SURGERY

MUKESH SAH
REGION 1 MEDICAL CENTER

INGUINAL HERNIA

DEFINITION AND BACKGROUND

An inguinal hernia occurs when tissue, such as part of the intestine, protrudes
through a weak spot in the abdominal muscles. The resulting bulge can be painful,
especially when you cough, bend over or lift a heavy object.

An inguinal hernia isn't necessarily dangerous. It doesn't improve on its own,

however, and can lead to life-threatening complications. Your doctor is likely to
recommend surgery to fix an inguinal hernia that's painful or enlarging. Inguinal
hernia repair is a common surgical procedure.

Symptoms

Inguinal hernia signs and symptoms include:

 A bulge in the area on either side of your pubic bone, which becomes more
obvious when you're upright, especially if you cough or strain
 A burning or aching sensation at the bulge
 Pain or discomfort in your groin, especially when bending over, coughing or
lifting
 A heavy or dragging sensation in your groin
 Weakness or pressure in your groin
 Occasionally, pain and swelling around the testicles when the protruding
intestine descends into the scrotum

You should be able to gently push the hernia back into your abdomen when you're
lying down. If not, applying an ice pack to the area may reduce the swelling enough
so that the hernia slides in easily. Lying with your pelvis higher than your head also
may help.

Incarcerated hernia

If you aren't able to push the hernia in, the contents of the hernia can be trapped
(incarcerated) in the abdominal wall. An incarcerated hernia can become strangulated,
which cuts off the blood flow to the tissue that's trapped. A strangulated hernia can be
life-threatening if it isn't treated.

Signs and symptoms of a strangulated hernia include:

 Nausea, vomiting or both

 Fever
 Sudden pain that quickly intensifies
 A hernia bulge that turns red, purple or dark
 Inability to move your bowels or pass gas

If any of these signs or symptoms occurs, call your doctor right away.

Causes

Some inguinal hernias have no apparent cause. Others might occur as a result of:

 Increased pressure within the abdomen

 A pre-existing weak spot in the abdominal wall
 A combination of increased pressure within the abdomen and a pre-existing
weak spot in the abdominal wall
 Straining during bowel movements or urination
 Strenuous activity
 Pregnancy
 Chronic coughing or sneezing

Risk factors

Factors that contribute to developing an inguinal hernia include:

 Being male. Men are eight times more likely to develop an inguinal hernia
than are women.
 Being older. Muscles weaken as you age.
 Being white.
 Family history. You have a close relative, such as a parent or sibling, who has
the condition.
 Chronic cough, such as from smoking.
  Chronic constipation. Constipation causes straining during bowel
movements.
 Pregnancy. Being pregnant can weaken the abdominal muscles and cause
increased pressure inside your abdomen.
 Premature birth and low birth weight.
 Previous inguinal hernia or hernia repair. Even if your previous hernia
occurred in childhood, you're at higher risk of developing another inguinal
hernia.

Complications

Complications of an inguinal hernia include:

 Pressure on surrounding tissues. Most inguinal hernias enlarge over time if

not repaired surgically. In men, large hernias can extend into the scrotum,
causing pain and swelling.
 Incarcerated hernia. If the contents of the hernia become trapped in the weak
point in the abdominal wall, it can obstruct the bowel, leading to severe pain,
nausea, vomiting, and the inability to have a bowel movement or pass gas.
 Strangulation. An incarcerated hernia can cut off blood flow to part of your
intestine. Strangulation can lead to the death of the affected bowel tissue. A
strangulated hernia is life-threatening and requires immediate surgery.

Diagnosis

A physical exam is usually all that's needed to diagnose an inguinal hernia. Your
doctor will check for a bulge in the groin area. Because standing and coughing can
make a hernia more prominent, you'll likely be asked to stand and cough or strain.

If the diagnosis isn't readily apparent, your doctor might order an imaging test,
such as an abdominal ultrasound, CT scan or MRI.

Treatment

If your hernia is small and isn't bothering you, your doctor might recommend
watchful waiting. In children, the doctor might try applying manual pressure to reduce
the bulge before considering surgery.

Enlarging or painful hernias usually require surgery to relieve discomfort and prevent
serious complications.
There are two general types of hernia operations — open hernia repair and
laparoscopic repair.

Open hernia repair

In this procedure, which might be done with local anesthesia and sedation or general
anesthesia, the surgeon makes an incision in your groin and pushes the protruding
tissue back into your abdomen. The surgeon then sews the weakened area, often
reinforcing it with a synthetic mesh (hernioplasty). The opening is then closed with
stitches, staples or surgical glue.

After the surgery, you'll be encouraged to move about as soon as possible, but it might
be several weeks before you're able to resume normal activities.

Laparoscopy

In this minimally invasive procedure, which requires general anesthesia, the surgeon
operates through several small incisions in your abdomen. Gas is used to inflate your
abdomen to make the internal organs easier to see.

A small tube equipped with a tiny camera (laparoscope) is inserted into one incision.
Guided by the camera, the surgeon inserts tiny instruments through other incisions to
repair the hernia using synthetic mesh.

People who have laparoscopic repair might have less discomfort and scarring after
surgery and a quicker return to normal activities. However, some studies indicate that
hernia recurrence is more likely with laparoscopic repair than with open surgery.

Laparoscopy allows the surgeon to avoid scar tissue from an earlier hernia repair, so it
might be a good choice for people whose hernias recur after traditional hernia surgery.
It also might be a good choice for people with hernias on both sides of the body
(bilateral).

Some studies indicate that a laparoscopic repair can increase the risk of complications
and of recurrence. Having the procedure performed by a surgeon with extensive
experience in laparoscopic hernia repairs can reduce the risks.
BURNS

There are three primary types of burns: first, second, and third-degree. Each
degree is based on the severity of damage to the skin, with first-degree being the most
minor and third-degree being the most severe. Damage includes:

 first-degree burns: red, nonblistered skin

 second-degree burns: blisters and some thickening of the skin
 third-degree burns: widespread thickness with a white, leathery appearance

There are also fourth-degree burns. This type of burn includes all of the symptoms of
a third-degree burn and also extends beyond the skin into tendons and bones.

Burns have a variety of causes, including:

 scalding from hot, boiling liquids

 chemical burns
 electrical burns
 fires, including flames from matches, candles, and lighters
 excessive sun exposure

Epidemiology

2015 fire and heat resulted in 67 million injuries.This resulted in about 2.9
million hospitalizations and 238,000 dying. This is down from 300,000 deaths in
1990. This makes it the 4th leading cause of injuries after motor vehicle collisions,
falls, and violence. About 90% of burns occur in the developing world.This has been
attributed partly to overcrowding and an unsafe cooking situation. Overall, nearly
60% of fatal burns occur in Southeast Asia with a rate of 11.6 per 100,000. The
number of fatal burns has changed from 280,000 in 1990 to 176,000 in 2015

The type of burn is not based on the cause of it. Scalding, for example, can cause all
three burns, depending on how hot the liquid is and how long it stays in contact with
the skin.

Chemical and electrical burns warrant immediate medical attention because they can
affect the inside of the body, even if skin damage is minor.

First-degree burn

First-degree burns cause minimal skin damage. They are also called “superficial
burns” because they affect the outermost layer of skin. Signs of a first-degree burn
include:

 redness
 minor inflammation, or swelling
 pain
 dry, peeling skin occurs as the burn heals

Since this burn affects the top layer of skin, the signs and symptoms disappear once
the skin cells shed. First-degree burns usually heal within 7 to 10 days without
scarring.

You should still see your doctor if the burn affects a large area of skin, more than
three inches, and if it’s on your face or a major joint, which include:

 Knee, ankle, foot, spine, shoulder, elbow, forearm

First-degree burns are usually treated with home care. Healing time may be quicker
the sooner you treat the burn. Treatments for a first-degree burn include:

 soaking the wound in cool water for five minutes or longer

 taking acetaminophen or ibuprofen for pain relief
 applying lidocaine (an anesthetic) with aloe vera gel or cream to soothe the
skin
 using an antibiotic ointment and loose gauze to protect the affected area

Make sure you don’t use ice, as this may make the damage worse. Never apply cotton
balls to a burn because the small fibers can stick to the injury and increase the risk of
infection. Also, avoid home remedies like butter and eggs as these are not proven to
be effective.

Second-degree burn

Second-degree burns are more serious because the damage extends beyond the top
layer of skin. This type burn causes the skin to blister and become extremely red and
sore.

Some blisters pop open, giving the burn a wet or weeping appearance. Over time,
thick, soft, scab-like tissue called fibrinous exudate may develop over the wound.

Due to the delicate nature of these wounds, keeping the area clean and bandaging it
properly is required to prevent infection. This also helps the burn heal quicker.

Some second-degree burns take longer than three weeks to heal, but most heal within
two to three weeks without scarring, but often with pigment changes to the skin.

The worse the blisters are, the longer the burn will take to heal. In some severe
cases, skin grafting is required to fix the damage. Skin grafting takes healthy skin
from another area of the body and moves it to the site of the burned skin.

As with first-degree burns, avoid cotton balls and questionable home remedies.
Treatments for a mild second-degree burn generally include:

 running the skin under cool water for 15 minutes or longer

 taking over-the-counter pain medication (acetaminophen or ibuprofen)
 applying antibiotic cream to blisters

However, seek emergency medical treatment if the burn affects a widespread area,
such as any of the following:

 Face, hands, buttocks, groin, feet.

Third-degree burn
Excluding fourth-degree burns, third-degree burns are the most severe. They cause the
most damage, extending through every layer of skin.

There is a misconception that third-degree burns are the most painful. However, with
this type of burn the damage is so extensive that there may not be any pain because of
nerve damage.

Depending on the cause, the symptoms third-degree burns can exhibit include:

 waxy and white color

 char
 dark brown color
 raised and leathery texture
 blisters that do not develop

Without surgery, these wounds heal with severe scarring and contracture. There is no

set timeline for complete spontaneous healing for third-degree burns.

Never attempt to self-treat a third-degree burn. Call AMBULANCE immediately.

While you’re waiting for medical treatment, raise the injury above your heart. Don’t
get undressed, but make sure no clothing is stuck to the burn.

Complications

Compared with first- and second-degree burns, third-degree burns carry the most risk
for complications, such as infections, blood loss, and shock, which is often what could
lead to death. At the same time, all burns carry the risk of infections because bacteria
can enter broken skin.

Tetanus is another possible complication with burns of all levels. Like sepsis, tetanus
is a bacterial infection. It affects the nervous system, eventually leading to problems
with muscle contractions. As a rule of thumb, every member of your household
should receive updated tetanus shots every 10 years to prevent this type of infection.

Severe burns also carry the risk of hypothermia and hypovolemia. Dangerously low

body temperatures characterize hypothermia. While this may seem like an unexpected
complication of a burn, the condition is actually prompted by excessive loss of body
heat from an injury. Hypovolemia, or low blood volume, occurs when your body loses
too much blood from a burn.

Preventing all degrees of burns

The obvious best way to fight burns is to prevent them from happening. Certain jobs
put you at a greater risk for burns, but the fact is that most burns happen at home.
Infants and young children are the most vulnerable to burns. Preventive measures you
can take at home include:

 Keep children out of the kitchen while cooking.

 Turn pot handles toward the back of the stove.
 Place a fire extinguisher in or near the kitchen.
 Test smoke detectors once a month.
 Replace smoke detectors every 10 years.
 Keep water heater temperature under 120 degrees Fahrenheit.
 Measure bath water temperature before use.
 Lock up matches and lighters.
 Install electrical outlet covers.
 Check and discard electrical cords with exposed wires.
 Keep chemicals out of reach, and wear gloves during chemical use.
 Wear sunscreen every day, and avoid peak sunlight.
 Ensure all smoking products are stubbed out completely.
 Clean out dryer lint traps regularly.

It’s also important to have a fire escape plan and to practice it with your family once a
month. In the event of a fire, make sure to crawl underneath smoke. This will
minimize the risk of passing out and becoming trapped in a fire.

Outlook for burns

When properly and quickly treated, the outlook for first- and second-degree burns is
good. These burns rarely scar but can result in a change in pigment of the skin that
was burned. The key is to minimize further damage and infection. Extensive damage
from severe second-degree and third-degree burns can lead to problems in deep skin
tissues, bones, and organs. Patients may require:

 surgery
 physical therapy
 rehabilitation
 lifelong assisted care

It’s important to gain adequate physical treatment for burns, but don’t forget to find
help for your emotional needs. There are support groups available for people who
have experienced severe burns, as well as certified counselors. Go online or talk to
your doctor to find support groups in your area. You can also use other resources such
as Burn Survivor Assistance and the Children’s Burn Foundation.

Pathophysiology

At temperatures greater than 44 °C (111 °F), proteins begin losing their three-
dimensional shape and start breaking down.This results in cell and tissue
damage.Many of the direct health effects of a burn are secondary to disruption in the
normal functioning of the skin.They include disruption of the skin's sensation, ability
to prevent water loss through evaporation, and ability to control body
temperature.Disruption of cell membranes causes cells to lose potassium to the spaces
outside the cell and to take up water and sodium.
In large burns (over 30% of the total body surface area), there is a significant
inflammatory response.This results in increased leakage of fluid from
the capillaries, and subsequent tissue edema. This causes overall blood volume loss,
with the remaining blood suffering significant plasma loss, making the blood more
concentrated.Poor blood flow to organs such as the kidneys and gastrointestinal
tract may result in renal failure and stomach ulcers.
Increased levels of catecholamines and cortisol can cause a hypermetabolic
state that can last for years. This is associated with increased cardiac
output, metabolism, a fast heart rate, and poor immune function

Diagnosis

Burns can be classified by depth, mechanism of injury, extent, and associated

injuries. The most commonly used classification is based on the depth of injury. The
depth of a burn is usually determined via examination, although a biopsy may also be
used. It may be difficult to accurately determine the depth of a burn on a single
examination and repeated examinations over a few days may be necessary. In those
who have a headache or are dizzy and have a fire-related burn, carbon monoxide
poisoning should be considered. Cyanide poisoningshould also be considered

Management

Resuscitation begins with the assessment and stabilization of the person's airway,
breathing and circulation. If inhalation injury is suspected, early intubation may be
required.This is followed by care of the burn wound itself. People with extensive
burns may be wrapped in clean sheets until they arrive at a hospital.As burn wounds
are prone to infection, a tetanus booster shot should be given if an individual has not
been immunized within the last five years. In the United States, 95% of burns that
present to the emergency department are treated and discharged; 5% require hospital
admission. With major burns, early feeding is important. Hyperbaric oxygenation may
be useful in addition to traditional treatments.
Intravenous fluids

In those with poor tissue perfusion, boluses of isotonic crystalloid solution should

be given. In children with more than 10–20% TBSA burns, and adults with more than
15% TBSA burns, formal fluid resuscitation and monitoring should follow. This
should be begun pre-hospital if possible in those with burns greater than
25% TBSA.The Parkland formula can help determine the volume of intravenous
fluids required over the first 24 hours. The formula is based on the affected
individual's TBSA and weight. Half of the fluid is administered over the first 8 hours,
and the remainder over the following 16 hours. The time is calculated from when the
burn occurred, and not from the time that fluid resuscitation began. Children require
additional maintenance fluid that includes glucose. Additionally, those with inhalation
injuries require more fluid. While inadequate fluid resuscitation may cause problems,
over-resuscitation can also be detrimental. The formulas are only a guide, with
infusions ideally tailored to a urinary output of >30 mL/h in adults or >1mL/kg in
children and mean arterial pressure greater than 60 mmHg

NEPHROLITHIASIS
BACKGROUND
The term nephrolithiasis specifically refers to calculi in the kidneys, but this
article discusses both renal calculi (see the first image below) and ureteral calculi
(ureterolithiasis; see the second image below). Ureteral calculi almost always
originate in the kidneys, although they may continue to grow once they lodge in the
ureter.

ANATOMY

Most of the pain receptors of the upper urinary tract responsible for the
perception of renal colic are located submucosally in the renal pelvis, calices, renal
capsule, and upper ureter. Acute distention seems to be more important in the
development of the pain of acute renal colic than spasm, local irritation, or ureteral
hyperperistalsis.
Stimulation of the peripelvic renal capsule causes flank pain, while stimulation of the
renal pelvis and calices causes typical renal colic (see the image below). Mucosal
irritation can be sensed in the renal pelvis to some degree by chemoreceptors, but this
irritation is thought to play only a minor role in the perception of renal or ureteral
colic.

PATHO PHYSIOLOGY
Formation of stones
Urinary tract stone disease is likely caused by two basic phenomena. The first
phenomenon is supersaturation of the urine by stone-forming constituents, including
calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which
ions from the supersaturated urine form microscopic crystalline structures. The
resulting calculi give rise to symptoms when they become impacted within the ureter
as they pass toward the urinary bladder.

The overwhelming majority of renal calculi contain calcium. Uric acid calculi
and crystals of uric acid, with or without other contaminating ions, comprise the bulk
of the remaining minority. Other, less frequent stone types include cystine,
ammonium acid urate, xanthine, dihydroxyadenine, and various rare stones related to
precipitation of medications in the urinary tract. Supersaturation of the urine is likely
the underlying cause of uric and cystine stones, but calcium-based stones (especially
calcium oxalate stones) may have a more complex etiology.

The second phenomenon, which is most likely responsible for calcium oxalate
stones, is deposition of stone material on a renal papillary calcium phosphate nidus,
typically a Randall plaque (which always consists of calcium phosphate). Evan et al
proposed this model based on evidence accumulating from several laboratories.

Calcium phosphate precipitates in the basement membrane of the thin loops of

Henle, erodes into the interstitium, and then accumulates in the subepithelial space of
the renal papilla. The subepithelial deposits, which have long been known as Randall
plaques, eventually erode through the papillary urothelium. Stone matrix, calcium
phosphate, and calcium oxalate gradually deposit on the substrate to create a urinary
calculus.

Development of renal colic pain and renal damage

The colicky-type pain known as renal colic usually begins in the upper lateral
midback over the costovertebral angle and occasionally subcostally. It radiates
inferiorly and anteriorly toward the groin. The pain generated by renal colic is
primarily caused by the dilation, stretching, and spasm caused by the acute ureteral
obstruction. (When a severe but chronic obstruction develops, as in some types of
cancer, it is usually painless.)
 In the ureter, an increase in proximal peristalsis through activation of intrinsic
ureteral pacemakers may contribute to the perception of pain. Muscle spasm,
increased proximal peristalsis, local inflammation, irritation, and edema at the site of
obstruction may contribute to the development of pain through chemoreceptor
activation and stretching of submucosal free nerve endings.

The following are the four main chemical types of renal calculi, which together are
associated with more than 20 underlying etiologies:

Calcium stones

Struvite (magnesium ammonium phosphate) stones

Uric acid stones

Cystine stones

Calcium stones

Calcium stones account for 75% of renal calculi. Recent data suggest that a low-
protein, low-salt diet may be preferable to a low-calcium diet in hypercalciuric stone
formers for preventing stone recurrences. [7] Epidemiological studies have shown that
the incidence of stone disease is inversely related to the magnitude of dietary calcium
intake in first-time stone formers.

Struvite (magnesium ammonium phosphate) stones

Struvite stones account for 15% of renal calculi. They are associated with chronic
urinary tract infection (UTI) with gram-negative, urease-positive organisms that split
urea into ammonia, which then combines with phosphate and magnesium to crystalize
into a calculus. Usual organisms include Proteus. Escherichia coli is not capable of
splitting urea and, therefore, is not associated with struvite stones. Because ammonia,
a base, is produced during the catalytic process, the urine pH is typically greater than
7.

Uric acid stones

Uric acid stones account for 6% of renal calculi. These are associated with urine
pH less than 5.5, high purine intake (eg, organ meats, legumes, fish, meat extracts,
gravies), or malignancy (ie, rapid cell turnover). Approximately 25% of patients with
uric acid stone have gout.
Cystine stones

Cystine stones account for 2% of renal calculi. They arise because of an intrinsic
metabolic defect resulting in failure of renal tubular reabsorption of cystine, ornithine,
lysine, and arginine. Urine becomes supersaturated with cystine, with resultant crystal
deposition.

Prognosis

Approximately 80-85% of stones pass spontaneously. Approximately 20% of

patients require hospital admission because of unrelenting pain, inability to retain
enteral fluids, proximal UTI, or inability to pass the stone.

The most morbid and potentially dangerous aspect of stone disease is the
combination of urinary tract obstruction and upper urinary tract infection.
Pyelonephritis, pyonephrosis, and urosepsis can ensue. Early recognition and
immediate surgical drainage are necessary in these situations.

Because the minimally invasive modalities for stone removal are generally
successful in removing calculi, the primary consideration in managing stones is not
whether the stone can be removed but whether it can be removed in an uncomplicated
manner with minimum morbidity.

Serious complications of urinary tract stone disease include the following:

Abscess formation

Serious infection of the kidney that diminishes renal function

Urinary fistula formation

Ureteral scarring and stenosis

Ureteral perforation

Extravasation

Urosepsis

Renal loss due to long-standing obstruction

Differential Diagnoses

Abdominal Abscess

Acute Epididymitis

Acute Glomerulonephritis

Appendicitis Imaging

Biliary Colic

Cholecystitis

Urinary Tract Infection (UTI) and Cystitis (Bladder Infection) in Females

Diverticulitis

Emergent Management of Pancreatitis

Intravenous Pyelography (Urography)

Before the advent of helical CT, IVP, also known as intravenous urography
(IVU), was the test of choice in diagnosing ureterolithiasis. IVP is widely available
and fairly inexpensive but less sensitive than noncontrast helical CT. CT scanning
with delayed contrast series and thin slices has reduced the need for IVP in the
evaluation of problematic ureteral stones. European Association of Urology
guidelines recommend non-contrast CT to confirm the diagnosis in patients with acute
flank pain, as it is superior to IVP. 

The main advantage of IVP is the clear outline of the entire urinary system that it
provides, making visualization of even mild hydronephrosis relatively easy. IVP is
helpful in identifying the specific problematic stone among numerous pelvic
calcifications, as well as in demonstrating renal function and establishing that the
other kidney is functional. These determinations are particularly helpful if the degree
of hydronephrosis is mild and the noncontrast CT scan findings are not definitive. IVP
can also show nonopaque stones as filling defects.
Computed Tomography Scanning

At most institutions that offer this examination, CT scanning has replaced IVP,
the historic criterion standard, for the assessment of urinary tract stone disease,
especially for acute renal colic. CT scans are readily available in most hospitals and
can be performed and read in just a few minutes. Numerous studies have
demonstrated that CT has a sensitivity of 95-100% and superior specificity and
accuracy when compared with IVP.

About 15-20% of patients require invasive intervention due to stone size,

continued obstruction, infection, or intractable pain. Techniques available to the
urologist when the stone fails to pass spontaneously include the following :

Stent placement
Percutaneous nephrostomy
Extracorporeal shockwave lithotripsy (ESWL)
Ureteroscopy (URS)
Percutaneous nephrostolithotomy
Open nephrostomy
Anatrophic nephrolithotomy

Emergency Management of Renal Colic

Initial treatment of a renal colic patient in the ED starts with obtaining IV access
to allow fluid, analgesic, and antiemetic medications to be administered. Many of
these patients are dehydrated from poor oral intake and vomiting. Although the role of
supranormal hydration in the management of renal (ureteral) colic is controversial
(see below), patients who are dehydrated or ill need adequate restoration of
circulating volume.

ACUTE CHOLANGITIS
RR, 55y/o, male, married, Catholic

DEFINITION

Acute cholangitis is a bacterial infection superimposed on an obstruction of the biliary

tree most commonly from a gallstone, but it may be associated with neoplasm or
stricture. The classic triad of findings is right upper quadrant (RUQ) pain, fever, and
jaundice. 

PATHOPHYSIOLOGY

The main factors in the pathogenesis of acute cholangitis are biliary tract obstruction,
elevated intraluminal pressure, and infection of bile. A biliary system that is colonized
by bacteria but is unobstructed, typically does not result in cholangitis. It is believed
that biliary obstruction diminishes host antibacterial defenses, causes immune
dysfunction, and subsequently increases small bowel bacterial colonization. Although
the exact mechanism is unclear, it is believed that bacteria gain access to the biliary
tree by retrograde ascent from the duodenum or from portal venous blood. As a result,
infection ascends into the hepatic ducts, causing serious infection. Increased biliary
pressure pushes the infection into the biliary canaliculi, hepatic veins, and perihepatic
lymphatics, leading to bacteremia (25-40%). The infection can be suppurative in the
biliary tract.

The bile is normally sterile. In the presence of gallbladder or common duct stones
(CBD), however, the incidence of bactibilia increases. The most common organisms
isolated in bile are Escherichia coli (27%), Klebsiella species
(16%), Enterococcusspecies (15%), Streptococcus species (8%), Enterobacter species
(7%), and Pseudomonas aeruginosa (7%). Organisms isolated from blood cultures are
similar to those found in the bile. The most common pathogens isolated in blood
cultures are E coli (59%), Klebsiella species (16%), Pseudomonas aeruginosa (5%),
and Enterococcus species (4%). In addition, polymicrobial infection is commonly
found in bile cultures (30-87%) and less frequent in blood cultures (6-16%).

Primary sclerosing cholangitis is a chronic liver disease that is thought to be due to an

autoimmune mechanism. [2] It is characterized by inflammation and fibrosis of the
intrahepatic and extrahepatic bile ducts. This condition ultimately leads to portal
hypertension and cirrhosis of the liver with the only definitive treatment being a liver
transplant.

Etiology

In Western countries, choledocholithiasis is the most common cause of acute

cholangitis, followed by ERCP and tumors.
Any condition that leads to stasis or obstruction of bile in the CBD, including benign
or malignant stricture, parasitic infection, or extrinsic compression by the pancreas,
can result in bacterial infection and cholangitis. Partial obstruction is associated with a
higher rate of infection than complete obstruction.

Common bile duct stones

CBD stones predispose patients to cholangitis. Approximately 10-15% of patients

with cholecystitis have CBD stones.

Approximately 1% of patients post cholecystectomy have retained CBD stones. Most

CBD stones are immediately symptomatic, while some remain asymptomatic for
years.

Some CBD stones are formed primarily rather than secondarily to gallstones.

Obstructive tumors

Obstructive tumors cause cholangitis. Partial obstruction is associated with an

increased rate of infection compared with that of complete neoplastic obstruction.
Obstructive tumors include the following:

Pancreatic cancer

Cholangiocarcinoma [4]

Ampullary cancer

Porta hepatis tumors or metastasis

Other causes

Additional causes of cholangitis include the following:

Strictures or stenosis

Endoscopic manipulation of the CBD

Choledochocele

Sclerosing cholangitis (from biliary sclerosis)

 AIDS cholangiopathy

Ascaris lumbricoides infections

Prognosis

The prognosis depends on several factors, including the following [6] :

Early recognition and treatment of cholangitis

Response to therapy

Underlying medical conditions of the patient

Mortality rate ranges from 5-10%, with a higher mortality rate in patients who require
emergency decompression or surgery.

Complications

Patients are increasingly likely to have complications with greater degrees of illness,
as follows:

Liver failure, hepatic abscesses, and microabscessess

Bacteremia (25-40%); gram-negative sepsis

Acute renal failure

Catheter-related problems in patients treated with percutaneous or endoscopic

drainage include the following:

 Bleeding (intra-abdominally or percutaneously)

 Catheter-related sepsis
 Fistulae

 Bile leak (intraperitoneally or percutaneously

Symptoms:

 Charcot's triad consists of fever, RUQ pain, and jaundice. It is reported in up to

50-70% of patients with cholangitis. However, recent studies believe it is more
likely to be present in 15-20% of patients.

 Fever is present in approximately 90% of cases

 Abdominal pain and jaundice is thought to occur in 70% and 60% of patients,
respectively.

 Patients present with altered mental status 10-20% of the time and hypotension
approximately 30% of the time. These signs, combined with Charcot's triad,
constitute Reynolds pentad.

Consequently, many patients with ascending cholangitis do not present with the
classic signs and symptoms.-Most patients complain of RUQ pain; however, some
patients (ie, elderly persons) are too ill to localize the source of infection.

Other symptoms include the following:

 Jaundice

 Fever, chills, and rigors

 Abdominal pain

 Pruritus

 Acholic or hypocholic stools

 Malaise
The patient's medical history may be helpful. For example, a history of the following
increases the risk of cholangitis:

 Gallstones, CBD stones

 Recent cholecystectomy

 Endoscopic manipulation or ERCP, cholangiogram

 History of cholangitis

 History of HIV or AIDS: AIDS-related cholangitis is characterized by

extrahepatic biliary edema, ulceration, and obstruction. The etiology is uncertain,
but it may be related to cytomegalovirus or Cryptosporidiuminfections. The
management of this condition is described below, although decompression is
usually not necessary

Physical Examination

In general, patients with cholangitis are quite ill and frequently present in septic shock
without an apparent source of the infection.

Physical examination may reveal the following:

Fever (90%), although elderly patients may have no fever

RUQ tenderness (65%)

Mild hepatomegaly

Jaundice (60%)

Mental status changes (10-20%)

 Sepsis

Hypotension (30%)

Tachycardia

Peritonitis (uncommon, and should lead to a search for an alternative diagnosis)

Differential Diagnoses

 Cholecystitis and Biliary Colic

 Diverticulitis

 Emergent Management of Pancreatitis

 Mesenteric Ischemia Imaging

 Septic Shock

 Viral Hepatitis

MANAGEMENT

Management of acute cholangitis in the emergency department includes the

following:
 After assessment of the ABCs (airway, breathing, circulation), place the patient
on a monitor with pulse oximetry, provide oxygen via nasal canula, and obtain an
electrocardiogram (ECG). Draw and send laboratory studies (including blood
cultures) when the intravenous line is placed.

 Provide fluid resuscitation with intravenous (IV) crystalloid solution (eg, 0.9%
normal saline).

 Administer parenteral antibiotics empirically after blood cultures are drawn. Do

not delay administration of antibiotics if blood cultures cannot be drawn.

 Correct any electrolyte abnormalities or coagulopathies.

 Standard therapy for cholangitis consists of broad-spectrum antibiotics with close

observation to determine the need for emergency decompression of the biliary
tree. [17]

 A nasogastric tube may be helpful for patients who are vomiting.

 Patients should be nothing by mouth (NPO). Place a Foley catheter in ill patients
to monitor urine output.
 PEPTIC ULCER DISEASE

DEFINITION AND BACKGROUND

Peptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the
submucosa or deeper. They may be acute or chronic and, ultimately, are caused by an
imbalance between mucosal defenses and acid/peptic injury.

PUD is one of the most common GI disorders in the United States with a prevalence
of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age
70 years.Recent studies have shown an increase in the rates of hospitalization and
mortality in elderly patients for the peptic ulcer complications of bleeding and
perforation.
PATHOPHYSIOLOGY AND ETIOLOGY:

Large majority of duodenal and gastric ulcers are caused by H. pylori infection
and/or NSAID use.The final common pathway to ulcer formation is acid-peptic injury
of the gastroduodenal mucosal barrier.

H.pylori predisposes to ulceration, both by acid hypersecretion and by

compromise of mucosal defense mechanisms. NSAID use causes ulcers
predominantly by compromise of mucosal defenses.A variety of other diseases are
known to cause peptic ulcer, including ZES (gastrinoma), antral G-cell hyperfunction
and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic
stress. Other causative agents include drugs (all NSAIDs, aspirin, and cocaine),
smoking, and psychologic stress.More than 90% of serious peptic ulcer complications
can be attributed to H. pylori infection, NSAID use, and/or cigarette smoking.

H. PYLORI INFECTION:

With specialized flagella and a rich supply of urease, H. pylori is uniquely

equipped for survival in the hostile environment of the stomach.The enzyme urease,
which converts urea into ammonia and bicarbonate, thus creating an environment
around the bacteria that buffers the acid secreted by the stomach. The ammonia is
damaging to the surface epithelial cells.

One of the mechanisms by which Helicobacter causes gastric injury may be

through a disturbance in gastric acid secretion. This is due, in part, to the inhibitory
effect that H. pylori exerts on antral D cells that secrete somatostatin, a potent
inhibitor of antral G-cell gastrin production.

ACID SECRETION AND PEPTIC ULCER

A variety of abnormalities related to mucosal acid exposure have been described

in patients with duodenal ulcer.Duodenal ulcer patients do produce excessive gastric
acid.The buffering capacity of the duodenum in many patients with duodenal ulcer is
compromised due to decreased duodenal bicarbonate secretion.
 The most common, Johnson type I gastric ulcer, is typically located near the
angularis incisura on the lesser curvature, close to the border between antral and
corpus mucosa. Patients with type I gastric ulcer usually have normal or
decreased acid secretion.

 Type II gastric ulcer is associated with active or quiescent duodenal ulcer disease,
and type III gastric ulcer is prepyloric ulcer disease.

 Both type II and type III gastric ulcers are associated with normal or increased
gastric acid secretion.

 Type IV gastric ulcers occur near the GE junction, and acid secretion is normal or
below normal.

 Type V gastric ulcers are medication induced and may occur anywhere in the
stomach.
NSAIDS AND PEPTIC ULCERS

Chronic use of NSAIDs (including aspirin) increases the risk of peptic ulcer
disease about 5-fold and upper GI bleeding about 4-fold.Complications of PUD
(specifically hemorrhage and perforation) are much more common in NSAID use.

SMOKING,STRESS AND OTHER FACTORS:

 Smokers are about twice as likely to develop PUD as nonsmokers.

 Smoking increases gastric acid secretion and duodenogastric reflux.

 Smoking decreases both gastroduodenal prostaglandin production and
pancreaticoduodenal bicarbonate production.

 Both physiologic and psychologic stress undoubtedly play a role in the

development of peptic ulcer in some patients.

 The use of crack cocaine has been linked to juxtapyloric peptic ulcers with a
propensity to perforate.

 Alcohol is commonly mentioned as a risk factor for PUD

CLINICAL MANIFESTATIONS:

 More than 90% of patients with PUD complain of abdominal pain.

 The pain is typically nonradiating, burning in quality, and located in the

epigastrium.

 Patients with duodenal ulcer often experience pain 2 to 3 hours after a meal and at
night.

 Two thirds of patients with duodenal ulcers will complain of pain that awakens
them from sleep.

 The pain of gastric ulcer more commonly occurs with eating and is less likely to
awaken the patient at night.
DIAGNOSIS:

In the young patient with dyspepsia and/or epigastric pain, it may be appropriate
to initiate empirical PPI therapy for PUD without confirmatory testing.

All patients more than 45 years old with the above symptoms should have an
upper endoscopy, and all patients, regardless of age, should have this study if any
alarm symptoms are present.

A double-contrast upper GI X-ray study may be useful.

Once an ulcer has been confirmed endoscopically or radiologically, obvious

possible causes (Helicobacter, NSAIDs, gastrinoma, cancer) should always be
considered.

All gastric ulcers should be adequately biopsied, and any sites of gastritis should
be biopsied to rule out H. pylori, and for histologic evaluation.

A baseline serum gastrin level is appropriate to rule out gastrinoma.

COMPLICATIONS:

The three most common complications of PUD, in decreasing order of frequency, are
bleeding, perforation, and obstruction.

Bleeding peptic ulcers are by far the most common cause of upper GI bleeding.

Patients with a bleeding peptic ulcer typically present with melena and/or
hematemesis.

Nasogastric aspiration is usually confirmatory of the upper GI bleeding.

Abdominal pain is quite uncommon.

Shock may be present, necessitating aggressive resuscitation and blood transfusion.

Early endoscopy is important to diagnose the cause of the bleeding and to assess
the need for hemostatic therapy.Three-fourths of the patients who come to the hospital
with bleeding peptic ulcer will stop bleeding if given acid suppression and nothing by
mouth. However, one fourth will continue to bleed or will rebleed after an initial
quiescent period.

Shock, hematemesis, transfusion requirement exceeding four units in 24 hours,

and certain endoscopic stigmata (active bleeding or visible vessel) define this high-
risk group.The most common endoscopic hemostatic modalities used are injection
with epinephrine, and electrocautery. In a case with exposed vessel, mechanical
hemostasis using a clip is useful to control the bleeding.
 Persistent bleeding or rebleeding after endoscopic therapy is an indication for
operation.Elderly patients and patients with multiple comorbidities may benefit from
early elective operation after initially successful endoscopic treatment.

Deep bleeding ulcers on the posterior duodenal bulb or lesser gastric curvature
are high-risk lesions.Because they often erode large arteries not amenable to
nonoperative treatment, and early operation should be considered.Perforated peptic
ulcer usually presents as an acute abdomen.Patient can often give the exact time of
onset of the excruciating abdominal pain.

Initially, a chemical peritonitis develops from the gastric and/or duodenal

secretions, but within hours a bacterial peritonitis supervenes. The patient is in
obvious distress, and the abdominal examination shows peritoneal signs. Usually,
marked involuntary guarding and rebound tenderness is evoked by a gentle
examination. Fluid sequestration into the third space of the inflamed peritoneum can
be impressive, so preoperative fluid resuscitation is mandatory.

Sometimes, the perforation has sealed spontaneously by the time of presentation,

and surgery can be avoided if the patient is doing well.Nonoperative management is
appropriate only if there is objective evidence that the leak has sealed (i.e., radiologic
contrast study), and in the absence of clinical peritonitis. Gastric outlet obstruction
occurs in no more than 5% of patients with PUD.

It is usually due to duodenal or prepyloric ulcer disease, and may be acute (from
inflammatory swelling and peristaltic dysfunction) or chronic (from cicatrix).Patients
typically present with nonbilious vomiting and may have a profound hypokalemic
hypochloremic metabolic alkalosis.Pain or discomfort is common. Weight loss may
be prominent, depending on the duration of symptoms.

MEDICAL TREATMENT OF PUD:

 PPIs are the mainstay of medical therapy for PUD.

 High dose H2RAs and sucralfate are also quite effective.

 When discharged, should be considered for lifelong PPIs unless the definitive
cause is eliminated or a definitive operation performed.

 Should stop smoking and avoid alcohol and NSAIDs (including aspirin).

 Patients who require NSAIDs or aspirin to treat other medical conditions should
always take concomitant PPIs or high dose H2 receptor blockers.

SURGICAL TREATMENT OF PUD

The indications for surgery in PUD are bleeding, perforation, obstruction, and
intractability or nonhealing.

Gastric cancer must always be considered in patients with gastric ulcer or gastric
outlet obstruction.
The vast majority of peptic ulcers are treated by a variant of one of the three basic
operations:

parietal cell vagotomy also called highly selective

vagotomy or proximal gastric vagotomy (HSV),

vagotomy and drainage (V+D),

vagotomy and distal gastrectomy.

HIGHLY SELECTIVE VAGOTOMY:

HSV severs the vagal nerve supply to the proximal two thirds of the stomach, where
essentially all the parietal cells are located, and preserves the vagal innervation to the
antrum and pylorus, and the remaining abdominal viscera.

Thus, the operation decreases total gastric

acid secretion by about 75%,

and GI side effects are rare.

VAGOTOMY AND DRINAGE PROCEDURES:

Truncal vagotomy and pyloroplasty, and truncal vagotomy and gastrojejunostomy.

HSV may be substituted for truncal vagotomy.

The advantage of V + D is that it can be performed safely and quickly.

The main disadvantages are the side effect profile (10% of patients have significant
dumping and/or diarrhea).
During truncal vagotomy care must be taken not to perforate the esophagus,

VAGOTOMY AND DISTAL GASTRECTOMY:

Distal gastrectomy without vagotomy (usually about a 50% gastrectomy to include

the ulcer) has traditionally been the procedure of choice for type I gastric ulcer.

The addition of vagotomy should be considered for type II and III gastric ulcers.

CHOICE OF OPERATION FOR PUD:

Factors include:

the type of ulcer (duodenal, gastric, recurrent, or marginal),

the indication for operation,

the condition of the patient.

Other important considerations are:

intraabdominal factors (duodenal scarring/inflammation, adhesions, or difficult

exposure),

the ulcer diathesis status of the patient,

the surgeon’s experience and personal preference, whether H. pylori infection is

present, the need for NSAID therapy,

previous treatment,

the likelihood of future compliance with treatment.

 APPENDICITIS

DEFINITION
Appendicitis is defined as an inflammation of the inner lining of the vermiform
appendix that spreads to its other parts.
EPIDIMEOLOGY:
 The life time risk of developing appendicitis is 8.6% in males and 6.7%in
females.

 The rate of appendectomy for appendictis has been decreasing since 1950s in
most countries.

 Since then there has been increasing in the incidence rate of non perforated
appendicitis.

ETIOLOGY AND PATHOGENESIS:

 The etiology and pathogenesis of appendicitis are not clearly understood.

 Obstruction of lumen due to fecaliths or hypertrophy of lymphoid tissue is

proposed as the main etiologic factor in appendicitis.

 The frequency of obstruction rises with the severity of inflammatory process.

 Fecaliths and calculi are found in 40% of cases in smple acute appendictis, in
65% of cases of gangrenous appendicitis without rupture, in nearly 90% of cases
of gangrenous appendictis with rupture

 Traditionally, the beliefhas been that there is a predictable sequence of events

leading to eventual appendiceal rupture.

 The proximal obstruction of the appendiceal lumen produces a closed-loop

obstruction, and contuining normal secretion by appendiceal mucosa rapidly
produces distension.

 Distension of appendix stimulates the nerve endings of visceral afferent stretch

fibers, produces vague, dull,diffuse pain in the mid abdomen or lower
epigastrium.
 Distension increases from continued mucosal secretionand from rapid
multiplication of the resident bacteria of the appendix.

 This causes reflex nausea and vomiting, and the visceral pain increases. As
pressure in organ increases, venous pressure is exceeded.

 Capillaries and venules are occluded, but arterial inflow continues, resulting in
engorgment and vascular congestion.

 The inflammatory process soon involves the serosa of the appendix and in turn
the parietal peritoneum.

 This produces characteristic shift of pain to the right lower quadrant.

 The mucosa of appendix is susceptible to impairment of blood supply : thus its

integrity is compromised early in the process, which allows the bacterial invasion.

 The area with the poorest blood supply suffers the most ; ellipsoidal infarcts
develop in the antimesenteric border

As distension, bacterial invasion, compromise of the vascular supply, and infarction

progress, perforation occurs usually on the anti mesenteric border just beyond the
point of obstruction.

CLINICAL PRESENTATION

The inflamatory process in the appendix presents as pain, which initially is of diffuse
visceral type and later becomes more localized as the peritoneal lining gets irritated.

SYMPTOMS :

 Appendicitis usually starts with the periumbilical and diffuse pain that eventually
localizes to the right lower quadrant

 Although right lower quadrant pain is the most sensitive signs of appendcitis
 Appendicitis is also accompanied by gastrointestinal symptoms like nausea,
vomiting and anorexia

CLINICAL SCORING SYSTEMS:

The clinical diagnosis of appendicitis is the subjective estimate of probability of

appendcitis.

This can be made more objective by the use of clinical scoring systems.

The alvarado score is the most widespread scoring systems.

It is especially useful for ruling out appendicitis and selecting patients for further
diagnostic workup.

DIFFERENTIAL DIAGNOSIS
The differential diagnosis of acute appendicitis is acute abdomen.

The most common findings in the case of preoperative diagnosis of apendicitis ,

accounting for more than 75% of cases are in descending order of frequency :
1. Acute mesenteric adenitis
2. Acute pelvic inflammatory disease
3. twisted ovarian cyst
4. Acute gastroenteritis

MANAGEMENT:

UNCOMPLIACATED APPENDICITIS

In patients with uncomplicated appendicitis, surgical treatment has been the standard
of treatment.

In patients whom non operative treatment fails, nearly half of patients have
comlicated appendictis

Patients pursuing non operative management should be carefully counseled regarding

the risks of treatment failure and recurrent appendicitis.

COMPLICATED APPENDICITIS

Complicated appendicitis typically refers to perforated appendicitis commonly

associated with an abscess or phlegmon.

Children less than 5 yrs old and patients more than 65 yrs of age have the highest
rates of perforation.The proportion of perforation increases with increasing duration
of symptoms.Perforated appendicitis has been suggested to increase the risk of female
infertility due to impaired tubal function.Rupture should be suspected in the presence
of generalized peritonitis and a strong inflammatory response.In many cases rupture is
contained and patients display localized peritonitis.
 Distinguishing acute, uncomlicated appendicitis from acute appendicits with
perforation based on clinical findins if often difficult but it is important to make
because treatment may differ.In this case CT scan may be beneficial.

OPERATIVE VS NON OPERATIVE MANAGEMNT OF COMPLICATED

APPENDICITIS:

Patients who present with signs of sepsis and generalized peritonitis should be
taken to the operating room immediately with concurrent resuscitation.Non opearative
managemnt included IV fluids minimizing gastrointestinal stimulation, parenteral
antibioticsand percutaneous drainage.

POSTOP CARE AND COMPLICATIONS:

Following uncomplicated appendectomy comlication rates are low and most

patients can quickly start on a diet and discharged home same day.Alternatively,
patients with complicated appendictis complications are increased.They should be
continued on broad spectrum antibiotcsfor 4- 7 days

Post op ileus may occur and so diet should be started based on clinical evaluation
In patients with incisional surgical site infection treatment should be opening of the
incision and obtaining the culture. Patients with post op intraabdominal abscess can
present in variety ways in which fever,leukocytosis, and abdominal pain are common.
Most commonly percutaneous drainage with CT or ultrasoung guidance is effective
FEMORAL FRACTURE
Case discussion
Fracture Shaft Of Femur

Anatomy:
Long tubular bone, anterior bowed forward and has oblique course from the neck to
distal end.

FEMUR FRACTURE CLASSIFICATION:

 Femoral Head Fractures
 Femoral Neck Fractures
 Intertrochanteric Fractures
 Subtrochanteric Fractures
 Femoral Shaft Fractures
 Distal Femur Fractures

Fracture Shaft Of Femur: A femoral shaft fracture is a fracture of the femoral

diaphysis occurring between 5 cm distal to the lesser trochanter and 5 cm proximal to
the adductor tubercle

Epidemiology: Common injury due to major violent trauma. It is more common in

people < 25 yr or >65 yr

Mechanism Of Injury
• In Young Adults, almost always the result of high-energy trauma, – Motor vehicle
accident – Gunshot injury, or – Fall from a height
• Pathologic fractures, especially in the elderly, commonly occur following a trivial
fall
• Stress fractures occur mainly in military recruits or runners

Symptoms
 Diffuse pain or ache, and tenderness and swelling in the thigh or groin.
 Bleeding and bruising in the thigh (uncommon).
 Weakness and inability to bear weight on the injured leg.
 Paleness and deformity
Clinical Evaluation
• A full trauma survey is indicated (ABC)
• The patient is –Non ambulatory with pain
– Variable gross deformity of thigh
– Swelling,
– Shortening of the affected extremity.
• A careful neurovascular examination is essential.
• Thorough examination of the ipsilateral hip and knee should be performed
• Knee ligament injuries are common, however, and need to be assessed after fracture
fixation

Types of Fracture:
 Type 0 - No commination
 Type 1 - Insignificant butterfly fragment with transverse or short oblique
fracture,
 Type 2 - Large butterfly of less than 50% of the bony width, > 50% of cortical
contact
 Type 3 - Larger butterfly leaving less than 50% of the cortex in contact
 Type 4 - Segmental commination

Diagnostics:
 X-ray Will confirm the diagnosis and establish the sites ,line ,extent and
displacement
 AP and Lateral views of the femur, hip, and knee

Management:
1) Non operative
 Traction- Skeletal, thomas splint
 Cast braces- uncommonly used
2) Operative
 For patients in whom surgery needs to be delayed, temporary stabilisation with
Skeletal traction is required
A) Operative Fixation Options
o Intramedullary Fixation
o Open Reduction and Plate Fixation
o External Fixation (For Open/ Infected Fractures

Complications:
 Vascular injury
 Nerve injury-iatrogenic(femoral, sciatic, pudendal, peroneal)
 Thromboembolism
 Compartment syndrome(1-2%)
 Infection
 Delayed union and non-union
 Joint stiffness, knee & hip pain
 Heterotrophic ossification
 SMALL BOWEL OBSTRUCTION
DEFINITION

SBOs can be partial or complete, simple (ie, nonstrangulated) or strangulated.

Strangulated obstructions are surgical emergencies. If not diagnosed and properly
treated, vascular compromise leads to bowel ischemia and further morbidity and
mortality.

EPIDEMIOLOGY:
Mechanical small bowel obstruction: Most frequently encountered surgical disorder
of the small intestine
Obstructing lesion is conceptualized according to its Anatomic relationship to
intestinal wall:
1. Intraluminal (foreign bodies, gallstones or meconium)
2. Intramural ( tumors, crohn’s disease)
3. Extrinsic ( adhesions, hernias, carcinomatosis)

ETIOLOGY
Intraabdominal adhesions - 75%
Less common: Hernia, malignant bowel obstruction, crohn’s disease
Rare: Superior mesenteric artery syndrome

Gas and fluid accumulate within the intestinal lumen proximal to the site of
obstruction
Intestinal motility increases
Colicky abdominal pain
Diarrhea
Bowel distention
Intraluminal and intramural pressure rises
If the intramural pressure becomes high enough, intestinal microvascular
perfusion is impaired
Ischemia and, ultimately, necrosis
This condition is termed strangulated bowel obstruction

PARTIAL SMALL BOWEL OBSTRUCTION:

Portion of the intestinal lumen is occluded Allowing passage of some gas and fluid
Occur more slowly than with complete small bowel obstruction,
Less likely to become strangulated

CLOSED LOOP OBSTRUCTION:

Segment of intestine is obstructed both proximally and distally
Gas and fluid cannot escape either proximally or distally from the obstructed segment
Rapid rise in luminal pressure and a rapid progression to strangulation.

SYMPTOMS:

Colicky abdominal pain, nausea, vomiting, obstipation

Vomiting - proximal than distal obstruction
Feculent?  bacterial overgrowth (more established)
Continuous passage of flatus/stool >6-12 hours=
Partial Obstruction
SIGNS
Abdominal distention (more in distal ileum, may be absent in proximal SI)
Initially hyperactive bowel sounds minimal
Later minimal bowel sounds

LAB FINDINGS:
Intravascular volume depletion
Hemoconcentration
Electrolyte abnormalities
Mild leukocytosis
STRANGULATED OBSTRUCTION
Abdominal pain disproportionate to degree of abdominal findings
- suggestive of intestinal ischemia
Tachycardia
Localized abdominal tenderness
Fever
Marked leukocytosis
Acidosis

DIAGNOSIS:
The diagnostic evaluation should focus on the following goals:
1.-Distinguishing mechanical obstruction from ileus
2.-Determine the etiology
3.-Discriminate partial from complete
4.-Discriminate simple from strangulated

ABDOMINAL SERIES:
Dx. Of small bowel obstruction- confirmed by radiographic examination
Abdominal series consist of:
(a) a radiograph of the abdomen with the patient in a supine position
(b) a radiograph of the abdomen with the patient in an upright position, and
(c) a radiograph of the chest with the patient in an upright position
Triad:
dilated small bowel loops (>3 cm in diameter)
air-fluid levels seen on upright films, and
paucity of air in the colon

ABDOMINAL RADIOGRAPHS

Sensitivity - 70% to 80%

Specificity - low (ileus and colonic obstruction can be associated with findings that
mimic those observed with small bowel obstruction)
False-negative findings - result when the site of obstruction is located in the proximal
small bowel and when the bowel lumen is filled with fluid but no gas, thereby
preventing visualization of air-fluid levels or bowel distention
Abdominal radiographs - important study in patients with suspected small bowel
obstruction because of their widespread availability and low cost

CT SCAN

Sensitivity - 80% to 90%

Limitation: Low sensitivity <50% in detection of low grade or partial bowel
obstruction and subtle transition zone
Specificity - 70% to 90%
Findings:
1. discrete transition zone with dilation of bowel proximally, decompression of
bowel distally,
2. intraluminal contrast that does not pass beyond the transition zone, and
3. colon containing little gas or fluid
CT scan : evidence for presence of closed-loop/strangulation
CT also reveals the etiology of obstruction

MANAGEMENT
Marked depletion of Intravascular volume – fluid resuscitation is integral to treatment
 Isotonic fluid IV + Bladder catheter
Broad-spectrum Antibiotics are given ( translocation of bacteria)
NGT
Evacuation of air and fluid from stomach
Gastric decompression decreases: nausea, vomiting, distention and aspiration

LAPAROSCOPIC SURGERY
Laparoscopic procedure have a
- quicker recovery
- less complications, and
- lower costs
Presence of bowel distention and multiple adhesions can cause these procedures to be
difficult and potentially hazardous

PERIORBITAL CELLULITIS

GENERAL DATA:

This is a case of patient S.W, 49 years old, male, single, Roman Catholic, Filipino
with a Chief complaint of itching of right eye for 2 weeks who was admitted at TPH
for the first time.
Introduction

Periorbital cellulitis is an infection of your eyelid or the skin around your eyes. Adults
can get it, but children under 2 are most likely to have it.

It happens when bacteria attack the soft tissue around your eye, including your eyelid.
These germs can get into your skin through a cut or scratch, or they can get to the area
through an infection in your sinuses. It also can be a reaction to a stye (a tender bump
on your eyelid that forms when a gland on your eyelid gets infected).

person with Periorbital cellulitis is sometimes called preseptal cellulitis because it

happens outside a part of your skull called the orbital septum. A layer of tissue keeps
the infection from spreading to your eye, so it usually doesn’t affect your

Pathophysiology

Periobital cellulitis is inflammation of eye tissues behind the orbital septum. It most
commonly refers to an acute spread of infection into the eye socket from either the
adjacent sinuses or through the blood. It may also occur after trauma.

Causes

The bacteria might also spread to your eye as a result of a sinus infection or another
upper respiratory infection. They can also lead to impetigo, which is a highly
contagious skin

infection that causes minor blisters and crusting. The bacteria that most commonly
cause this condition are: Haemophilus influenzae.

Signs and symptoms

The most common signs of periorbital cellulitis are:

Redness and swelling around the eye

A cut, scratch, or insect bite near the eye

The skin in the affected area is tender to the touch and might feel a little tough.

The white of the eye might look red.

Periorbital cellulitis doesn’t cause a fever or pain. If you or your child has a fever and
swelling and it hurts to move the affected eye, get medical help right away. These
things can be caused by a more serious condition called orbital cellulitis that affects
the eye itself.

Treatment

If you or your child has periorbital cellulitis, the doctor will prescribe antibiotics like
gentamycin and cloramphenicol, and these should start to work within 24 to 48 hours.
You’ll probably need to schedule a follow-up visit or two to make sure the infection is
completely gone.

CEREBRAL CONCUSSION

DEFINITION AND BACKGROUND:

Concussion, or mild traumatic brain injury (MTBI), is common among contact

and collision sports participants. One definition of concussion is a condition in which
there is a traumatically induced alteration in mental status, with or without an
associated loss of consciousness (LOC).  A broader definition is a traumatically
induced physiologic disruption in brain function that is manifested by LOC, memory
loss, alteration of mental state or personality, or focal neurologic deficits.
Signs and symptoms

An athlete suffering from an MTBI may demonstrate the following:

 Confusion: Athletes with an MTBI often appear acutely with a confused or blank
expression or blunted affect

 Delayed responses and emotional changes: Delayed response to simple

questioning may be demonstrated, along with emotional lability; the emotional
lability may become more evident as the athlete attempts to cope with his or her
confusion.

 Pain/dizziness: Many athletes report an associated headache and dizziness

 Visual disturbances: Visual complaints may include seeing stars, blurry vision, or
double vision

 Amnesia: Pretraumatic (retrograde) and posttraumatic (antegrade) amnesia may

be present; usually, the duration of retrograde amnesia is quite brief, while the
duration of posttraumatic amnesia is more variable (lasting seconds to minutes),
depending upon the injury

 Signs of increased intracranial pressure: A history of persistent vomiting may

suggest a significant brain injury with associated elevated intracranial pressure;
other signs of increased intracranial pressure include worsening headache,
increasing disorientation, and a changing level of consciousness

Physical examination

The physical examination should include assessment of the following:

 Appearance: The initial clinical examination should include a careful inspection
of the athlete's general appearance

 Head and neck: Palpating the head and neck is important when looking for an
associated skull or cervical injury

 Facial bones: Palpate the facial bones and the periorbital, mandibular, and
maxillary areas after any head trauma

 Jaws: Open and close the mouth to help in the evaluation of possible
temporomandibular joint (TMJ) pain, malocclusion, or mandibular fracture

 Nose: Inspect the nose for deformity and tenderness, which may indicate a
possible nasal fracture

 Presence of discharge: Persistent rhinorrhea or otorrhea (clear) indicates a

possible associated skull fracture.

 Vision: Perform a careful, detailed neurologic examination that includes

evaluation of the visual fields, extraocular movements, pupillary reflexes, and
level of the eyes

 Strength and sensation: Assess upper-extremity and lower-extremity strength and

sensation.

 Coordination and balance: Concussed patients often have difficulty with the
finger-nose-finger test and will use slow, purposeful movements to complete the
task

Postconcussive syndrome
Postconcussive syndrome consists of prolonged symptoms that are related to the
initial head injury. Symptoms usually consist of the following:

Persistent, recurrent headaches

Dizziness

Memory impairment

Loss of libido

Ataxia

Sensitivity to light and noise

Concentration and attention problems

Depression

Anxiety

Diagnosis

Imaging

The following imaging studies can be used in the examination of head injury (Note:
Although the following studies may be useful in the evaluation of head trauma, they
will be negative for a concussion with no other injury.):

 Computed tomography scanning: CT scanning continues to be the imaging study

of choice for evaluating acute head injury

 Magnetic resonance imaging: MRI is the imaging study of choice for patients
who have prolonged symptoms (>7 days) or when a late change occurs in an
individual's neurologic signs or symptoms
Although positron emission tomography (PET) scanning and functional MRI (fMRI)
may be used in evaluating patients with concussion, their clinical application in most
cases of MTBI is uncertain.

Neuropsychological testing

Detailed neuropsychologic testing is employed more often at the professional level

and in research in athletes with MTBI.

Management

Most patients with MTBI recover in 48-72 hours, even with detailed
neuropsychological testing, and are headache free within 2-4 weeks of the injury.

A clinical report by the American Academy of Pediatrics (AAP) on the diagnosis and
management of sports-related concussions in adolescents and children noted the
following :

Cognitive and physical rest is the mainstay of management of patients with

concussion

Ongoing neuropsychological testing is a helpful tool during management

Although several different guidelines regarding return to play have been established,
the main criteria for an athlete's return to play after a concussion include the
following:

Complete clearing of all symptoms

Complete return of all memory and concentration

No symptoms after provocative testing: Provocative testing includes jogging,

sprinting, sit-ups, or pushups (ie, exercise that raises the athlete's blood pressure
and heart rate)
Highlights from the revised recommendations include the following  :

There is no evidence that medication improves recovery after concussion

The risk for concussion is greatest in football and rugby, followed by hockey
and soccer; for young women and girls, the risk is greatest in soccer and
basketball

An athlete who has a history of 1 or more concussions is at greater risk for being
diagnosed with another concussion

The first 10 days after a concussion appears to be the period of greatest risk for
being diagnosed with another concussion