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 are prolonged
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 the anorectal region

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

Conservative therapies are the initial treatment for patients with most patients with symptomatic
hemorrhoids. These include:
 ↑ fiber intake

 Exercise

 Sitz baths

 Stool softeners

 Topical analgesics & steroids

 Topical Ca2+ blockers, nitrates

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
Hesselbach’s triangle

 Direct inguinal hernias occur medial to the inferior epigastric artery, “directly” entering
Hesselbach’s triangle

The boundaries of Hesselbach’s 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.
Indirect inguinal hernias are covered by all 3 layers of spermatic fascia (i.e., external spermatic fascia,
cremasteric fascia, and internal spermatic fascia), whereas direct inguinal hernia sacs are covered by
only the external spermatic fascia.
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 the
location, an ultrasound may be useful.
On physical exam, patients with an inguinal hernia typically have:
 A reducible bulge in the groin if unincarcerated
  An 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 palpation)
signs and symptoms may be present)

 Necrotic

Hydrocele, Varicocele, and 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 may be asymptomatic or present with:
 Scrotal swelling

 Aching scrotal pain

 Sense of fullness in the scrotum

 Testicular atrophy

Symptoms are typically exacerbated by standing and relieved by lying down due to the pooling of venous
blood.
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

Untreated varicoceles can lead to infertility because of testicular atrophy and hypogonadism secondary
to increased scrotal temperature.
A hydrocele is a collection of peritoneal fluid 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. A closed processus vaginalis
prevents communication of fluid into the abdominal cavity.

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,and ultrasound.

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.

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 tenderness that is relieved by
supporting the scrotum, which relieves tension on the spermatic cord and the epididymis. Other symptoms
include dysuria and induration.
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.

Testicular Cancer

Testicular cancer is the most common solid malignancy in males between the ages 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 a 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 markers 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 and choriocarcinoma.

Note: serum beta-hCG is also elevated in 15-25% of patients with seminomas.

Serum alpha fetoprotein (AFP) may also be elevated in nonseminomatous germ cell tumors, but is
essentially never elevated in seminomas. Therefore, seminomas can 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 recurrence than for diagnostic purposes.
Men with suspected testicular cancer undergo a radical inguinal orchiectomy for 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)

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.
Richter’s hernia occurs when only half of the intestinal wall is protruding, seen commonly in femoral and
obturator hernias.
Littre’s hernia describes a hernia sac that contains Meckel’s diverticulum.
(Think “Littreckel”)
Garengoff’s hernia and Amyand's hernia describe femoral and inguinal hernia sacs, respectively, that include 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)
Cooper’s 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.

Meckel's Diverticulum

Meckel’s diverticulum is an anomalous remnant of the vitelline duct present in the terminal ileum that
results from incomplete obliteration of the omphalomesenteric duct. It is a true diverticulum.
It is the most common congenital abnormality of the gastrointestinal tract, with an incidence ranging from 1
to 4% and a male-to-female ratio of 2:1.
50% of the diverticula contain heterotopic tissue, with gastric mucosa as the most common type. A few
diverticula contain pancreatic tissue.
For exam purposes, it is good to know the five rules of 2s:
 2 types of ectopic tissue

 Within 2 years of life

 2% of population

 2 feet from ileocecal valve

 2 inches long

Meckel’s diverticulum causes lower GI bleeding resulting from the ulceration of adjacent ileal mucosa by
acid-secreting heterotopic gastric mucosa contained in the diverticulum. Bleeding is often brisk and
painless.
Meckel’s diverticulum is the most common cause of significant lower GI bleeding in infants and young
children.
Abdominal findings on physical examination are usually benign.
Provided that gastric mucosa is present, the diagnosis of Meckel’s diverticulum can be made with an 85 to
90% sensitivity by a radionuclide 99mTc pertechnetate scan (also called a Meckel’s scan).
Radionuclide scan findings associated with Meckel’s diverticulum show the presence of heterotopic gastric
mucosa in the right lower quadrant of the abdomen.
If radionuclide scan results are equivocal, arteriography may be used which will show an anomalous
branch of the superior mesenteric artery feeding the diverticulum.
The treatment of choice for Meckel’s diverticulum is surgical excision.
Meckel’s diverticulum can cause intestinal obstruction and has been associated with the following
complications:
 Intussusception

 Volvulus

 Abdominal wall hernia

 Meckel’s diverticulitis

Acute Abdomen

The definition of acute abdomen is the sudden onset of severe abdominal pain usually due to peritoneal
inflammation.
The differential diagnoses of acute abdomen is wide and highly dependent on the clinical history. Some
highlights include 4 "-itis" pathologies and the "three 3's":
 4 -itis's: Appendicitis, diverticulitis, cholecystitis, acute pancreatitis

 3 miscellaneous GI: Small bowel obstruction, peptic ulcer disease, GI perforation

 3 reproductive: Ectopic pregnancy, pelvic inflammatory disease, ovarian torsion

 3 cardiovascular: Myocardial infarction, mesenteric ischemia, AAA rupture

Since abdominal pain is the primary complaint of acute abdomen, characterization of the pain is the most
important part of the HPI (history of present illness). The following questions should be asked:
 Where is the pain localization? (e.g., RLQ- appendicitis, LLQ- diverticulitis, RUQ- cholescysitis)

 Does the pain radiate? (e.g., cholecysitis- right scapula, pancreatitis- back)

 What makes the pain worse (i.e. precipitating factors)? (e.g., eating- mesenteric ischemia)

 What makes the pain better (i.e., relieving factors)? (e.g., fetal position- peritoneal inflammation)

 What are the associated symptoms?

 Medical history (e.g., atrial fibrillation- mesenteric ischemia, STDs- pelvic inflammatory disease)

 Surgical history (e.g., past abdominal surgery- adhesions/small bowel obstruction)

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

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.
Imaging tests used to diagnose low implantation of the ureter include:
 Renal ultrasound (initial diagnostic test)

 MRI or CT with contrast

 Voiding cystourethrogram

Posterior urethra valves is the 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 by cystoscopy 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 intrinsic 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 reflux

 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 the prepuce is needed during surgical
correction.
Epispadias is caused by faulty positioning of the genital tubercle during development and is
characterized by the external urethral orifice opening on the dorsal surface of the penis.
Epispadias is associated with exstrophy of the bladder.
Urethral Stricture

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

Urologic 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

Pelvic fractures are most commonly associated with injuries to the:

 Bladder (either sex)

 Vagina (women)

 Posterior urethra (men)

Urethral injuries most commonly occur in men and classically manifest with:
 Blood at urethral meatus

 Inability to urinate

 High-riding prostate on DRE

 Perineal or scrotal hematoma

 Resistance to catheter during urethral catheterization*

*Urethral catheterization should be deferred in these patients until additional evaluation (eg, retrograde
urethrogram) is performed. DRE = digital rectal exam.
Retrograde urethrogram (RUG) must be performed prior to urethral catheterization in the setting of
suspected urethral injury (eg, blood at meatus). RUG results are interpreted as follows:
NO DISRUPTION:
 All contrast enters bladder, no urethral extravasation

PARTIAL DISRUPTION:
 Some contrast enters bladder, some extravasates via urethra

COMPLETE DISRUPTION:
 No contrast enters bladder, all extravasates via urethra
Urinary drainage is the mainstay of the management of bladder and urethral injuries and should be
performed after initial evaluation and imaging (eg, retrograde urethrogram or cystogram). Acceptable
methods include:
 Urethral catheter

 Suprapubic catheter

The urogenital diaphragm divides the male urethra into the anterior and posterior urethra:
 Anterior: bulbous & pendulous urethra

 Posterior: prostatic & membranous urethra

The acute management of most penetrating urethral injuries is classically guided by whether the injury is
localized to the anterior vs. posterior urethra:
ANTERIOR URETHRA:
 Open exploration with repair

POSTERIOR URETHRA:
 Diversion with suprapubic cystostomy → urethroplasty in 3-6 months

Delay is classically indicated for posterior injuries because it allows for anatomic stabilization (eg, prostate
descends from high-riding position) and resolution of the associated pelvic hematoma (thereby avoiding
infection with catheterization).
Bladder injuries are associated with pelvic fractures and classically present with:
 Gross hematuria

 Suprapubic tenderness

 Difficulty voiding

Retrograde cystography using plain films, fluoroscopic, or CT imaging is used to evaluate and diagnose
suspected bladder injuries.

It is performed by filling the bladder with ≥300 mL of water-soluble contrast via a urinary catheter.
Extraperitoneal leaks can be difficult to visualize on retrograde cystography when the bladder is full; thus,
post-drainage films (in addition to films at capacity) must be performed to identify these leaks when plain
films or fluoroscopy are used for retrograde cystography.
Retrograde urethrogram should be performed before cystography if a trauma patient presents with clinical
manifestations of both urethral and bladder injuries.

Retrograde cystography is still required to evaluate the bladder regardless of the results of an initial
retrograde urethrogram.
The management of traumatic bladder injuries is classically guided by whether the injury is intraperitoneal
or extraperitoneal:
 Intraperitoneal: surgical repair

 Extraperitoneal: urethral catheter placement → spontaneous healing

CT urography (using contrast) is the preferred test to diagnose suspected renal injuries in hemodynamically
stable patients.

Intravenous pyelogram (IVP) is a second-line, less accurate alternative.

Surgical repair (by endoscopic stenting or open laparotomy and reconstruction) is indicated for all ureteral
injuries.
These are rare injuries that are usually found while working up suspected renal injuries.
Nonoperative management is initially indicated for most renal injuries in hemodynamically stable patients.
Renal arteriovenous (AV) fistulae are a classical complication of penetrating trauma that involves the renal
pedicle; congestive heart failure is a common presentation.

Renal catheterization and angioembolization are used to ablate the fistulae.

Penile fracture is a urologic emergency that is caused by the traumatic rupture of the corpus cavernosum ±
tunica albuginea and urethra.

It classically occurs during vigorous sexual intercourse with thefemale partner on top and presents with
an audible “pop”, rapid detumescence (loss of erection), and penile shaft hematoma(“eggplant sign”).
Retrograde urethrogram should be performed in patients with an acute penile fracture to assess for
associated urethral injuries.

Additional imaging studies are not required, as penile fracture is a clinical diagnosis.
Emergent surgical repair of the penis ± urethra is the definitive treatment for penile fracture.
The formation of arteriovenous shunts leads to impotence in patients with penile fractures that are not
repaired.
Urological Emergencies

Testicular torsion classically presents in adolescent males with acute-onset pain following vigorous
exercise (esp. involving trauma) most commonly presents with:
 Acute testicular or abdominal pain

 Nausea, vomiting

 High-riding testicle w/ horizontal lie

 Absent ipsilateral cremasteric reflex

Testicular torsion has a bimodal age of distribution with peaks during the:
 Neonatal period (extravaginal torsion)

 Puberty (intravaginal torsion)

Presentation during puberty (12-18 years of age) is most common; increased testicular weight due to
hormonal changes in puberty is likely a contributing factor.
Inadequate anchoring of the testis to the posterior scrotal walldue to congenital defects of the
processus vaginalis allows the testis to hang freely (and often horizontally) within the scrotum.

This is known as the “bell clapper” deformity and is the most common congenital anomaly associated with
testicular torsion. It is typically bilateral.
Testicular torsion is primarily a clinical diagnosis.

Color Doppler ultrasound (US) of the scrotum can be used to support the diagnosis in equivocal cases;
decreased testicular perfusion is consistent with a diagnosis of torsion.
Emergent bilateral orchiopexy within 4 to 6 hours of onset is the preferred acute treatment of testicular
torsion. The surgery is performed bilaterally because the contralateral testicle is at risk for torsion (the bell
clapper deformity usually is bilateral).

There is nearly 100% testicular viability if orchiopexy is performed within 4-6 hours of onset vs. 20%
testicular viability after 12 hours of onset. Orchiectomy is performed for nonviable/necrotic testicles.
Manual detorsion can be attempted in the emergency department if surgery is not immediately available.

Medial to lateral rotation ("opening a book") of the testicle is attempted initially; it results in substantial
pain alleviation if successful. If the initial rotation exacerbates or fails to improve the pain, it can be
subsequently attempted in the opposite direction.

Surgical exploration is still necessary following successful detorsion because partial torsion often persists
following manual detorsion. Additionally, bilateral orchiopexy is prophylactic.
Key findings that distinguish testicular torsion from torsion of the appendix testis or epididymis include:
Testicular torsion Appendix testis or epididymis torsion

Adolescents (12-18 years) Children (7-12 years)

High-riding testicle w/ horizontal lie Palpable nodule w/ blue dot

Absent cremasteric reflex Intact cremasteric reflex

Absent or ↓ perfusion on Doppler US Normal or ↑ perfusion on Doppler US

Emergent bilateral orchiopexy Supportive (analgesia, ice, rest)*

*Appendix testis or epididymis torsion typically resolves spontaneously in 1-2 weeks. Surgical removal of
the affected testicular appendix (no contralateral exploration) can be performed in refractory cases.
Priapism is a 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 >12 hours)

Intracavernosal injection of phenylephrine, an alpha agonist, is the preferred medical treatment

for ischemic priapism in most patients.
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 catheterizationor percutaneous nephrostomy
  IV antibiotics

Fournier gangrene is a necrotizing fasciitis of the perineum that typically presents with intense
pain localized to the abdominal wall that subsequently migrates to the thigh, scrotum, and penis.

Physical exam reveals characteristic crepitus (indicating subcutaneous gas) as well as systemic signs (eg,
fever, tachycardia, and hypotension) that appear out of proportion to the local extent of the disease. Tense
edema outside the immediately involved skin may also be seen, and frank skin necrosis is a late finding.
Fournier gangrene is a polymicrobial, mixed aerobic and anaerobic infection.

Commonly implicated aerobes include E. coli, Klebsiella, and enterococci; commonly implicated anaerobes
include Bacteroides, Fusobacterium, Clostridium, and anaerobic streptococci.
Fournier gangrene is most common in males; major risk factors include:
 Diabetes mellitus

 Alcohol misuse

 Immunosuppression

CT scan is the preferred imaging study for the evaluation of potential Fournier gangrene in equivocal
patients; characteristic findings include:
 Gas in soft tissues

 Fascial thickening

 Fat stranding

Imaging studies should NOT delay surgical intervention in patients with more characteristic presentations
of Fournier gangrene (eg, crepitus), who can be presumptively diagnosed clinically and definitively
diagnosed upon surgical debridement.
The cornerstones of Fournier gangrene treatment are:
 Hemodynamic support

 Broad-spectrum IV antibiotics

 Urgent surgical debridement

Patients typically require multiple debridement procedures (average of 3.5 procedures per patient).
Triple antibiotic therapy is commonly used in the empiric treatment of Fournier gangrene; the most
commonly used regimen consists of the combination of:
 Clindamycin plus

 Vancomycin plus

 Carbapenem or beta-lactam w/ beta-lactamase inhibitor

Carbapenems: imipenem, meropenem, ertapenem.

Beta-lactam with beta-lactamase inhibitors: piperacillin-tazobactam, ampicillin-sulbactam, or ticarcillin-
clavulanate.

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)

Electrical Shock and Burn

Electric shock and burn occurs via current flow through the body.
Young men and children are disproportionately injured.
Both the type of current and the amount of voltage affect the extent of damage from a shock.
The skin is a barrier to injury from electric shock.
However, wet skin and breaks in the skin both reduce this resistance.
Electrical burns to internal organs may be hidden by small external burns.
Skin necrosis and sloughing may not occur for days.
Third spacing of fluid occurs with internal organ injury.
Rhabdomyolysis can occur.
Electrical shocks are managed by freeing the patient from the current either by turning off the power, severing the
wire, or by prying them or hitting them away with a non-conductive material (e.g. wooden board).
Cardiac and ventilatory statuses should be checked immediately. CPR must be initiated if necessary.
Electrical burns are treated conservatively.
Give an intravenous infusion of crystalloid solutions if the patient is in circulatory shock.
Acidosis may require the infusion of intravenous bicarbonate therapy.
Mannitol may be given to those with very low urine output.
A fasciotomy may be necessary, but the full extent of an electrical burn may not be apparent until 7-10 days after the
burn.
Electric shocks cause general, neurologic, orthopedic, and cardiovascular clinical findings.
General clinical findings: Pain, fatigue, and headache.
Neurologic clinical findings: Nervous irritability, seizures, deafness, and blindness.
Orthopedic clinical findings: Shoulder dislocation and femoral neck fractures, for example.
Cardiovascular clinical findings: ectopic beats, sinus tachycardia, bradycardia, atrial fibrillation, asystole, and
ventricular fibrillation.

Transplant Selection and Rejection

Organ transplant donors are most commonly brain-dead or living voluntary donors without cancer,
sepsis, or organ insufficiency. HIV is no longer an absolute contraindication for transplantation; patients
with a well-controlled HIV infection are eligible.
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 is monocyte/macrophage.
Acute transplant rejection is treated with intravenous steroids (e.g. methylprednisolone) and is frequently
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 is mediated 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.
Kidney, Pancreas, 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

Existing kidneys are NOT removed due to increased rates of surgical morbidity. The donated kidney is
usually placed in the iliac fossa (pelvis).
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.
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:
 Viral: HCV and HBV

 Steatohepatitis: Alcoholic and Non-Alcoholic

 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

 Hepatocellular carcinoma with metastases

 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.
Heart and Lung Transplantation
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 confirmed 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

 α1-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

Absolute contraindications for lung transplantation include:

 Active TB

 Malignancy in last 2 years

 BMI ≥35 kg/m2

 Severe cardiac, renal, hepatic, or CNS disease

 Substance abuse: active tobacco smoking, drug/alcohol dependency

 Noncompliance with medical therapy

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

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 (intraperitoneal, 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 0.9%

Two risk factors 6.6%

Three or more risk factors 11.0%

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 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.
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.
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.
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 onlyreceive 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 undergoingintermediate-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).
Chest Pain
Post-operative chest pain should alert the clinician to 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. Chronic elevation should be ruled out with baseline values or preoperative residual samples.
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 5-7. 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

Postoperative Fever

Immediate postoperative fever (ie, onset within the OR or within hours of the surgery) is commonly associated with:

 Adverse drug or transfusion reactions

 Pre-existing trauma or infections

Malignant hyperthermia has a characteristically high (>40°C or 104°F) fever that occurs in the peri- or immediate
postoperative period in patients exposed to volatile anesthetics (eg, halothane, isoflurane) or succinylcholine.

Surgical site infections (SSI) rarely occur within hours of surgery; when fulminant SSI do occur in the immediate
postoperative period, the most likely pathogens are:

 Group A streptococcus

 Clostridium perfringens

The 5 classical “W’s” of postoperative fever are:

Wind (lungs)  Atelectasis

 Pneumonia

 PE

Water  UTI

Wound  Surgical site infection

 Abscess

 Indwelling lines

Walk  Deep vein thrombosis

  Thrombophlebitis

Wonder drugs & products  Drug reaction

 Transfusion reaction

Atelectasis is classically considered to be the most common cause of postoperative fever during postoperative day
(POD) 1.

(Note: While the causal relationship of atelectasis and fever has been debated, the NBME still tests on this concept.)

Pneumonia classically presents during POD 3 and can be superimposed upon pre-existing atelectasis. It is
typically nosocomial.

Long periods of mechanical ventilation predispose to ventilator-associated pneumonia, while postoperative vomiting
and NG tubes predispose to aspiration pneumonia.

UTI classically presents during POD 3-5.

Fever in thrombophlebitis classically presents on POD 5; it may be superimposed on a pre-existing DVT.

Note that this can also present after POD 5.

Common causes of postoperative fever ≥1 week after surgery include:

 Febrile drug reactions

 Central venous catheters

 Surgical site infections

 C. difficile colitis

 Deep abscesses

Thrombophlebitis is also a common etiology of fever in this period.

Drugs are the most common noninfectious cause of postoperative fever. Commonly implicated agents include:

 Heparin

 Antibiotics (esp. sulfa drugs & β-lactams)

Fever due to deep abscesses classically presents during PO days 10-15.

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 out dehydration 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 than 40 mEq/L is suggestive
of acute renal failure.

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 is 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.

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 administration postoperatively 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.

Airway & Breathing

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

Airway Management

Tongue prolapse into the posterior pharynx due to loss of muscle tone is the most common cause of
airway obstruction unconscious patients.
Airway obstruction due to tongue prolapse in unconscious patients can be corrected with the following
maneuvers:
 Head-tilt chin-lift (if no c-spine injury)

 Jaw-thrust (if concern for c-spine injury)

Airway adjuncts prevent the tongue from occluding the airway. They include oropharyngeal airways
(OPA) and a nasopharyngeal airways (NPA). Relative contraindications to each airway include:
 OPA: avoid if intact gag reflex

 NPA: avoid if facial/skull trauma

Insertion of an OPA in a semiconscious patient with an intact gag reflex can cause vomiting and aspiration,
while insertion of a NPA in a patient with facial or skull trauma can lead to inadvertent intracranial
placement of the NPA.
Indications that intubation is typically necessary include:
 Glasgow Coma Scale ≤8

 Pooling secretions, inability to swallow

 Loss of protective reflexes (eg, cough, gag)

 Anticipated need (eg, smoke inhalation, angioedema)

Failure of oxygenation or ventilation can also indicate that intubation is necessary if the patient is not a
good candidate for noninvasive positive pressure ventilation.
Inhalation injury (eg, due to heat, smoke, chemicals or toxic gases) is an indication for early intubation if
there is swelling of the neck or any indication of respiratory distress (eg, stridor, wheezing, hypoxemia).

Intubation is often performed in the field to secure the airway en route to the emergency department.
Upper airway edema can occur rapidly and unexpectedly in patients with inhalation injuries and is
exacerbated by intravenous fluid administration.

Thus, there is an extremely low threshold to perform early intubation in patients with inhalation injuries.
Common indications for flexible (formerly known as fiberoptic) scope intubation include:
 Limited mouth opening

 Unstable cervical spine

 Abnormal airway anatomy*

*Includes blunt or penetrating anterior neck trauma, angioedema, inhalation injuries, and subcutaneous
emphysema of the neck (aka pseudoangioedema).
Rapid sequence intubation (RSI) is the most common technique used in the emergency setting to secure a
patient's airway.

It involves concurrent administration of an anesthetic induction agent and a neuromuscular blocking agent
to facilitate rapid intubation.
The key steps to RSI are the 7 P’s:
1. Preparation

2. Preoxygenation

3. Pretreatment

4. Paralysis & induction

 5. Positioning

6. Placement with proof

7. Postintubation management

Preoxygenation consists of 3-5 minutes of high-flow oxygen, which displaces nitrogen and other gases
from the lung and creates a large pulmonary oxygen reservoir.

This allows for a longer period of apnea without desaturation.

Pretreatment may not be performed in all patients. When done, it consists of:
 Hemodynamic optimization (eg, IV fluids, vasopressors)

 Fentanyl plus lidocaine (if ↑ ICP)

 Atropine (select patients with bradycardia)

Fentanyl plus lidocaine attenuate the reflex sympathetic response to laryngoscopy, which is particularly
important in patients with elevated intracranial pressure (ICP).
Paralysis and induction involves the simultaneous administration of an anesthetic agent and a paralytic
agent.
Positioning for RSI in adults is the “sniffing” position, which consists of:
 Forward flexion of the neck

 Hyperextension of the head

End-tidal carbon dioxide assessment (colorimetric or quantitative) is the most accurate way to confirm
endotracheal tube placement.

A CXR is also typically obtained to assess the depth of tube placement; however, it cannot distinguish
endotracheal vs. esophageal placement.
Postintubation management consists of:
 CXR to assess for procedure complications & tube depth

 Mechanical ventilation initiation

 Longer-acting sedative, analgesic, & paralytic agent administration

Succinylcholine is an analogue of acetylcholine that acts as a depolarizing neuromuscular blocking agent.

It is the preferred paralytic agent for RSI in most patients given its shorter duration of action than the
nondepolarizing agents.
Hyperkalemia caused by K+ efflux at the motor end plate is the most important adverse effect of
succinylcholine. Thus, succinylcholine is contraindicated in patients with current hyperkalemia or who are at
high risk for hyperkalemia, including:
 Rhabdomyolysis, tumor lysis syndrome

 Acute renal failure

 Burns or crush injuries >72 hours

 Inherited muscular dystrophies

 Denervating injuries >72 hours (stroke, spinal cord injury) or chronic diseases (eg, ALS, MS)
Patients at risk for hyperkalemia should be treated with a nondepolarizing neuromuscular blocking agent
(eg, rocuronium) instead.
Acetylcholine receptor upregulation at the neuromuscular junction is responsible for the profound
hyperkalemia seen with succinylcholine administration in many injuries and diseases (eg, denervations &
burns >72 hours, inherited muscular dystrophies).
A family history of malignant hyperthermia is an absolute contraindication to succinylcholine use.

Malignant hyperthermia is an autosomal dominant condition triggered by administration of inhaled

anesthetics or succinylcholine that presents with sympathetic hyperactivity, hypercapnia, and generalized
muscle rigidity. The antidote is dantrolene.
Succinylcholine should be avoided in acute cocaine intoxication since both succinylcholine and cocaine
are metabolized by plasma cholinesterase.

Succinylcholine administration in this setting thus impairs metabolism of both drugs, resulting in prolonged
paralysis and cocaine intoxication.
Rocuronium is the preferred nondepolarizing neuromuscular blocking agent for RSI because it has a more
rapid onset (45 to 60 seconds) and shorter duration of effect (30 to 45 minutes) than other nondepolarizing
paralytic agents.

Nondepolarizing paralytic agents competitively antagonize acetylcholine at the neuromuscular junction.

Etomidate is a nonbarbiturate sedative-hypnotic with rapid onset (15 to 45 seconds) and short duration of
effect (3 to 12 minutes) that potentiates GABAA receptors.

It is the most hemodynamically neutral (ie, negligible change in heart rate, cardiac output, or blood
pressure) of the induction agents used for RSI. It also has anticonvulsant properties attributed to its
decreasing cerebral metabolic rate of oxygen consumption.
Common adverse effects of etomidate include:
 Pain during injection

 Transient adrenal suppression (<24 hrs)

 Myoclonic jerking

Myoclonic jerking is accompanied by EEG changes and can be mistaken for seizures; it is clinically
insignificant with concurrent administration of a paralytic agent.
Etomidate inhibits 11-beta-hydroxylase, which catalyzes the conversion of 11-deoxycortisol to cortisol.
This causes transient adrenal suppression.

Thus, some clinicians prefer an alternative induction agent in patients with septic shock.
Ketamine is a dissociative anesthetic with quick onset (45 to 60 seconds) and a relatively short duration of
effect (10-20 minutes). It is structurally similar to PCP. It has the following mechanisms of action:
 Anesthesia: NMDA receptor antagonism

 Analgesia: central opioid receptor agonism

 Elevated sympathetic tone: ↑ catecholamine release

Ketamine-induced catecholamine release causes bronchodilation via β2 receptor agonism.

Thus, ketamine is often used for induction in patients with reactive airway disease (eg, severe asthma
exacerbations).
Due to its sympathomimetic effects, ketamine is typically avoided in patients with:
 Ischemic heart disease
  HTN (MAP >120 mmHg)

 Signs of cerebral herniation

Ketamine-induced catecholamine release increases heart rate, contractility, mean arterial pressure (MAP),
and cerebral blood flow (CBF). Increased CBF, in turn, leads to increased intracranial pressure, which can
exacerbate cerebral herniation.
Ketamine-induced emergence reaction is a common adverse effect in adults. It is characterized by:
 Hallucinations, illusions

 Vivid dreams

 Depersonalisation

 Disorientation

This can be treated with benzodiazepines and is less common in the emergency department given
concomitant benzodiazepine-induced sedation that lasts well beyond ketamine duration of action.
Propofol is a highly lipophilic anesthetic with quick onset (15 to 45 seconds) and a short duration of effect
(5-10 minutes) that potentiates GABAA receptors and is a weak NMDA receptor antagonist.

Like ketamine, propofol also induces bronchodilation and can be used for induction in patients with reactive
airway disease (eg, severe asthma exacerbations).
Propofol causes dose-dependent hypotension (average ↓10 mmHg MAP) upon bolus infusion and is
typically avoided in patients with hypovolemia or hypotension.

Contributing mechanisms include propofol-mediated L-type Ca2+channel antagonism, increased NO

synthesis/release, depressed myocardial contractility, and a blunted baroreceptor response.
Additional adverse effects of propofol include:
 Injection-site pain

 Anaphylaxis (rare, egg or soy allergies)

 Dose-dependent respiratory depression (ie, apnea) with induction

Injection-site pain from propofol administration can be minimized by using a large antecubital vein or by
pretreatment with lidocaine along with proximal venous occlusion.
Midazolam is the most common benzodiazepine used for RSI induction; it has a rapid onset (30 to 60
seconds) and a relatively short duration of effect (15-30 minutes).

Like other benzodiazepines, midazolam is an allosteric modulator of GABAA receptors that increases the
frequency of GABA-induced Cl-channel opening.
Midazolam causes dose-dependent hypotension upon induction and is typically avoided in patients with
hypovolemia or hypotension.

Midazolam-induced hypotension is caused by myocardial depression and systemic vasodilation.

Midazolam causes dose-dependent respiratory depression, which is potentiated by concurrent opioid
administration.

Thus, ventilation and oxygenation should be monitored closely in these patients.

Preferred agents for RSI induction in patients with shock include either:
 Ketamine (↑ BP, HR), or
  Etomidate (hemodynamically neutral)

Glucocorticoids (eg, hydrocortisone) can be used to counteract the transient adrenal suppression induced
by etomidate in patients with septic shock and refractory hypotension (ie, insufficient response to treatment
with fluids plus vasopressors).
First-line agents for RSI induction in patients with severebronchospasm (eg, acute asthma
exacerbation) include:
 Ketamine (preferred)

 Propofol (avoid if hypotensive)

Recall that both agents induce bronchodilation.

Preferred agents for RSI induction in patients with head injury or stroke include either:
 Etomidate, or

 Ketamine (avoid if HTN or signs of herniation)

Etomidate is the preferred agent for RSI induction in patients with cardiovascular disease since it is
hemodynamically neutral.
Ketamine is typically avoided for RSI induction in patients withstatus epilepticus given its stimulatory
effects. Preferred agents for RSI induction in patients with status epilepticus include either:
 Propofol, or

 Etomidate, or

 Midazolam

Propofol, etomidate, and midazolam all modulate GABAA receptors and have anticonvulsant properties.
Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) is an acute-onset respiratory failure characterized by bilateral alveolar
infiltrates and hypoxemia that is refractory to 100% oxygen (requires high PEEP to open collapsed alveoli).

ARDS is caused by inflammation — in particular, pro-inflammatory cytokine secretion, neutrophil infiltration, and
increased alveolar capillary permeability and damage that leads to pulmonary edema, atelectasis, and pulmonary
vascular obliteration.

Etiologies of ARDS include (mnemonic: AAAARDDDSSS):

 Aspiration

 Acute pancreatitis

 Air or Amniotic embolism

 Radiation

 Drug overdose

 DIC

 Drowning
  Shock

 Sepsis

 Smoke inhalation

Sepsis is the most common cause of ARDS.

ARDS typically presents with acute-onset:

 Dyspnea

 Tachypnea

 Tachycardia

 Diffuse crackles

The Berlin Definition of ARDS requires that all of the following are present:

 Acute onset respiratory distress (<1 week)

 Bilateral (patchy or ground glass) diffuse infiltrates on chest imaging

 Cardiogenic pulmonary edema excluded

 PaO2/FiO2 ≤300 mmHg with PEEP or CPAP ≥5 cm H2O

PaO2 = arterial partial pressure of oxygen. FiO2 = fraction of inspired oxygen.

PEEP = positive end-expiratory pressure. CPAP = continuous positive airway
pressure.

Acute cardiogenic pulmonary edema is the most important diagnosis to exclude in the workup of ARDS; this is most
commonly accomplished by:

 Physical exam — absence of: S3 or S4 gallop, JVD, leg edema in ARDS

 BNP or NT-proBNP — normal in ARDS

 ± TTE — absence of valvular dysfunction & normal EF in ARDS

JVD = jugular venous distension. BNP = brain natriuretic peptide. NT-proBNP = N-

terminal proBNP. TTE = transthoracic echocardiography. EF = ejection fraction.

PCWP <18 mmHg via flow-directed pulmonary artery (Swan-Ganz) catheterization suggests ARDS and excludes
cardiogenic pulmonary edema.

Right heart catheterization is not routinely performed in the workup of ARDS; its use is limited to equivocal
cases. PCWP = pulmonary capillary wedge pressure.

Pulmonary contusion is more likely when diffuse infiltrates on CXR present within 24 hours of an injury as
superimposed ARDS typically takes >1 day to develop.

Traditional settings for mechanical ventilation in the treatment of ARDS include:

  ↓ TV — less likely to cause alveolar overdistension

 ↑ PEEP — opens collapsed alveoli

TV = tidal volume. PEEP = positive end-expiratory pressure.

Fluid volumes should be kept low to prevent pulmonary edema.

In patients with ARDS on mechanical ventilation, target arterial partial pressure of oxygen (PaO2) and hemoglobin
oxygen saturation (SaO2) is:

 PaO2: 55-80 mmHg

 SaO2: 88-95%

In mechanical ventilation, the arterial partial pressure of oxygen (PaO2) is primarily influenced by:

 FiO2

 PEEP

Fraction of inspired oxygen = FiO2. Positive end-expiratory pressure = PEEP.

In mechanical ventilation, the arterial partial pressure of carbon dioxide (PaCO2) is primarily influenced by minute
ventilation, ie:

 Respiratory rate

 Tidal volume

Pulmonary minute ventilation = respiratory rate x tidal volume.

FiO2 <60% is the target in patients with ARDS on mechanical ventilation to prevent free-radical-induced alveolar
damage and absorptive atelectasis (due to washout of alveolar nitrogen).

Prone ventilation can improve oxygenation in patients with severe ARDS who are refractory to traditional (ie,
supine) mechanical ventilation.

However, prone ventilation is not the preferred treatment in patients experiencing a rapidly progressive ventilatory
decline or life-threatening hypoxemia; ECMO is more appropriate in this situation.

Venovenous extracorporeal membrane oxygenation (ECMO), which provides respiratory support only, can be used
to treat ARDS that is refractory to traditional mechanical ventilation and supportive care.

In contrast, saturation ECMO provides both hemodynamic and respiratory support and is used in patients with
cardiac failure.

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 patient’s head and applying suction to
allow drainage of the oropharynx.
If an unwitnessed or intraoperative aspiration is suspected, supportive therapy and watchful waiting for
48 hours is useful.
Prevention of pulmonary aspiration is the best therapy:
 Nil per os (NPO) preoperatively

 Elevate 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 become progressively 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.
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.
Injuries to the diaphragm and structures in the abdomen should be considered with penetrating thoracic
trauma (eg, bullets) that enters or exits below the:
 Nipple line anteriorly

 Tip of the scapula posteriorly

These often necessitate exploratory laparotomy.

Nipple line = 4th intercostal space; tip of the scapula = 7th intercostal space.
Pneumonia due to pain-induced hypoventilation and subsequent atelectasis is a major complication of rib
fractures in older (>45 years) adults.
Intercostal nerve blocks (eg, ropivacaine or bupivacaine with epinephrine) improves pulmonary mechanics
and reduces the incidence of pneumonia in patients with multiple rib fractures.

In contrast, opioids can exacerbate hypoventilation by decreasing respiratory drive.

Chest radiography is the initial diagnostic study to evaluate for blunt aortic injury in stable patients that
have sustained chest trauma.
Application of an occlusive dressing that is taped on 3 sides is the preferred first aid of a sucking chest
wound (ie, air enters pleural cavity on inspiration and closes with expiration).

This prevents the development of a tension pneumothorax by acting as a one-way valve to let air out of the
thorax.
Beck's triad is a classical presentation of cardiac tamponade and includes:
 Hypotension

 Dilated neck veins

 Muffled heart sounds

The triad is only seen in a minority of cases.

Manifestations of cardiac tamponade on echocardiography include:
 Diastolic collapse of right heart chambers

 Hepatic venous flow abnormalities

 Interventricular septum bulging into left ventricle

However, under no circumstances should the definitive treatment of clinically evident or suspected
hemodynamically significant tamponade be delayed for the purpose of confirming the diagnosis by
echocardiography.
ECG findings associated with cardiac tamponade include:
 Sinus tachycardia

 Low QRS voltage

 Electrical alternans

Electrical alternans = beat-to-beat alterations in the QRS complex due to the swinging movement of the
heart in a large pericardial effusion.
Emergent pericardiocentesis with ultrasound guidance is the preferred initial treatment of patients with
cardiac tamponade who are hemodynamically unstable.

If ultrasound is not available, the needle is typically inserted in the subxiphoid area below the rib margin
and advanced while angled towards the shoulder.
Both hemothorax and tension pneumothorax can acutely present with hypotension, tachycardia,
tachypnea, tracheal deviation to the contralateral side, and absence of breath sounds on the ipsilateral side.
The lung is the most common source of bleeding in hemothorax; bleeding is typically self-limited in these
situations.
Intercostal arteries are the most common source of profusebleeding in the setting of hemothorax.
Tube thoracostomy with a large chest tube (≥ 36 French) to facilitate drainage is the initial management
of hemothorax.
Key the indications for surgical thoracotomy after tube thoracostomy in the treatment of hemothorax
include:
 ≥1500 mL blood via immediate drainage

 ≥150–200 mL blood per hour over 3 hours

Key differentiating features and emergent treatments are highlighted in the table:
Hemothorax Tension pneumothorax

Flat neck veins JVD

Dull to percussion Hyperresonant to percussion

Tube thoracostomy Needle thoracostomy

JVD = jugular venous distension.

Flail chest is the most severe form of chest wall injury due to blunt thoracic trauma (eg, forceful contact of
steering wheel with chest). It occurs with fracture of:
 ≥3 contiguous ribs in

 ≥2 separate locations

This results in a free-floating segment of the chest wall.

Paradoxical motion of the chest wall with respiration is the classic clinical manifestation of flail chest.

Chest pain often leads to involuntary chest splinting as well as reduced inspiratory effort with associated
tachypnea and short, shallow breaths on exam.
Pulmonary contusion is the most common injury associated with flail chest and is highly associated with
respiratory failure.
Supplemental oxygen and pain control (eg, analgesics or epidural analgesia) are the key components of the
early management of flail chest in patients without severe respiratory compromise.

Since these patients are at risk for rapid respiratory failure, this typically occurs in the ICU setting.
Positive pressure ventilation (either invasive or noninvasive) with or without bilateral chest tube
placement is used for patients with flail chest and severe respiratory compromise.

Chest tubes prevent the development of tension pneumothorax caused by a fractured rib.
There are 4 signs of trauma that are extreme enough to warrant active investigation for occult secondary
complications of trauma. These signs are:
 1st rib fracture

 Sternum 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, ECG, and cardiac enzymes for these complications.
Rapid deceleration — most often due to high-speed MVCs or falls from height (>10 feet) — is the major
risk factor for blunt thoracic aortic injury.
The isthmus of the aorta is the most common site of blunt thoracic aortic injury.

The isthmus is the segment of the aorta immediately distal to the left subclavian artery at the site of the
ligamentum arteriosum.
Findings on CXR suggestive of blunt thoracic aortic injury in patients that have sustained blunt trauma to
the thorax include:
 Widened mediastinum

 Obscured aortic knob

 Left apical cap

 Large left hemothorax

 Right tracheal, NG tube deviation

 Left mainstem bronchus depression

On CXR, a widened mediastinum is defined as:

 >8 cm supine

 >6 cm upright
Contrast-enhanced multidetector CT angiography of the chest is the first-line imaging modality for the
diagnosis of blunt aortic injury in hemodynamically stable patients following CXR.

Transesophageal echocardiography is an alternative imaging modality that is preferred in

hemodynamically unstable patients with equivocal presentations.

These imaging studies are performed in patients with either suggestive findings of aortic injury on CXR
— or — a normal CXR but a high clinical suspicion of aortic injury.
Thoracic aortography is the historical "gold standard" for the diagnosis of blunt aortic injury but is now
rarely used due to the time-intensive nature of the study.
Pulmonary contusion develops within the first 24 hours post-injury and presents with dyspnea and
hypoxemia that directly correlates with the size of the contusion. It is frequently notevident on the initial
radiograph (~⅓ of patients).

Unilateral irregular, non-lobar infiltrates (ie, “white-out”) on CXR is the diagnostic hallmark.

In contrast, bilateral infiltrates are present in ARDS.

Pulmonary contusion is the most common lung injury identified in the setting of blunt chest trauma.

Pneumonia and superimposed ARDS are the major complications associated with mortality.
Contused lung is highly sensitive to fluid overload and overly-aggressive repletion can exacerbate
pulmonary edema.

Thus, fluid repletion to euvolemia should be performed carefully in the setting of pulmonary contusion.

Pain control with analgesics or epidural analgesia, supplemental oxygenation, and airway management (if
indicated) are the other key components of the management of pulmonary contusion.
Diaphragmatic rupture classically presents with abdominal viscera (eg, spleen, stomach) and/or a NG
tube in the thorax on chest radiography.

The treatment is surgical correction.

Left-sided rupture is more common because it is not protected by the liver like the right hemidiaphragm.
Tracheobronchial injuries (eg, rupture) classically present with:
 Subcutaneous emphysema

 Dyspnea, hoarseness

 Persistent pneumothorax

 Pneumomediastinum that re-accumulates despite chest tube placement

The right main bronchus is most commonly involved in traumatic tracheobronchial injuries (eg, rupture).
Fiberoptic bronchoscopy is used to definitively diagnose tracheobronchial injuries (eg, rupture) and secure
an airway in affected patients.

The management of severe cases is surgical repair or lung resection.

Abdominal Injuries

Abdominal trauma can be caused by a variety of mechanisms including penetrating 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 Kehr’s sign.
Unstable patients with peritoneal signs (e.g. pain, rebound tenderness, guarding) or evisceration status post
trauma warrant immediate surgery.
Patients should be kept on hemodynamic monitoring and followed clinically with serial abdominal
exams.

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 patient’s 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 or evidence of a fracture (e.g., point
tenderness on c-spine palpation), then a CT scan of the cervical spine is indicated.

Shock
Hypovolemic shock due to hemorrhage is the most common cause of shock in the trauma setting. Additional
etiologies include:

 Cardiac tamponade

 Tension pneumothorax

 Myocardial or pulmonary contusion

 High-spinal cord injury (ie, neurogenic shock)

Fat or air emboli can also cause shock in the trauma setting, although they are relatively rare.
The presence of high central venous pressure (CVP) in the following injuries distinguishes them from
hypovolemic/hemorrhagic shock in tachycardic trauma patients:

 Pericardial tamponade

 Tension pneumothorax

 Myocardial contusion

In contrast, hypovolemic/hemorrhagic shock presents with low CVP. CVP is assessed by examination of neck veins;
the right internal jugular vein is typically preferred although other neck veins can be used.
Two large-bore (≥16 gauge) peripheral IVs is the standard approach to deliver fluid resuscitation in trauma.

Common refrain: "two is one and one is none" (referring to the requirement of placing 2 IVs). Rationale: if only a
single IV is placed and is subsequently lost, the patient can no longer be resuscitated with existing lines.

Peripheral IV lines are typically preferable to central lines in trauma patients. If peripheral IV access cannot be
established quickly, preferred alternatives include:

 Femoral central venous catheter in adults

  Tibial intraosseous cannulation in children

Jugular vein catheters and surgical venous (eg, saphenous) cutdowns are alternative approaches.
After establishing an airway, controlling breathing, and applying pressure to bleeding from external wounds, the
next steps (in order) of the management of trauma patients with hypovolemic shock due to hemorrhage are:

 IV fluids (normal saline or lactated ringers)

 Give only until blood is available or SBP =90 mmHg

 Blood product transfusion in 1:1:1 ratio

 PRBCs:FFP:platelets

 ± Tranexamic acid (if ≤3 hrs of injury)

Classically, 2 L of IV fluids are transfused in the initial step. Packed red blood cells (PRBCs) should be type O negative if
the patient’s blood type is unknown. FFP = fresh frozen plasma. SBP = systolic blood pressure.
Common targets for volume replacement in trauma patients with hypovolemic shock include:

 SBP: 90 mmHg

 Urine output: 0.5-2.0 mL/kg/h

 CVP ≤15 mmHg

A patient with pericardial tamponade will have the following clinical features:

 Trauma to the chest (eg, penetrating chest trauma)

 Distended head & neck veins (↑ 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.

Tension pneumothorax classically presents with:

 Hypotension

 Dyspnea, tachypnea

 Unilateral pleuritic chest pain

 Hyperresonance to percussion

 Jugular venous distention ( ↑ JVP)

 Absent breath sounds (on affected side)

Tension pneumothorax is diagnosed clinically.

While CXR classically shows tracheal deviation to the unaffected side, it should NOT be performed in the setting of
suspected tension pneumothorax because it will delay intervention for this life-threatening emergency.

The sequential steps of the emergent and definitive management of tension pneumothorax are:

 Needle thoracostomy* (emergent)

 Thoracostomy tube placement (definitive)

*Performed at the 2nd or 3rd intercostal space at the midclavicular line above the rib.
Obstructive shock is the most common cause of death in tension pneumothorax. The pathophysiology entails:

1. Increased pleural pressure

2. Mediastinal shift

3. Kinking of SVC & IVC

4. Increased venous pressure

5. Decreased venous return

6. Insufficient cardiac preload

Bradycardia is the key finding that distinguishes neurogenic shock from the other forms of shock in the setting of
trauma. Additional clinical manifestations of neurogenic shock include:

 Flaccid paralysis

 Hypotension

 Cutaneous vasodilation

Neurogenic shock is a sub-type of distributive shock.

Other sub-types of distributive shock include anaphylactic shock, septic shock, and endocrine shock.

Lack of sympathetic discharge due to high (cervical or high thoracic) spinal cord injuries abrogates sympathetic
arterial tone, leading to extreme vasodilatation and hypotension in the setting of neurogenic shock. This is also the
cause of the key physical exam findings:

 Bradycardia (unopposed parasympathetic tone)

 Peripheral vasodilation (lack of sympathetic tone)

Surgical 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) include the epidermis and some of the dermis, and is usually 10/1000 to 18/1000
of an inch thick.
Full thickness skin grafts (FTSG) include the epidermis and all of the 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.

Wounds

The four types of wounds include:

 Clean

 Clean-contaminated

 Contaminated

 Dirty

A clean wound is defined as 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 the GI, GU, or respiratory tracts.

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 staples, 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.

Finally, wound healing with skin grafts most commonly entails the use of split-thickness skin grafts, which consist of
epidermis and a portion of dermis.
Dressings are required for open 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.

Enteric fistulas most commonly occur in the postoperative setting; they are abnormal connections between the GI
tract and other abdominal organs, chest, or skin.

Abdominal CT scan with and without oral and intravenouscontrast is the preferred initial imaging study for the
evaluation of a suspected enteric fistula.

The initial management of freely-draining, uninfected enteric fistulas consists of:

 NPO w/ TPN initiation

 Abdominal skin protection*

 Fluid and electrolyte repletion

*Can be accomplished with bag drainage and/ or somatostatin analogs (eg, octreotide), which reduce fistula output.
Most enteric fistulas heal spontaneously in several weeks; etiologies of non-healing fistulas include
(mnemonic: FRIENDS):

 Foreign body in the wound

 Radiation damage
  Infection or Inflammatory bowel disease

 Epithelialization of the fistulous tract

 Neoplasm

 Distal bowel obstruction

 Steroids

Peripheral Vascular Disease

Atherosclerotic plaques that progressively impair lower extremity blood flow are the central pathologic
cause of peripheral artery disease (PAD).

Note that this is distinct from the causes of acute limb ischemia — acute thrombosis or embolization.
Smoking is the most important risk factor in PAD.

Other risk factors for atherosclerosis (eg, hypertension, hyperlipidemia, diabetes) are also associated with
PAD.
Claudication in lower extremity PAD is a 3-part definition that consists of all of the following:
 Leg pain with walking

 Several minutes of rest alleviate pain

 Pain is reproducible at the same walking distance and intensity

The superficial femoral artery (SFA) at the level of the adductor (Hunter's) canal is the most common
site of peripheral atherosclerosis.

Since calf muscles are perfused by the SFA, this muscle group is most commonly affected by claudication
in PAD.
Aortoiliac occlusive disease (ie, Leriche syndrome) is due to atherosclerosis of the infrarenal aorta or
common iliac arteries and presents with the classic triad of:
 Claudication of low back, buttocks, hip, or thigh

 Absent or diminished femoral pulses

 Erectile dysfunction

Dry, shiny, scaly skin without hair along with brittle, thickenedtoenails is indicative of lower extremity
PAD.
Ischemic rest pain indicates severe PAD and impending limb loss.

Ischemic rest pain is an indication for surgical intervention given the substantial risk of future amputation.
Nighttime forefoot or toe pain that awakens patients from sleepand is alleviated by placing the leg in a
dependent position (ie, dangling over the side of the bed, walking) is characteristic of ischemic rest pain.

Mechanism: laying in bed (vs. standing or sitting) reduces gravity-assisted blood flow to the foot, leading to
ischemia in the middle of the night.
Buerger test is performed by observing foot perfusion with the patient in the supine position by sequentially:
1. Raising legs to 45° for 1-2 min, followed by

2. Placing legs in a dependent position (eg, over the edge of the bed)
A positive Buerger test is indicative of severe PAD (ie, PAD with ischemic rest pain) and differentiates
PAD from cellulitis. It consists of foot:
 Pallor on elevation

 Rubor when placed in the dependent position*

*Due to compensatory arteriolar dilation and reactive hyperemia.

Nerve root compression in the setting of lumbar spinal stenosiscauses so-called neurogenic claudication,
which presents with bilateral, asymmetric leg pain, sensory loss, and weakness that is:
 Exacerbated by walking & erect postures

 Relieved by sitting, lying down & leaning forward, thus straightening the spine*

*Common examples include pain relief with pushing a shopping cart or leaning against a wall.
Acute lumbosacral radiculopathy (eg, S1 radiculopathy) is a more likely cause of lower back pain that
radiates down the posterior thigh into the foot since hamstring muscles are not substantially taxed during
normal walking.

Patients may also experience reduced sensation that is localized to the posterior thigh and the lateral edge
of the foot as well as loss of the ankle reflex.
A resting ankle-brachial index (ABI) is the initial test-of-choice to confirm the diagnosis of arterial
stenosis or occlusion in the setting of suspected PAD.

ABI compares the ratio of systolic pressures in the lower versus upper extremities.
ABI values and interpretations (in ascending order) include:
 <0.4: severe PAD (rest pain)

 0.4—0.9: moderate PAD (claudication)

 0.91—1.3: normal

 >1.3: unreliable (incompressible vessel)

Diabetes mellitus and end-stage renal disease are associated with ABI >1.3 due to medial calcinosis that
renders lower extremity vessels incompressible.

Patients with DM and PAD may also have falsely normal ABI values — additional vascular studies should
be pursued in these patients.
Arterial duplex scans are non-invasive tests that are commonly used to localize the level of the occlusion in
PAD. They involve a combination of:
 Ultrasound to identify arterial plaques

 Doppler to detect elevated blood flow velocity, which indicates stenosis that is hemodynamically
relevant

Arterial Doppler velocity waveforms in the context of peripheral artery disease (PAD) can be interpreted as
follows:
 Triphasic: normal

 Biphasic: single-level (moderate) PAD

 Monophasic: multi-level (severe) PAD

The triphasic waveform is due to rapid forward blood flow during systole, retrograde flow at the end of
systole (due to elastic recoil of the vessel), and slow outflow during diastole. Atherosclerosis diminishes
vessel elasticity; thus, the period of retrograde flow is lost in single-level PAD (biphasic waveform).
CT-angiography is the gold standard for localizing areas of vessel stenosis but is largely reserved for
patients that are planning to undergo invasive therapeutic interventions.
Supervised exercise therapy plus smoking cessation (if indicated) are the initial steps in the initial
management of patients with mild-to-moderate PAD that manifests as claudication.

Exercise promotes collateral circulation.

The following pharmacologic therapies that reduce cardiovascular risk are indicated in most patients with
mild-to-moderate PAD:
 Antihypertensive agent

 Statin (even with normal serum LDL)

 Antiplatelet agent (aspirin or clopidogrel)

Cilostazol is a phosphodiesterase III (PDE3) inhibitor that improves walking distance in patients with
claudication that is refractory to lifestyle modifications (eg, exercise smoking cessation) and medical
therapies that reduce cardiovascular risk.

PDE3 inhibition reduces platelet aggregation, promotes vasodilation, and inhibits vascular smooth muscle
cell proliferation.
Invasive revascularization is indicated in patients with PAD and any of the following:
 Lifestyle-limiting claudication

 Ischemic rest pain

 Tissue loss (eg, ischemic ulcerations)

Common invasive techniques include percutaneous transluminal angioplasty with or without stenting
OR bypass grafting. Limb amputation may be indicated instead, depending on the patient’s medical status
and disease severity.
Acute lower extremity occlusion refers to a sudden-onset of impaired perfusion that threatens limb
viability. It is classically characterized by the six Ps:
 Pulselessness (defining feature)

 Pain (at rest)

 Pallor

 Poikilothermia (cold)

 Paresthesia

 Paralysis (most ominous sign)

Cardiac emboli are the most common cause of acute lower extremity occlusion; frequently associated
etiologies include:
 Atrial fibrillation (most frequent)

 Post-myocardial infarction

 Valvular disease
  Atrial myxoma

 CHF/cardiomyopathy

The left atrium is the most common site of embolus origin.

The common femoral artery bifurcation into the superficial femoral and profunda femoris arteries is the
most common location of arterial embolization and acute lower extremity occlusion.

Patients present with unilateral calf and foot pain with pulses that are absent or markedly diminished
throughout the affected limb.
Skeletal muscle ischemia >6 hours results in complete cell damage, leading to a severely impaired limb that
may necessitate amputation.
The initial management of an acute lower extremity occlusion consists of:
 Heparin

 IV fluids

 Affected limb placement in a dependent position

This should be initiated before imaging studies are obtained.

CT angiography is the gold standard test for acute lower extremity occlusion; it can be performed
intraoperatively in patients that require immediate revascularization.
Emergent open embolectomy (ie, balloon catheter embolectomy or Fogarty catheter embolectomy) is the
procedure of choice for most patients with acute lower extremity occlusion, especially those with both
sensory and motor deficits on exam.

Select patients with mild occlusion (ie, sensory deficits without motor impairment) can be treated with
endovascular thrombolysis.
Primary amputation is indicated in patients with an acute lower extremity occlusion that has caused
irreversible damage (ie, completely anesthetic tissue with paralysis or rigor).
Abdominal Aortic Aneurysm

The infrarenal aorta (ie, abdominal aorta below the renal arteries) is the most common location of
abdominal aortic aneurysms (AAA).

An abdominal aorta with a maximum diameter ≥3.0 cm is considered aneurysmal in most adults (normal
infrarenal diameter = 2.0 cm).
The key pathophysiological event in abdominal aortic aneurysm development is atherosclerosis.
Nonmodifiable risk factors for abdominal aortic aneurysm (AAA) development include:
 Advancing age (esp. >60)

 Caucasian race

 Male sex

 Family history of AAA

 Another large vessel aneurysm*

*For example, 85% of patients with femoral artery aneurysms have a concomitant AAA and 60% of patients
with popliteal aneurysms have a concomitant AAA.
Modifiable risk factors for abdominal aortic aneurysm (AAA) development, expansion, and rupture include:
  Smoking (strongest)

 Atherosclerotic risk factors except diabetes (eg, hypertension, hyperlipidemia, coronary artery
disease)

Counterintuitively, diabetes mellitus is negatively associated with AAA.

AAAs are most commonly asymptomatic.

A pulsatile abdominal mass is present on physical exam in 30% of patients with asymptomatic AAAs.
Aneurysm size and the patient's abdominal girth are the major limiting factors for detecting AAA on exam.

Note that an isolated pulsatile abdominal mass is not considered "symptomatic"; thus, it is not a finding that
can be used to justify surgical intervention.
Patients with symptomatic, unruptured AAAs most often present with:
 Abdominal, back, or flank pain (most common)

 Limb ischemia

 Fever, malaise*

*Seen in infected (mycotic) aneurysms.

The classic clinical triad of AAA rupture is seen in 50% of patients and consists of:
 Acute-onset abdominal, back, or flank pain (most common)

 Pulsatile abdominal mass (>60% of patients)

 Hypotension

Retroperitoneal hematoma due to a ruptured AAA can lead to ecchymosis at several sites, including:
 Flank ecchymosis (Grey-Turner sign)

 Periumbilical ecchymosis (Cullen's sign)

 Proximal thigh ecchymosis (Fox's sign)

 Scrotal ecchymosis (Bryant's sign)

Aortocaval fistulas are most commonly formed from rupture or erosion of an AAA into the inferior vena
cava. These fistulas can present with:
 Congestive heart failure

 Hematuria

 Leg swelling & cyanosis without distal ischemia

Abdominal ultrasound is the initial diagnostic modality for AAA in asymptomatic patients.

Ultrasound should be performed following a period of fasting since overlying bowel gas can make the aorta
difficult to visualize.
The initial approach to patients with symptomatic AAA depends on the hemodynamic stability of the
patient:
 Abdominal CT w/ IV contrast if stable

 Emergent surgery ± bedside FAST if unstable

FAST = Focused Assessment with Sonography in Trauma.
AAA ruptures are most commonly retroperitoneal and are notvisible on bedside ultrasound, which
detects intraperitoneal fluid.

Thus, patients with symptoms suggestive of rupture and a seemingly intact AAA on ultrasound should be
taken to the OR.
Men 65-75 years of age who have smoked (current smokers or lifetime history of ≥100 cigarettes) should
receive a one-time screening for AAA by ultrasonography, per USPSTF guidelines.
Additional recommendations from the Society for Vascular Surgeryregarding AAA screening broaden the
screening population, recommending a one-time ultrasound in:
 Women 65-75 years old who have smoked

 Men & women >75 years old who have smoked & have not undergone prior screening*

 First-degree relatives of patients with AAA between 65-75 years of age or >75 years of age*

*Requires that patients are in otherwise good health.

Indications for surgical repair of an abdominal aortic aneurysm (AAA) include any of the following:
 ≥5.5 cm diameter in men

 ≥5.0 cm diameter in women*

 Growth rate >0.5 cm/6 months or >1 cm/year

 Symptomatic aneurysms (eg, abdominal/back/flank pain, limb ischemia)

*Although AAA are less common in women than in men, when present, they are more likely to rupture in
women.
AAAs can be surgically repaired via either:
 Open surgery

 Endovascular aneurysm repair (EVAR)

All things being equal, EVAR is associated with a lower perioperative (30-day) morbidity and mortality,
while long-term mortality is roughly equivalent for both approaches to date.
Myocardial infarction is the most common cause of death following the surgical repair of an AAA.
While there are no medical interventions that have been clearly demonstrated to reduce AAA growth and
prevent rupture, conservative management of patients with asymptomatic AAAs includes:
 Smoking cessation

 Cardiovascular disease treatment*

 Ultrasound screening at 6- to 12-month intervals

*Rationale: AAA is a coronary risk equivalent. Entails antiplatelet agent (eg, aspirin), statin, and
antihypertensive agent(s) as indicated.
Complications of surgical abdominal aortic aneurysm (AAA) repair include:
 Ischemic colitis (early)

 Renal failure (early)

  Sexual dysfunction (early)

 Graft infection (late)

 Aortoenteric fistulae (late)

Early = initial week after surgery. Late = months to years after surgery.
Postoperative ischemic colitis due to interruption of the inferior mesenteric artery is a feared
complication of AAA repair. It typically presents in the first 3 days after surgery and almost always affects
the rectosigmoid segment. Classical clinical manifestations include:
 Bloody or liquid diarrhea

 Abdominal pain, ileus, or distension

 Leukocytosis

Immediate sigmoidoscopy to assess the viability of the colonic mucosa should be performed in patients
with suspected postoperative ischemic colitis.

Patients with full-thickness ischemia are treated with colon resection, while those with partial thickness
ischemia are managed conservatively (eg, NPO, antibiotics, hydration, and repeat sigmoidoscopy).
Etiologies of postoperative renal failure following AAA repair include:
 Atherosclerotic renal artery embolization

 Ischemia due to clamping of the aorta

 Contrast-induced nephropathy*

*Contrast is required in endovascular approaches.

A history of erectile dysfunction (ED) should be assessed prior to elective AAA repair since iatrogenic ED
can be caused by intraoperative damage to the pelvic nerves (eg, pelvic splanchnic, hypogastric nerves).
Skin flora such as S. epidermidis and S. aureus are the most common causes of graft infections following
AAA repair. These infections can present years after AAA repair, especially in the setting of S.
epidermidis infection. Clinical manifestations include:
 Fever

 Wound abscess, sinus tract

 Abdominal/back pain

Aortoenteric fistulae (AEFs) most commonly involve the 3rd & 4th portions of the duodenum and are a late
complication of AAA repair. They are caused by erosion of a prosthetic aortic graft into the intestine. The
classical presenting clinical triad is:
 GI bleeding

 Abdominal pain

 Palpable mass

AEFs may initially present as a self-limited bleed (ie, herald bleed) that precedes a future
potentially catastrophic hemorrhage.
CT scans of patients with aortoenteric fistulae (AEFs) classically show:
 Peri-aortic ectopic gas
  Aortic wall discontinuity

 Focal bowel wall thickening

 Contrast extravasation into the bowel lumen

Patients with vascular graft infections and aortoenteric fistulae (AEFs) are managed with:
 Removal of the graft

 Revascularization via axillofemoral bypass

 Broad-spectrum antibiotics

Surgical repair of the GI tract is also performed in the setting of AEFs.

Thoracic Aortic Aneurysm
Thoracic aortic aneurysms are 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 weakens 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, smokingand hypercholesterolemia are the three most important risk factors for
thoracic aneurysm formation 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.
Syphilis is an important infectious cause of thoracic aortic aneurysms. 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 a syphilitic aneurysm in a patient with long standing syphilis and a new diastolic murmur in the right
2nd intercostal space indicating aortic valve insufficiency due to dilation of the aortic valve and valve ring.

Aortic Dissection
A tear in the tunica intima is thought to be the primary event leading to an 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 an aortic dissection includes 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.
Unequal pulses in the upper extremities are sometimes observed due to (partial) occlusion of the left subclavian
artery or brachiocephalic trunk.
Under systemic pressures, this initial intramural aortic hemorrhage quickly gives rise to an unstable medial hematoma
which may:
 1. 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.

3. Rupture into pericardial sac can cause cardiac tamponade.

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.

Chest x-ray is a common radiograph in patients with suspected aortic dissection who are stable. The most classic
finding on chest x-ray in patients with an aortic dissection is a 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 diagnosis 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 at 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 a dissection is suspected and the 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
requiresurgery.
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 are given beforenicardipine/clevidipine/nitroprusside to prevent reflex tachycardia.

Malrotation

During embryologic development of the midgut, the bowel lengthens, herniates into a U-shaped (around
33 days) loop into the base of the umbilical cord and rotates around the SMA axis 270° counterclockwise
(after 44 days). It then reenters the abdomen and undergoes fixation.
Malrotation is defined as a failure of normal rotation of any portion of the gastrointestinal tract. It also
implies abnormal fixation, which is the predisposing factor for the development of a volvulus.
Intestinal malrotation is associated with the following conditions:
 Diaphragmatic hernia

 Duodenal atresia

 Jejunoileal atresia
Intestinal malrotation is twice as common in males as in females.
Omphalocele occurs when the midgut loop fails to return to the abdomen, which presents with an intact
shiny mesenteric covering.
Gastroschisis is a defect in the ventral abdominal wall due to failure of closure of the lateral folds.
The viscera extrude from the peritoneal covering without the shiny mesenteric coveringseen in
omphalocele. The umbilical cord is also to the left of the defect as opposed to omphalocele where it
goes through the defect
The clinical presentation of acute midgut volvulus includes:
 Occurrence in the first decade of life

 Sudden onset bilious vomiting

 Diffuse abdominal pain out of proportion to physical exam

Chronic midgut volvulus typically presents with recurrent abdominal pain and intestinal malabsorption.
Some degree of abdominal distention should be seen on physical examination.
The gold standard for diagnosing intestinal malrotation is an upper gastrointestinal contrast series*.
Ultrasound imaging is also associated with a 0% false positive rate in the hands of an experienced user.

*X-ray visualization of the esophagus, stomach, and duodenum using barium as a contrast agent.
Intestinal congenital defects, such as malrotation, require surgical correction. The most effective procedure
done for malrotation is the Ladd procedure which involves a reduction of the volvulus (if present),
division of the mesenteric bands, placing the small bowel on the right, the large bowel on the left of the
abdomen, and an appendectomy.

Small Bowel Obstruction

The most frequent causes of mechanical small bowel obstruction (SBO) in developed countries are:
 Postoperative adhesions (most common)

 Neoplasms

 Hernias

In contrast, hernias are the most common cause of SBO worldwide and are more likely in patients without a
history of abdominal or pelvic surgeries.
Other less common causes of SBO include:
 Appendicitis/diverticulitis/intraabdominal abscess

 Intussusception

 Volvulus

 Crohn disease

 Congenital stricture

 Traumatic intramural hematoma

 Gallstone
Closed-loop obstruction refers to obstruction of the intestine at two contiguous points that results in a
portion of intestine with neither a proximal or distal outlet.

Closed-loop obstructions can progress rapidly to strangulation, ischemia, and necrosis.

Continued passage of gas and stool >6-12 hours following symptom onset and the presence of residual
colonic gas on imaging are characteristic of a partial SBO and can help to differentiate it from complete
SBO.

In contrast, patients with complete SBO have no gas in the distal bowel segments or colon.
The most common clinical manifestations of small bowel obstruction are:
 Nausea, vomiting

 Obstipation

 Cramping, paroxysmal abdominal pain

High-pitched, tinkling bowel sounds on auscultation caused by a compensatory increase in GI tract

peristalsis are indicative of early mechanical SBO.

Hypoactive or absent bowel sounds due to progressive intestinal dilation and atony are characteristic
of prolonged mechanical SBO.
High-pitched, tinkling bowel sounds are initially present in mechanical SBO (eg, due to adhesions,
hernias).

Hypoactive or absent bowel sounds are early findings in ileus or pseudo-obstruction.

Classic radiographic findings in SBO include:
 Proximal air-fluid levels

 Gasless abdomen

 String of beads or pearls sign

 Proximal loops of dilated bowel with distal bowel collapse

Imaging studies indicative of a complicated SBO (eg, ischemia, necrosis, perforation) include:
 Abdominal free air (eg, under diaphragm)

 Bowel wall thickening

 Reduced bowel wall enhancement

Clinical and laboratory manifestations indicative of a complicated SBO (eg, ischemia, necrosis, perforation)
include:
 Fever

 Tachycardia

 WBC >10,000/mm3

 Peritoneal signs (eg, rigidity, guarding, rebound tenderness)

 Atypical abdominal pain (ie, localized, continuous, or worsening)

Conservative management with frequent reassessment can be attempted if signs of a complicated or
complete SBO are absent. Management includes:
 NPO w/ IV fluids

 Nasogastric decompression

 ± PO water-soluble contrast (eg, Gastrografin)

Early exploratory laparotomy is indicated in patients with a SBO that is complicated by bowel ischemia,
necrosis, or perforation.
Anus

Anal fissures are linear tears in the anal mucosa below the dentate line, most commonly found in the
posterior midline.
Primary anal fissures are caused by local trauma, such as:
 Constipation, diarrhea

 Vaginal delivery

 Anal sex
Anal fissures classically present with pain that is present at restbut severely exacerbated by
defecation along with blood-streaked stools and blood-stained toilet paper.

Constipation is a common complication and is caused by withholding bowel movements to avoid the
exquisite, "tearing" pain of defecation.
Supportive measures plus topical vasodilators are the preferred initial treatment for patients with typical
anal fissures. This entails:
 ↑ fiber & water intake

 Stool softeners (eg, docusate)

 Sitz baths

 Topical analgesics (eg, 2% lidocaine jelly)

 Topical vasodilators (nifedipine or nitroglycerin)

Endoscopy to rule out underlying Crohn disease is indicated in patients with persistent/refractory anal
fissures after 2 months of medical therapy with supportive measures and topical vasodilators.
Anal fissures that do not respond to medical therapies (and are not associated with Crohn disease) can be
treated with surgical therapies. The risk of developing fecal incontinence guides the selection of treatment:
 Low risk: lateral internal sphincterotomy

 High risk: botulinum toxin injection or anal advancement flap

Examples of patients at high risk for fecal incontinence include multiparous women and the elderly.
Perianal abscesses (aka anorectal abscesses) are caused by an obstruction of an anal crypt gland,
resulting in bacterial overgrowth and abscess formation.
Risk factors for a perianal abscess include:
 Constipation

 Diarrhea

 Inflammatory bowel disease

 Immunosuppression or chemotherapy

 Diabetes mellitus

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, usually including the surrounding area

 Purulent drainage

Incision & drainage is the mainstay of treatment for perianal abscesses.

Poorly managed diabetics are predisposed to necrotizing tissue infections from a perianal abscess.
Anorectal fistulas originate from either:
 Anal abscesses within anal crypt glands (most common)

 Deep, penetrating inflammation in Crohn disease

By definition, a fistula is an abnormal connection between two epithelialized surfaces that is lined with
granulation tissue.
Risk factors for developing an anorectal fistula include:
 Perianal abscesses (most common)

 IBD (Crohn disease >ulcerative colitis)

 Local radiation

 Foreign bodies

IBD = inflammatory bowel disease.

Anorectal fistulas classically present with constant, purulent perianal discharge that is associated with a
firm mass. A history of perianal abscess drainage, as well as rectal pain associated with defecation and
sitting and/or pruritis, are additional common features of the clinical history.

On exam, a cordlike tract can often be palpated that may express discharge.
Simple anorectal fistulas are diagnosed clinically without imaging studies. They can be differentiated from
other perirectal conditions by:
 Absence of fever (vs. anal abscess)

 Presence of an anorectal tract (vs. Hidradenitis)

 Perianal location (vs. gluteal cleft location in pilonidal disease)

Anorectal tracts can be explored using a fistula probe.

Fistulotomy is the preferred treatment for simple anorectal fistulas; it involves examination under
anesthesia to identify the internal opening, passage of a probe throughout the fistula tract, incision of the
tract, and curettage. The tract can then be marsupialized.

Curettage of the internal opening of the fistula is the key to reducing fistula recurrence.
Goodsall’s 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

Fecal incontinence and Crohn disease are major contraindications to fistulotomy, even in the setting of
simple fistulas.

Placement of a draining seton for >6 weeks is the initial treatment in these patients. A sphincter-sparing
procedure can subsequently be performed.
Anorectal fistulas that diverge from Goodsall’s rule should raise suspicion of Crohn’s disease.
Anal cancer is a relatively rare form of cancer; key risk factors include:
 Receptive anal intercourse

 HPV infection (HPV 16 most common)

 Cigarette smoking
  Chronic immunosuppression (eg, HIV infection, chronic glucocorticoids, post-transplant)

While HPV 6 and HPV 11 are the most common causes of anorectal condylomas, HPV 16 is the most
common type of HPV associated with anal cancer.
Squamous cell carcinoma (SCC) is the most common histopathology associated with anal cancer. Anal
SCC frequently metastasizes to the:
 Inguinal lymph nodes (most common)

 Superior rectal lymph nodes (up to 50% of patients)

History of an anorectal condyloma is common in patients who later present with anal cancer. Clinical
manifestations of anal cancer include:
 Rectal bleeding (most common)

 Anorectal pain

 Sensation of a rectal mass (ie, perianal fullness)

Up to 20% of patients may also be asymptomatic at the time of diagnosis.

In addition to physical exam and biopsy, anal cancers are staged clinically via:
 Abdominopelvic CT scan or MRI

 Chest CT scan

 ± PET scan

In women, cervical cancer screening and a gynecologic exam should also be performed.
Combined chemoradiotherapy with fluorouracil plusmitomycin (ie, modified Nigro or Wayne State
protocol) is the standard of care for the initial treatment of most patients with localized anal cancer, even in
the presence of positive lymph nodes.

This is both highly effective and preserves the anal sphincter, which is the rationale for its strong
preference over surgery in this setting.
Abdominoperineal resection is indicated for patients with locally recurrent (ie, after chemoradiotherapy
treatment) anal cancer.
Pilonidal disease is caused by the recurrent penetration of gluteal (aka natal) cleft skin pores by ingrown
hairs, which induces a foreign body reaction and formation of a sinus tract.

It can present as a painless cyst, an acute abscess, or as chronic/recurrent cysts with draining sinuses.
Risk factors for pilonidal disease include:
 Obesity

 Hairy or deep gluteal cleft

 Sedentary lifestyle, prolonged sitting

A tender, fluctuant mass in the posterior midline over the sacrum and coccyx is the most common
manifestation of pilonidal disease.

This finding, along with the presence of fever, malaise, and/or overlying cellulitis is indicative of a pilonidal
abscess.
Maneuvers that stretch the gluteal cleft skin (eg, bending down, sit-ups) typically exacerbates pain.
Pilonidal disease a purely clinical diagnosis; any of the following findings are diagnostic on exam of the
gluteal cleft region (ie, superior/dorsal to the anus):
 Midline skin pits

 Tender, painful mass

 Chronically draining sinus tracts

This is a purely clinical diagnosis; additional tests are not necessary.

Incision & drainage with unroofing, hair debridement and curettage of the abscess cavity is the
preferred initial treatment of an acute pilonidal abscess. The wound is packed and left open to heal by
secondary intention.

Antibiotics are reserved for patients with concomitant cellulitis.

Gluteal hair removal and meticulous perineal hygiene can reduce the risk of recurrent pilonidal
abscesses.

Hair removal can be accomplished via shaving, laser removal or depilatory creams (eg, Nair).
Surgical excision of the pilonidal sinus tracts down to the level of the sacrococcygeal fascia is the
definitive treatment of pilonidal disease.

It is indicated for patients with recurrent pilonidal abscesses or who experience persistent drainage and
inflammation.
Benign Prostatic Hyperplasia

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 prostate leading 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 evaluate patients
with lower urinary tract symptoms (LUTS) associated with BPH:
 Urinalysis to look for infection or blood (associated with bladder cancer or renal calculi)

 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
are initially treated with an alpha-blocker (e.g. tamsulosin, terazosin), which provide immediate
benefits. Combination of an alpha-blocker and a 5-alpha-reductase inhibitor (e.g. 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.
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 normally asymptomatic 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 manifestations
include 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

 Laparoscopic

 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 menare 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.
An 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.
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.
These occur most commonly in the greater saphenous vein and its tributaries, esophagus, anorectum, and
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 uncomplicated superficial thrombophlebitis
as it is not a risk factor for PE or DVT.
Deep Venous Thrombosis
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. 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.
Virchow’s 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 patient’s 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 Virchow’s 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
the lower extremities. Veins with DVTs will have a non-compressible venous lumen.
In patients with low pre-test probability of DVT, a negativecompression 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 with anticoagulation (e.g. warfarin, heparin, low-
molecular-weight heparin, or factor Xa inhibitors).
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 embolismunless otherwise contraindicated.

Postoperative Paralytic Ileus

Postoperative ileus typically lasts 3-5 days following surgery and is characterized by a transient decrease or
arrest of bowel motility after surgery that manifests with obstipation and intolerance of oral intake.

It is a normal physiologic response to the operation.

Prolonged postoperative ileus lasts >3-5 days post-surgery.
Surgeries involving the abdomen, GI tract, or pelvis (esp. those with GI tract manipulation) are at risk for
prolonged postoperative ileus. Other major surgical risk factors include:
 Prolonged surgeries

 Perioperative opioids

 Delayed enteral nutrition

 Routine NG tube placement

 Open surgery (vs. laparoscopic)

 Postoperative fever (pneumonia)

 Intra-abdominal infection (peritonitis, sepsis, abscess)

NG = nasogastric tube.
Prolonged postoperative ileus lasts >3-5 days post-surgery and manifests with:
 Nausea, vomiting
  Failure to tolerate oral diet

 Abdominal distention, bloating

 Diffuse, constant abdominal pain

 Delayed passage of stool, flatus

X-ray is typically the initial imaging study ordered to evaluate prolonged postoperative ileus.

Abdominal CT with oral contrast is highly sensitive and specific for distinguishing ileus
from complete small bowel obstruction; it is the next diagnostic imaging modality in equivocal cases.

CT scan is less effective in distinguishing ileus from a partial small bowel obstruction.
Upper gastrointestinal contrast studies (ie, enteroclysis) withwater-soluble contrast (eg, Gastrografin)
can effectively distinguish prolonged postoperative ileus from from a partial small bowel obstruction.
Abdominal imaging findings classically seen in prolonged postoperative ileus include:
 Dilated bowel loops

 Free air in colon

 No transition point*

In contrast to ileus, a mechanical SBO has an identifiable transition point on abdominal imaging.
*Transition point = point between proximal, dilated bowel and distal, nondilated bowel, indicating location
of mechanical obstruction in SBO.
Supportive care with serial abdominal exams is the mainstay of treatment for prolonged postoperative ileus.
Cornerstones of management include:
 Minimizing & reducing opioids

 NPO w/ IV fluids*

 Electrolyte abnormality correction

 ± Nasogastric decompression**

*Small sips of clear fluids are typically permitted.

**Especially useful with persistent nausea/vomiting.
Hypokalemia exacerbates and prolongs postoperative ileus and should be corrected.

Serum magnesium levels should also be assessed since hypokalemia is refractory to K+ supplementation in
the setting of hypomagnesemia.
Both postoperative ileus and mechanical small bowel obstruction (ie, due to postoperative adhesions) can
present within days of a surgery with abdominal distention, nausea, vomiting, and failure to tolerate oral
intake.

Key features that distinguish prolonged postoperative ileus from early small bowel obstruction (SBO)
include:
Prolonged postoperative ileus Early SBO

No initial return of bowel function Initial bowel function return prior to onset
Hypoactive or absent bowel sounds High-pitched bowel sounds

Constant, dull abdominal pain Paroxysmal, cramping abdominal pain

NO air-fluid levels on x-ray Air-fluid levels on x-ray

CT scan w/ contrast: CT scan w/ contrast:

 Air in distal bowel  NO air in distal bowel

 NO transition point  Transition point* present

*Transition point = point between proximal, dilated bowel and distal, nondilated bowel, indicating location
of mechanical obstruction in SBO.
Acute colonic pseudo-obstruction (Ogilvie syndrome) is an idiopathic disorder in which acute dilatation
of the colon occurs in the absence of a mechanical obstruction. It usually involves the cecum and right
hemicolon.

It most commonly occurs in elderly patients who are severely ill, immobilized, hospitalized, and/or
institutionalized.
A markedly distended and tympanitic abdomen is the cardinal clinical feature of acute colonic pseudo-
obstruction. Patients also present with findings characteristic of bowel obstruction (eg, nausea, vomiting,
constipation). Other notable manifestations include:
 Bowel sounds present (90%)

 Paradoxical diarrhea (40%)

Treatment of underlying medical conditions along with conservative therapy for 24-48 hours is the
preferred initial management strategy of acute colonic pseudo-obstruction in the absence of substantial
abdominal pain or extreme colonic dilatation (>12 cm). This entails:
 NPO w/ IV fluids

 Electrolyte abnormalities correction

 Nasogastric decompression

 Discontinue potentially offending medications*

*Examples include: narcotics, anticholinergics, sympathetic agents, antiparkinson agents, calcium channel
blockers.
Neostigmine, a short-acting acetylcholinesterase inhibitor, is the first-line pharmacologic therapy for
patients with acute colonic pseudo-obstruction (Ogilvie syndrome) who have failed 1-2 days of conservative
therapy or are at risk for perforation (cecal diameter >12 cm).

Mechanical bowel obstruction should be definitively ruled out prior to initiating neostigmine since it is
potentially lethal in this setting. During treatment, patients should be placed on continuous cardiac
monitoring and atropine should be readily available to treat bradycardia.
Colonoscopic decompression is performed in patients who are refractory to neostigmine or have
contraindications to cholinergic agents (eg, bradycardia, hypotension, current bronchospasm).

While colonoscopy can be used for treatment, it should NOT be used for diagnosis because it increases the
risk of perforation.
Cecostomy or partial resection with anastomosis can be performed in patients with acute colonic pseudo-
obstruction who are refractory to colonoscopic decompression and who do not have perforation.
Abdominal CT scan is the preferred imaging modality to support the diagnosis of acute colonic pseudo-
obstruction and exclude a mechanical etiology since this is a diagnosis of exclusion.

Proximal colonic dilation with an intermediate transition pointat the level of the splenic flexure is the
characteristic finding.

Since this is pseudo-obstruction, a transition zone is characteristic on imaging, similar to radiographic

findings in mechanical bowel obstructions.
Acute Mesenteric Ischemia
Mesenteric ischemia is a reduction of blood flow to the intestines.
Patients have severe periumbilical abdominal pain that is out of proportion to the findings on physical examination.
Mesenteric ischemia is either due to occlusions, vasospasm, or hypoperfusion. Acute mesenteric ischemia is the
sudden onset of decreased blood flow to the intestines.
Superior mesenteric artery embolism occurs in 50% of cases.
Superior mesenteric artery thrombosis occurs in 15-25% of cases.
Nonocclusive ischemia occurs in 20-30% of cases.
Mesenteric venous thrombosis occurs in 5% of cases.
75% of patients with a mesenteric venous thrombosis have an inherited thrombotic disorder.
Diagnosis depends on clinical suspicion, laboratory studies, and radiographic studies.
Leukocytosis may be present.
A non-elevated serum lactate may be helpful to rule out mesenteric ischemia.
Abdominal CT may be helpful by showing focal or segmental bowel wall thickening.
Mesenteric angiography is the gold standard for diagnosis.
Treat with fluids, antibiotics, correction of metabolic acidosis, and surgery if necessary.
Necrotic bowel appears dusky and blue on gross pathologic examination.
Exploratory laparatomy with small bowel resection is indicated in patients with potential infarction, perforation, or
arterial thrombosis.

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). For more information on peripheral
vascular disease see https://med.firecracker.me/topics/1215.
Unlike venous stasis and diabetic ulcers, arterial ulcers are painful.

Arterial Venous

Site Dorsum of toes, feet and Medial gaiter region (between knee
ankle, and ankle)
sites of increased pressure

Wound Necrotic tissue Granulation tissue

base

Appearance "Punched out" Shallow, irregular margins

Pain Painful Generally painless

Thoracic Outlet Syndrome and Subclavian Steal Syndrome

Thoracic outlet syndrome is the compression of the neurovascular bundle at the thoracic outlet.
Causes of thoracic outlet syndrome include anomalous ribs, congenital cervical fibro-cartilagionous bands, muscular
anomalies, and injury.
Three distinct types of thoracic outlet syndrome (TOS) exist:
 Neurogenic TOS

 Venous TOS

 Arterial TOS

Neurogenic thoracic outlet syndrome is due to brachial plexus compression. True neurogenic thoracic outlet
syndrome is rare.
Venous thoracic outlet syndrome is due to subclavian veincompression.
Arterial thoracic outlet syndrome is due to subclavian arterycompression.
Electrophysiological evaluation and imaging are used for diagnosis.
The first line imaging modality is usually arterial or venous duplex ultrasound. If that is equivocal, CT or MRI should
be ordered.
Management includes physical therapy, anticoagulation, embolectomy, and thoracic outlet decompression.
Surgery is indication only for patients who are symptomatic.
Symptoms depend on the type of thoracic outlet syndrome.
Patients with true neurogenic thoracic syndrome develop unilateral atrophic weakness in the intrinsic muscles of the
hand. The thenar musculature is affected more than the hypothenar musculature is.
Venous TOS occurs in patients who uses an upper extremity repetitively. Swelling pain and cyanosis may be present
in the affected extremity.
Arterial TOS is typically associated with a cervical or anomalous rib. Patients present with hand
ischemia and pain, pallor, and paresthesia.
In subclavian steal syndrome, stenosis or occlusion of the proximal subclavian artery leads to reversal of blood flow
through the ipsilateral vertebral artery.
The subclavian artery normally supplies blood to the upper extremity. One branch of the subclavian artery is the
vertebral artery. If the proximal subclavian is obstructed, then blood will flow to the region of lowest pressure. Blood
travels through the intracranial vasculature including the circle of willis and basilar artery. From the basilar artery it
travels in a retrograde fashion through the vertebral artery and then to the distal subclavian artery (past the
obstruction) and into the upper extremity. The subclavian artery is "stealing" blood from the vertebrobasilar system.
Symptoms of subclavian steal syndrome are mostly related to ischemia of the upper extremity, and less often due to
vertebrobasilar ischemia. Symptoms include:
 Arm ischemia

 Exercise-induced pain

 Fatigue

 Coolness

 Paresthesias

 Vertebrobasilar ischemia

 Dizziness
  Vertigo

 Ataxia

 Dysequilibrium

 Tinnitus

 Hearing loss

 Blurred vision

 Diplopia

The primary physical exam finding of subclavian steal syndrome is >15 mmHg difference in pressure between upper
extremities.
Diagnosis is done with continuous wave doppler, MRA, CTA, and contrast angiography.
Treatment for patients with symptomatic subclavian steal involves surgical revascularization of the affected area. The
most common surgical procedures include carotid-subclavian bypass, carotid transposition, and percutaneous
angioplasty with stenting.

Congenital Heart Defects

Right-to-left shunts — 5 T’s:

 Tetralogy of Fallot

 Transposition of great vessels

 Tricuspid atresia

 Truncus arteriosus

 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:
 VSD (ventricular septal defect): holosystolic harsh murmur
  ASD (atrial septal defect): loud S1 with wide, fixed split S2

 PDA (patent ductus arteriosus): continuous machine like murmur

Children with Down syndrome often have an endocardial cushion defect with VSD, 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.
A 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 an ASD, the treatment is a patch that can be placed surgically or through cardiac catheterization.
Tetralogy of Fallot has 4 different components:
 Pulmonary stenosis aka right ventricular outflow tract obstruction

 Over-riding aorta

 Ventricular septal defect

 Right ventricle hypertrophy

The degree of right ventricular outflow tract obstruction 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 an anterosuperior displacement of the
infundibular septum, and infundibular spasm is hypothesized to contribute to "cyanotic spells".
Children with tetralogy of Fallot learn to squat to improve oxygenation: increased femoral artery
compression → increases arterial resistance → decreased R- L shunt gradient.
CXR finding will likely show a boot shaped heart due to progressive right ventricular hypertrophy from the
pressure generated against a stenotic pulmonary valve.
TOF is 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).
Diagnosis of TOF is by echocardiogram and definitive treatment is surgery (guided by size of pulmonary
arteries vs. ascending aorta).
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 or PFO), 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.

Note: 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.
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 a decrease in PGE levels (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 a 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 continuous “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.
Coil embolization is performed in older children, unless a large diameter or a short length of ductus requires
surgery.
Eisenmenger’s 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. Heart–lung transplantation is
the only definitive treatment.
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

 Osteoporosis, osteonecrosis

 Acne

 Skin thinning

 Myopathy

 Psychosis

 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.

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:
 Older than 65

 Who do not want anticoagulation

 Women of childbearing age

The major risk associated with mechanical valves is the 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.