bullae w/ central clearing
9) stasis dermatitis = dermal fibrosis and brawny edema secondary to venous incompetence
DM patient w/ painful, erythematous, swollen leg with bullae and violaceous skin along w/ radiographic evidence of gas bubbles?
Necrotizing soft tissue infection (NSTI)
RF for NSTI?
DM, malnutrition, IVDU, obesity, chronic alcohol abuse, CLL, chronic steroid use, renal failure, peripheral arterial dz, cirrhosis
Implication of bullae and violacious skin in NSTI?

Bullae implies partial tissue death within layers of the skin that allows for collection of fluid between tissue layers

Violaceous skin implies discoloration secondary to ischemia

Hard signs of NSTI?
Hypotension, crepitus, skin necrosis, bullae
Cellullitis vs. NSTI?
Cellulitis reqs abx; NSTI emergent surgical debridement
What organnisms are seen in NSTI?
Type 1 = polymicrobial
Type 2 = Group A strep
Type 3 = clostridium perfrigens
What is clostridium septicum associated w/?
occult malignancies, most often colon cancer
Term for NSTI that involves the scrotum or perineum?
Fournier’s gangrene
Initial steps in managing NSTI?
IV fluids, broad spectrum abx, aggresive surgical debridement = gold standard
Intraoperative findings that confirm NSTI?
Murky fluid, gray discoloration of fascia, lack of bleeding from fascia
Current recommendations of a second look operation in NSTI?
24 hours after initial debridement to ensure that the infection has not reemerged
Ddx surgical causes of neonatal respiratory distress
1) choanal atresia = cant place NGT
2) congential diaphragmatic hernia
3) cystic lesions
4) esophageal atresia + transesophageal fistula = scaphoid abdomen, excessive salivation, stomach bubble
5) pneumothorax
What accounts for 40% of neonatal resp distress in term babies? Premies? Postterm?

Transient tachypnea of newborn 2/2 residual pulmonary fluid in the lung after tissue delivery;

Hyaline membrane disease/respiratory distress syndrome 2/2 decrease in surfactant prod by type 2 alveolar cells

Meconium aspiration syndrome

Pathophys of congenital diaphragmatic hernia?
Failure of septum transversum to completely divide the pleural and coelomic cavities during fetal development. Leads to herniation of intra-abd contents. Pulmonary hypoplasia results from decreased pulmonary mass and bronchiolar branching and dysfunctional surfactant production
Most common variant of congenital diaphargmatic hernia?

Bochdalek hernia = posterolateral defect.

Anteromedial defects aka Morgagni are mostly asymptomatic and present w/ GI sx or obstruction if sx.

Most extreme form of congenital diaphragmatic hernia?
Diaphragmatic agenesis = complete absence of hemidiaphragm
How does CDH affect neonatal resp system upon first breath?

The pulomnary hypoplasia combined w/ muscular hyperplasia of the pulmonary arterial tree causes high resistance in the pulmonary arterial bed that does not reverse w/ the infeant’s first breath

–> hypoxemia, acidosis, hypotension –> pulmonary vasoconstriction –> decreased gas exchange and carbon dioxide retention

Best initial diagnostic test in newborn resp distress?
Placement of orogastric tube followed by CXR.
Timing for surgical repair in CDH?

Pts w/ mild sx requirling minimal support = 48-72 hours

In most pts, it is generally delayed. Provide cardiopulmonary support and avoid lung injury while awaiting lung maturation and reversal of pulmonary hypertension. Time will improve.

Ddx of bilious emesis in newborn
1) duodenal atresia = double bubble on ACR, no distal bowel gas
2) hirschsprung dz = transition zone on contrast enema, absence of ganglion cells w/ hypertrophied nerve trunks on rectal bipsy
3) imperporate anus = bowel gas present, no anus on physical exam
4) inarcerated inguinal hernia
5) jejunoileal/colonic atresia = distal obstruction, microcolon on contrast enema
6) malrotation
7) meconium ileus/plug = no passage of meconium, distended abd
8) necrotizing enterocolitis
Significance of bilious vomiting?

Reflux of enteric contents from distal to the ampula of Vater. Pylorus is patent and rules out common stomach pathology such as pyloric stenosis.

Surgical problem until proven otherwise

Ddx for polyhydramnios?

Impaired swallowing = CDH, duodenal atresia, esophageal atresia, gastrochisis, neck mass, TEF)

Decreased urine production = maternal diabetes, twin pregnancy

What does meconium consist?
Lanugo (fine body hair), amniotic fluid, bile, mucus, and shed epithelium
What percent of duodenal atresia will be proximal to ampulla of vater?
20%. Sx: nonbilious vomiting instead of bilious
Associated anomalies of duodenal atresia?
Down Syndrome 28%
Annular pancreas 23%
CHD 23%
Malrotation 20%
First imaging to obtain in suspected duodenal atresia?

in stable patient: 2-view plain abd radiograph after naso-or orogastric tube placement

unstable: abx and OR for exploratory laparotomy

If double bubble is seen + distal bowel gas, what is the diagnosis?
Malrotation + midgut volvulus
Inadequate preoperative resuscitation for duodenal atresia can result in?
Worsening of exisiting hypotension or seizures due to electrolyte imbalances, end organ damage from hypoperfusion, or CV collapse
If cardiac defects are found concomitantly w/ duoudenal atresia, what do you do?
Repair cardiac stuff first
Ddx for bilious emesis in an infant
1) adhesions = prior abd surgery, dilated loops of bowel w/ transition point to decompressed bowel on contrast study
2) enteric duplication cyst = fluid filled structure not contiguous w/ stomach or small bowel
3) gastroenteritis = fever, diarrhea, initial nonbilious emesis
4) hirschsprung
5) ileus secondary to other medical disease
6) incarcerated inguinal hernia
7) intussuception = target sign, currant jelly stools
8) malrotation w/ midgut volvulus = corkscrew appearance of duodenum on contrast UGI
What percent of children w/ malrotation present before 1 month of age?
33% between 1 mo and 1 yo
RF/assoc of malrotation?
Heterotaxy syndrome
Duodenal atresia
If plain abd XR shows free air under diaphragm, what do you do?

There is perforation. Urgent laparotomy

If no air is seen –> UGI contrast study to visualize duodenum and proximal small intestine

Define the midgut

Second part of duodenum to 2/3 way across the transverse colon.

Supplied by the SMA

Classic variant of malrotation?

Ligament of Treitz is situated to the right of midline and the cecum fails to rotate the final 180degrees down the right lower quadrant, placing it in the epigastrum

Corkscrew appearance

Important imeediate management principles in midgut volvulus?
*orogastric or nasogastric tube to decompress stomach
*broad spectrum abx
*fluid resuscitation
*rugent laparotomy
Delays in OR in midgut volvulus may result in what?
Complete infarction –> necessitating small bowel resection –> short bowel syndrome –> lifelong parenteral nutrition OR small intestinal transplantation (may develop TNP-associated liver failure and require liver transplantation as well)
Sequence of Ladd’s procedure for midgut volvulus?
1) gently rotate the gut counter-clockwise
2) divide peritoneal attachments from RUQ to the ascending colon
3) straighten duodenum and examine for intrinsic obstruction
4) small bowel is positioned on the right side of abd and large bowel on the left, in complete nonrotation
How can you exclude duodenal stenosis or atresia in infants w/ malrotation?
A large bore orogastric or nasogstric tube must be passed through the second part of the duodenum during surgery
Ddx for infant w/ nonbilious emesis
1) acute gastro
3) metabolic (CAH, electrolyte imbalances, glycogen storage dz)
4) pylorospasm
5) antral web
6) enteric duplication cyst
7) pyloric atresia / stenosis
Classic hx for hypertrophic pyloric stenosis?
Projectile, nonbilious vomiting. Progressively more forceful and voluminous. Typically between 4-8 weeks old
Classic PE findings for pyloric stenosis?

Dehydrated, sunken fontanelle, olive shaped mass in RUQ

Olive = thickened and elongated pyloric muscle

Pathophys of hypertrophic pyloric stenosis?
Hypetrophy and hyperplasia of circular muscle layer of the pylorus –> narrowing and elongated –> gastric outlet obstruction –> smooth muscle of stomach hypertrophies and dilates in response to vigorous peristalsis against an obstructed pylorus
First imaging study in hypertrophic pyloric stenosis?

If no palpable mass = US (careful in premature or small infants because this grows over time and may lead to false-negative)

If equivocal = UGI contrast study (have high risk of aspiration in infants)

Electrolyte abnl in hypetrophic pyloric stenosis

Hypochloremic, hypokalemic metabolic alkalosis


Important immediate management issue in hypertrophic pyloric stenosis?
*secure IV access and begin fluid resuscitation
*once child urinates, 20mEq/L KCl should be added to IV fluids
Procedure of choice for pyloric stenosis?
Ramstedt pyloromyotomy. Incision is made in pylorus through overlying serosa and thickened pyloric muscularis. Muscle is spread apart until intact submucosa and mucosa are seen. Instill air or methylene blue to confirm there is no leak
Why may a patient vomit after resuming feeds following pyloric stenosis surgery?
Postop edema around pylorus. Should resolve within 3-4 days, and if it does not, then this suggests incomplete pyloromyotomy and may need repeat operation
If emesis persists beyond 3-4 days following pyloromyotomy, what do you order?
UGI evaluation
What can result if incision is made too deep in pyloromyotomy?
Leakage of gastric secretions and/or enteric contents –> may present w/ fever and tachy post op w/ feeding intolerance and leukocytosis –> may develop peritonitis and sepsis
Ddx for newborn w/ abd wall defect
1) gastroschisis = medial defect w/ evisceration of abd contents. NO MEMBRANE over contents. To the RIGHT of umbilical stalk. Dx impossible <12wks
2) omphalocele = midline abd defect w/ herniation of abd contents; COVERED BY AMNIOPERITONEAL MEMBRANE; umbilical cord inserts into membrane; dx possible <12wks if liver herniation present
3) bladder or cloacal exstrophy = extra-abd/pelvic sac containing herniated hemibladders, urethra, kidney, and intestine; INFERIOR to umbilical stalk
4) prune belly syndrome = abd wall hypoplasia; assoc w/ hypoplastic prostate, bilateral undescended testes, infertility, bladder outlet obstruction
5) urachal abnormality = communication of bladder and anterior abd wall; assoc w/ omphalocele and NTDs
Mother RF for gastrochisis?
Young age, caucasian, low BMI, singleton prego, recent tobacco use, frequent UTIs
Gastroschisis vs. omphalocele?
Location: G = Right; O = umbilical, epigastric, hypogastric
Defect size: G = <5cm; O = often large
Membrane: G = absent; O = present
GI funct: G = ileus; O = normal
Mother RF for omphalocele?
<20yo or >40yo; high BMI; SSRI use
Pathophys of gastroschisis?
Vascular accident within the umbilical ring leading to local defect in developing body wall and evisceration
Pathophys of omphalocele?
Arrest of lateral-body fold migration and body wall closure. Persistent herniation of viscera contained within a sac that never returned to the abdomen during development
Significance of liver being involved in omphalocele?
Suggests chromosomal abnormality is unlikely
Why is gastroschisis more urgent?
Not covered by membrane –> markedly inflammed bowel
What assoc are significant in omphalocele?
Pentalogy of Cantrell, trisomy 13, trisomy 18
What is a dacron-coated silastic silo?
Used for gastroschisis and large omphaloceles over the herniated contents to allow gradual resolution of visceral inflammation and reduction into the peritoneal cavity
What needs to be avoided in protecting protruded bowel?

Moist gauze dressings bc can lose sig fluid and heat without a watertight plastic dressing.

Saran Wrap reasonable if silo takes long to acquire

What signs should you look for in observing infant post eviscerated abd content repair?
Low urine output, insufficient ventilation, positive fluid balance = COMPARTMENT SYNDROME
Ddx for excessive drooling/feeding intolerance in newborn?
1) choanal atresia
2) cleft palate
3) esophageal atresia w/ or w/o TEF
4) esophageal web or ring
5) food sensitivity = normal anatomy; accompanying rash or diarrhea, specific foods
7) laryngotracheoesophageal cleft = midline defect between posterior wall of larynx/trachea and anterior esophagus
8) mediastinal or tracheal compression
9) neuro disorder = patent esophagus, uncoordinated peristalsis on swallow study
Focal infiltrates on newborn w/ esophageal atresia w/ TEF suggests?
Pneumonia secondary to aspiration of gastric contents or feedings
How may patients w/ H type EA w/ TEF present?
Later in life w/ recurrent pna or resp distress with feeding
Pathophys of EA w/ or w/o TEF?
Defect in the dev of longitudinal tracheoesophageal fold that separates the most caudal part of the primitive foregut into the trachea and esophagus
Anomalies found in VACTERL?
Vertebral = hypoplastic or hemivertebrae
Anorectal = anal atresia or imperforate anus
Tracheoesophageal = TEF
Esophageal = esophageal atresia
Renal = renal agenesis, hypoplastic/dysplastic kidney, renal ectopia
Limb = displaced or hypoplastic thumb; polydactyly; syndactyly
Most common EA and TEF?
Type C = proximal esophageal pouch w/ distal TEF. 85% of cases
CHARGE anomalies?
Heart defect
Atresia choanae
Retarded growth and development
Genital abnormality
Ear anbl
Best initial diagnostic test in EA +/- TEF?

CXR after placement of nasogastric or orogastric tube. Need anteroposterior PLUS lateral to confirm that the tube is curled in the upper esophageal pouch and not the trachea or larynx

*can ID right sided aortic arch which will change surgical approach (typically done via right thoracotomy incision)

How can EA be manifested prenatally on ultrasound?
Preoperative management for EA +/- TEF?
1) if in resp distress = intubation and mech ventilation
2) minimize risk of aspiration via continuous suctioning of blind upper esophageal pouch
3) elevation of infant’s head
4) abx if they have developed pna
5) gastrostomy tube may be placed to prevent further reflux into trachea
Timing of surgical repair for EA +/- TEF?
If healthy = within first few days of life
If severe anomalies or resp failure = ligation of TEF and placement of gastrostomy tube for feeding. Definitive repair shoul be delayed until clinical status improves
Definitive surgical treatment for EA +/- TEF?
Surgical division of fistula tract w/ repair of trachea and primary anastomosis of the esophagus
Complications after surgical repair of EA +/- TEF?
15% have a leak at the esophageal anastomosis
All have GERD w/ increased risk for Barrett’s esophagus and esophageal cancer. Of these, 30% will need anti-reflux procedure long term
Significance of azygous system in EA +/- TEF repair?
It is divided to allow access to the TEF. Some patients, rarely, have IVC that drains into the right atrium via the azygous system. In this case, interrupting the IVC will disrupt all venous return from abdominal viscera/lower extremities and lead to patient demise
What do you need to avoid in presence of TEF?
Intubation and mechanical intubation bc gastric and abd distention 2/2 air
Ddx of scrotal pain?
1) testicular torsion = tender, swollen testicle displaced superiorly. ABSENT cremasteric reflex. N/v
2) torsion of testicular or epididymal appendage = common cause of hemiscrotum in child. Blue dot sign is classic fingind. Onset more gradual. MAINTAINED cremasteric reflex
3) epididymitis and/or orchitis = pain relieved by supporting the scrotum. Classically from mumps
4) hydrocele = fluid in tunica vaginlasis. TRANSILLUMINATES
5) varicocele = bag of worms. DOES NOT TRANSILLUMINATE
6) appenciitis
7) fournier’s gangrene = uncontrolled DM/immunocompromised
8) traumatic testicular rupture
9) testis tumor
Pathway of cremasteric reflex
When medial thigh is stroked –> sensory fibers from femoral branch of genitofemoral nerve (L1-L2) are stimulated –> travels to spinal cord to L1/L2 to activate cremasteric muscle –> ipsilateral elevation of the testis
What is Prehn’s sign?
Pain relief w/ elevation of scrotal contents. Classically seen in epididymitis; negative in testicular torsion
What is blue-dot sign?
Pathognomonic for testicular or epididymal appendage torsion
4 cardinal sx of testicular torsion?
Testicular pain <24 hrs duration
Superiorly displaced testicle
Absent cremasteric reflex
Differences b/t testicular torsion and appendix testes torsion?

TT: sudden onset; absent cremasteric; management = detorsion followed by bilateral orchioplexy

ATT: gradual onset, blue dot sign; present cremasteric; management = NSAID, ice packs, scrotal support

What congenital defect predisposes children to devlop testicular torsion?
Bell-clapper deformity = failure of normal posterior anchoring of the gubernaculum, testes, epididymis, allowing testes to freely rotate and swing within the tunica vaginalis of the scrotum similar to the gong inside a bell. Usually present bilaterally
If suspicion for testicular torsion is low, what should you do?

UA to r/o UTI or epidymo-orchitis

Doppler blood flow US to assess presence of torsion

What do you look for in doppler ultrasound in trauma setting of test torision?

Determine if tunica albuginea is violated as this would warrant surgical repair.

Absence of arterial flow suggests torsion or severe trauma that has disrupted the blood supply

What can be done in the ED if duration of sx is <6h for testicular torsion.
Manual detorsion by twisting testis laterally. Can be followed w/ elective orchiopexy (fixing testicle to scrotum to prevent retorsion)
How do you manage minor trauma to testes?
Scrotal support, ice packs, NSAIDs, bed rest
Operative indications for testicular trauma
1) violation of tunica albuginea
2) rapidly expanding testicular hematoma
3) avulsion
4) scrotal degloving
5) absence of blood flow as evidenced on doppler US
How can loss of testicle lead to infertility?
Formation of antisperm antibodies w/ subsequent decrease in sperm count and decrease in motility. Not common.
Ddx Scrotal masses involving the skin?
1) epidermoid or pilar cysts = painless, slow growing, mobile, fluid filled nodules. Occur in areas that have a lot of hair such as scrotum and chest
2) SCC = ulcerated, nodular mass w/ no telagniectasias. 5th/6th decade; assoc w/ HPV and occup exposure (soot, oil, petroleum workers)
Ddx scrotal masses involving spermatic cord
1) indirect inguinal hernia
2) hydrocele = painless, transilluminates
3) varicocele = bag of worms, assoc w/ infertility
Ddx scrotal mass involving the epididymis?
1) epididymitis = painful, tender, Prehns sign
2) spermatocele = aka epididymal cyst. Painless, fluid filled, distinct from testis, may transilluminate
3) torision fo testicular epidiymal appendix
ddx scrotal mass involving the testes?
1) orchitis = painful, tender testicle. MUMPS, STD
2) testicular torsion
3) testicular cancer = firm, painless testicular mass that does not transiluminate. Germ cell tumor (usually within the testicle)
How can specific constitutional sx associated w/ painless testicular mass help you distinguish different metastases?

Back/abd pain, weight loss, nausea = retroperitoneal lymph node mets

Cough, SOB = pulmonary mets

RF for testicular cancer
Personal hx of testicular cancer
FHx of testicular cancer
White race
Which benign testicular processes are benign?
Spermatocele, varicocele, hydrocele
Most common subtype of testicular tumor?
Seminoma, a germ cell tumor. Malignant.
Features of seminoma
Most common type in adults, highly responsive to radiotherapy. Metastasize late; excellent prognosis. Rare hCG production
Organisms causing epididymitis <35yo?
Chlamydia trachomatis (D-K)
N gonorrhea
Organisms causing epididymitis >35yo?
E coli
What causes gyencomastia w/ testicular cancers?

Choriocarcinoma, a germ cell tumor = hCG ectopic production

–> breast development; hyperthyroid sx w/o goiter

Difference b/t epididymitis and spermatocele?
E: dysuria and tender epididymitis
S: asymptomatic often, painless, transilluminates w/ light
Why does varicocele form and where is it more common?
Impaired venous drainage over time. More common on left
Thrombosis of left renal vein (renal cell carcinoma) can lead to what in testicle?
Sudden onset of left-sided varicocele
Communicating vs. noncommunicating hydroceles?
Communicating ones change in size w/ valsalva. Noncommunicating remain the same size
Imaging of choice for testicular cancer
Ultrasound. Solid mass = likelihood of cancer high
*if cystic, fluid-filled = unlikely to be malignant
If confirm testicular cancer on US, what next?

CT scan of abd and pelvis to look for retroperitoneal lymph node mets and CXR to look for pulm meds.

If retroperitoneal node mets are found, get CT of chest

What blood tests should be obtained in testicular cancer?
AFP only in nonseminomatous cancer*these are helpful in staging, prognosis, and following treatment

How is pathologic confirmation of testicular cancer determined?
Radical inguinal orchiectomy is performed
Why is inguinal incision preferred over scrotal one?
Trans-scrotal is assoc w/ higher rate of local recurrence
What must patients be advised about who receive retroperitoneal lymph node dissection in testicular cancer?
Can injure nerves and affect erectile function
Key differences between seminoma vs. nonseminoma?
Seminoma is more common, no/rare AFP, bCG levels; RADIOSENSITIVE, does not require retroperitoneal lymph node dissection
Ddx for gross hematuria?
1) acute cystitis = E coli. +frequency, urgency, burning; pyuria
2) bladder cancer = painless hemaaturia. RF = tobacco, exposure to automobile exhaust or industrial solvents
3) BPH = +freq, urgency, hesitancy, slow stream, NOCTURIA
4) nephrolithiasis
5) benign essential hematuria = dx of exclusion
6) prostatitis = +fever, dysuria, perineal/back pain
7) renal cancer = most asymptomatic. Smoking is RF
8) pyelo = CVA tenderness
9) prostate cancer = most common non-skin malignancy in males; hematuria is rare
10) urethral stricture
11) PKD = +flank pain, enlarged liver, kidney stones, HTN
12) menstruation = blood can mix w/ urine
Hematuria <2wks <20yo?
UTI, foley trauma, exercise
Hematuria >2wks, <20yo?
IgA nephropathy
Hematuria <2wks, 20-50yo?
UTI, foley trauma, exercise, nephrolithiasis
Hematuria >2wks, 20-50yo?
PKD; bladder, kidney or prostate cancer
Hematuria <2wks, >50yo?
UTI, foley trauma, neprholithiasis
Hematuria >2wks, >50yo?
BPH; PDK; bladder, kidney, prostate cancer
Rf for urologic malignancy?
Elderly male, persistent gross hematuria, absence of pain, hx of smoking, possible exposure to carcinogens such as paint
When is a complete hematuria workup warranted?
Presence of >3 RBCs/HPF on 2 of 3 properly collected urine specimens
Brown blood in urine is consistent w/?
Old blood; glomerular bleeding
Other thanblood, what can make urine appear red?

Drugs = rifampin, sulfonamides, phenazopyridine, nitrofurantoin, phenytoin, levodopa, chloroquine

Conjugated bili in biliary obstruction or certain metabolic diseases of liver

Pain w/ hematuria makes what more likely?
UTI, pyelo, nephrolithiasis
Classic presentation for nephrolithiasis?

Acute colicky flank pain that may extend into groin area. Patient will typically move around in attempt to relieve pain, which distinguishes it from peritonitis who remain rigid.

+n/v, dysuria

RF for nephrolithiasis
prior episodes
high protein diet
males > females
low fluid intake
recurrent UTI
renal tubular acidosis
certain meds = acetazolamide, furosemide, allopurinol
Triad for kidney cancer?
Flank pain, abd mass, hematuria. Seen only in 10-15% of patients
RF for renal cancer?
Most common presentation for bladder cancer? RF?

Painless gross hematuria

RF smilar to renal cancer

How does prostate cancer present?
Most discovered incidentally bc of PSA screening. May present similar to BPH sx
Most common causes of glomerular hematuria?
IgA nephropathy (bergers)
Thin glomerular basement membrane disease
Hereditary nephritis (alports)
Where do renal stones develop?
Anywhere along urinary tract but typically from kidney or renal pelvis. Cause sx when they get lodged somwehre in the tract, most commonly at hte URETEROPELVIC JUNCTION (UPF) and URETEROVESICAL JUNCTION (UVJ)
Calcium oxalate stone features?
Etiology: hypercalciuria, Chrohns
Most common type
Struvite stone features
Etiology: UTI 2/2 urease+ organisms (proteus, klebsiella)
Women affected more;
Staghorn calculi
Calcium phosphate stone features
Etiology: Renal tubular acidosis, HYPERparathyroid
Form in alkalnizied urine
Uric acid stone features
Etiology: low urinary pH, gout, chemo, patients w/ ileostomies
Can be treated by increasing urinary pH
Why do high protein diets increase risk of developing renal stones?
Protein breakdown lowers urinary pH and incrases excretion of uric acid
Most common type of kidney cancer?
Renal cell carcinoma arises from renal tubule cells; 1/3 have mets at time of presentation
Clear cell (70%)
Papillary (15%)
Chromophobe (5%)
Most common location for RCC mets?
Genetic syndromes assoc w/ RCC?
von Hippel-Lindau = AD, mut on 3p
Tuberous sclerosis = AD, mut on chrom 9
Birt-Hogg-Dube = AD, mut 17
What paraneoplastic syndromes are assoc w/ RCC?
1) polycythemia via increased EPO prod
2) hypercalcemia via PTH-like hormone
3) HTN via increased renin production
4) cushings via ectopic cortisol production
5) stauffers via reversible liver dysfunction
Most common type of bladder cancer?
Urothelial cell carcinoma
Most common type of prostate cancer?
Prostatic adenocarcinoma
First step in workup of pt w/ gross hematuria?
UA to confirm red blood cells in urine
Next step in workup?
Microscopic UA
What urinalysis findings suggest glomerular source?
Brown-colored urine, red cell casts, dysmorphic RBCs, significant proteinuria
What workup is recommended for non-glomerular hematuria?
Symptomatic = usually assoc w/ stones and infection. Give abx if necessary.
Best diagnostic test for nephrolithiasis?

non-contrast helical CT scan (CT-KUB)

US is procedure of choice in pregnant women and women of childbearing age

In HIV+ = contrast-enhanced CT scan

Further workup in presence of gross hematuria?
CT urogram, urine cytology, cystourethroscopy (for bladdeer and urethral pathology)
What can you give pts w/ stones <5mm to help them pass them?
Alpha blockers such as tamsulosin to relax the ureteral wall
Emergent surgical indications for renal stones?

Uresepsis, intractable pain, progressive renal damage, solitary kidney

Will require ureteral stent placement or percutaneous nephrostomy tube placement

Treatment options for masses concerning for RCC?
Radical or partial nephrectomy. Radical = removal of kidney, perinephric fat, Gerota’s fascia, ureter, lymph nodes, and possibly ipsilateral adrenal gland
How is urotheilial carcionma of the bladder treated?

Transurethral resection for diagnosis and staging.

Standard = radical cystectomy w/ urinary diversion

What is a radical cystectomy?
Removal of entire bladder and pelvic lymph nodes
Which patients are appropriate candidates for radical prostatectomy?
Contained disease to prostate
Life expectancy of at least 10 years
What are next steps in pt w/ persistent significant hematuria despie foley catheter placement and manual irrigation?
3-way foley catheter
OR for cystoscopy
Ddx for transient monocular vision loss
1) embolus from carotid artery
2) central retinal artery occlusion
3) severe orthostatic hypotension as seen on diabetics
4) giant cell arteritis
5) retinal vein occlusion = assoc w/ chronic glaucoma, DM, coagulopathy; painless, monocular, cloudy vision. COTTON WOOL SPOTS, retinal hemorrhages
6) retinal detachment = “floaters”
7) open angle glaucoma = gradual loss of vision from periphery to central
8) pailledema
9) optic neuritis = assoc w/ MS, inflamm of optic nerve, painful visual loss
10) retinal migraine or aura
What is associated w/ amarousis fugax?
Curtain shade descending down the field of vision in one eye.
Result of atherosclerotic debris from a plaque in the internal carotid artery (ICA) that embolizes to the opthalmic artery.
In patient w/ carotid embolus to eye, what will you see on fundoscopic exam?
Hollenhorst plaques = cholesterol microemboli seen within the retinal arterioles that have a bright, yellow, and refractile appearance
What can cause neck bruit?

Typically due to internal carotid artery atherosclerosis.

But also: aortic stenosis; stenosis of external carotid artery; stenosis of subclavian artery

RF for carotid stenosis?
Old age
ICA vs. ECA in neck?
ICA has no branches in the neck
What are the branches of the ECA?
Superior Thyroid
Ascending Pharyngeal
Posterior auricular
Superficial Temporal
“some attendings like freaking out potential medical students”
What is the first branch of the internal cartotid artery?
What is the most common location for an anterior circulation stroke?
MCA territory
Presentation of opthalmic artery stroke?
Supplies Retina
Amarousis fugax; sudden onset painless vision loss
Where do carotid plaques embolize more to?
Main causes of hemorrhagic stroke?
1) intracerebral hemorrhage due to poorly controlled HTN, congenital AVMs
2) subarachnoid hemorrhage 2/2 ruptured intracranial aneurysm
Main source of cerebral emboli?
ICA at the carotid bifurcation from the heart
What is a lacunar stroke?
Ischemic stroke caused by occlusion of the deep penetrating arteries. RF = severe HTN, DM
What promotes atherosclerotic plaque build up?
Low shear stress as seen in the outer walls of arteries
If patient has had multiple TIAs w/ the same Sx each time, what is the most likely source of TIA?
Carotid artery bc it travels along the same path.
VS atrial fib embolization which can go anywhere in the systemic circulation and can result in stroke, limb ischemia, bowel ischemia
What can help differentiate high grade stenosis s. occlusion of vascular lumen?
Diagnostic test of choice for possible carotid stenosis?

Carotid duplex scan. This gives a range of stenosis.

Second study – CTA or MRA – gives exact percent

Management of 100% carotid stenosis?
ASA, statin and/or clopidogrel
Management of 70-99% carotid stenosis?
CEA for men and women
Management of 50-69% carotid stenosis
CEA Is of less benefit
Management of <49% stenosis?
ASA, statin, clopidogrel
At what percent of ICA stenosis should CEA be considered in sx patients?
High grade 70-99%. Benefit greater in men, with hemispheric symptoms
Following stroke or TIA, what is the optimal timing of CEA?
Within 2 weeks
At what percent of ICA stenosis should CEA be considered in asymptomatic patients?
Those w/ 80-99% stenosis.
Why is there less benefit from CEA in women?
Smaller caliber vessels putting them at risk for developing recurrent stenosis and perioperative carotid thrombosis
Presentation of cerebral hyperperfusion sydrome following CEA?
1% of pateitns about 2-7 days post surgery
Sx: severe headaches, neuro deficits, and/or seizures leading to intracerebral hemorrhageMech: ischemia-reperfusion injury

What cranial nerves can be damaged in CEA?
VII – droop in corner of mouth
IX – difficulty in swallowing
X – hoarseness
XI – dimished or absent function of SCM and trapezius
XII – tongue deviation to side of injury
Ddx for calf pain when walking?
1) claudication = pain w/ walking, relieved w/ rest, reproducible at same distance. Atherosclerotic plaque obstructing blood flow
2) osteoarthritis of hip/knee = not relieved w/ few mins rest; not reproducible w/ walking
3) spinal stenosis = generalized weakness of both legs that worsen w/ walking; relieved by leaning forward
4) sciatica = buttock pain, leg pain, shooting down the posterior thigh
5) chronic venous stasis = worse after prolonged standing, leg swelling, relieved by elevating legs
What 3 part definition of claudication should be obtained by history?
Caused by reduction in blood flow to the leg muscles, most commonly by an atherosclerotic plaque.
1) leg pain with walking
2) relieved by few mins of rest
3) reproducible at same walking distance each time
Claudication is sx of what underlying dz?
peripheral artery disease. Leads to chronic limb ischemia
RF for PAD
Advanced age
Male gender
Sedentary lifestyle
Heart attack
At what rutherford classification is there ischemic rest pain?
1-3 mild, mod, severe claudication
5-6 minor, major tissue loss
What is ischemic rest pain?
Presents in foot, most commonly in toes. Occurs at night. Patient wakes up w/ toes aching or feeling numb and is forced to get up and walk around or dangle.
What is buerger’s sign?
Sign of advanced chronic ischemia. Affected foot turns pale after it is elevated. Once the patient sits up and dangles the foot down, it becomes ruborous
Ddx of ischemic rest pain?
1) DM neuropathy = bilateral burning in feet; not relieved by dependency; stocking glove, no rubor.
2) night cramps
3) gout = pain and redness in big toe. HyperuricemiaIschemic rest pain = awaken at night pain in forefoot, relieved by standing or dangling feed, dependent rubor

What other findings would support PAD?
Calf muscle atrophy; hair appendages die; dry scaly skin; development of ulceration; cap refill prolongation
What supplies the calf muscles?
Superficial femoral artery, the most comomn site for atherosclerosis in the lower extremities
Most common location of arterial emboli?
Common femoral artery
Pathophys of dependent rubor?
It is a sign of advanced chronic ischemia. The dermal arterioles no longer constrict when subjected to high hydrostatic pressure, so they are just dilated so that they can increase the amount of blood supply to the area (since they are so chronically ischemic). So when in dependent positions, blood will extravasate and pool, leading to rubor.
What other diseases can cause claudication?
Buerger’s disease
Chronic embolization
Entrapment of popliteal artery
What condition is assoc w/ claudication in upper extremities?
Subclavian steal syndrome. An atherosclerotic plaque contributes to narrowing of subclavian artery –> retrograde flow in vertebral artery during arm exercise
What is beurger’s disease?

AKA thromboangiitis obliterans.

Seen in: <40yo, M>F, SMOKERS

Path: inflammatory and thrombotic process that causes occlusion of distal arteries below the knee & hands

Tx: smoking cessatino

Calf claudication is typically due to what?
Superficial femoral artery disease
What is Leriche syndrome?

Chronic, slowly developing occlusion of the infrarenal aorta most often seen in smokers.

Triad: 1) buttock and thigh claudication. 2) impotence 3) absent femoral pulses

Next step in diagnostic workup for claudication?

Ankle brachial index (ABI) and arterial duplex scan

normal ABI = 1-1.2. Ratio of highest systolic pressure at ankle/foot over the highest brachial systolic pressure.

What can falsely elevate the ABI?
PAD categories by ABI?

PAD defined by ABI <0.9.

Mild disease = 0.7-0.9
Moderate disease = 0.4-0.7
Severe disease/rest pain = <0.4

What tests are recommended in patients in whom an intervention is being planned for claudication?
Risk of limb loss for patients w/ claudication?
As long as no ischemic rest pain, 5 year risk is 5%.
10 year is 10%
Risk of limb loss for patients w/ ischemis rest pain?
50% at one year without intervention
Initial management of claudication?

Primary treatment is lifestyle and risk factor modification. Smoking cessation and exercise.

Control HTN, DM, diet may halt progression of atherosclerosis

What drugs are approved by FDA for claudication?

Cilostazol is a quinolone derivative primarily inhibits platelet aggregation and is a vasodilator. Drug of choice. CI in patients w/ heart failure

Pentoxifylline has not been supported recently

Does a statin improve claudication?
Yes. Via anti-inflamm effect and reduction of risk of stroke and MI.
Is aspirin recommended in claudication?
Yes, since there is strong assoc b/t PAD and coronary and carotid atheroscelrosis
Do anticoagulants have a role in reducing claudication?
No. It is not a blood clot or embolization problem
What treatment is preferred in most patients for claudication?

Invasive. Endovascular angioplasty/stenting

Or endardectomy or bypass

Which patients are candidaes for invasive therapeutic approach for claudication if medical management fails?
Rutherford class 2 or 3 provided:
1) good risk candidates for intervention
2) sx are significantly affecting lifestyle
Which patients go directly to invasive therapy?
Rutherford class 4-6
Ddx sudden onset severe left-sided abd pain
1) ruptured AAA = elderly, white male, left flank and groin pain, goes to back. Pulsatile abd mass, tachycardia, hypotension
2) perforated gastric or duodenal ulcer
3) aortic dissection = hx of HTN
4) pancreatitis
5) diverticulitis begins in LLQ and may become diffuse +n/d. elderly
Typical presentation for AAA
For most, first sx is rupture which is fatal.
Otherwise, incidentally found. As it enlarges, can produce abd pain and lower back pain
RF for AAA
Smoking, >60yo, caucasian, male, CAD, hx of extra-abd aneurysms, atherosclerosis, FHx, HTN
Diabetes assoc w/ AAA?
It is protective. Hypothesis = glycation of matrix metalloproteinases leads to deactivation and thus decreases aortic remodeling
Screening guidelines for AAA?

physical exam and one-time abd US fo rmen 65-75 who have ever smoked.

First degree relatives of a patient w/ AAA should be screened at 60yo

If AAA found, follow yearly if 3-4cm; biannually if 4-4.5cm

What other arteries assoc w/ AAA?

Femoral and popliteal

Screen w/ duplex ultrasound

Presentation of thoracic aortic aneurysm?
Dysphagia, hoarseness, dyspnea, upper extremity edema
Normal diameter of infrarenal aorta?
Men 2cm
Women 1.8cm
What is the defect in AAA?
Degeneration of medial layer through degradation of elastin and collagen
Def of anerysm in terms of artery diameter?
When it is 1.5x larger than it should be. In infrarenal = 3cm or more.
Matrix metalloproteinase role in AAA formation?
Important for collagen turnover –> vital to inflammation and wound healing.
Patients w/ AAA have high levels of MMP acvitiy in aortic wall –> weakens the arterial wall and contributes to dilation of aneurysm over time*Statin drugs decrease activity of MMPs

Where does an AAA typically ruptures?
Into the retroperitoneum and on the left side
RF for AAA rupture
Poorly controlled HTN
First step in eval of patient w/ suspected AAA?
ABCs. 2 large-bore IVs should be established, one in each antecubital fossa
Goal of fluid resuscitation in suspected ruptured AAA?

Receive no more than 1L crystalloid followed by admin of blood products w/ goal to maintain SBP greater than 70mmHg.

Massive resuscitation tends to exacerbate hemorrhage by diluting coag factors and raising SBP

Recommended imaging for suspected ruptured AAA?

CTA in hemodynamically stable

If hemodynamically UNstable = take to OR for exploratory laparotomy

AAA size/growth rate effect on management?
3-4.4cm = annual US
4.5-5.5cm = US every 3 months
>5.5cm = elective repair
Enlarging >1cm/year or symptomatic = elective repair
What 2 options available for nonruptured asymptomatic AAA?
Open repair
Endovascular Aneurysm repair (EVAR)
Main source of perioperative morbidity and mortality following both open and EVAR is?
Myocardial infarction
Surgical options for ruptured AAA?
Open vs. EVAR
What makes an AAA unsuitable for EVAR?
If the aortic neck is too short
Why do patients require at least an annual lifetime follow up after EVAR?

To check if there is an endoleak present (persistent arterial flow into the aneurysm sac in the case that there is failure to exclude the aortic aneurysm)


Features of endoleak type 1
Anterograde or retrograde flow from inadequate proximal or distal seal of the stent graft w/ arterial wall
Features of endoleak type 2
Retrograde flow from patent visceral branches within the aneurysm sac
Which type of endoleak is most common? Most dangerous?

Common = 2

Dangerous = 1 bc persistent flow from aorta or iliac vessels in the aneurysm sac will maintain high pressures and continue to enlarge

What are you concerned about if patient develops diarrhea following AAA repair?

Postop ischemic colitis 2/2 ligating the inferior mesenteric artery.

tx: fluids, NPO, broad spectrum IV abx

Which portion of duodenum rests next to aorta? what does this mean for post AAA repair?
4th portion. An aortoenteric fistula can develop months or years after AAA repair and can present w/ upper GI bleeding or melena
Ddx for cold, painful lower extremity?
1) acute limb ischemia = pain pallor, pulselesness, paresthesias, paralysis, poikilothermia; hx of PAD, A fiub
2) compartment syndrome = severe pain in calf w/ passive motion of ankle, tense leg edema, recent trauma, PULSE PRESENT
3) phlegmasia cerulea dolens = cyanotic leg and edema, massive DVT, assoc w/ malignancy
4) CVA = numbness and weakness but not pain or pulselessness
5) disk herniation = history of back pain, DJD
6) spinal cord tumor = presents similarly to herniation
Timing of acute limb ischemia?
Acute if <2 weeks; chronic if longer
What is considered the defining feature of acute limb ischemia?

PULSELESSNESS; pain is the presenting symptom most often

others: pallor, paresthesias, paralysis, poikilothermia

Etiologies of acute limb ischemia?
1) thrombosis. Look for vascular risk factors, claudication history, coagulopathies
2) emboli, 80% from heart. Look for A fib, valvular dz, CHF, MI, aneurysms
3) acute aortic dissectioni
4) systemic shock
Most common cause of acute arterial emboli?
Atrial fibrillation
Why is it important to check the other leg in acute leg ischemia?

Bc if the other leg has signs consistent w/ PAD (hairlessness, ischemic ulcers, absent pulses, atrophic skin changes), then this may suggest a thrombotic etiology

lack of these signs makes embolic causes more likely

How do you assess a patient’s atherosclerotic disease history?
Smoking, hypercholesterolemia, coronary artery disease, DM, history of intermittent claudication
Why is it important to ask about past interventions for PAD?
Thrombosis of a previous graft is frequent cause of ALI
Where is the most common place for an embolus to lodge in the lower extremity?
Bifurcation of common femoral artery into the superficial femoral and profunda femoris arteries
Sx if embolic occlusion at aortic bifurcation
Pulses absent bilaterally
Sx: bilateral pain/weakness of thighs/calves, mottling of skin distal to umbilicus
Sx if embolic occlusion at common femoral bifurcation?
Pulses absent throuhgout affected limb.
Sx: unilateral calf and foot pain
Sx if embolic occlusion at popliteal bifurcation?
Femoral pulse present, pedal pulses absent
Sx: unilateral foot pain; calf pain may be present as well
How do you use doppler for acute limb ischemia?
Normal artery has triphasic signal. ALI has absent, or monophasic at best.
What imaging modality is recommendded for acute limb ischemia?

Duplex signaling is simple and convenient in initial evaluation


What imaging should be done if an embolus is suspected as cause for ALI?
Cardiac workup w/ transthoracic echocardiography should be performed; venous duplex should be performed if clues suggest venous thrombosis w/ paradoxical embolus
What are the 3 important initial management principles in ALI?
1) anticoagulation w/ heparin
2) IV fluids
3) patient in dependent position to improve flow
What stage of ALI is amputation indicated?
Stage 3 = irreversible = major tissue loss or permanent nerve damage
2 mainstay treatment options for ALI?

Endovascular and open surgical revascularization;

in some cases, heparin alone may be the best treatment option

What must you do in anticipation of sequela of reperfusion?
Monitor CPK and myoglobinuria. Need to watch out for rhabdomyolysis –> if suspected, start IV fluids and bicarb infusion
First line treatment for stage I and IIa ALI?
Catheter directed thrombolysis. Takes 24-48 hours to complete.
Treatment for Stage IIb ALI?
Surgical revascularization

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