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CARDIOTHORACIC SURGERY

Coronary artery bypass graft:

A coronary artery bypass graft (CABG) utilizes arteries or veins from elsewhere in the patient's body to bypass
atherosclerotic stenosis and improve coronary blood flow. The 2 primary indications for coronary artery bypass graft
(CABG) are patients with:
Left main coronary stenosis of 50%

3-vessel disease

Grafts used in coronary artery bypass surgery include the internal thoracic artery and saphenous vein, among
others. Internal thoracic arteries are more commonly used as they have been shown to have the best long term
patency.
Percutaneous coronary intervention is indicated in patients with single or two vessel disease and normal LV
function.

General considerations for prosthetic valves:

The two categories of valve replacement are tissue and mechanical.


The major risk associated with a tissue valve is structural deterioration of the valve requiring 30% of patients in need
of replacement in 10 years and 50% in 15 years.
Tissue valves are indicated in patients:
Patients older than 65

Those who do not want to take anticoagulation

Women of childbearing age

The major risk associated with mechanical valves is a need for lifelong anticoagulation. Mechanical valves are
indicated in patients:
Younger than 65

That have no contraindications to anticoagulants

Who are reliable to take anticoagulants

The St. Jude mechanical valve is the most commonly used valve in aortic and mitral valve replacement due to
its double-disk tilting, hemodynamics, and low thrombogenicity.
Valve obstruction can result from thrombosis due to:
Poor anticoagulation

Formation of a fibrous tissue ingrowth called a pannus (less common)

Vegetations due to poor antibiotic prophylaxis

Non-structural dysfunction is a general term for valve complications that arise and include:
Inappropriate sizing

Hemolysis

Tissue or suture entrapment

Paravalvular leak
Operated prosthetic valvular endocarditis can be early (<60 days following implantation) or late. Early prosthetic
valve endocarditis is when the valve is seeded intraoperatively or via catheters, cannulas, or wound infections.
Organisms involved in early prosthetic valve endocarditis include
Staphylococcus aureus

Staphylococcus epidermidis

Gram-negative bacteria

HACEK organisms

Haemophilus

Aggregatibacter (formerly Actinobacillus)

Cardiobacterium

Eikenella

Kingella

Pseudomonas

Late prosthetic valve endocarditis is typically due to noncardiac sepsis arising from dental, gastrointestinal, or
genitourinary tracts.
Organisms involved in late prosthetic valve endocarditis include Streptococcus spp. and Staphylococcus
spp. with viridans streptococci being the most common.

GENERAL SURGERY

Acute abdomen:

The common symptoms of acute abdomen include:


Pain

Fullness, bloating

Nausea/vomiting

Dyspnea (due to decreased diaphragmatic excursion)

Fever

The treatment for most causes of acute abdomen is surgery. However, the following are causes of acute abdominal
pain that do not require surgery:
Pelvic inflammatory disease

Spontaneous bacterial peritonitis

Diverticulitis (sometimes)

Sickle cell crisis

Psychological
Diabetic ketoacidosis

Pancreatitis

Anus:

Anal fissures are linear tears in the anal mucosa below the dentate line, most commonly found in the posterior
midline.
Anal fissures typically occur in the setting of repetitive local trauma (e.g. childbirth, repetitive constipation/diarrhea,
anal sex, etc.).
Patients with an anal fissure typically present with:
Blood on the toilet paper following defecation

Pain

First line therapy for an anal fissure is conservative therapy (e.g. sitz baths, fiber, lidocaine, stool softeners).
If conservative therapy fails in the management of an anal fissure, a lateral internal sphincterotomy or botulinum
toxin injection may be beneficial.
Crohns disease should be suspected in cases when an anal fissure, perianal abscess, or an anorectal fistula fail to
heal.
Perianal abscesses (aka anorectal abscesses) are caused by an obstruction of an anal crypt gland, resulting in
bacterial overgrowth and abscess formation.
Patients with a perianal abscess typically present with:
Severe anal or rectal pain not associated with bowel movements

Fever

Malaise

On physical exam, a patient with a perianal abscess typically displays:


A fluctuant mass

Overlying erythema

Purulent drainage

Perianal abscesses are treated by incision and drainage.


Poorly managed diabetics are predisposed to necrotizing tissue infections from a perianal abscess.
Risk factors for a perianal abscess include:
Constipation

Diarrhea

Inflammatory bowel disease

Immunosuppression or chemotherapy

Diabetes mellitus

An anorectal fistula is a track from the rectum to the perianal skin, most commonly due to reepithelialization of a
ruptured perianal abscess.
Risk factors for developing an anorectal fistula include:
Perianal abscesses (most common cause)
Inflammatory bowel disease

Local radiation

Foreign bodies

Patients with an anorectal fistula typically present with:


Perianal drainage of fecal or purulent material

Itching

Intermittent pain

The diagnosis of an anorectal fistula relies upon visual inspection of an anorectal track. A probe may be used to
confirm the presence of a track.
Anorectal fistulas are treated preferentially with a fistulotomy.
Goodsalls rule is used to facilitate a surgical plan:
Anterior fistulas connect with rectum in a straight line

Posterior fistulas go towards a midline internal opening in the rectum

Anorectal fistulas that diverge from Goodsalls rule should raise suspicion of Crohns disease.
Anal cancer is an uncommon form of cancer. Risk factors for its development include:
Anal intercourse

Multiple sexual partners

Human Papillomavirus (HPV) infections (16 is the most common subtype)

HIV

Immunosuppressive therapies

Smoking

Anal cancer is most commonly of the squamous cell carcinoma histological type.
Patients with anal cancer typically present with:
Bleeding

Feeling of perianal fullness

May be asymptomatic

Anal cancer is definitively diagnosed with biopsy and CT or MRI imaging is used for staging.
The initial treatment for anal cancer is chemoradiotherapy with 5-fluorouracil and mitomycin (aka modified Nigro
or Wayne State protocol).
Anal cancer refractory to chemoradiotherapy should be treated withabdominoperineal resection as indicated.

Hemorrhoids:

Hemorrhoids are dilations in the rectal and anal veins. The two types of hemorrhoids are:
Internal hemorrhoids which are dilated veins of the superior rectal plexus, located above the dentate line

External hemorrhoids which are dilated veins of the inferior rectal plexus, located below the dentate line
Internal hemorrhoids are lined by columnar epithelium, whereas external hemorrhoids are lined by squamous
epithelium.
Some of the most important risk factors for developing hemorrhoids areprolonged
sitting, constipation, and pregnancy. Other risk factors for developing hemorrhoids include:
Increased age (tissue scaffolding weakening)

Portal hypertension

Pelvic tumors

Patients with hemorrhoids typically present with:


Hematochezia

Rectal prolapse

Itching

Sense of fullness in anorectal region

Acute pain from thrombosis (only if external, because of somatic innervation)

The first line therapy for hemorrhoids is conservative therapy such as sitz baths, stool softeners, OTC remedies and
a high fiber diet.
Hemorrhoids refractory to conservative management may be managed surgically. Indications for surgery also include
thrombosed or necrotic external hemorrhoids. Surgical management depends on the type of hemorrhoid:
Internal hemorrhoids: Rubber band ligation

External hemorrhoids: Hemorrhoidectomy

If left untreated, hemorrhoids may:


Strangulate leading to gangrene

Thrombose

Bleed leading to iron deficiency anemia

Inguinal hernias:

Inguinal hernias are classically categorized based on location:


Indirect inguinal hernias occur lateral to the inferior epigastric artery, indirectly entering Hesselbachs
triangle

Direct inguinal hernias occur medial to the inferior epigastric artery, directly entering Hesselbachs
triangle

The boundaries of Hesselbachs triangle are:


Inguinal ligament inferiorly

Inferior epigastric artery laterally

Rectus abdominus muscle medially


An indirect inguinal hernia is caused by the failure of the processus vaginalis to close, allowing intestines to enter
the inguinal canal.

Direct inguinal hernias are usually caused by inguinal canal floor weakness.
Direct inguinal hernia sacs are covered by the external spermatic fascia, whereas indirect inguinal hernias have no
additional fascial covering.
Risk factors for an inguinal hernia include:
Prior history of groin herniation

Caucasian

Elderly

Male

Previous abdominal wall surgeries

Anything that causes increased intra-abdominal pressure

Connective tissue abnormalities

Patients with an inguinal hernia typically present with:


Heaviness in the groin mostly at times of increasing intra-abdominal pressure (e.g. weight lifting)

Pain in the groin or testicles (if incarcerated or strangulated)

Changes in bowel movements

Asymptomatic

The diagnosis of an inguinal or femoral hernia is based upon physical exam, and when in doubt of location an
ultrasound may be useful.
On physical exam, patients with an inguinal hernia typically have:
A reducible bulge in the groin if unincarcerated

A irreducible bulge in the groin if incarcerated

Increased size of bulge with coughing or Valsalva

The definitive treatment for inguinal hernias is surgery; however, for patients with no symptoms and an easily
reducible hernia, watchful waiting is appropriate.
If left untreated, an inguinal hernia may become:
Incarcerated (irreducible bulge, not always strangulated)

Strangulated (systemic (e.g., fever, nausea, vomiting) and local (e.g., erythema, painful to palpitation) sign
and symptoms may be present)

Necrotic

Large Bowel Obstruction:

Large bowel obstruction is a mechanical or functional obstruction of the large intestines.


The etiologies of large bowel obstruction include:
Colon cancer (primary concern)

Hernias

Adhesions

Volvulus

Diverticulitis/Diverticulosis

Inflammatory bowel disease

In severely ill patients, acute dilation of the colon can occur in the absence of any actual mechanical obstruction. This
pseudo-obstructive phenomenon is known asOgilvie syndrome.
Symptoms include constipation, abdominal discomfort, and feculent emesis.
On physical exam, the abdomen may be distended, tympanic, and tender.
Diagnosis can be made with abdominal x-ray or CT imaging. Multiple air-fluid levels and dilated air-filled proximal
colon with air-absent distal colon is highly suggestive of LBO. The clinician should also be vigilant to look for any
masses.
Other pertinent studies to evaluate for the presence and/or cause of obstruction may
include contrast enema or sigmoidoscopy/colonoscopy.
Treatment is aimed at relief of obstruction by enema, decompression with rectal tube, or colonoscopy. In severe
cases, surgery may be required.

Other Hernias:

Femoral hernias anatomically occur through the femoral ring, which is the most medial aspect of the femoral
sheath, lateral to the lacunar ligament, and inferior to the inguinal ligament.
Femoral hernias are typically acquired secondary to aging or injury.
Richters hernia occurs when only half of intestinal wall is protruding, seen commonly in femoral and obturator
hernias.
Littres hernia describes a hernia sac that contains Meckels diverticulum.
(Think Littreckel)
Garengoffs hernia and Amyand's hernia describe femoral and inguinal hernia sacs, respectively, that includes the
appendix.
A pantaloon hernia describes a combination of a direct and an indirect inguinal hernia.
(The hernia is divided by the inferior epigastric vessels so that it is reminiscent of a pair of pantaloons)
Spigelian hernia describes a hernia sac passing through the spigelian (aka semilunaris) fascia.
(Think of Smeagol, sounds like SPIGELian, standing in front of the moon, semiLUNAris fascia)
Coopers hernia describes a femoral hernia with two sacs, the first being in the femoral canal, and the second
passing through a defect in the superficial fascia and appearing immediately beneath the skin.
An incisional hernia describes a hernial sac passing through a previous surgical incision, associated with obesity,
diabetes, and infection.

Small Bowel Obstruction:

The most common causes of small bowel obstruction are:


Adhesions from prior abdominal surgery (most common cause in US)

Hernias (most common cause worldwide)

Cancer
Other less common causes of small bowel obstruction include:
Appendicitis/diverticulitis/intraabdominal abscess

Intussusception

Volvulus

Crohn's disease

Congenital stricture

Traumatic intramural hematoma

Gallstone

The most common presenting symptoms of small bowel obstruction (SBO) are:
Nausea

Vomiting

Abdominal pain

Obstipation

The severity of the symptoms of SBO can vary depending on the location of the obstruction. Nausea and
vomiting are prominent in proximal obstruction, whereas abdominal pain and distention is more severe
in distal obstruction.
Small bowel obstruction (SBO) is usually diagnosed based on history and physical examination. Physical examination
may show any or all of the following:
Signs of dehydration (e.g., tachycardia, orthostatic hypotension, decreased urine output)

High-pitched "tinkling" and hyperactive bowel sounds (though they may be later reduced/absent)

Abdominal tenderness and/or distention

Abdominal mass related to cause (e.g., tumor, hernia, volvulus)

Complete blood count with differential (CBC with diff) and basic metabolic panel (BMP) are the most common
laboratory studies ordered and are not specific or sensitive for SBO, but are used to identify possible
complications. The results show any or all of the following:
Hypovolemia

Leukocytosis

Hyponatremia or hypokalemia

Elevated lactate (not part of CBC or BMP, but sensitive for acute intestinal ischemia)

Anemia (cancer or Crohn's disease)

Note: In patients with chronic small bowel obstruction, such as from Crohn's disease or slowly progressing tumors, no
lab abnormalities may be present.
Imaging is used to identify the location, partial vs. complete obstruction, and the possible cause. Plain abdominal x-
ray films may show dilated small bowel loops with multiple air-fluid levels and lack of gas in the colon. CT scans
have utility when high clinical suspicion remains despite negative or relatively unremarkable radiograph.

Management of small bowel obstruction requires volume resuscitation, electrolyte abnormality corrections, and
determining if surgery is necessary. Surgery is required for complete obstruction and for clinical or radiographic
signs of ischemia, necrosis, or perforation.
Non-operative management should be attempted if signs of a complete or complicated obstruction are absent.
Management includes:
Bowel rest by making the patient NPO

Nasogastric suctioning to decompress the bowel

IV fluids to maintain electrolytes and hydration

MINIMALLY INVASIVE SURGERY

Laparoscopic surgery is a form of minimally invasive surgery in which operations in the abdomen are performed
through small incisions as opposed to the larger incisions needed in laparotomy.

This is mainly a topic for surgical wards.


Laparoscopic surgery poses several advantages including:
Reduced bleeding

Smaller incision leads to reduced pain and need for pain medications

Less scarring

May reduce intestinal adhesion development

Shorter hospital stay

Laparoscopic surgery has several disadvantages including:


Loss of dexterity

Poor depth perception


Longer surgery and anesthesia duration

Risk of IVC compression from insufflation pressures

Laparoscopic surgery poses several risks including:


Initial blind insertion of the trocar leading to an increased chance of injuring blood vessels or intestines

CO2 is used to inflate the abdomen and is absorbed into the blood stream leading to an increased
pulmonary work

Inadvertently injury of adjacent structures

Following laparoscopic surgery, patients may complain of shoulder pain. This is caused by irritation of the
diaphragm by CO2 (either by direct pressure or cellular death from temperature change) used to inflate the
abdomen. The phrenic nerve, which innervates the diaphragm, crosses with cervical nerves presenting as shoulder
pain.

NEUROSURGERY

Spinal cord:

Myelopathy refers to compression of the spinal cord. Depending on the location of injury, various neurological
symptoms can ensue. It commonly produces upper motor neuron signs.
Radiculopathy refers to compression of the nerve roots. It commonly produces lower motor neuron signs.

Neurosurgical emergencies:

Intracranial hypertension is defined as intracranial pressure (ICP) greater than 20 mmHg. ICP can be monitored with
a number of pressure transducers inserted into the ventricles, parenchyma, epidural space, etc.
Monro-Kellie doctrine states the cranial compartment volume is fixed and consists of blood, CSF, and brain tissue.
Any increase in volume of one must becompensated by a decrease in volume of another, or the pressure will rise.
Cushings triad is a late sign of increased ICP and is defined as
Hypertension

Bradycardia

Respiratory depression

Uncal (transtentorial) herniation is where the uncus (medial part of the temporal lobe) is pushed over the tentorium
cerebelli and puts pressure on the brainstem.
Uncal (transtentorial) herniation can result in several deficits:
Ipsilateral CN3 palsy

Ipsilateral hemiparesis (compression of contralateral crus cerebri)

Contralateral homonymous hemianopsia (compression of ipsilateral PCA)


Central herniation is where the diencephalon and parts of the temporal lobes are squeezed downward through a
notch in the tentorium cerebelli. Duret hemorrhages (intraparenchymal bleeds due to shearing of the basilar artery)
are associated with central and uncal herniations.

Subfalcine (cingulate) herniation is where the cingulate gyrus is pushed under the rigid falx cerebri. This is the
midline shift that is commonly measured on CT scans.
If severe, the anterior cerebral arteries can be occluded in subfalcine herniations.

Tonsillar herniation is a herniation syndrome in which cerebellar tonsils move downward through the foramen
magnum.
Tonsillar herniation is feared because it can cause rapid compression of the lower brainstem, resulting in central
respiratory failure.

OPHTHALMOLOGY

ARMD:

Age-related macular degeneration is the most common cause of vision loss in patients over age 65 in industrialized
countries.
Risk factors for age related macular degeneration include:
Increasing age (specifically over age 50)

Smoking

Cardiovascular diseases (such as coronary heart disease)

Family history

Medications (such as aspirin)

Exudative, or wet, age related macular degeneration results from the growth of abnormal blood vessels into the
retina, which begin leaking serous fluid and blood behind the retina.
Nonexudative, or dry, age related macular degeneration is caused by atrophy of the retina and/or deposition of
drusen, which are deposits of extracellular matrix.
Vision loss caused by exudative age related macular degeneration occurs more rapidly than the nonexudative
variant.
Patients with age related macular degeneration generally present with:
Progressive loss of vision initially central, spreading peripherally

Scotomas

Blurred vision

Distortion of straight lines


Most patients remain asymptomatic in early disease

Pharmacological treatment of exudative ARMD includes intraocular injections of VEGF (vascular endothelial growth
factor A) inhibitors, such as bevacizumab or ranibizumab. Other treatments include:
Photocoagulation

Vitamin cocktails which include beta-carotene

Nonexudative age related macular degeneration therapies include:


Lifestyle modifications (e.g. quit smoking)

Antioxidants

Vitamin cocktails containing zinc and beta-carotene

Cataracts and Glaucoma:

A cataract is a painless opacification of the lens leading to a decrease in vision. Cataracts are the most common
cause of blindness in the world.
Risk factors for cataracts include:
Increased age

Cigarette smoking

Steroid use

Prolonged UV radiation exposure

Trauma

Uncontrolled diabetes mellitus (sorbitol accumulation)

Wilsons disease

Down syndrome

Alcohol

Classic galactosemia

Infections such as congenital CMV, congenital syphilis, congenital HSV

Patients with cataracts characteristically present with progressively worsening night vision.
The definitive treatment for cataracts includes phacoemulsification or conventional cataract extraction.
Glaucoma is a progressive irreversible loss of vision thought to be due to increased intraocular pressure and is the
second leading cause of blindness worldwide.
Glaucoma may arise either from increased aqueous humor production by the ciliary processes or decreased
drainage by the trabecular meshwork.
The risk factors for glaucoma include:
Increasing age

African heritage

Family history
Steroid use

Trauma

Open angle glaucoma presents as progressive loss of vision in an otherwise asymptomatic patient.
Closed angle glaucoma presents acutely with:
Blurred vision

Headache

Painful eye

Seeing halos

Nausea, vomiting

Rock hard eye

Glaucoma is diagnosed using tonometry, which measures intraocular pressure.


On ophthalmoscopy, cupping of the optic disk may be present due to atrophy of the optic disk.
Open angle glaucoma is treated with topical medications such as:
Beta-blockers (e.g. Timolol)

Alpha agonists

Carbonic anhydrase inhibitors (e.g. acetazolamide)

Prostaglandin analogues (e.g. latanoprost)

Closed angle glaucoma requires laser iridotomy immediately. If that fails, then surgical iridectomy is the next step.
Closed angle glaucoma is an ophthalmologic emergency that leads to irreversible vision loss within hours if left
untreated.

Vascular disorders of the retina:

Occlusions of the central retinal artery, a branch of the internal carotid, typically occur in patients who are:
Over the age of 65

Diabetic

Hypertensive

Smokers

Have other cardiovascular risk factors

The etiology of a central retinal artery occlusions may be due to:


Carotid artery atherosclerosis

Cardiogenic embolizations

Inflammatory diseases (e.g. Temporal arteritis)

Hematologic diseases (e.g. Sickle Cell)


The vision loss in patients with a central retinal artery occlusion generally presents as:
Painless

Acute onset

Monocular

On fundoscopy, patients with a retinal artery occlusion may present withwhitening of the fundus and a cherry red
spot with decreased blood vessel sizes.
Amaurosis fugax is a transient loss of vision, either monoocular or biocular, resulting from carotid artery disease.
Little can be done to reverse a retinal artery occlusion, however hyperbaric oxygen and ocular massage (to dislodge
the embolus further down the arterial tree) en route to the hospital.
Thrombolytic therapy within 4 hours of arrival at the emergency room is the emergent therapy for a central retinal
artery occlusion.
Central retinal vein occlusions typically occur in patients with:
Increased age

Hypertension

Diabetes

Obesity

Smoking

Patients with a central retinal vein occlusion present with:


Blurred vision

Graying of vision

Painless vision loss

The diagnosis of a central retinal vein occlusion depends upon the history, fundoscopic exam, and confirmed with
fluorescein angiography.
Fundoscopy of a patient with a central retinal vein occlusion may show:
Cotton wool spots

Dilated retinal blood vessels

Hemorrhages

Edema

Patients with a central retinal vein occlusion may be treated with:


Laser photocoagulation

Intraocular anti-VEGF injections (e.g. bevacizumab)

Steroids

Conjunctivitis:

Conjunctivitis is inflammation of the conjunctiva, which lines the inside of the eyelid and the globe up to the
limbus. Conjunctivitis is the most common cause of red eye.
Viruses, such as adenovirus, are the most common cause of conjunctivitis.
Bacterial conjunctivitis is typically caused by:
Staphylococcus aureus (most common in adults)

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Adult patients may present with Neisseria gonorrhoeae and Chlamydia trachomatis conjunctival
infections following sexual contact. Neonates may present following birth.
Allergic conjunctivitis is caused by an allergen that activates mast cell degranulation leading to an IgE mediated
inflammatory reaction.
Conjunctivitis can arise from several etiologies:
Infectious (e.g. bacterial, viral, parasitic, fungal)

Hyperacute (e.g. Neisseria gonorrhoeae)

Chemical irritation (e.g. chlorine gas, tear gas, bleach)

Allergic (e.g. Hay fever, seasonal allergies, dryness)

Skin disorders (e.g. Stevens-Johnson syndrome)

Systemic disorders (e.g. Sjogrens syndrome, Kawasakis disease)

Nutrient deficiencies (e.g. vitamin A deficiency)

Foreign bodies (e.g. contact lenses)

Patients with infectious conjunctivitis typically present with:


Unilateral redness of the eye that may eventually become bilateral

Difficulty opening the eye in the morning

White or yellow (purulent) discharge if bacterial

Upper respiratory symptoms and watery discharge if viral

Patients with an allergic conjunctivitis typically present with:


Bilateral redness of the eyes

Thin, watery discharge

Itchiness (key symptom for distinguishing from a viral cause)

A history of allergies

Hyperacute conjunctivitis caused by Neisseria gonorrhoeae uniquely presents with:


Symptoms appearing within 24 hours of infection

Copious purulent (white or yellow) discharge


Urethritis

Red eye

On physical examination, a patient with infectious conjunctivitis may have:


Diffuse redness of the eye (no localized spots)

No loss of visual acuity

Purulent or watery discharge

Lymphadenopathy

Classically on ophthalmologic exam, chlamydial conjunctivitis presents with:


Follicular involvement

Pannus formation (from neovascularization and inflammation of corneal blood vessels)

Chronic infection may cause corneal scarring from the eyelashes rubbing on the globe

Patients with conjunctivitis may be managed according to the etiology, with viral and non-STI bacterial etiologies
receiving largely supportive care. Notably, contact lens wearers should receive fluoroquinolone eyedrops in the
setting of conjunctivitis due to the high incidence of Pseudomonas conjunctivitis in this population.
Chlamydial conjunctivitis is preferentially treated with oral erythromycin. Azithromycin is an appropriate
alternative to erythromycin.
Neisseria gonorrhoeae conjunctivitis is preferentially treated with intramuscularceftriaxone (Rocephin).
Hyperacute conjunctivitis caused by Neisseria gonorrhoeae is a medical emergency requiring an ophthalmology
referral to prevent:
Corneal scarring

Blindness

Perforation

Keratitis

Patients with allergic conjunctivitis are managed supportively with hydrating eye drops, cool compresses, and
antihistamines.

Corneal abrasions:

The cornea overlies the iris to offer protection, UV light filtering, and refractory of light onto the retina.
Abrasions are commonly caused by:
Contact lens wear

Fingernails

Makeup brushes

Foreign objects blown into eyes.

A corneal abrasion often presents with:


Tearing
Foreign-body sensation

Conjunctival injection

Blurry vision

Photophobia

The diagnosis of corneal abrasion is confirmed by fluorescein dye staining examination under a blue light, as corneal
abrasions are often not visible upon gross examination.
Complications of corneal abrasions include:
Hypopyon

Traumatic iritis

Corneal ulcer

Overall, treatment is aimed at relieving pain and preventing infection. Nonsteroidal anti-inflammatory ophthalmic
drops offer long term pain control.
Short-acting cycloplegics such as cyclopentolate or homatropine can diminish pain caused by ciliary spasms and are
especially useful in patients complaining ofheadache and photophobia.
Topical antibiotics such as erythromycin are indicated for fingernail or contact lens induced abrasions.
Eye patches may be used for large abrasions, but are not for corneal abrasions caused by contact lenses or other
contaminating sources.

Diabetes:

Diabetic retinopathy causes progressive vision loss in diabetic patients due to microvascular changes associated with
chronic hyperglycemia. Diabetic retinopathy is a leading cause of blindness in the United States and is divided into
two types Nonproliferative (Background) and Proliferative.
Patients with diabetes should be screened initially at the time they are diagnosed with diabetes (type 1 or type
2) and every year after.
The most accurate way to further assess diabetic retinopathy is to use fluorescein angiography.
Nonproliferative (Background) retinopathy is characterized by:
Microinfarcts (Cotton wool spots)

Microaneurysms

Blot and Dot hemorrhages

Hard exudates

The goal of nonproliferative retinopathy is tight glycemic and blood pressurecontrol to slow the progression of
retinopathy. Laser photocoagulation for treatment of affected areas.
Proliferative retinopathy is characterized by:
Neovascularization

Vitreous hemorrhage

Retinal detachment

Panretinal laser photocoagulation is the mainstay of treatment for proliferative retinopathy.


Vascular endothelial growth factor (VEGF) inhibitors like ranibizumab and pegaptanib serve as an adjunct therapy
for photocoagulation and can be injected into the vitreous of some patients to control neovascularization.
Ophthalmic pediatrics:

Strabismus occurs when misalignment of the two eyes results in reduced visual acuity and disconjugate gaze. It is the
most common cause of amblyopia.
When the brain is presented with 2 overlapping images it will suppresses 1 image leading to cortical blindness of the
affected eye. Amblyopia (permanent visual deficit of the suppressed eye) occurs if strabismus is not corrected by the
time the normal neuronal connections in the visual system are finalized by age 7 or 8.
Two key tests are used in the detection of strabismus:
The corneal light reflex (reflection) test: The child is asked to affix his or her gaze to an object while a pen
light is directed at the patients eyes. If the patient has strabismus, the reflection of the light on the cornea will
be different in each eye with respect to the cornea.

The cover/uncover test: The child is asked to fixate on an object, then an eye is covered. If strabismus occurs
after covering an eye, the test is positive. The test is also positive when strabismus is corrected upon
uncovering.

Intermittent strabismus is considered normal in infants during the first 3 months of life and often corrects
spontaneously. Strabismus lasting greater than 3 months requires ophthalmologic intervention.
Strabismus is classically treated with occlusion/penalization therapy of thenormal eye (not the strabismic eye!) to
encourage use of the strabismic eye. Either atropine eyedrops inducing reversible cycloplegia or an eyepatch may be
used.

If amblyopia develops, treatment still centers around maximizing use of the abnormal eye.
Amblyopia, also known as "lazy eye", is a vision deficiency in an eye that is physically normal, or a vision deficiency
out of proportion to associated structural abnormalities of the eye.
There are three primary causes of amblyopia:
Strabismus-induced amblyopia occurs when misalignment of the two eyes results in diplopia and
suppression of the image of one of the eyes

Refractive or anisometropic amblyopia occurs when the eyes are presented with different images due to
unequal refractive errors.

Deprivation or occlusion amblyopia occurs when opacities (cataracts/corneal haziness) within the eye
prevent visual input from reaching the optic nerve disrupting development.

Congenital glaucoma is a rare clinical condition in infants and children that can either occur spontaneously or
secondarily from a genetic syndrome. The classic description is an infant with large, shiny eyes; glaucoma must be
ruled out to prevent blindness.
Retinoblastoma is the most common pediatric intraocular tumor.

Orbital fractures:

Orbital floor or blow out fractures occur when there is a rapid increase in intraorbital pressure from trauma to the
face that is relieved by rupture of the orbital floor, the weakest portion of the eye socket. This allows fracture to the
orbit without significant injury to the globe.
The classic symptom associated with orbital floor fractures is restricted upward gaze due to entrapment of the
inferior rectus muscle.
Patients will have several other findings on physical exam besides restricted upward gaze including:
Infraorbital anesthesia - due to damage to the infraorbital nerve (V2)

Enophthalmos - posterior displacement of the globe into the orbit

Diplopia
Patients with orbital floor fractures with associated entrapment of extraocular muscles, such as the inferior rectus
muscle, can stimulate the oculocardiac reflex, producing nausea, vomiting as well as bradycardia.
If orbital floor fracture is suspected following trauma, the imaging study of choice is coronal computed tomography
(CT).
Patients with confirmed orbital floor trauma should receive antibiotics andurgent referral to ophthalmologist for
further management.

Periorbital cellulitis:

Periorbital (preseptal) cellulitis is an infection anterior to the orbital septumwhich is a barrier to the spread of
infection into the orbit.
Periorbital cellulitis presents with erythema, tenderness, and swelling of the eyelid and periorbital area.
As opposed to orbital cellulitis, there is no impairment of extraocular muscles, proptosis, diplopia, vision loss, or
pain with eye movement.
Infection is caused by three categories:
Local infection (from conjunctivitis, hordeolum, dacrocystitis, etc.)

Hematogenous spread (especially in children with recent URIs)

Extension of sinusitis (especially from S. pneumoniae, M. catarrhalis, and nontypable H. influenzae)

CT scan of the orbits and sinuses is used to determine the extent of orbital involvement and distinguish periorbital
cellulitis from orbital cellulitis.
Well appearing or afebrile patients can be treated as outpatients with oral antibiotics.
More toxic patients or those in which hematogenous spread is suspected require hospitalization and empiric oral
antibiotics.
Antibiotic regimens include clindamycin or trimethoprim-sulfamethoxazoleplus amoxicillin, amoxicillin-clavulanic
acid, or a third generation cephalosporin.

Retinal detachment:

Retinal detachments occur when the neurosensory retina separates from the underlying pigmented epithelium,
leading to ischemia of the sensory layer of the retina.
Risk factors for retinal detachments include:
Trauma

Myopia (myopic eyes tend to have a thinly stretched retina)

Proliferative retinopathies such as diabetic retinopathy (abnormal blood vessels in the vitreous can pull the
retina away from the pigment epithelium)

Previous cataract surgery

Family history

Patients with a retinal detachment may present with:


Increasing number of floaters

Bright flashes of light

Dense shadow that starts peripherally and moves centrally

A curtain or veil blocking the peripheral vision


May be asymptomatic if small

The diagnosis of a retinal detachment is based upon a fundoscopic exam or an ocular ultrasound if vitreous view is
blocked by hemorrhage.
An ophthalmologic exam is required emergently when suspecting a retinal detachment to avoid permanent vision
loss.
The treatment of a retinal detachment includes:
Laser photocoagulation

Scleral buckles

Injection of vitreal gas bubbles

Vitrectomy

Specific vision abnormalities:

Specific pupillary abnormality patterns are characteristic of specific disorders such as syphilis and the Argyll
Robertson pupil in which the pupil accommodates, but is unreactive to light.
The Marcus Gunn pupil is an afferent pupillary defect in which decreased bilateral pupillary constriction is observed
when light is shone into the affected eye. Normal pupillary constriction and visual acuity is otherwise observed. This
defect is most often observed in optic nerve pathologies such as optic neuritis, giant cell arteritis, and radiation
neuritis.
Horners syndrome is characteristically associated with a cervical sympathetic nerve lesion causing ptosis, miosis,
and anhydrosis.

Uveitis:

Uveitis is divided into anterior and posterior inflammatory locations:


Anterior uveitis affects the iris and the ciliary bodies

Posterior uveitis affects the choroid

Panuveitis describes inflammation of both the anterior and posterior chambers

Uveitis may be caused by many etiologies including:


Infectious (e.g. CMV, HSV, herpes zoster virus, syphilis, toxoplasmosis)

Autoimmune (e.g. reactive arthritis, ankylosing spondylitis, inflammatory bowel disease, sarcoidosis,
Behcets disease, juvenile idiopathic arthritis, SLE, Sjogrens syndrome)

Patients with uveitis generally present with symptoms depending upon the compartment involved:
Anterior compartment: pain, photophobia

Posterior compartment: painless, floaters, decreased visual acuity

Anterior uveitis is diagnosed by slit lamp exam which demonstrates white blood cell and protein accumulation
within the aqueous humor of the anterior chamber.
Posterior uveitis is diagnosed by fundoscopy or a focused slit lamp exam which shows white blood cells within the
vitreous humor and chorioretinal inflammation.
Viral uveitis is managed with the appropriate anti-viral therapy (e.g. valacyclovir for herpes simplex virus
infections) plus topical glucocorticoids,whereas bacterial uveitis is managed by solely treating the infection with
the appropriate antibiotics.
Autoimmune uveitis is managed by topical glucocorticoids, with resistant cases necessitating systemic
glucocorticoids.

ORTHOPEDICS

Hip dislocation:

90% of hip dislocations occur in the posterior direction and are usually associated with a high-energy athletic events
or trauma (eg. motor vehicle accident).
Posterior hip dislocations present with legs that appear shortened, internally rotated, and adducted.
Anterior hip dislocations can be either superior or inferior. Superior hip dislocations present with a hip that
is extended and externally rotated. Inferior hip dislocations present with a hip that is flexed and externally rotated.
Many hip dislocations are associated with acetabular fractures and less often with fractures of the femoral head.
Plain film radiography should be used in the initial assessment of suspected pelvic and hip injury.
MRI is used to determine extent of ligamentous injury and is the gold standard imaging study in ruling out
avascular necrosis of the femoral head. It is recommended that patients receive MRI 3-4 weeks post reduction to rule
out any complications from avascular necrosis.
Isolated hip dislocation can be life-threatening and require emergent reduction. A closed reduction should be
performed as soon as possible to decrease the risk of avascular necrosis and sciatic nerve damage.
Long term complications of hip dislocation include:
Avascular necrosis

Neurovascular compromise

Posttraumatic arthritis

Recurrent dislocation

OTOLARYNGOLOGY

Head and neck cancer:

Head and neck cancers are becoming more common in younger patients. Risk factors for its development include:
Smoking tobacco products (including second hand smoking)

Alcohol (may be synergistic with tobacco)

Epstein-Barr Virus (nasopharyngeal carcinoma or lymphoma)

Human Papillomavirus (type 16)

HIV (predisposes to lymphoma)

Occupational exposures (e.g. formaldehyde, hydrocarbons)

Prior radiation therapy

Plummer Vinson syndrome

The most common type of head and neck cancer in children is lymphoma.
The human papillomavirus (HPV) is becoming an increasingly recognized cause of squamous cell head and neck
cancer in young, non-smokers. This is thought to be transmitted sexually.
The most common histological type of head and neck cancers in adults issquamous cell carcinoma. Squamous cell
carcinoma is predominately secondary to alcohol, smoking, and HPV infections.
Oral cavity cancers typically present with symptoms of:
Oral pain

Non-healing ulcers

Difficulty swallowing

Weight loss

Ear pain (referred pain)

Dysarthria

Pharyngeal cancers typically present with symptoms of:


Throat pain

Bleeding

Difficulty sleeping secondary to breathing difficulties

Trouble swallowing

Referred ear pain

May be asymptomatic

Laryngeal cancers typically present with symptoms of:


Hoarseness

Trouble swallowing

Coughing

Hemoptysis

The diagnosis of a head and neck cancer relies upon a history and a physical exam which includes direct
laryngoscopy for visualization of any masses.
Head and neck cancers may present with a single, painless, enlarged jugular lymph node.
Human Papillomavirus (HPV) induced cancers may present initially as a cystic mass, in which fine needle aspiration
would not be effective.
Imaging studies include CT, MRI, and PET scan are used to stage malignancies. This should be done prior to biopsy
to prevent false readings on PET imaging.
Fine needle aspiration of an enlarged lymph node has a high diagnostic probability. Sentinel lymph node biopsies
may be used for both staging and diagnosis.
Open biopsy should never been done as it could alter staging and surgical management of the tumor.
Head and neck cancers are typically treated depending on the extent of malignancy involvement:
Localized tumors are treated by radiation or resection (resection for oral cavity tumors)

Advanced malignancies are treated with a combination of resection, radiation, and chemotherapy
(resection for oral cavity tumors)

Nasopharyngeal carcinomas are preferentially treated with radiation therapy.


Human papillomavirus (HPV) related head and neck cancers may be prevented with the tetravalent HPV vaccine
(Gardasil).

Head and neck infections:

Ludwigs angina is a form of cellulitis located in the submandibular space bilaterally and is typically secondary to
a dental infection.
Patients with Ludwig's angina symptomatically present with:
Pain

Drooling

Dysphagia

Fevers

Chills

Difficulty breathing in advanced disease

Ludwig's angina is diagnosed by both physical exam and CT imaging.


On physical examination, Ludwig's angina typically presents with:
An erythematous and raised floor of the mouth

Cyanosis (present in advanced stages)

Leaning forward (helps maintain a patent airway)

The initial therapy for Ludwig's angina is supportive therapy, however advanced cases require:
Airway protection via nasal intubation (tracheostomy if emergent)

Antibiotics such as ampicillin-sulbactam (Unasyn)

If left untreated, Ludwig's angina may cause airway obstruction and asphyxiation.
Epiglottitis is the inflammation of the epiglottis commonly caused by:
Haemophilus influenzae type b, although the rates are declining due to vaccinations

Nontypeable Haemophilus influenzae species

Staphylococcus aureus

Streptococcus species

Trauma (e.g. foreign body irritation)

Patients with epiglottitis typically present with acutely developing symptoms of:
Dysphagia

Drooling

Anxiety

No cough (versus croup)


Fever

Muffled voice

Dyspnea (lessened by leaning forward)

Stridor

The diagnosis of epiglottitis depends on visualization of an inflamed epiglottis and lateral neck radiographs which
classically demonstrates the thumb print sign.
The management of epiglottitis involves:
Airway management

Antibiotic regimens such as ceftriaxone (Rocephin) and vancomycin(Vancocin)

If left untreated, patients with epiglottitis may develop:


Airway compromise

Abscess formation

Mastoiditis, the inflammation of the mastoid air cells, is usually caused by direct extension of an acute otitis media.
Mastoiditis is typically caused by:
Streptococcus pneumoniae

Streptococcus pyogenes

Staphylococcus aureus

Patients with mastoiditis typically present with:


Overlying acute otitis media

Fever

Postauricular pain

Postauricular mass

Displacement of the ear inferiorly

May be asymptomatic

Mastoiditis is diagnosed by history and physical exam, with CT scan used to confirm the diagnosis.
Mastoiditis is managed depending on its severity:
If no involvement of adjacent structures, use intravenous antibiotics such as vancomycin (Vancocin) and
myringotomy

If adjacent structures are involved, use intravenous antibiotics such as vancomycin, myringotomy, and
mastoidectomy

If left untreated, patients with mastoiditis may develop:


Facial nerve palsy

Hearing loss
Vertigo

Intracerebral lesions

Epidural abscesses

Otitis externa:

Otitis externa is the inflammation of the external auditory canal. Risk factors for otitis externa include:
Trauma

Cerumen removal with a cotton swab (causing microperforations)

Swimming or water exposure in general (changes external auditory canal flora to gram negative
predominantly)

Foreign bodies (e.g., headphones)

The most common microbiological causes of otitis externa include:


Pseudomonas aeruginosa (associated with water exposure)

Staphylococcus epidermidis

Staphylococcus aureus

Patients with otitis externa typically present with the following symptoms:
Localized ear pain

Pruritus

Fluid discharge

Changes in hearing

The diagnosis of otitis externa is typically made through history and physical exam, which must include otoscopy.
On physical exam, patients with otitis externa typically have:
A tender auricle or tragus when palpated

White discharge may be present

Erythematous external auditory canal on otoscopy

Mobile tympanic membrane on pneumatic insufflation (versus otitis media)

No granulation tissue or mastoid tenderness (versus malignant otitis externa)

Patients with otitis externa are typically managed through:


Cleaning of the ear canal using otoscopy and a cotton swab

Otic antibiotic drops such as ofloxacin (Floxin), ciprofloxacin (Cipro),polymyxin B, neomycin, or


tobramycin (Tobrex)

Topical hydrocortisone to reduce swelling


Acetic acid drops (a low pH limits bacterial growth)

If left untreated, patients with otitis externa may develop:


Malignant otitis externa

Otomycosis (following an antibiotic regimen)

Abscess formation

Tympanic membrane perforation

Malignant (or necrotizing) otitis externa is an infection of the external auditory canal and the surrounding bony
skull.
Malignant otitis externa typically occurs in elderly diabetic patients.
Malignant otitis externa is most commonly caused by Pseudomonas aeruginosa.
Patients with malignant otitis externa typically present with:
Severe ear pain (out of proportion to simple otitis externa)

Drainage from the ear

Granulation tissue visible with otoscopy

Advanced cases may have cranial nerve involvement

The diagnosis of malignant otitis externa is dependent upon:


History and physical exam

CT imaging showing bony erosions

Biopsy to distinguish from squamous cell carcinoma

Bacterial culture for Pseudomonas aeruginosa

Malignant otitis externa is treated with an antipseudomonal such as ciprofloxacin (Cipro).

Otitis media:

Otitis media refers to an infection of the middle ear.


The most common causes of otitis media include:
S. pneumonia

H. influenzae

M. catarrhalis

S. pyogenes

Viruses

Children are more at risk for developing otitis media than adults due to a shorter and more horizontal eustachian
tube, pacifier use, and hypertrophic tonsillar tissue.
Symptoms and signs of otitis media include:
Ear pain and decreased hearing
Fever

A bulging tympanic membrane with decreased mobility and poor light reflex

Pneumatic otoscopy is the standard examination technique for diagnosing otitis media.
Complications of acute otitis media occur primarily due to local spread of the infection and include:
Mastoiditis

Meningitis

Hearing loss

Sigmoid sinus thrombosis

Brain abscess

Complications of chronic or recurrent otitis media include:


Extracranial and intracranial spread of infection

Facial paralysis

Cholesteatoma

The initial treatment of otitis media is observation and supportive care, withamoxicillin use for 10 days in
unresolved cases.
Resistant cases may require amoxicillin and clavulanic acid or a stronger cephalosporin.
Surgical placement of tympanostomy tubes into the tympanic membrane is indicated in recurrent cases to help
promote drainage of the middle ear.

Peritonsillar abscess:

Peritonsillar abscesses are loculations of purulence located between the palatine tonsillar capsule and the
pharyngeal muscles.
Peritonsillar abscesses are typically polymicrobial, including:
Streptococcus pyogenes

Staphylococcus aureus

Anaeorbes (e.g. Fusobacterium)

On physical exam, patients with a peritonsillar abscess are toxic-appearing and have concerning symptoms
of trismus (inability to fully open mouth), muffled voice, odynophagia and respiratory distress.
Differential diagnoses that may resemble peritonsillar abscess include other deep tissue infections of the head and
neck (e.g. retropharyngeal abscess) and epiglottitis. The presence of uvular deviation and unilateral cervical
lymphadenopathy are relatively unique to peritonsillar abscess and can aid in diagnosis.
A CT scan with IV contrast is the imaging modality of choice for confirming the diagnosis of a peritonsillar abscess
and also see the extent of spread.
The initial management of a peritonsillar abscess without respiratory distress involves supportive therapy and a 24
hour trial of empiric antibiotics such as:
Ampicillin-sulbactam (Unasyn)

Clindamycin
Vancomycin may be additionally used if the above regimen does not produce an adequate response.
Patients with a peritonsillar abscess and respiratory distress or failing a 24 hour trial of antibiotics requires incision
and drainage.
If left untreated, a peritonsillar abscess may cause:
Respiratory obstruction

Septic shock

Necrotizing fasciitis

Vascular compromise (internal jugular vein thrombosis)

Salivary gland tumors:

Salivary gland tumors are rare, representing 6 - 8% of all head and neck tumors in the United States.
Risk factors for salivary gland tumors include:
Radiation

Viral infections (HIV, EBV)

Smoking (Warthins tumors)

Industrial exposures

Salivary gland tumors in order of prevalence:


Pleomorphic adenoma (~60%)

Mucoepidermoid carcinoma (~8%)

Warthins tumor (~7%)

The most common benign tumor of the salivary glands is the pleomorphic adenoma (aka mixed tumor).
The most common salivary gland malignancy is the mucoepidermoid tumor, which typically arises in the parotid
glands and involves the facial nerve. (Malignant = Mucoepidermoid)
Warthins tumors are benign cystic tumors most commonly in the parotid glands.
Patients with salivary gland tumors typically present with:
Painless swelling or mass in the face and neck

Facial muscle paralysis from parotid gland invasion of the facial nerve

Swollen lymph nodes in the neck

Diagnosing salivary gland tumors requires either a fine needle aspiration (FNA) or a ultrasound-guided core needle
biopsy to determine whether the tumor is benign or malignant.
Staging requires a CT or MRI.
The treatment of salivary gland tumors generally involves surgery such as a parotidectomy.
Complications of parotidectomy include:
Facial paralysis from facial nerve irritation or transection

Frey syndrome (sweating over parotid area while chewing)


PEDIATRIC SURGERY

Congenital heart defects:

Right-to-left shunts 5 Ts:


1. Tetralogy of Fallot
2. Transposition of great vessels
3. Tricuspid atresia
4. Truncus arteriosus
5. Total anomalous pulmonary venous return
The R- L shunts cause early hypoxia, so the patients manifest cyanosis as children. Generally, the shunts result from a
high pulmonary venous resistance and low systemic vascular resistance. Anything that further increases PVR (crying,
hypoventilation, and acidosis) or decreases SVR (hypotension, histamine release, sepsis) will increase the shunting
and worsen the hypoxia.
Left-to-right shunts:
1. VSD (ventricular septal defect): holosystolic harsh murmur
2. ASD (atrial septal defect): loud S1 with wide, fixed split S2
3. PDA (patent ductus arteriosus): continuous machine like murmur
Children with Down syndrome often have an endocardial cushion defect withVSD, ASD, or AV septal defects. While
healthy children usually have a higher baseline heart rate, children with Down syndrome and a congenital heart
defect typically have a low baseline heart rate.
Small, restrictive VSD low in the muscular septum produces only a heart murmur with otherwise no symptoms and is
likely to close spontaneously within the first 2 or 3 years of life
For ASD, the treatment is a patch that can be placed surgically or through cardiac catheterization
Tetralogy of Fallot has 4 different components:
1. Pulmonary stenosis aka right ventricular outflow tract obstruction (RVOTO)
2. Over-riding aorta
3. Ventricular septal defect
4. Right ventricle hypertrophy
Children with tetralogy of Fallot learn to squat to improve oxygenation: increased femoral artery compression,
arterial side systemic pressure increased, thus decreasing the R- L shunt gradient.
The degree of RVOTO is the most important determinant of cyanosis. With severe pulmonary stenosis, all the venous
mixture is shunted to the left arterial circulation.
Clinically, these children may suffer "cyanotic spells", especially when they exert themselves during crying or feeding.
Their fingers and lips turn blue. TOF is caused by anterosuperior displacement of the infundibular septum, and
infundibular spasm is hypothesized to contribute to "cyanotic spells".
Diagnosis is by echocardiogram and definitive treatment is surgery (guided by size of pulmonary arteries vs.
ascending aorta).
CXR finding will likely show a boot shaped heart due to progressive right ventricular hypertrophy from the pressure
generated against a stenotic pulmonary valve.
Associated with the 22q11 syndrome (DiGeorge syndrome CATCH 22: which includes: cardiac defects, abnormal
facial features, thymic aplasia, cleft palate, hypocalcemia and chromosome 22 deletion).
Transposition of the Great Vessels: caused by failure of the aorticopulmonary septum to spiral in which there is a
separation of systemic and pulmonary circulation (RV attaches to Aorta and LV attaches to pulmonary trunk)
Without a L-R shunt (through an existing or surgically constructed VSD, PDA orPFO), this syndrome is incompatible
with life.
This defect is more often seen in infants of diabetic mothers.
Most common association: 50% of children with transposition of the great vessels have co-existing VSD.
Diagnosis is by echocardiogram and definitive treatment is surgery (technical details are complex and unnecessary for
Step 2).
Patent Ductus Arteriosus: a failure of the ductus arteriosus to close after birth can lead to a L-R shunt, causing
excessive pulmonary blood flow
Coil embolization is performed in older children, unless large diameter or short length of ductus requires surgery.
In utero, a patent ductus arteriosus (PDA) is normal and the right to left shunt is a normal part of the fetal
cardiovascular circulation.
3 days after birth, the ductus arteriosus will functionally close due to in PGElevels (PGE promotes ductus arteriosus
patency). This drop is triggered by the post-natal increase in PaO2 (O2 inhibits PGE synthesis). PVR also falls in
response to lung expansion and rise in PaO2.
If the ductus arteriosus continues to remain open after birth, an L-R shunt develops, leading to excessive pulmonary
blood flow and a machine-like murmur. Complications resulting from a large shunt may include: pulmonary artery
hypertension, pulmonary vascular resistance.
Diagnosis is by echocardiogram.
Indomethacin successfully treats most cases but surgery is indicated for premature infants who are refractory to
medication.
Unless CHF develops, elective surgery can be performed in full-term infants between 6 months and 2 years.
Eisenmengers syndrome: a left to right shunt can reverse to become a right to left shunt if there is progressive
pulmonary hypertension from increased pulmonary circulation. Heartlung transplantation is the only definitive
treatment.

PLASTIC SURGERY

Reconstructive and cosmetics:

Reconstructive surgery is a method by which surgeons restore function and structure to various organs and tissues.
Examples of various reconstructive surgeries include:
Trauma reconstruction

Cleft lip and palate repair

Breast reconstruction or reduction

Using skin grafts or flaps to repair skin wounds

Repair of epispadias

Cosmetic surgery is a method by which surgeons may alter the aesthetics of the body. These surgeries are generally
electively performed.
Examples of various cosmetic surgeries include:
Rhinoplasty

Removal of birthmarks and scars

Breast enhancement

Blepharoplasty

Panniculectomy

Grafts and Flaps:

A surgical graft is the transfer of tissue without its blood supply to a new location, requiring a new blood supply to
form.
Initially, the graft survives by plasmatic imbibition, or the absorption of transudate. Capillaries begin to form 48
hours following grafting, with full vascular flow developing 7 days postoperatively.
Surgical grafts are indicated when the patient experiences:
Trauma

Tumor removal

Burns

Poor approximation of wound edges

Chronic ulcers

Split thickness skin grafts (STSG) includes the epidermis and some of the dermis, and is usually 10/1000 to 18/1000 of
an inch thick.
Full thickness skin grafts (FTSG) includes the epidermis and dermis. The donor location requires a surgical flap to
repair the extraction site.
Full thickness skin grafts are used in locations where cosmetic appearance is important (e.g. the face) or in areas
with increased mobility (e.g. around joints).

Split thickness skin grafts contract more than full thickness skin grafts, making them undesirable except when large
grafts are required (e.g. large burns). They are used in cases of large grafts because of the simple healing process of
the donor site.
Failure of a surgical graft may occur secondarily to:
Graft movement

Infection

Poor neovascularization

Diabetes mellitus

Malnutrition

Smoking

Corticosteroid therapy

Graft failure may be treated depending on the extent of failure:


Partial loss is managed with moist dressing

Complete loss requires surgical assessment

A surgical flap is defined as the transfer of tissue with its original blood supply to a new location.
Surgical flaps are indicated when:
The wound area is poorly vascularized

The wound cannot be closed without high tension

A large wound occurs in a cosmetically delicate location (e.g. breast reconstruction)

Surgical flaps may be categorized by location of original tissue such as:


Simple flaps: skin that is adjacent to the wound

Regional flaps: skin is found nearby, but not immediately adjacent to the wound
Distant flaps: tissue taken from a distant region of the body

Surgical flaps may be categorized by route of vascularization:


Free flaps have a blood supply that was reconnected microvascularly

Prefabricated flaps have a blood supply connected from a distal site

Surgical flap failure is most commonly secondary to poor vascularization of the flap.
Surgical flaps that have become necrosed require surgical debridement.

POST OPERATIVE CARE

Chest pain:

Post-operative chest pain should alert the clinician two main diagnoses:myocardial infarction (MI) and pulmonary
embolism (PE).
Myocardial infarction (MI) may occur during or after the operation. The greatest risk of MI perioperatively is 48
hours after the operation. MI can be triggered by hypotension (e.g. blood loss, anesthetic vasodilation) and/or
tachycardia (e.g. pain) which may result in a mismatch of myocardial oxygen supply and demand.
Diagnosis of MI during surgery is based on elevated troponin or creatinine kinase MB levels along with symptoms
of ischemia or electrocardiographic (EKG) changes.

Diagnosis of MI postoperatively requires only elevated troponin or creatinine kinase MB levels without another
clear etiology.
Troponin measurements are recommended in the following situations:
All patients with symptoms or EKG changes. At least two serial measurements are recommended

All patients with high cardiac risk and some with low cardiac risk (see Cardiac Risk for
definition). Measurements at 6-12 hours after surgery and days 1-3 after surgery are recommended

Mortality (50%-90%) in patient with postoperative MI is much higher than MI not associated with surgery,
since thrombolytics and anticoagulation are typically contraindicated in the peri-operative setting.
All patients with symptoms of ischemia or MI and all patients with high cardiac risk (see Cardiac Risk for
definition) should receive 12-lead EKG.
The treatment for MI during surgery and MI postoperatively is statin and aspirin therapy.
Pulmonary embolism (PE) typically occurs around post-operative day 7. Cancer patients and immobilized
patients are at highest risk.
D-dimer is typically not useful in the post-operative period as it is very often elevated due to the surgery itself (i.e.
bleeding, thrombosis, inflammatory response).
The following therapies are used to prevent atelectasis, pneumonia, and pulmonary embolism, postoperatively:
Incentive spirometry (especially in high-risk patients)

Deep breathing exercises (especially in high-risk patients)

Pain control

Physical therapy

Malignant hyperthermia:
Malignant hyperthermia is a hereditary condition induced by certain anesthetic agents characterized by massive
release of intracellular calcium from the sarcoplasmic reticulum.
The inheritance of malignant hyperthermia is autosomal dominant. Malignant hyperthermia is associated with
mutations in the ryanodine receptor and, less commonly, the dihydropyridine receptor.
The most common pharmacologic causes of malignant hyperthermia are:
Inhalational halogenated anesthetics (e.g., halothane)

Succinylcholine

The increased intracellular calcium within muscle cells leads to a hypermetabolic state and are a direct cause of the
presenting signs and symptoms, which include:
Hyperthermia (usually very rapid, may climb 1 to 2 every 5 minutes)

Rigidity (due to sustained muscle contractions)

Tachycardia

Cyanosis

Systemic and local conditions related to unmanaged hyperthermia include:


Compartment syndrome

Myoglobinuria (due to rhabdomyolysis)

Arrhythmias (due to hyperkalemia and hypercalcemia from rhabdomyolysis)

Disseminated intravascular coagulation (DIC)

The initial step in management of malignant hyperthermia is discontinuing the offending agent. The only treatment
for malignant hyperthermia is dantrolene, a muscle relaxant that disrupts excitation-contraction coupling in muscle
cells. Supportive management of hyperthermia (e.g., evaporative cooling, cold inhaled O2, cold GI lavage, cool IV
fluids) should be initiated as needed.

Perioperative pulmonary complications:

Pulmonary aspiration is the process of introducing a nonpulmonary substance to the tracheobronchial tree. Risk
factors for a pulmonary aspiration include:
Altered mental status (such as sedation, neurological disorders, dementia)

Decreased gag reflex

Dysphagia

Traumatic brain injuries

Intubation and extubation

Tracheostomies

Alcoholism

Seizures
Vomiting

Esophageal problems (such as acid reflux)

Aspiration contents are usually located in characteristic locations due to the increased diameter and more vertical
angle of the right bronchus compared to the left:
Upper segment of the right lower lobe (if supine)

Lower segment of the right lower lobe (if standing or sitting)

Upper segment of the right upper lobe (if patient is prone)

A pulmonary aspiration is typically diagnosed both clinically (if witnessed) and by chest x-ray.
On physical exam, patients with a pulmonary aspiration typically present with:
Wheezing

Pulse-ox desaturation

Tachypnea

Fever (classically postop day 3 pneumonia)

Dullness to percussion (if obstruction)

Crackles on auscultation

A witnessed pulmonary aspiration may be treated by turning the patients head and suction to allow drainage of the
oropharynx.
If an unwitnessed or intraoperative aspiration is suspected, supportive therapy watchful waiting for 48 hours is
useful.
Prevention of pulmonary aspiration is the best therapy:
Nil per os (NPO) preoperatively

Elevated the head of the bed

Nasogastric tube for altered mental status patients

Smoking cessation (allows for improved cilia motility)

If left untreated, a pulmonary aspiration may cause:


Chemical pneumonitis (e.g., gastric acid)

Aspiration pneumonia (e.g., oropharyngeal flora)

Lung collapse (e.g., foreign body)

Lung abscess

An intraoperative tension pneumothorax may develop in patients with weak or traumatized lungs during positive
pressure ventilation (e.g. chronic tuberculosis or recent blunt trauma with broken ribs).
Classically, patients with an intraoperative tension pneumothorax becomeprogressively harder to ventilate with
deteriorating vital signs and decreased breath sounds unilaterally.
An intraoperative tension pneumothorax may be managed by needle decompression through the midclavicular
second intercostal space, followed by a chest tube after stabilization.
If a tension pneumothorax develops during an abdominal surgery, needle decompression may be achieved through
the diaphragm.

Postoperative fever:

Causes of postoperative fever begin with malignant hyperthermia. Suspect this etiology in a patient that develops
high fever (typically > 104 F) shortly after administration of the anesthetic. IV dantrolene, 100% O2, and cooling
blankets are warranted.
Bacteremia is a cause of fever within hours of the surgery. Blood cultures and empiric antibiotics are warranted.
Five Ws of Postoperative Fever:
1. Wind (e.g., pneumonia, pulmonary embolism)

2. Water (e.g., urinary tract infection, pyelonephritis)

3. Walking (e.g., deep venous thrombosis)

4. Wound (e.g., wound/catheter infection)

5. Wonder drugs (e.g., antibiotics or heparin, most commonly)

6. Wonder where/why (e.g., abscess)

Atelectasis is the most common cause of postoperative fever on days 0-1.

(Note: While the causal relationship of atelectasis and fever has been debated, the NBME still tests on this concept.)
Pneumonia is a cause of postoperative fever between days 1-3, and is typically suspected when an initial fever on
postoperative day 0-1 persists for 2-3 days.
Post operative urinary tract infections typically present between postoperativedays 3-5.
Thrombophlebitis may be a source of fever on postoperative days 4-6.
Postoperative wound or catheter infection usually present between postoperativedays 5 to 8. The first step to treating
postoperative wound infections is to remove some staples from the fluctuant wound to allow any fluid collection (e.g.,
pus) to drain from beneath the skin.
Drug fever should always be considered in the differential of postoperative fever, and may have a varied
presentation. It can occur at any time, but classically presents on postoperative day >7.

Paralytic ileus:

A postoperative paralytic ileus refers to the severe constipation and overall intestinal atony following an abdominal
or non-abdominal surgery.
Postoperative paralytic ileuses are typically benign, occurring anywhere from the stomach through the large intestines
as a result of:
Inflammatory responses to mechanical movement or trauma

Inhibitory neural reflexes within the sympathetic ganglia

Nitric oxide and VIP inhibitory peptide release

Opioid medications

Hypokalemia, hypomagnesemia

Risk factors for a postoperative paralytic ileus include:


Abdominal or pelvic surgery

Prolonged surgical time

Open surgery (versus laparoscopic)

Obesity

Transfusions

Perioperative intestinal inflammation

Patients with a postoperative paralytic ileus symptomatically present with:


Abdominal distention

Nausea

Vomiting

Intolerance to oral foods/drinks

Delayed flatulence or stool passage

Pain

The diagnosis of a postoperative paralytic ileus is typically a diagnosis of exclusion, however an abdominal x-ray
may be used to rule out obstruction.
Patients with a postoperative paralytic ileus typically present with the following physical exam findings:
Abdominal distention

Tympanic on percussion

Diffuse tenderness

Decreased bowel sounds (vs. small bowel obstruction which has increased bowel sounds)

Classically on abdominal imaging, patients with a postoperative paralytic ileus demonstrate:


Dilated bowel loops (x-ray)

Free air in the colon (x-ray)

No transition zone (CT)

Notably, a mechanical small bowel obstruction will have an identifiable transition zone on abdominal CT, in contrast
to ileus.
The management of a postoperative paralytic ileus is typically supportive therapy including:
Correcting electrolyte abnormalities

Weaning off pain medications

Bowel rest

Laxatives such as docusate (Colace, Dulcolax)


Acute colonic psuedo-obstruction (aka Ogilvie's syndrome) should be suspected inseverely ill patients with a dilated
cecum and right hemicolon and is typically managed through supportive therapy and neostigmine.

Urinary complications:

Urinary retention is common problem postoperatively. Risk factors for postoperative urinary retention include:
Pain medications (e.g. opioids)

Anticholinergic medications

Spinal anesthesia

Long duration of anesthesia

Pelvic surgeries/manipulation (e.g. rectal stimulation can reflexively inhibit bladder contraction)

Postoperative day 1 - 3

Postoperative urinary retention is common after surgery in the abdomen, pelvis, rectum, or groin. Patients will
present with:
Urgency

Discomfort

Fullness on palpation of bladder

Inability to void

The first step in managing a postoperative patient with bladder distention and urinary retention is in and out
catheterization (straight catheterization).
Patients with low urinary output, less than 0.5mL/kg/hour, who have had urinary retention ruled out via straight or
current indwelling catheterization in the presence of normal perfusing blood pressure should be worked up to rule
outdehydration or acute renal failure.
Fluid challenge (bolus of ~ 1 liter of normal saline) is an appropriate first step in the evaluation of a postoperative
patient with oliguria without urinary retention. Urine output will increase in a dehydrated patient with prerenal
azotemia and will remain the same in patients with renal failure.

Urinary sodium less than 20 mEq/L is suggestive of dehydration while more than40 mEq/L is suggestive of acute
renal failure.

Wounds:

The four types of wounds include:


Clean

Clean-contaminated

Contaminated

Dirty
A clean wound is defined as a atraumatic and having no gastrointestinal (GI), genitourinary (GU), or respiratory
tract involvement. An example is surgical incision.
A clean-contaminated wound is similar to a clean wound, but with GI, GU, or respiratory tract involvement. An
example is a minor sterile break into GI, GU, or respiratory tract.
A contaminated wound is direct contact of GI, GU, or respiratory contents with wound. An example is traumatic
wound with GI, GU, or respiratory matter.
A dirty wound is active infection within wound. An example is infected surgical wound with abscess.
The four types of wound healing include:
Primary intention

Secondary intention

Delayed primary closure

Skin grafts

Wound healing by primary intention refers to any technique where the epidermal edges of the wound are
approximated. Examples include the surgical incisions or lacerations closed with staple, sutures, or adhesive.
Wound healing by secondary intention leaves the wound open. These wounds are treated with "wet-to-dry"
dressings. Examples include subcutaneous abscess after incision and drainage and open appendectomy for
perforated appendicitis.
Delayed wound closure (or wound healing by tertiary intention) is left to heal by secondary intention for up to 5
days then the wound edges are approximated and closed as in wound healing by primary intention. This type of
wound healing is possible due to the highly vascular granulation tissue of secondary intention wound healing making
it more resistant to infection.
Wound healing with skin grafts refers to the use of split-thickness skin grafts consisting of epidermis and a portion
of dermis.
Dressings are required for closed wounds for the first 48 hours after closure.
Systemic factors that may inhibit and/or delay wound healing are:
Malnutrition

Corticosteroids

Smoking

Hepatic and/or renal failure

Diabetes mellitus

Local factors that may inhibit and/or delay wound healing are:
Radiation

Infection

Bleeding/hematoma (can lead to infection)

Improper wound management (e.g., not keeping the wound clean, debrided, dry, closed)

Wound dehiscence is when a wound breaks open along surgical suture, typically occurs around post-operative day
5.
Wound dehiscence can appear to be intact, but large amount of salmon-colored (peritoneal) fluid soaks the
dressing.
The most common cause of wound dehiscence is wound infection.
Wound dehiscence requires re-operation to prevent evisceration.
Surgery may not be necessary in cases where only part of the incision has opened and where the fascia remains
intact. To assess whether the patient needs surgery, sutures or staples must be removed from the affected portion of
the incision and the wound must be probed with cotton-tipped applicators.
Gastrointestinal fistula usually occur as a complication of abdominal surgery and are usually recognized when bowel
contents leak through a surgical wound or drain site.
General management of a freely draining fistula centers on ordering NPO status, fluid and electrolyte replacement,
and intensive protection of the abdominal wall to prevent erosion.
Most will heal in several weeks; however, when fistulas fails to heal use the FRIEND mnemonic to remember
possible explanations.
Foreign body in the wound

Radiation damage

Infection or Inflammatory bowel disease

Epithelialization of the fistulous tract

Neoplasm

Distal bowel obstruction

PRE-OPERATIVE CARE

Cardiac risk:

An initial estimate of perioperative cardiac risk is calculated with the revised Goldman cardiac risk index (RCRI),
which is based on the following 6 independent predictors:
High risk surgery (intraperotineal, intrathoracic, vascular)

History of ischemic heart disease

History of congestive heart failure

History of cerebrovascular disease

Diabetes mellitus requiring insulin treatment

Pre-operative creatinine >2.0 mg/dL

Total Risk of Peri-operative Cardiac Complications


Points for noncardiac surgery

Zero risk factors 0.4%

One risk factor 1.0%

Two risk factors 2.4%

Three or more risk factors 5.4%

Patients with a score of 1 or 0 on RCRI are considered low risk for major cardiac events (<1%).
Patients with low risk for major cardiac events undergoing can be cleared for surgery without further cardiac testing
or risk stratification.
Patients with 2 or more RCRI are considered elevated risk for major adverse cardiac event.
Functional status has been found to be an accurate predictor of perioperative and long-term cardiac events. Metabolic
equivalents are measures of functional status estimated from activities of daily living and can be used to further risk
stratify patients with elevated risk for major adverse cardiac events.
Patients with an elevated risk of major adverse cardiac event need not require further cardiac testing if they have >4
metabolic equivalents (METs) which is considered moderate to excellent.
A question stem can provide information on a patient's functional status or METs implicitly. A patient who can
perform the following or more should be understood to have adequate functional status and not require further
testing:
Climbing a flight of stairs

Walking up a hill

Performing heavy household work

Rigorous sports activities

A patient with known or suspected heart disease should only receive a cardiac stress test or echocardiography before
surgery if it is indicated in the absence of proposed surgery. Patients with the following conditions warrant further
study:
Unstable angina

Significant arrhythmia

Uncompensated CHF

Severe valvular disease

Elective surgery should be delayed at least 8 weeks post-myocardial infarction.


It is recommended that an ECG be obtained in patients undergoing intermediate-risk procedures or in patients with
at least 1 clinical risk factor identified by RCRI, in order to compare it to a postoperative ECG in the event the
postoperative ECG is abnormal.

ECG is unnecessary in all patients undergoing low risk surgery (eg. cataract surgery).

Hepatic risk and hematologic assessment:

Child-Pugh score is used to predict mortality and short term survival in patients with liver disease. While the
classification of patients based on the Child-Pugh score is beyond the scope of Step 2, the following measures of
hepatic function are used in scoring:
Albumin

Bilirubin

Encephalopathy

Ascites

PT (INR)

Mnemonic: "A BEAP"


Acute hepatitis is a contraindication for elective surgery.
Patients with liver disease should have their medical therapy optimized prior to undergoing surgery. The following
should be evaluated in a patient with liver disease prior to surgery:
Renal function

Electrolyte abnormalities

Bleeding time / PT (INR) / PTT

Encephalopathy

Nutritional status

Prolonged bleeding time can be corrected in a patient with liver disease withdesmopressin (DDAVP).
If coagulopathy is present, attempt to normalize INR prior to surgery with:
1. Vitamin K

2. Fresh frozen plasma (FFP)

Patients who are taking warfarin should discontinue medication 3 to 4 days before the surgery. This timing is based
on warfarin's half-life, which is approximately 36-42 hours.
For surgeries with a high risk of bleeding the international normalized ratio (INR) should be kept below 1.5.
A history of thromboembolism indicates anticoagulation with heparin or low molecular weight heparin (LMWH)
(e.g., enoxaparin, dalteparin) after discontinuing warfarin until surgery then restarted warfarin postoperatively.
Heparin or LMWH is resumed 12 hours after surgery.

Metabolic and renal risk:

Patients with diabetes mellitus have the following surgical complications:


Increased risk of infection

Delayed wound healing

Increase risk of cardiac complications

Increased mortality postoperatively

Diabetic patients may require greater than normal insulin administrationpostoperatively due to glycemic
fluctuations.
Preoperative dialysis may be necessary for patients with renal insufficiency to control creatinine and electrolytes.
Acetylcysteine may be used to prevent contrast-induced nephropathy in patients with renal insufficiency, who are
expected to receive intraoperative contrast. In addition, volume depletion and NSAIDs should be avoided. Isotonic
IV fluid administration hours before can prevent volume depletion.

Nutritional risk:

If the patient shows severe nutritional depletion, elective surgery should be postponed until optimized.
Severe malnutrition increases operative risk. Indicators of severe nutritional depletion include:
1. Anergy to skin antigens

2. Serum albumin < 3 g/dL

3. Serum transferrin < 200 mg/dL

4. Significant weight loss (e.g., loss of 20% total body weight) over a span of only a few months
The best lab test to determine acute nutritional status is prealbumin, due to its short half life (2-3 days). The normal
range is 16-40 mg/dL. Values <16 mg/dL are associated with malnutrition.
However, prealbumin is expensive and may be decreased in patients with the following conditions:
Physiological stress

Infection

Liver dysfunction

Over-hydration

Pulmonary risk:

Preoperative pulmonary function tests serve as the best predictors of postoperative pulmonary complications.
Patients with known lung disease (eg. COPD, asthma) and smokers should be considered for preoperative pulmonary
function tests (PFTs) if after clinical evaluation it is still unclear whether the patient is at their best baseline and
that airflow obstruction is optimally reduced. Routine PFTs in patients with stable symptoms and optimized
management of their lung disease is NOT recommended.
The most effective way to reduce postoperative respiratory complications is smoking cessation at least 8 weeks prior
to surgery.
A preoperative FEV1 of > 1.5 liters is required for lobectomy.
A preoperative FEV1 of > 2 liters is required for pneumonectomy.

TRANSPLANTATION SURGERY

Heart and Lung transplant:

Heart transplantation is performed on patients with end-stage heart failure or severe coronary artery disease.
Indications for heart transplant include:
Severe cardiac disability on maximal medical therapy

Symptomatic ischemia or recurrent ventricular arrhythmia on maximum medical therapy, with left
ventricular ejection fraction less than 30%

Unstable angina and not a candidate for CABG or percutaneous transluminal coronary angioplasty

Donor matching is based on several donor-recipient compatibilities including:


ABO compatibility

Body size

Weight similarity

Contraindications for heart transplantation include:


Pulmonary hypertension

Smoking tobacco within six months

COPD

Acute rejection is the most common form of rejection following heart transplantation.
Rejection is diagnosed and conrmed by endomyocardial biopsy via the right internal jugular vein.
The complications of heart transplantation include:
Infection

Pulmonary hypertension

Graft failure

Lung transplantation is performed on patients with end-stage lung disease who are refractory to all other available
medical treatments, most commonly secondary to:
COPD

Idiopathic pulmonary fibrosis

Cystic fibrosis

Primary pulmonary hypertension

1-antitrypsin deficiency

Donor-recipient compatibility for lung transplantation is based upon several criteria:


ABO compatibility

Pulmonary gas exchange

No smoking history

Similar donor-recipient lung volumes

Contraindications for lung transplantation include:


Smoking within six months

Cardiac, renal, or hepatic failure

HIV

Terminal illness

Chronic rejection is the most common form of rejection following lung transplantation.
Rejection is confirmed by biopsy through bronchoscopy and has several findings including:
Fever

Dyspnea

Decreased PaO2

Decreased FEV1

Chest x-ray demonstrating interstitial infiltrate

Complications following lung transplantation include:


Infection

Rejection
Immunosuppressive drugs:

All patients receiving allografts require immunosuppressive therapy. The only exception is recipients of a
transplanted organ from an identical monozygotic twin (isograft).
Most immunosuppressive agents covered in this topic are used in maintenance therapy to prevent acute rejection of the
graft.
Immunosuppressive agents carry a complex array of morbidities. The most important morbidities to broadly associate
with the various immunosuppressive agents are nephrotoxicity, myelosuppression, and metabolic syndrome.
Glucocorticoids suppress B and T cell function and inhibit the release of IL-1 from macrophages. Prednisone is the
most commonly used glucocorticoid used in transplantation.
The adverse effects of glucocorticoids include:
Cushing syndrome

Cataracts

Dyspepsia

Osteonecrosis

Acne

Glucose intolerance

Cyclosporine (CsA, Sandimmune, Neoral, Gengraf) is a calcineurin inhibitor that binds cyclophilin and inhibits the
secretion and formation of IL-2.
Tacrolimus (FK506, Prograf) is a calcineurin inhibitor that binds FK506 binding protein (FKBP) and inhibits the
secretion and formation of IL-2 and other cytokines. It is the most commonly used calcineurin inhibitor in
immunosuppressive drug regimens.
In contrast to cyclosporine (another commonly-used calcineurin inhibitor),tacrolimus exhibits less severe androgenic
effects.
Azathioprine (Imuran) is an antimetabolite precursor of 6-mercaptopurine, which inhibits nucleotide synthesis. It is
being replaced with mycophenolate mofetil (MMF, CellCept).
Sirolimus or rapamycin (Rapamune) exhibits a unique molecular target by inhibiting mTOR (mammalian Target Of
Rapamycin) by complexing with FKBP to inhibit T-cell proliferation.
Sirolimus is unique for exhibiting minimal nephrotoxicity.
Muromonab-CD3 (Orthoclone OKT3) is a monoclonal antibody that depletes the T-cell population.
Muromonab-CD3 can induce a one-time cytokine release (fever, bronchospasm) upon use. It can only be used in
short-term therapy.

Kiney, pancreas and liver transplantation:

Kidney transplantation is the most common solid organ to be transplanted.


There are multiple causes of end stage renal disease that may warrant transplantation including:
Diabetes

Hypertension

Glomerular nephritis

Congenital urologic anomalies

Focal segmental glomerular sclerosis


Left kidney is preferred as a donor because it has a longer renal vein (remember the inferior vena cava is on the right
side of the body, so the left kidney needs a longer vein).
Early complications of kidney transplant include oliguria or anuria that may result from graft thrombosis or urine
leak.
Late complications of kidney transplant include ureteral stricture ( creatinine)and arteriosclerosis of the renal
artery.
Existing kidneys are NOT removed due to increased rates of surgical morbidity. The donated kidney is usually placed
in the iliac fossa (pelvis).
Pancreas transplantation is performed on individuals with type 1 diabetes with end-stage renal disease (majority of
these are simultaneous pancreas-kidney transplantations).
Type II diabetes is a contraindication to pancreas transplantation.
There are multiple causes of liver failure that are indications for transplantation:
Chronic hepatitis B

Chronic hepatitis C

Alcoholic sclerosis

Biliary disease - primary sclerosing cholangitis, primary biliary cirrhosis, biliary atresia

Wilson disease

Absolute contraindications for liver transplantation include:


Active drug or alcohol abuse

Uncontrolled metastatic cancer outside liver

Liver cancer

Active systemic infection

Individuals with hepatitis B or C may be used as donors for patients with the same infection if there is no organ
damage detected in the donor liver.

Transplant selection and rejection:

Organ transplant donors are most commonly brain-dead or living voluntary donors without HIV, cancer, sepsis, or
organ insufficiency.
Selection of organ transplant donors is based on the following criteria:
ABO blood group compatibility

Cross match compatibility (i.e., antidonor antibodies on recipient T cells)

HLA antigen matching

HLA antigen matching is more significant for pancreas and kidney transplants and less significant
for heart and liver.
Organs from individuals with a specific infection (e.g., hepatitis) with no significant organ damage may be
transplanted into a recipient with the same infection.
The three types of transplant rejection are:
Hyperacute

Acute
Chronic

Hyperacute transplant rejection occurs immediately or within hours (< 24 hours) of the transplantation.
Preformed recipient antibodies against donor tissue, usually directed toward ABO blood group or HLA antigens,
mediate the reaction leading to vascular thrombosis and necrosis. Histologically, the predominant cell infiltrate of
hyperacute transplant rejection is polymorphonuclear leukocytes.
Hyperacute transplant rejection is untreatable, but rarely occurs due to cross-matching and blood group matching.
Acute transplant rejection usually occurs 7-10 days after transplantation, but may occur up to a year.
Antidonor T-cells proliferate in the recipient and mediate the reaction leading to mononuclear infiltration into
vascular and interstitial spaces. For this reason, histologically, the predominant cell infiltrate of acute transplant
rejection ismonocyte/macrophage.
Acute transplant rejection is treated with immunosuppressive agents and isfrequently reversible. If reversed, the
graft has a good prognosis.
Chronic transplant rejection occurs years after transplantation.
The pathogenesis of chronic transplant rejection is poorly understood, but ismediated by both cellular and humoral
immune reactions. The donor tissue is characterized by vascular intimal hyperplasia and lymphocytic infiltration.
There is no effective treatment for chronic transplant rejection.

TRAUMA

Abdominal trauma:

Abdominal trauma can be caused by a variety of mechanisms includingpenetrating trauma (e.g. from a stab wound
or gunshot wound) or blunt trauma (e.g. from a motor vehicle accident).
The liver and spleen are at high-risk for injury during blunt abdominal trauma.
Rib fractures may be a cause or complication of these injuries.
Clinical presentation may include:
Abdominal distension

Tenderness or fullness on palpation

Guarding

Bowel sounds in the thorax

Crepitation of lower thoracic cage

The goal of the primary survey of a patient that has sustained abdominal trauma is to identify and treat life-
threatening injuries. This is dictated by the Advanced Trauma Life Support protocol, and includes:
Airway maintenance, with cervical spine precautions

Breathing

Circulation

Disability

Exposure

Focused abdominal sonography for trauma (FAST) scan can be used to evaluate potential areas of blood collection
within the peritoneum.
CT scan of the abdomen gives detailed information about the pathology and source of hemorrhage (if present). It
may also assist in planning of operative intervention.
Complications of abdominal trauma to the liver and spleen may include:
Hypovolemic shock

Infection

Diaphragmatic rupture

Hematoma rupture

Abscess formation

Bowel obstruction or ileus

Abdominal compartment syndrome

Irritation of the diaphragm (e.g. due to splenic rupture) may cause referred pain to the shoulder area, typically the
left shoulder. This is known as Kehrs sign.
Unstable patients with peritoneal signs or evisceration status post trauma warrant immediate surgery.
Patients should be kept on hemodynamic monitoring and followed clinically with serial abdominal exams.

Airway:

In trauma resuscitation, always secure the airway first.


If the patient is speaking in a normal tone of voice, s/he has a patent airway.
If emphysema in the neck or an expanding neck hematoma is noted, the patient has a threatened airway, requiring
airway management.
Intubation is indicated in all patients with a Glasgow Coma Scale (GCS) score equal to or less than 8.
Neck hyperextension in patients with possible cervical spine injury should be avoided; in-line
stabilization and/or fiberoptic intubation should be used when intubating.
The three main ways to secure an airway are:
Cricothyroidotomy

Orotracheal intubation

Percutaneous tracheostomy

In the field without access to orotracheal intubation, cricothyroidotomy is most commonly used.
In the emergency department, use rapid sequence induction and orotracheal intubation. Avoid nasal intubation if the
patient has facial fractures.
In a patient with extensive maxillofacial injuries (preventing passage of an endotracheal tube),
perform cricothyroidotomy or percutaneous tracheostomy.
Breathing is assessed by the movement of air:
Breath sounds in both right and left lung fields

Normal pulse oximetry

Head injuries:

Every patient who sustains head trauma and becomes unconscious for any period of time requires a head CT scan.
Patients who sustain head trauma and become unconscious for any period of time do not need to be hospitalized if
the following conditions are met:
There is no intracranial bleeding on CT scan.
The patient is neurologically intact.

The patient has someone who will check on him/her frequently for 24 hours to ensure the patient is not
becoming comatose and to bring the patient back to the ER if signs and symptoms of traumatic brain injury
(e.g., headache, vomiting, dizziness, confusion) persist or worsen.

Generally, the rules for linear skull fractures are the following:
If the fracture is closed (no overlying wound), it requires no direct treatment.

If the fracture is open, the wound needs to be closed.

If the fracture is comminuted and/or depressed, it must surgically repaired in OR.

Signs of skull base fractures are:


Periorbital ecchymoses (i.e., raccoon eyes)

Rhinorrhea (CSF dripping from nose)

Otorrhea (CSF leaking from ears)

Ecchymosis behind the ear (i.e., Battles sign)

If skull base fracture is suspected in a conscious patient, a CT of the c-spine is indicated to check for cervical spine
fractures.

If skull base fracture is suspected in a patient who was unconscious, a CT of the head including the c-spine is
indicated to check for intracranial bleeding and cervical spine fractures.
Epidural hematoma is usually caused by tearing of the middle meningeal arterydue to head trauma. Classically, the
patient will initial lose consciousness from the initial trauma then have a "lucid interval" followed by rapid neurologic
deterioration. The clinical course is commonly described as "talk and die."
Head CT scan provides the most definitive diagnosis of an epidural hematoma. It will classically show a biconvex,
lens-shaped hematoma.
Once diagnosed by head CT scan, the treatment for epidural hematoma is rapid craniotomy to evacuate the
hematoma. Generally, a good outcome is expected if treated promptly.
If not treated with craniotomy, the expanding hematoma can lead to compression of CN3 resulting in ipsilateral fixed
dilated pupil and a subfalcine herniation with compression of the cerebral cortex and brainstem resulting
in contralateral hemiparesis with decerebrate posturing.
Acute subdural hematoma is usually caused by tearing of the bridging veins in the subdural space. Classically, there
is more severe trauma than that associated with an acute epidural hematoma. A patient may be immediately knocked
unconscious and never fully regain consciousness due to the severity of the initial injury. Mass effects of the acute
subdural hematoma may cause a midline shift.
Head CT scan provides the most rapid and definitive diagnosis of acute subdural hematoma. It will classically show
a semilunar crescent-shaped hematoma.
Once diagnosed by head CT scan, the treatment for an acute subdural hematoma depends on whether there is an
midline shift.
If midline brain structures are displaced by the hematoma, craniotomy may help.

If midline brain structures are not deviated, craniotomy will not help and the patient should be managed
medically to prevent or minimize subsequent development of increased ICP (intracranial pressure).

Increased ICP is managed in the following ways:


ICP monitoring

Elevate head of bed


Hyperventilate

Avoid fluid overload with gentle diuresis with mannitol or furosemide

Chronic subdural hematomas are most commonly seen in alcoholics andthe elderly. These patients have significant
brain atrophy causing an increased susceptibility to bridging vein tearing.
Once diagnosed by head CT scan, craniotomy may result in dramatic improvement of a chronic subdural hematoma.
Penetrating head trauma requires immediate surgery to repair damage.
Diffuse axonal injury is seen in severe trauma. Head CT scan shows no mass lesion, but multiple small lesions
involving the gray-white matter interface.

Neck injuries:

In order to help guide management, the neck is divided into the following 3 zones:
Zone I: Inferior to the cricoid cartilage

Zone II: Between the cricoid cartilage and angle of the mandible

Zone III: Superior to the angle of the mandible

Penetrating neck injuries warrant surgical exploration if any of the following conditions are present:
The patients vitals are deteriorating (i.e., hemorrhagic shock)

There is an expanding hematoma, which can acutely compromise the airway

There are signs of tracheal or esophageal injury (e.g., hemoptysis, subcutaneous emphysema)

In patients with penetrating neck injuries (e.g., gun shot or stab wounds), the following tests are necessary to rule out
surgical intervention or determine surgical approach:
Arteriography

Esophagogram (water-soluble, then barium if negative)

Esophagoscopy

Bronchoscopy

If patients with severe blunt trauma to the neck have neurologic deficits orevidence of a fracture (e.g., point
tenderness on c-spine palpation), then a CT scan of the cervical spine is indicated.

Shock:

In the setting of traumatic injury, shock is usually caused by:


Hypovolemia/hemorrhage (most common cause in trauma patients)

Acute pericardial tamponade

Tension pneumothorax

Neurogenic (spinal cord injury)

The most important clinical feature that distinguishes hypovolemia/hemorrhage from tension pneumothorax and
pericardial tamponade in a tachycardic trauma patient is flat neck veins (low CVP).
The first step in management of a patient with hypovolemia/hemorrhagic isvolume replacement with intravenous
fluids. 2 liters of normal saline or lactated ringers are given as fast as possible through large-bore (e.g., 14-gauge)
peripheral IVs. This is followed by blood (packed red cells). The general rule for trauma resuscitation is 3 ml of fluid
is need for each ml of blood lost ("3-to-1 rule"). Note: Colloids (vs. crystalloids) have not been shown to improve
mortality in hemorrhagic patients.
During trauma resuscitation of a hypovolemic/hemorrhagic patient, the target urine output is 0.5-2.0
ml/kg/h. However, the central venous pressure (CVP) should not exceeded 15 mmHg.
If peripheral IV access cannot be established quickly, alternatives include:
Intraosseous cannulation (e.g., proximal tibia) (most common in modern trauma setting)

Percutaneous femoral/jugular vein catheters

Saphenous vein cut-downs

A patient with pericardial tamponade will have the following clinical features:
Trauma to the chest (e.g. penetrating chest trauma most common)

Distended head and neck veins (high CVP)

Hypotension

Muffled heart sounds

Beck Triad = Hypotension, JVD, muffled heart sounds


Pericardial tamponade is a medical emergency and is usually diagnosed clinically. When diagnosis is
unclear, sonogram is used for confirmation. Immediate pericardial sac evacuation by pericardiocentesis, tube,
pericardial window, or open thoracotomy is required for treatment.
A patient with a tension pneumothorax will have the following clinical features:
Trauma to the chest (e.g., GSW, stabbing)

Distended head and neck veins (high CVP)

Hypotension

Severe respiratory distress

On physical exam of the chest of a patient with tension pneumothorax, the affected side has no breath sounds and
is hyperresonant to percussion. On x-ray, the mediastinum is displaced to the opposite side, marked most notably by
tracheal deviation.
Since a tension pneumothorax is a clinical diagnosis and a medical emergency,NO chest x-ray or other study is
necessary and is contraindicated. Management is insertion of a large-bore needle or IV catheter into the pleural
space(inserted high on anterior chest wall in the second intercostal space) then insertion of a chest tube and connect it
to underwater seal and suction (chest tube also inserted high on anterior chest wall).
The most important clinical feature to distinguish neurogenic shock from the other forms of trauma shock
is bradycardia. Other signs and symptoms include:
Flaccid paralysis

Hypotension

Cutaneous vasodilation
Thoracic injuries:

Thoracic trauma is unique in that blunt trauma may cause secondary penetrating trauma via fractured rib
penetration. Therefore, penetrating trauma must be considered in any case of thoracic trauma.
Due to the curvature of the diaphragm, one cannot rule out abdominal trauma that occurs below the nipple line.
Pain on breathing from rib fractures and other injuries in thoracic trauma may limit chest wall excursion.
Management in these cases centers around local anesthesia, as opposed to pain medications that may decrease
respiratory drive.
Both tension pneumothorax and pericardial tamponade can cause extrinsic compression of the heart and acute heart
failure, and must be considered as differential diagnoses of hypotensive tachycardia in the setting of thoracic trauma.
Note that these are both clinical diagnoses; taking time for diagnostic imaging risks increased mortality.

Both of these pathologies are differentiated from hypovolemic shock by the presence of distended neck veins.
In the setting of thoracic trauma, hypotensive tachycardia with distended neck veins is suspected to be either cardiac
tamponade or a tension pneumothorax (though more rare pathologies could be causative). Distant, muffled heart
sounds are indicative of cardiac tamponade.

Blood will also be found in the pericardial sac on emergent bedside ultrasound examination (the "FAST" exam).
The best next step in treatment of cardiac tamponade is emergent pericardiocentesis, without waiting for diagnostic
imaging.
Further information regarding cardiac tamponade can be found in the Cardiac Tamponade topic and the Shock topic.
In the setting of thoracic trauma, hypotensive tachycardia with distended neck veins could be either cardiac
tamponade or a tension pneumothorax. Pulmonary exam findings of decreased breath sounds and hyperresonant
percussion are indicative of tension pneumothorax.
Sucking chest wounds are those that visibly can be seen to suck in air, and can lead to a tension pneumothorax.
Management is bandaging with an occlusive dressing taped at only 3 points, which acts as a one-way valve to let air
out of the thorax. Intubation and further surgical management may be needed.
The first three steps in management of a tension pneumothorax are:
1. Emergent needle decompression, inserted into the 2nd intercostal space

2. Chest tube (tube thoracostomy), inserted into the 5th intercostal space

3. Intubation, if still necessary

Note that diagnostic imaging plays no role in the emergent stabilization of these patients.
Further information regarding pneumothoraces can be found in thePneumothorax topic and the Shock topic.
Hemothorax, an accumulation of blood outside the visceral lung pleura, is a differential diagnosis of decreased breath
sounds along with pneumothorax. However, it is differentiated by the presence of dullness to percussion on physical
exam.
The management of hemothorax is often non-emergent, as parenchymal lung bleeding is often self-limiting. Initial
management is a chest tube (tube thoracostomy).
Either a massive immediate drainage (greater than 1.5 L) or large ongoing drainage of the chest tube (200 to 300 ml per
hour) warrants surgical intervention with thoracotomy to ligate the vessel. Bleeding in this manner is known to be
thoracic (e.g. intercostal artery), as opposed to pulmonary parenchymal.
A flail chest is a segment of chest wall that exhibits paradoxical respiratory mechanics (i.e. expansion on
expiration) correctable by PEEP (positive end-expiratory pressure). It occurs when segments of ribs are broken in two
places to create a separate segment of chest wall.
The best early treatment of a flail chest is pain control and supplemental oxygen to maximize excursion and
oxygenation.
If patients with flail chest are intubated and PEEP is utilized, prophylactic chest tubes on the side where rib fractures
are located are warranted to prevent pneumothorax.
There are 4 signs of trauma that are extreme enough to warrant active investigation for occult secondary
complications of trauma. These signs are:
Sternum fracture
1st rib fracture

Scapula fracture

Flail chest formation

If any of these four signs of extreme thoracic trauma are present, the patient must be prophylactically evaluated for
the following complications:
Pulmonary contusion

Myocardial contusion

Aortic rupture

Initial evaluation includes chest radiograph, EKG, and cardiac enzymes for these complications.
The first diagnostic study to evaluate a patient for a traumatic aortic rupture is achest x-ray. Finding of a widened
mediastinum on chest x-ray is highly concerning.
Regardless of CXR results, if clinical suspicion of traumatic aortic rupture is high, the next diagnostic study to perform
is either a chest CT or a transesophageal echocardiogram (TEE). The two tests have comparable sensitivity and
specificity, with TEE being preferable in unstable patients.
The final diagnostic study that may be needed in the evaluation of a potential aortic rupture is
an arteriogram. Arteriograms are only indicated in the case of apositive chest radiograph and negative follow-up
CT/TEE with high clinical suspicion.
Pulmonary contusions are parenchymal injuries that can cause hypoxia in the acute setting. Classically, pulmonary
contusions may not be immediately apparent radiographically, but later show a bilateral "white-out" appearance due
to diffuse opacities.
Pulmonary contusions have a similar pathophysiology to ARDS in that they are characterized by increased vascular
permeability. Besides breathing and oxygenation monitoring, treatment of pulmonary contusion centers around fluid
restriction and diuretics.
Diaphragmatic ruptures most commonly occur on the left, because the liver prevents right-sided rupture. Two
radiographic findings on chest x-ray aremultiple air-fluid levels and presence of nasogastric tube in the thorax.

Treatment is via surgical correction.


Tracheobronchial injury can lead to extravasation of air into other tissues and persistent respiratory trouble. Suspect
rupture of the trachea or bronchi when apneumothorax persists despite chest tube placement and other stabilization
measures.
The next best step in evaluation of a tracheobronchial injury is bronchoscopy.

Urological injuries:

Urological injuries are often overlooked in the initial evaluation of a trauma patient but need to be suspected in the
following situations:
Straddle injury

Penetrating injury to lower abdomen

Fall from a height

Gross hematuria

Pelvic fracture

The most common signs and symptoms of urethral injury include:


Blood at the urethral meatus
Ecchymoses or hematoma involving penis, scrotum, or perineum

"High riding", or superiorly displaced, prostate

Inability to void

When an urethral injury is suspected, before a Foley can be placed retrograde urethrogram must be done to evaluate
the extent of the urethral injury.

(Note: While the digital rectal exam is classically taught to be useful in the initial valuation of urethral injury, multiple
retrospective and observational studies demonstrate a lack of sensitivity and utility in the DRE.)
Anterior urethral injury is treated with immediate surgery; posterior urethral injury is treated with suprapubic
cystostomy tube placement and delayed repair.
Bladder injuries are usually associated with pelvic fractures. Intraperitoneal bladder rupture is treated
with surgery; extraperitoneal bladder rupture is treated with non-surgical management by Foley drainage or
suprapubic cystotomy tube.
Abdominal CT scan with contrast is used to diagnose renal and ureteral injuries. Intravenous pyelogram (IVP) is also
used to diagnose ureteral injuries.
Ureteral injuries, usually found searching for renal injuries, are the least common GU tract injury and must
be surgically repaired.
Renal injuries can be usually managed conservatively. Only severe injuries, such as vascular injury or parenchymal
laceration extending through the renal cortex, medulla, and collecting system, warrants surgery.
Penis fractures usually occur when the penis is erect during vigorous sexual intercourse.
The signs and symptoms of a fracture of the penis are:
Sudden pain

Hematoma of the penis shaft

Normal appearing glans

Fracture of the penis (i.e., fracture of the corpus cavernosa, fracture of the tunica albuginea) requires immediate
urethrogram to evaluate urethral damage followed by surgical intervention.
Complications of a untreated penis fracture include development of an arteriovenous shunt and impotence.

UROLOGY

Acute urinary retention:

Acute urinary retention, the inability to pass urine, is the most common urologic emergency, typically occurring in
men over the age of 60 with benign prostatic hyperplasia.
Risk factors for acute urinary retention include:
Benign prostatic hyperplasia (prostatic volume greater than 30 mL)

Advanced age

Use of anticholinergic or sympathomimetic medications

Over-distention of the bladder

Spinal cord injuries or other neurological disorder

Tumors (e.g. fibroids in women)


Patients with acute urinary retention typically present with:
Inability to urinate

Lower abdominal pain or discomfort

Fullness on suprapubic palpation

The management of acute urinary retention includes:


Immediate bladder catheterization for decompression (may require suprapubic catheterization if the
obstruction is severe)

BPH drugs in men (e.g. tamsulosin, finasteride)

Surgery (e.g. transurethral resection of the prostate)

BPH:

Benign prostatic hyperplasia (BPH) is a disease of middle-aged and older men, with the prevalence increasing with
increasing age (19-46% over the age of 50).
BPH develops in the periurethral zone (transitional zone) of the prostateleading to the obstructive symptoms seen in
patients with BPH.
BPH DOES NOT predispose patients to prostate cancer.
The clinical presentation of BPH is related to the obstructed urine flow and includes:
Hesitancy

Weak urine stream

Frequency

Urgency

Dysuria

Nocturia

The diagnostic workup of BPH begins with a history and physical. A DRE (digital rectal exam) will reveal
a uniformly enlarged, rubbery prostate. Contrast with prostate cancer, in which the prostate is non-uniformly
enlarged with lumps and bumps.
There may be a mild increase in prostate specific antigen (PSA), which is age-dependent. For instance, the normal
serum PSA for men 40 to 49 years old is 0-2.5 ng/mL, and for men 70 to 79 years old; 0-6.5 ng/mL. In addition the
race of the patient should be considered when evaluating a serum PSA level.
The American Urological Association (AUA) recommends two laboratory studies to evaluation patients with lower
urinary tract symptoms (LUTS) associated with BPH:
1. Urinalysis to look for infection or blood (associated with bladder cancer or renal calculi).

2. Serum PSA to screen for prostate cancer.

There are several complications of untreated BPH from urinary obstruction:


Bilateral hydronephrosis

Bladder diverticula and smooth muscle hypertrophy

Predisposition to infection due to urine stasis


Prostatic infarct: painful, enlarged, firm gland with increased PSA

Behavior modifications are advised, which includes avoiding liquids before going out or going to bed, reduced
caffeine and alcohol, and double voiding to completely empty bladder. Mild to moderate symptoms is initially
treated with an alpha-blocker (tamsulosin, terazosin), which provide immediate benefits. Combination of an alpha-
blocker and a 5-alpha-reductase inhibitor (finasteride) is suggested for patients with severe symptoms, large
prostates, and/or failed response to an alpha-blocker.
If refractory to medication, BPH is treated with TURP (transurethral resection of the prostate).
If refractory to medication but the patient is not a good surgical candidate, the BPH is treated with transurethral
needle ablation.

Congenital urologic defects:

Low implantation of the ureter is usually asymptomatic in boys but leads to unusual urinary symptoms in
girls. Urine is deposited into the bladder by the normal ureter that allows appropriate voiding intervals. However,
the low implanted ureter leads to urine that drips into the vagina, causing constant urinary leakage in females.
Low implantation of the ureter is diagnoses by intravenous pyelogram. Corrective surgery is required.
Posterior urethra valves is most common cause of bladder outlet obstruction in male newborns resulting from an
obstructing membrane in the posterior urethra from abnormal in utero development.
Posterior urethra valves is diagnosed with voiding cystourethrogram (VCUG), which is characterized by an abrupt
tapering of urethral caliber. It is associated with vesicoureteral reflux in 50% of children. Diagnosis can also be made
bycystoscopy by direct visualization.
The treatment for posterior urethra valves is surgical endoscopic valve ablation. In select cases, fetal surgery is
necessary for those with severe oligohydramnios, in an attempt to limit the associated lung underdevelopment that is
seen at birth.
Vesicoureteral reflux (VUR) is an abnormal retrograde movement of urine from the bladder into the
ureters. Children with VUR are predisposed to UTIs that can present as lethargy and failure to thrive in newborns,
while infants and young children typically present with the following symptoms:
Dysuria

Increased urinary frequency and urgency

Malodorous urine

Low abdominal pain

Low-grade fevers.

There should be a high degree of suspicion for VUR when a child <2 years old is diagnosed with a febrile UTI. A first-
time febrile UTI in a child (boy or girl) younger than 2 years of age warrants a renal and bladder ultrasound.
Vesicoureteral reflux (VUR) is diagnosed with voiding cystourethrogram (VCUG) showing retrograde urine flow.
Two indications for getting a VCUG to diagnose VUR are:
Recurrent febrile UTIs in a child < 2 years of age

A positive renal ultrasound upon first febrile UTI < 2 years of age

Treatment of VUR is low dose antibiotic prophylaxis (often TMP-SMX) until resolution of VUR occurs, as most cases
will resolve spontaneously. Surgical treatment is only necessary in very severe cases that show pyelonephritic
changes or renal deterioration.
Ureteropelvic junction obstruction is most commonly caused by instrinic stenosis obstructing the flow of urine from
the renal pelvis to the proximal ureter. The obstruction is usually not symptomatic until a large diuresis (for
example, a first big drinking episode). Colicky flank pain is the most common clinical manifestation.
The work up for ureteropelvic junction obstruction consists of the following imaging studies:
Renal ultrasonography showing hydronephrosis
Voiding cystourethrogram to rule out vesicoureteral reflex

Diuretic renogram showing delayed clearance at the ureteropelvic junction

Most children are treated conservatively and monitored closely. Surgical intervention is indicated in the event of
significantly impaired renal drainage.
Hypospadias, which is more common than epispadias, is caused by failure of urethral folds to fuse completely and
is characterized by the external urethral orifice opening on ventral surface of the penis.
The treatment for hypospadias is corrective surgery in order to prevent urinary tract infections. Children with
hypospadias should never be circumcised since the skin of prepuce is needed during surgical correction.
Epispadias is caused by faulty positioning of genital tubercle during development and is characterized by the
external urethral orifice opening ondorsal surface of penis.
Epispadias is associated with exstrophy of the bladder.

Emphysematous pyelitis:

Emphysematous pyelitis is a rare complication of a pyelonephritis where gas forms in the urinary tract. This is an
emergent medical condition; rapid diagnosis and treatment is paramount.
The most common risk factors for emphysematous pyelitis are diabetes and a history of urinary tract
obstruction (e.g., nephrolithiasis). The classic patient is a women in her 60's with a history of struvite stones, staghorn
calculi, and/or recurrent UTIs.
Emphysematous pyelitis presents with sepsis. They can present with
Fevers

Chills

Abdominal/flank pain

Nausea/vomiting

Emphysematous pyelitis is best diagnosed by CT scan of the abdomen and pelvisshowing air in the upper urinary
tract.
The treatment of emphysematous pyelitis is rapid administration of parental antibiotics. Other interventions (such
as percutaneous catheter drainage, nephrectomy, cystectomy) may be warranted based on the severity of the
infection.

Epididymitis:

Epididymitis is inflammation of the epididymis, caused by testicular inflammation (orchitis).


Etiologies of epididymitis include:
Chlamydia trachomatis and N. gonorrhoeae (young, sexually active men)

Gram-negative aerobic rods (older men, > 35 years of age)

Local trauma

The classic symptom of epididymitis is unilateral testicular pain and tendernessthat is relieved by supporting the
scrotum, which relieves tension on the spermatic cord and the epididymitis. Other symptoms
include dysuria andinduration.
Part of the differential diagnosis of the acutely painful scrotum is testicular torsion. Patients with suspected
epididymitis should undergo testicular ultrasound to rule out testicular torsion.

(Note, however, that cases of suspected torsion are urological emergencies and should not be delayed by ultrasound
confirmation)
Urinalysis in cases of epididymitis will show WBCs, whereas urine studies in testicular torsion almost always lack
pyuria.
If caused by Chlamydia trachomatis and/or N. gonorrhoeae, epididymitis is treated
with ceftriaxone/doxycycline or ceftriaxone/fluoroquinolones.
If non-infectious, NSAIDs and scrotal support are the preferred treatment.

Erectile dysfunction:

Erectile dysfunction (ED), or male impotence, is defined as the inabiity to develop and maintain an erection. The
incidence of ED increases with age. The causes of ED are either organic or psychogenic. The easiest way to
distinguish between them is asking the patient if they have nocturnal erections. The ability to achieve and maintain
an erection at night indicates an organic cause is unlikely.
Organic causes of ED include:
Trauma to perineum

Radical prostatectomy

Drug-induced

Vascular disease (e.g., diabetes, artherosclerotic disease)

A majority of the most commonly prescribed drugs mention ED as a side effect. These drugs include:
Antidepressants (most commonly, serotonin selective reuptake inhibitors (SSRIs))

Spironolactone

Sympathetic blockers (e.g., clonidine)

Thiazide diuretics

Ketoconazole

Cimetidine

The clinical presentation of erectile dysfunction can either be sudden or gradual onset. Other than traumatic causes,
sudden onset usually indicates an psychogenic cause. Gradual onset due to a chronic disease process indicates
anorganic cause.
The nocturnal penile tumescence (NPT) test is used to distinguish between psychogenic and non-psychogenic
causes. The test can be performed with a specific device, such as the Rigi-Scan monitor, or even with a roll postage
stamps.
The workup for causes of erectile dysfunction should include:
Questioning of sexual history (rapidity of onset, erectile reserve)

Physical exam (looking for/at gynecomastia, peripheral vascular disease, testicular volume)

Serum testosterone levels

Treatment of erectile dysfunction (ED) should begin with treating the underlying cause, whether psychogenic or
organic. The first line pharmacologic therapy for ED is phosphodiesterase-5 (PDE-5) inhibitors, which include:
Sildenafil (Viagra)

Vardenafil (Levitra)

Tadalafil (Cialis), longest duration of action


Avanafil (Stendra)

Because of the effect on the peripheral vasculature, PDE inhibitors should not be combined with nitrates, such as
nitroglycerin, as it can cause significant hypotension.

Hydrocele, varicocele, spermatocele:

A spermatocele is a cystic structure containing sperm, located within the epididymis.


A spermatocele presents as a painless scrotal swelling which does not cause symptoms or infertility.
On physical exam, a spermatocele may present as:
A palpable mass

Separate from the testis on palpation

Transilluminates (versus testicular tumors which do not)

When in doubt about testicular cancers, an ultrasound is useful in confirming the diagnosis of a spermatocele.
Spermatoceles are managed supportively, but surgically excised if symptomatic.
A varicocele is a dilation of the pampiniform plexus of veins that surrounds the spermatic cord.
Varicoceles classically occur following blockage of the left spermatic vein as it enters the left renal vein, but may
occur in any instance that increases venous pressure.
Patients with a varicocele typically present with symptoms of:
Painless scrotal swelling

A sense of fullness in the scrotum, especially upon standing

Infertility

May be asymptomatic

On physical exam, a varicocele typically:


Feels like a bag of worms due to dilation of the pampiniform plexus

Increases in size with increased intra-abdominal pressure (e.g. Valsalva, standing)

Decreases in size while the patient is supine

Does not transilluminate

Varicoceles are usually managed supportively. Surgery is considered if one of the following criteria are met:
Decreased sperm count

Bilateral varicoceles

Pain

A hydrocele is a fluid-filled space between the visceral and parietal layers of the tunica vaginalis within the
scrotum.
Hydroceles come in two variants:
Communicating hydroceles develop from a closure defect of the processus vaginalis, allowing peritoneal
fluid to enter the cavity.

Noncommunicating hydroceles develop from local secretion of fluids.


Patients with a hydrocele generally present with symptoms of:
Painless scrotal swelling

Fullness of the scrotum

Worsening of symptoms throughout the day (due to peritoneal connection)

Hydroceles are diagnosed based on palpation, transillumination, andultrasound.


On physical exam, patients with a hydrocele typically have a scrotal swelling that:
Transilluminates (both communicating and noncommunicating)

Increases in size with standing or Valsalva (if communicating)

Does not reduce or change in size (if noncommunicating)

Hydroceles are typically managed supportively. Surgery is done if the hydrocele is symptomatic or persists for
greater than one year.

Male infertility:

Infertility is defined as the inability to conceive following 1 year of normal sexual activity without any contraception.
An infertile male will frequently have the one of the following historical or physical findings:
Testicular trauma

Surgery

Chemotherapy

Penile defects

Infection

Varicocele

Undescended testes

The workup for male infertility includes screening for hypogonadism. Total serum testosterone less than 300 ng/dL
and/or serum LH and FSH >8 mlU/mL may indicate hypogonadism.
Semen analysis is used to analyze:
Sperm motility

Number

Morphology

Concentration.

Treatment for male infertility begins with correction of any underlying disorderthen in-vitro fertilization.

Male urethritis:

Urethritis is an infection of the urethra, typically caused by N. gonorrhoeae and C. trachomatis.


The presentation of male urethritis includes the following symptoms:
Dysuria
Frequency

Urgency

Burning with urination

If infected with N. gonorrhoeae, there will also be purulent drainage from the penis.
If a man is suspected of having urethritis, Gram stain and culture of a urethral sample should be ordered. The gram
stain will show Gram- diplococci if positive for N. gonorrhoeae.
Thayer-Martin is used to culture N. gonorrhoeae.
If the patient is symptomatic for urethritis but the Gram stain is negative, it is most likely due to C. trachomatis, which
can then be confirmed with nucleic acid testing.
Urethritis can result in urethral strictures, and reinfection is common if any sexual partners are not treated.
Male urethritis is treated with ceftriaxone plus azithromycin or ceftriaxone plus doxycycline.
All sexual partners must be treated as well, or recurrence is very likely. In some states, this is a reportable disease.

Prostate cancer:

Prostate cancer (adenocarcinoma) is the most common nondermatologic malignancy in males at rate of 128.3 per
100,000 (2011).
In males, lung and prostate cancer are the first and second, respectively, most common causes of cancer-related
deaths.
Prostate cancer typically arises in the peripheral zones of the prostate.
Risk factors for prostate cancer include:
Advanced age*

Prostatitis

Family history of prostate cancer

High-fat diet

*Age is the most important risk factor. There is a strong relationship between age and rates of prostate cancer: 31-40
years, 9 to 31%; 81-90 years, 40 to 73%.
Since prostate cancer begins in the peripheral zones of the prostate, it is normallyasymptomatic until advanced.
Once symptomatic, urinary symptoms of prostate cancer are related to the obstruction of urine flow:
Urinary retention

Weak urine flow

Frequency

Hesitancy

The main site of prostate cancer metastasis is bone, in particular the vertebrae. The clinical manifestation includes
pain (most common) and pathologic fractures.
The treatment of prostate cancer depends on the stage.

If the cancer has not yet spread, it can be sucessfully treated with external beam
radiation or brachytherapy (radioactive seed implants).
More extensive tumors can be treated with a radical prostatectomy, through varying approaches:
Retropubic

Perineal
Laproscopic

Robotic

Impotence and incontinence are very common complications with a radical prostatectomy.
The following are used in treating metastatic prostate cancer:
GnRH agonist (e.g., leuprolide),

Androgen receptor antagonist (e.g., flutamide, bicalutamide)

Chemotherapy (not very effective)

Since many prostate cancers are very slow growing, older men are often observed because they are more likely to die
from something unrelated to their prostate cancer.
Once treated, PSA is regularly measured to monitor for metastases and recurrence.
Current guidelines conflict on prostate cancer screening. Due to the controversy in evidence-based
recommendations, PSA and/or digital rectal exam screening should be offered on a case-by-case basis. Societies that
do recommend prostate cancer screening suggest beginning screening around age 40-50.
Prostate-specific antigen (PSA) has historically been used as a screening test, in which concern for cancer arises in
large or acute changes in number. If the cancer has invaded, then alkaline phosphatase is often elevated as well.
A abnormal digital rectal exam should prompt a tissue biopsy regardless of PSA level. An abnormal digital rectal
exam includes:
Asymmtery

Nodularity

Induration

Needle core biopsy guided by transrectal ultrasound is the standard for definitive diagnosis of prostate cancer.

Prostatitis:

Prostatitis is an inflammation of the prostate that can cause urinary symptoms such as dysuria and urgency. There
are 4 types of prostatitis, which are:
Acute prostatitis

Chronic bacterial prostatitis

Chronic nonbacterial prostatitis/pelvic pain syndrome

Inflammatory

Non-inflammatory

Asymptomatic inflammatory prostatitis

For all diagnoses of prostatitis, nonbacterial prostatitis is more common than bacterial prostatitis. This is due to the
fact that chronic nonbacterial prostatitis/pelvic pain syndrome is the most common prostatitis diagnosis.
Acute and chronic bacterial prostatitis is usually caused by the same organisms that cause urinary tract infections
(UTIs) or sexually transmitted infections (STIs) in sexually active males. These include:
E. coli (most common)

Klebsiella spp
Proteus spp

Chlamydia trachomatis

Neisseria gonorrhoeae

Chronic nonbacterial prostatitis and asymptomatic inflammatory prostatitis have negative bacterial cultures and are
usually idiopathic.
Every type of prostatitis, except asymptomatic inflammatory prostatitis, is characterized by urinary symptoms
including:
Dysuria

Urgency

Increased frequency

Nocturia

In addition, these types of prostatitis may exhibits pain in the pelvic region, including lower back and perineum.
In addition to urinary symptoms, patients with acute bacterial prostatitis may exhibit systemic symptoms, such as:
Fever

Chills

Malaise

Myalgia

Asymptomatic inflammatory prostatitis is asymptomatic and is usually diagnosed incidentally when working up
another disease process by biopsy, elevated PSA, expressed prostatitic secretions, and/or third midstream bladder
specimen.
The diagnosis of acute bacterial prostatitis is a combination of the following:
Appropriate urinary and systemic symptoms

Edematous, tender, boggy prostate on digital rectal exam (DRE)

Positive urine gram stain and culture

In patients with suspected acute bacterial prostatitis, digital rectal exam (DRE)should performed gently and not
repeated. Vigorous massaging of the prostate does not add diagnostic or therapeutic benefit, is uncomfortable for the
patient, and can cause bacteremia.
A true diagnosis of chronic bacterial prostatitis requires a prostate biopsy.
Chronic nonbacterial prostatitis/pelvic pain syndrome is a diagnosis of exclusion. The patient will usually have
appropriate symptoms for greater than 3 months with a negative bacterial culture. There may be elevated
leukocytes in the urine, prostate secretions, or seminal plasma post massage.
The first line treatment for acute bacterial prostatitis is trimethoprim-sulfamethoxazole (TMP-SMX; Bactrim) or
a flouroquinolone, such as ciprofloxacin (Cipro) or levofloxacin (Levaquin), since they cover gram-negative organism
and are able to achieve a therapeutic dosage within prostate tissue.
The treatment of chronic bacterial prostatitis is similar to acute bacterial prostatitis. A flouroquinolone, such as
ciprofloxacin (Cipro) or levofloxacin (Levaquin), is the first-line treatment with trimethoprim-
sulfamethoxazole (TMP-SMX; Bactrim) an alternative. Longer and multiple courses of antibiotics may be required
due to the chronicity of chronic bacterial prostatitis.
An initial treatment of alpha-blocker and antibiotic therapy, usually tamsulosin (Flomax) and ciprofloxacin (Cipro),
should be tried for chronic nonbacterial prostatitis/pelvic pain syndrome. Additional treatments may be indicated if
symptoms persist, which is common. Symptomatic relief may be used, which includes:
Repetitive prostatitic massage (contraindicated in acute prostatitis)

5-alpha reductase inhibitors (finasteride, dutasteride)

NSAIDS

Pelvic floor physical therapy

Surgery

If bladder drainage is required in a patient with acute prostatitis, transurethral catheterization is contraindicated due
risk of prostatic abscess or septicemia. The preferred method is suprapubic catheterization.
Prostatic abscess should be considered in patients with acute prostatitis who fail to respond to appropriate antibiotic
therapy with 36 to 72 hours. Imaging studies (contrast enhanced CT or transrectal US, if impaired kidney function)
should be obtained to identify an abscess if present.

Testicular cancer:

Testicular cancer is the most common solid malignancy in males between theages of 15 and 35 (i.e., young men). It
occurs more commonly in whites than African-Americans.
Testicular lymphoma is an overall rare cause of testicular cancer, but is found in older men, greater than 50 years of
age. It can be a primary lymphoma arising from within the testicle or can be metastatic disease from other parts in the
body.
The risk factors for testicular cancer include:
Cryptorchidism (both testicles are at risk)

Testicular cancer in contralateral testicle.

Klinefelter syndrome

Correction of cryptorchidism does not remove the risk factor; it only allows for better surveillance.
The classifications of testicular cancer are determined by the histology and cell type by a pathologist and are divided
into the following types:
Germinal cell tumors (95% of all testicular cancers)

Seminoma (35% of all testicular cancers)

Nonseminoma

Embryonal carcinoma

Yolk sac (endodermal sinus tumor)

Choriocarcinoma

Teratoma

Mixed germ cell tumor (40% of all testicular cancers)

Stromal cell tumors (non-germinal cell) tumors


Leydig cell

Sertoli cell

Testicular lymphoma

The most common clinical presentation of testicular cancer is a painless testicular mass. Other symptoms include:
Weight loss

Pain in lower abdomen, perianal area, or scrotum

Gynecomastia (usually associated with hCG tumor production)

Hyperthyroidism (TSH and hCG have similar homology)

Symptoms of metastasis

Cough or dyspnea (pulmonary metastasis)

Bone pain (skeletal metastasis)

Leg swelling (iliac or caval venous obstruction)

Anorexia, nausea, vomiting, GI hemorrhage (GI metastasis)

The evaluation of a testicular mass begins with an ultrasound, which will show hypoechoic intratesticular mass if it
is a cancer.
The following studies may be needed in order to determine the histologic type and extent of disease:
CT/MRI of abdomen and pelvis

Measurement of serum tumor markers

Radical inguinal orchiectomy (biopsy and treatment)

Retroperitoneal lymph node dissection (due to high false negative rate of CT)

Trans-scrotal biopsy of the testis or a trans-scrotal orchiectomy should NOT be performed because a scrotal incision in
the presence of testicular cancer may cause local recurrence and/or metastasis.
The three most important serum tumor marker for testicular cancer are:
Beta human chorionic gonadotropin (beta-hCG)

Alpha fetoprotein (AFP)

Lactate dehydrogenase (LDH)

Beta-hCG is the most common serum tumor marker elevated in nonseminomatous germ cell tumors (NSGCTs) and is
produced by embryonal carcinomas andchoriocarcinoma. Note: serum beta-hCG is also elevated in 15-25% of
patients with seminomas.
Serum alpha fetoprotein (AFP) may also elevated in nonseminomatous germ cell tumors, but is essentially never
elevated in seminomas. Therefore, seminomascan almost completely be ruled out in the setting of elevated AFP.
Serum tumor markers should be measured before and after any treatment modalities are performed, since they are
more useful for detecting recurrencethan for diagnostic purposes.
Men with suspected testicular cancer undergo a radical inguinal orchiectomyfor definitive diagnosis and treatment.
Once an orchiectomy is performed, the cancer is staged by radiographic imaging (similar for seminomas and non-
seminomas):
Stage I: No clinical, radiographic, or marker evidence of tumor presence beyond the testis

Stage II: Retroperitoneal adenopathy on CT scan or palpable retroperitoneal adenopathy with disease
limited to lymph nodes below the diaphragm, normal serum tumor markers after orchiectomy

Stage III: Visceral involvement

For early stage seminomas, treatment is orchiectomy with or without chemotherapy and radiation therapy. For early
stage nonseminomas, treatment is the same, but with retroperitoneal lymph node dissection.
The most common chemotherapy used to treat testicular cancer is BEP:
Bleomycin

Etoposide

Platinum-containing chemotherapy (most commonly cisplatin)

Urethral strictures:

Urethral strictures are narrowings of the urethra which may be secondary to:
Inflammation (e.g. urethritis, sexually transmitted infections)

Scar formation (e.g. post-infectious, post-kidney stone passage)

Trauma to the urethral area (e.g. repeated catheterizations)

Pelvic fractures

Prior surgeries (e.g. hypospadias correction)

Prostate cancer radiation

Congenital causes

Patients with a urethral stricture typically present with difficulty voiding which may lead to acute urinary retention
if severe.
Urethral strictures are diagnosed through history and a physical exam which includes a retrograde urethrogram.
Urethral strictures are typically initially managed with:
Balloon urethral dilation is the most common therapy

Endoscopic urethrotomy (incision of the urethra)

Urethral stenting

Suprapubic catheterization if acute urinary retention is present

Urethral strictures that recur may be managed with:


Reconstructive urethral surgeries (e.g. perineal urethostomy)

Surgical flap or graft for urethroplasty


Urological emergencies:

The presentation of testicular torsion is usually an afebrile adolescent with acute onset of severe pain in a testicle,
lower abdomen, or the inguinal canal. The following are the most sensitive and important physical exam findings:
Pain not relieved upon elevation of testicle (pain relieved in epididymitis)

Absence of cremasteric reflex

Testicular torsion results from maldevelopment and xation between the enveloping tunica vaginalis and the
posterior scrotal wall.
Since testicular torsion is a clinical diagnosis and a medical emergency,immediate surgical repair is
indicated. Bilateral orchiopexy is usually done to prevent future occurrences on either sides. There is a salvage rate
of 80100% if pain presented less than 6 hours.
The feared complication of untreated testicular torsion is venous thrombosis followed by arterial thrombosis and
infarction.
Priapism is painful condition in which the erect penis does not return to its flaccid state within 6 hours, despite the
absence of physical and psychological stimulation.
Causes of priapism include:
Hematological disorders (e.g., sickle cell disease or trait, G6PD, leukemia,thalassemia)

Neurological disorders (e.g., spinal cord lesions or spinal cord trauma)

Medications (e.g. intracavernosal injections for treatment of erectile dysfunction and trazodone).

Since priapism in patients with sickle cell disease is a low flow priapism due to occlusion of venous drainage with
stasis and ischemia, the treatment is the following:
1. Aspiration of blood, followed by saline irrigation and injection of adrenergic agonist

2. If still refractory, blood exchange transfusion,

3. Surgical intervention (only considered if priapism lasts greater than 12 hours)

The treatment of priapism not associated with sickle cell for patients centers around intracavernosal phenylephrine.
Acute obstructive pyelonephritis (also called febrile renal colic) is an infection of the kidney with co-occurring
obstruction which is an urological emergency and can lead to rapid renal failure and potential sepsis.
The usual presentation of acute obstructive pyelonephritis starts as colicky lumbar pain (i.e. renal colic) that
suddenly develops into chills, acute high febrile spikes, and flank pain.
Diagnosis of acute obstructive pyelonephritis is made by non-contrast abdominal CT (may or may not show stone
depending on stone composition) and renal ultrasound, which will show urinary tract ectasia or hydronephrosis.
Since acute obstructive pyelonephritis is an urological emergency, immediate treatment is indicated requiring
Drainage of the urinary tract via ureteral catheterization or percutaneous nephrostomy

IV antibiotics

VASCULAR SURGERY

AAA:

The abdominal aorta is the most common site of an arterial aneurysm. Abdominal aortic aneurysms (AAA) are
usually located below the renal artery(infrarenal aorta).
The key pathophysiological event in abdominal aortic aneurysms isatherosclerosis. Risk factors for AAA include:
Age > 55 years
Smoking

Hypertension

Abdominal aortic aneurysms (AAA) diagnosed and followed byabdominal ultrasound, which has a near 100%
sensitivity and specificity.
The USPSTF recommends one-time screening for AAA by ultrasonography in men aged 65 to 75 who have ever
smoked (currently smoking or have smoked 100 cigarettes or more in the past).
Indications for surgical repair of abdominal aortic aneurysm (AAA) include:
1. Size at which the risk of rupture exceeds the risk of mortality from the operation repair (greater than 5.5 cm in
diameter)

2. Rapidly increasing size (greater than 0.5 cm in 6 months or greater than 1 cm in a year).

3. Symptomatic (e.g., abdominal/back/flank pain, limb ischemia)

AAAs can be surgically repaired via open surgery or endovascular aneurysm repair (EVAR). All things being equal
EVAR has been associated with a lower perioperative (30-day) morbidity and mortality.
Possible complications of abdominal aortic aneurysm (AAA) repair include:
1. Renal failure due to atherosclerotic emboli of the renal arteries, contrast (needed in endovascular approach)
induced nephropathy, or occlusion of renal arteries with graft placement.

2. Ischemic colitis due to inferior mesenteric artery occluded by stent-graft placement.

3. Spinal cord ischemia due to disruption of artery of Adamkiewicz at the T12 level leading to anterior cord
syndrome

Acute arterial limb ischemia:

Acute arterial limb ischemia is most often due to arterial embolization and is most commonly seen in the lower
extremity compared to the upper extremity.
Two common causes of arterial embolization are atrial thrombi in patients with underlying atrial fibrillation and
mural thrombus formation in patients with recent heart attack.
Symptoms of arterial occlusion (aka the 6 Ps):
Pain: severe, constant, ischemic rest pain, sudden onset.

Pulselessness: unilateral loss of previously palpable pulses distal to occlusion.

Paralysis: reflects degree of neural or muscle ischemia.

Pallor: skin is pale or cadaveric.

Paresthesias: pins and needles feeling that reflects peripheral nerve ischemia.

Poikilothermia: skin is cold distal to occlusion.

Reperfusion of the effected limb with via thrombolytics or surgery must be accomplished within 6 hours as skeletal
muscle can only tolerate this duration of ischemia before becoming necrotic.
The first step in treating a patient with suspected acute arterial occlusion is administering intravenous
heparin. Patients should receive an IV bolus followed by a continuous heparin drip.
Following anticoagulation with heparin, emergent referral for vascular surgical evaluation is required as acute
arterial ischemia is associated with high rates of morbidity and mortality.
Fogarty balloon catheter embolectomy is the surgical procedure of choice in patients with acute arterial limb
ischemia.
Fasciotomy should be performed to prevent compartment syndrome which can occur if there is significant edema of
the muscle following re-perfusion. Read more about compartment syndrome in the dedicated topic.

Aortic dissection:

A tear in the tunica intima is thought to be the primary event leading to aortic dissection.
Hypertension is thought to be the most important predisposing risk factor for aortic dissection in patients over 60
years old.
There are several risk factors that predispose patients younger than 40 to aortic dissection:
Connective tissue disorders - Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome

Bicuspid aortic valve

Coarctation

Vasculitis - Takayasu arteritis, giant cell arteritis, rheumatoid arthritis, syphilitic aortitis

Crack cocaine use

The classic presentation of aortic dissection include diaphoresis + sudden-onset severe tearing chest pain which
radiates to the back between the scapulae and migrates inferiorly as the dissection progresses soon after the onset
of the pain.
The Stanford Classification divides aortic dissections into Type A and Type B:
1. Type A dissections are proximal aortic dissections and must involve the ascending aorta. Type A
dissections can have ascending and descending aortic involvement. Type A dissections are the most
common and most dangerous.

2. Type B dissections are limited to the descending aorta ONLY.

Under systemic pressures, this initial intramural aortic hemorrhage quickly gives rise to an unstable medial
hematoma which may:
1. Dissection within the media can proceed proximally toward the heart and into the RCA causing posterior
MI (most common coronary vessel implicated in aortic dissection).

2. Rupture through the adventitia can cause massive hemorrhage (most common cause of death due to aortic
dissection).

3. Rupture into pericardial sac can cause cardiac tamponade.

Unequal pulses in upper extremities are sometimes observed due to (partial) occlusion of the left subclavian artery
or brachiocephalic trunk
Chest x-ray is a common radiographic in patients with suspected aortic dissection who are stable. The most classic
finding on chest x-ray in patients with aortic dissection is widened mediastinum (sensitive but nonspecific). Other
findings include:
Loss of the aortic knob

Tracheal deviation to the right

Calcium sign (displacement of the intimal calcium layer in the aorta)

Chest x-ray is NOT sufficient to make or rule out a diagnose of aortic dissection. Therefore, CT or transesophageal
echocardiography (TEE) are the two preferred radiographic studies due to their accuracy and speed of use. TEE has
the added benefit of being able to be performed bedside, is quicker and exposes the patient to less radiation compared
to CT. MRI is most accurate but is not used due to the relatively long time it takes to get results in an emergent
situation compared to CT or TEE.
If dissection is suspected and patient is unstable, CT, MRI, and angiogram should not be done. In this
situation, transesophageal echocardiography (TEE) is the best confirmatory test that can be used in unstable patients.
Type B dissections are medically managed while Type A dissections are considered medical emergencies and
require surgery.
The initial treatment of aortic dissection whether Type A or Type B involves rapid correction of blood pressure
using beta blockers (often labetalol) and an afterload reducing agent like clevidipine, nicardipine
or nitroprusside. It is important that beta blockers be given before nicardipine/clevidipine/nitroprusside to prevent
reflex tachycardia.

Arterial and venous ulcers:

Venous ulcers are caused by incompetent venous valves that prevent efficient venous return from the lower
extremities.
Venous ulceration should be considered when the patient has signs of venous insufficiency including:
Varicose veins

Venous stasis dermatitis - deposition of hemosiderin leading to hyperpigmentation

Heaviness and pain in the legs that decreases with elevation

Edema

Venous stasis ulcers are classically located on the medial aspect of the ankle and calf but can occur anywhere
between the ankle and knee. Ulcers on the dorsum of the foot or toes are NOT likely to be venous in origin.
The best initial assessment of venous insufficiency associated with venous stasis ulcers is doppler duplex
scan (duplex ultrasound).
Treatment of venous ulcers involves:
Elevation

Compression stockings

Unna's boots - a compression dressing impregnated with zinc oxide to promote healing

Arterial ulcers form secondary to occlusive arterial disease and should be suspected in a patient with significant risk
factors for peripheral vascular disease such as:
Smoking

Hypertension

High cholesterol

Diabetes

Patients with arterial ulcers will present with symptoms of claudication and leg pain that is worse at night since
keeping the legs at heart level will decrease perfusion compared to standing.
Arterial ulcers are a symptom of advanced peripheral vascular disease (PVD). The first step in working up a patient
for PVD with suspected arterial ulcers is taking the Ankle Brachial Index (ABI).

Unlike venous stasis and diabetic ulcers, arterial ulcers are painful.
Arterial Venous

Site Dorsum of toes, feet and ankle, Medial gaiter region


sites of increased pressure

Wound base Necrotic tissue Granulation tissue

Appearance "Punched out" Shallow, irregular margins

Pain Painful Generally painless

DVT:

Deep venous thrombosis (DVT) is the formation of a clot in a large vein, generally of the lower extremity.
Most DVTs occur in veins distal to the popliteal vein, such as in the posterior tibial, though many are
asymptomatic. Remember the saphenous vein is a superficial vessel.
Thrombi proximal to the popliteal vein, e.g. in the femoral or iliac veins, pose a risk of embolization to the
lungs. Patients with proximal thrombi often have concomitant pulmonary embolism, though they may not have
symptoms of PE.
Virchows triad describes the pathophysiological risk factors for venous clot formation:
Venous stasis, such as prolonged immobility or proximal occlusion

Damage to the vascular endothelium

Hypercoagulability, which may be from inflammation, inherited conditions (e.g. Factor V Leiden),
pregnancy, cancer, or cigarette smoking

Key elements of the patients history that suggest DVT include thrombotic risk factors such as:
Recent surgery, especially orthopedic surgery

Pregnancy, current OR recent

Cancer

Long-distance plane travel

Prolonged bedrest

Tip: You can remember historical elements as associated with one or more of Virchows triad (stasis, endothelial damage, and
hypercoagulability.)
While some DVTs are asymptomatic, classic signs and symptoms are unilateral leg pain, swelling, and warmth.
The diagnosis of DVT is most commonly confirmed by compression ultrasound(venous duplex ultrasonography) of
lower extremity. Veins with DVTs will have anon-compressible venous lumen.
In patients with low pre-test probability of DVT, a negative ultrasound OR D-dimer excludes the diagnosis. D-dimer
has a high negative predictive value for DVT and is considered comparable to ultrasound in excluding DVT.
In patients with moderate or high pre-test probability of DVT, the false-negative rate of d-dimer increases, and a
negative D-dimer is not sufficient to rule out DVT.
In patients with moderate or high pre-test probability of DVT, compression ultrasonography is the best initial test to
evaluate patients for DVT before starting anticoagulation.
Patients with proximal DVT or concomitant PE should be treated withanticoagulation (e.g. warfarin, heparin, low-
molecular-weight heparin, or factor Xa inhibitors)
Do NOT give anticoagulants to patients with isolated distal DVTs without major symptoms and without risk factors
for proximal extension (e.g., malignancy; hospitalization; DVT close to the proximal veins or >5 cm long). Treat
with early ambulation with follow-up ultrasonography to monitor progression.
In patients with a high risk of bleeding or contraindications to anticoagulation (e.g., current active bleeding, history of
severe GI bleeding or hemorrhagic stroke) should undergo placement of an inferior vena cava (IVC) filter to prevent
pulmonary embolism unless otherwise contraindicated.

Peripheral vascular disease:

Peripheral vascular disease (PVD) is the occlusion of the peripheral blood supply secondary to atherosclerosis. See
atherosclerosis topic for more details on pathogenesis and risk factors.
Cigarette smoking is by far the strongest risk factor for PVD, even more so than it is for coronary artery disease.
Many patients with PVD have concomitant coronary or carotid artery disease. Patients with PVD are therefore at
markedly higher risk of stroke and ischemic heart disease.
Since peripheral vascular disease is an occlusive disease, symptoms are related to peripheral ischemia, most
importantly intermittent claudication, or leg pain with activity that improves with rest, often described as
cramping, tightness, or tiredness. Severe disease may cause leg pain even at rest.
The most common site for peripheral artery occlusion or stenosis is in the superficial femoral artery (SFA) at the
level of the adductor (Hunter's) canal. Other sites include the popliteal and aortoiliac artery.

Decreased perfusion to the skin results in dry skin, skin ulcers, and loss of hair growth in the affected areas.
Aortoiliac disease may cause erectile dysfunction in addition to buttock and hip claudication.
The first step in diagnosing peripheral artery disease in patients with atypical leg symptoms or claudication is
the ankle-brachial index (ABI), the ratio of the systolic blood pressure of the ankle versus that of the arm.
A normal ABI is between .9 and 1.3. Patients with an ABI > 1.3have noncompressible vessels indicative of severe
arterial disease from calcified arteries.
An ABI <0.9 is diagnostic for peripheral arterial stenosis and occurs in patients with claudication without resting pain.
An ABI <0.4 is diagnostic for severe peripheral arterial stenosis and occurs in patients with claudication with resting
pain.
CT-angiography is the gold standard for locating areas of occlusion in patients with peripheral vascular disease.
The first treatment for PVD is always increased exercise to promote collateral circulation.
Cilostazol, a phosphodiesterase inhibitor, improves walking distance and is approved for treatment of intermittent
claudication. Although some sources recommend pentoxifylline, it has not consistently improved walking distance in
randomized clinical trials and is not recommended.
Patients who fail lifestyle and medical therapy or who have rest pain (ABI < .4), arterial ulcers, or gangrene should be
treated with surgical revascularization with percutaneous transluminal angioplasty (PTA) with or without stenting
OR bypass grafting.
If the limb ischemia is irreversible, amputation is the final treatment.

Thoracic aortic aneurysm:

Thoracic aortic aneurysm is usually clinically silent unless a complication such as an aortic dissection or rupture
occurs. Less common symptoms include hoarseness from recurrent laryngeal nerve compression and aortic
regurgitation from aortic valve stretching.
The majority of ascending thoracic aortic aneurysms are considered degenerative meaning that a combination of
genetic and mechanical factors results in cystic medial necrosis which in turn weakness the integrity of the aortic
wall.
The major cause of descending thoracic aortic aneurysms is atherosclerosis and its associated risk factors including
hypertension, smoking and hypercholesterolemia.
In older patients, hypertension, smoking and hypercholesterolemia are the three most important risk factors for
thoracic aneurysm with long standing hypertension being the most commonly tested.
Hypertension hypertrophy of media of vasa vasorum diminished blood flow to the aortic wall loss of
smooth muscle in aortic media aortic wall weakens
Younger patients with connective tissue disorders affecting the collagen and/or elastic tissue in the wall of the aorta
are especially prone to thoracic aortic aneurysms:
Marfan syndrome

Ehlers-Danlos syndrome

Loeys-Dietz syndrome

Defects in copper metabolism

The two major complications from thoracic aneurysm are aortic dissection and hemorrhage.

Syphilitic aneurysm is an important infectious cause of thoracic aneurysm. Treponema pallidum invades the vaso
vasorum of the ascending and transverse portions of the aortic arch resulting in a weakening of the aortic arch.
Suspect syphilitic aneurysm in a patient with long standing syphilis and new diastolic murmur in right 2nd
intercostal space indicating aortic valve insufficiency due to dilation of the aortic valve and valve ring.

Varicose veins and superficial thrombophlebitis:

Varicose veins are the most common form of venous disorder of the lower extremity and is the distention of the
tortuous superficial veins from incompetent valves in the deep, superficial, or perforator systems. Occurs most
commonly in greater saphenous vein and its tributaries, esophagus, anorectum, scrotum.
The main mechanism by which varicose veins occur is from incompetence of venous valves that cause elongation,
dilatation, and tortuosity.
There are multiple risk factors which increase the probability of developing varicose veins including:
Increasing age

Female gender

Oral contraceptives

Pregnancy

DVT

Diagnosis of varicose veins is based on clinical presentation and physical exam findings. Examination will reveal:
Visible long, dilated and tortuous superficial veins along the thigh and leg.

Evidence of venous stasis including ulceration, hyperpigmentation and induration.

Sensation of "heaviness" in the legs.


Patients with varicose veins will have a positive Brodie-Trendelenberg test or Trendelenberg Test (valvular
competence test). With patient supine, raise leg and compress saphenous vein at thigh, then have the patient stand; if
the veins fill quickly from top down then incompetent valves are present.
The best initial treatment for varicose veins is conservative management consisting of leg elevation and/or elastic
compression stockings.
If conservative management fails and/or patients request treatment for cosmetic reasons, the preferred treatment is
either injection sclerotherapy or laser ablation rather than surgery for vein ligation and stripping. Careful
consideration must be made before ligation is attempted since the saphenous vein may be needed should the patient
ever require bypass surgery (CABG).
Superficial thrombophlebitis is inflammation or thrombosis of a superficial vein that causes pain.
Clinical findings are classically:
Palpable cord

Pain

Mild fever

Superficial thrombophlebitis is most often associated with varicose veins in the lower extremity and the site of IV
infusion in the upper extremity.
Treatment for uncomplicated superficial thrombophlebitis is alleviation of symptoms with warm
compresses and aspirin for pain relief.
Anticoagulation is NEVER the answer as a treatment option for superficial thrombophlebitis as it is not a risk factor
for PE or DVT.

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