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Problem 4

Devin Alexander
405160054
Peritonitis
• an inflammation of the peritoneum, the tissue that lines the
inner wall of the abdomen and covers and supports most of
your abdominal organs.
• Caused by infection from bacteria or fungi
• Left untreated, peritonitis can rapidly spread into
the blood(sepsis) and to other organs, resulting in multiple
organ failure and death.
Etiology
• Primary peritonitis or spontaneous bacterial peritonitis (SBP)
1. ascetic fluid infection without an evident intra-abdominal surgically
treatable source
2. may be the result of contamination of the peritoneal cavity with
microorganisms, irritating chemicals, or both.

• secondary variety, an intraabdominal process, such as a ruptured appendix


or a perforated peptic ulcer is evident.
Pathogenesis
• Key step SBP  Bacterial translocation,
• is the “passage” of bacteria from the lumen to the mesenteric lymph nodes
and thereafter to the blood stream and other extra‐intestinal sites.
• Bacterial overgrowth in association with impairment of the intestinal
barrier, alterations of local immune defences, slow motility of the bowel
in patients with cirrhosis and reduced opsonic activity (hence decreased
reticulo‐endothelial system activity) precede the episodes of bacterial
translocation
• translocation of bacterial products, such as lipopolysaccharides (LPS)
from (Gram (-) bacteria) and peptidoglycans (Gram (+) bacteria) together
with bacterial DNA, through the intestinal wall has been associated with
production of many cytokines
• microorganisms more commonly isolated from cases of SBP are
Escherichia coli (∼70%), Klebsiella species (∼10%),
Diagnosic approach
• Sign & symptons :
1. First symptoms: poor appetite and nausea and a dull abdominal ache that
quickly turns into persistent, severe abdominal pain, which is worsened
by any movement.
2. Abdominal pain & tenderness
3. Fever
4. Not passing any urine, or passing significantly less urine than usual
5. Difficulty passing gas or having a bowel movement
• Examination:
1. Assessment of tension and tenderness in the abdomen.
2. Auscultation  absent of bowel sound
3. Palpation  muscle rigidity in whole abdomen

• Work up:
1. Blood
2. Imaging studies such as X-rays and computerized tomography (CT) scans
3. Ascitic fluid culture
Treatment
• intravenous antibiotics or antifungal medications
• Primary SBP – empiric antibiotic first
cefotaxime 2 g intravenously every eight hours
• Many cases - emergency surgery is required (appendicitis, a
perforated stomach ulcer, or diverticulitis)
• vigorous rehydration and correction of electrolyte disturbances
Hernia
• Hernia is defined as an abnormal protrusion of an organ or
tissue through a defect in its surrounding walls
• Abdominal wall hernias occur only at sites at which the
aponeurosis and fascia are not covered by striated muscle

Townsend CM, Beauchamp


RD, Evers BM, Mattox KL.
Sabiston textbook of surgery.
19th Ed. Philadelphia : Elsevier
Saunders; 2012
Inguinal hernia
• Etiology
1. Weak abdominal muscles
2. Weak connective tissues
3. Lifting heavy objects
4. Coughing & straining too
hard
• Risk factor :
• overweight  increases the pressure in your abdomen.
• Patent processus vaginalis
• Male gender
• weak abdominal muscles
• Smoking  increase risk for reccurence
• Pathophysiolog
y
• Diagnosis approach
• Sign & symptons
1. lump in the groin that goes away with minimal pressure or when the patient is lying down
2. Mild & moderate discomfort the increases with activity

• Examination
1. The doctor first takes a look while the patient is standing, after asking them to tense their
stomach muscles and cough. Then the patient is asked to lie down
2. can be pushed back into the abdominal cavity, and irreducible if it remains permanently
outside the abdominal cavity
• Examination of a patient with a suspected inguinal hernia
1. Examine the patient first when he or she is standing
2. Demonstrate lump with cough impulse
3. Then do an abdominal examination with the patient lying down
• Work up
1. Rarely needed
2. X-rays, CT (computed tomography) scans or MRI (magnetic resonance
imaging)
• If the hernia sac bulges directly through the posterior wall of
the inguinal canal  direct hernia
• If passes through the internal inguinal ring alongside the
spermatic cord, following the coursing of the inguinal canal 
indirect hernia
Treatment
• Surgery is the only option  pushing the hernia sac back into the abdomen or removing it, and closing
the gap in the abdominal wall with stitches.
• OS  arried out through a larger cut where the hernia is
• LS
1. longer operation times but less severe postoperative pain, fewer complications, and a more rapid return
to normal activities
2. associated with higher recurrence rates but causes less chronic pain
3. several smaller cuts are made

• Recover time needs 5-8 days


Prevention
• avoid strain due to things like carrying heavy objects
• Losing weight
Hernia umbilical
• Etiology
1. Infants & young children  failed closure of the umbilical ring during
gestation that ultimately results in a central defect in the linea alba
2. adult  acquired and are more common in women or patients with
increased intra-abdominal pressure as in pregnancy, obesity, ascites, or
chronic abdominal distention
• Pathophysiology
1. During the time between fifth and tenth weeks of gestation, the intestinal
tract undergoes rapid growth with protrusion of the abdominal content
outside the abdominal cavity, usually within the proximal portion of the
umbilical cord. This is followed by a gradual re-entry of the abdominal
cavity and then the ultimate narrowing of the umbilical ring which completes
the process of abdominal wall formation as fetal development concludes.

2. Failures of each fold will lead to different congenital disabilities at birth


• Diagnosis approach
• Sign & symptons
1. a large hernia (loss of domain), skin color changes consistent with
incarceration, thinning of the overlying skin
2. Spontaneous rupture of umbilical hernias in patients with ascites can
result in peritonitis and death.
• Examination
• careful examination of the entire abdominal wall, especially around scar
• Patients should be examined in the standing and supine positions (to
determine the size of a hernia +/- Valsalva maneuver) to determine the
edges of the fascial defect
• Treatment
• Child
1. Wait the defect close spontaneusly until age 2
2. If not  surgery

• Adults  open surgery/ laprascopy surgery

• Surgery  small curvilinear incision is made into the skin crease of the umbilicus, and the sac is dissected
free from the overlying skin as well the fascial defect to ensure not abdominal content are present prior
repair of the fascial defects. The skin is closed using subcuticular sutures, either monocryl or vicryl
Appendicitis
http://www.carnegiehillendo.com/webdocuments/CHE-Appendicitis.pdf
Etiology
• Obstruction caused by fecalith, which is accumulation and
inspissation of fecal matter around vegetable fiber
• Enlarged lymphoid follicles associated with viral infection
• Inspissated barium
• Tumor
• Appendiccal ulceration
• Infective
• Bacterial (Tuberculosis, Typhus, Actinomycosis, E.
coli and B. fragilis, Pseudomonas, Yersinia, Eikenella
corrodens infections)
• Viral (Adenovirus, Cytomegalovirus infections
• Fungal (Aspergillosis, Histoplasmosis)
Obstruction Pathogenesis

Mucous can’t be drained

Edema

Increase intraluminal pressure

Bacterial diapedesis

Mucosal Ulceration

Epigastric pain

Appendicitis acute focal


Mucous >>

Intraluminal pressure >>

Bacterial invasion of the


appendix wall

Vein obstruction Pathogenesis

Peritonitis

Pain in RLQ

Appendicitis supurative acute


Pathogenesis
Bad arterial flow

Gangren

Appendicitic gangrenosa

Infark

Appendicitis perforation
Diagnosis approach
• relies on a through history and examination
• History
1. Abdominal pain  most common
2. Colicky central abdominal followed by vomiting with migration of the pain to the right iliac fossa
3. patient describes a peri-umbilical colicky pain, which intensifies during the first 24 hours,
becoming constant and sharp, and migrates to the right iliac fossa
4. Lost of appetite
5. Nausea & vomitting
6. Patients at extremes of the age  diagnostic difficulty because of non-specific presentation
• Examination
1. flushed, with a dry tongue
2. Pyrexia with tachycardia
3. Palpation  localised tenderness and muscular rigidity after localisation
of the pain to the right iliac fossa
4. Rovsig's sign), psoas sign, and obturator sign  aid in diagnosis
https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC5082605
• Work up :
1. Imaging
2. Labolatory
 WBC
counts
3. Laprascopy

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082605/
Terminology
• Simple/ uncpmplicated appendicitis—Inflamed appendix, in the absence of
gangrene, perforation, or abscess around the appendix

• Complicated appendicitis—Perforated or gangrenous appendicitis or the presence of


periappendicular abscess

• Negative appendicectomy—Term used for an operation done for suspected


appendicitis, in which the appendix is found to be normal on histological evaluation
Treatment
• Uncomplicated appendicitis
1. Appendectomy is still considered to be the gold standard
2. Open approach & laprascopic approach
3. LA  associated with fewer superficial wound infections, less post-operative pain,
shorter hospital stay and earlier return to work, but the higher rate of IAA (intra
abdominal abcess) raised concerns

• Complicated appendicitis
1. drain the abscess of pus and fluid, then remove the appendix
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1562475/
• Complicated appendicitis
1. drain the abscess of pus and fluid, then remove the appendix
Prognosis
• Most people recover quickly after surgery if the appendix is removed before it ruptures.
• If your appendix ruptures before surgery, recover may take longer. You are also more
likely to develop or problems, such as:
• - An abscess
• - Blockage of the intestine
• - Infection inside the abdomen (peritonitis)
• - Infection of the wound after surgery

Harrison_s - Medicina Interna - 16th_Edition


COMPLICATION
• Abscess peri appendicitis
• Septicemia
• Peritonitis
Intutusepsion
• invagination of one segment of the bowel into an immediately adjacent
segment of the bowel.
• acquired invagination of the bowel into itself, usually involving both
small and large bowel, within the peritoneal cavity.
• It is an emergent condition where delay in diagnosis is not uncommon,
and leads to an increased risk of bowel perforation, obstruction, and
necrosis.
• The nomenclature of intussusception reflects location of both the
intussusceptum and intussuscipiens in the bowel: enteroenteric,
appendiceal, appendiceal-ileocolic, ileocolic, colocolic, rectoanal, and
stomal intussusception
Etiology
• Most cases - idiopathic
• Some reports have suggested a viral etiology, most commonly adenovirus
but also enterovirus, echovirus, rotavirus and human herpes virus 6
• noninfectious etiologies, such as intestinal allergies, Celiac disease, and
Crohn disease
• clinically symptomatic cases - age of 5 to 9 months
• may occur in children who present without the typical clinical
presentation of vomiting, bloody stools, palpable abdominal mass, and
colicky abdominal pain (7-20%), rare in adults
Diagnosis approach
• Sign & symptons:
1. marked by abdominal pain and signs of bowel obstruction  then vomiting
2. Children younger than 2 years  acute onset colicky abdominal pain, knees drawn
to chest, with excessive irritability and crying
3. stool mixed with blood and mucus, giving it a “currant jelly” appearance
4. Clasically presents with the triad of abdominal pain, vomiting, and blood in the
stools
5. Adut  small or large bowel obstruction, most common is abdominal pain
• Examination :
1. Palpation  “sausage-shaped mass” in the right upper quadrant or
epigastric region of the abdomen, but the mass is only detected in
2. Generally reveals a soft and nontender abdomen between episodes of
pain
3. Occasionally, the intussusceptum may be palpable in the rectum
4. Decreased or absent bowel sounds
• Work up :
1. An abdominal radiograph should be examined for a soft-tissue mass displacing
loops of bowel
2. CT-Scan
3. Colonoscopy
4. Barium or water-soluble contrast (Gastrografin) enema may be useful in adult
patients with colonic or ileocolic intussusception, revealing a characteristic
“cup-shaped” filling defect
Treatment
• Pediatric :
1. depends on the type of intussusception.
2. Ileocolic intussusception, the most common, requires reduction by ultrasound-guided
or fluoroscopic pneumatic or hydrostatic enema
3. Small bowel  reduce spontaneusly without surgery
4. Surgery  if there’re signs of bowel necrosis.

• Adults : surgery
Complications & Prognosis
• Relates directly to the duration of intussusception before reduction
• Mortality rate with treatment is 1-2 %

• Complications:
1. Perforation during nonoperative reduction.
2. Wound infection.
3. Internal hernias and adhesions causing intestinal obstruction.
4. Sepsis from undetected peritonitis (major complication from a missed diagnosis)
Ileus obstruction
https://www.ncbi.nlm.nih.gov/books/NBK13786/
https://www.ncbi.nlm.nih.gov/books/NBK441975/
• interference of the normal passage of luminal contents through the
gastrointestinal tract, caused by an extrinsic compression
• mechanical or functional obstruction of the small or large intestines
• obstruction can be partial or complete
• Ileus  failure of normal intestinal motility in the absence of mechanical
obstruction
Etiology
• classified as either extrinsic, intrinsic, or intraluminal
• Extrinsic
1. post-surgical adhesions
2. cancer  compression of the small bowel  obstruction
3. inguinal and umbilical hernias  Untreated hernias may eventually
become kinked  small bowel protrudes through the defect in the
abdominal wall  entrapped in the hernia sack
• Intrinsic
1. bowel wall thickening
2. Crohn's disease

• Intraluminal
1. ingested foreign body  causes impaction within the lumen of
the bowel
Diagnosic approach
• Sign & sympton:
1. abdominal pain, vomiting, abdominal distention, and obstipation
2. intermittent and colicky pain but improves with vomiting
3. Vomitting  more frequent, in larger volumes, and bilious
4. Obstipation and failure to pass gas
5. Hyperactive bowel sound
• Examination
1. Inspection  may reveal distention, previous surgical scars, hernias, or
masses
2. Palpation  tenderness focal, rigidity
3. Auscultation  reveal periods of increasing bowel sounds with periods
of relative quiet, usually high-pitched
• Work up
• Abdominal radiography
1. complete abdominal series (upright
chest film, upright and supine
abdominal, and lateral decubitus)
2. dilated intestinal loops proximal to
the obstruction and no gas in the
colon or rectum
3. multiple air-fluid levels with
distended loops of bowel

http://www.learningradiology.com/archives06/COW%20216-SBO/sbocorrect.htm
X-ray Finding
Air fluid level Herring bone
Stepladder appearance
Absent colonic gases
Partial obstruction
Treatment
• low-fiber diet  if doesn’t work  surgery to repair or move
the affected portion of the bowel may be needed.
• nasogastric tube decompression

Complete obstruction
• Abdominal surgery to remove the blockage or the damaged
intestine portion
• Limiting oral intake
• Intravenous antibiotics covering gram-negative and anaerobic
bacteria  cases of suspected inflammatory mass or perforation.
Prognosis
• Patients treated in a timely manner have a very good prognosis.
• In untreated patients, obstruction progresses to intestinal necrosis,
perforation, sepsis, and multi-organ failure.
Ileus paralitic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569564/
https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC2501703/pdf/postm
edj00517-0028.pdf
• Also called pseudo-obstruction
• occlusion or paralysis of the bowel preventing the forward passage of the
intestinal contents, causing their accumulation proximal to the site of the
blockage.

• Causes of paralytic ileus may include:


• Chemical, electrolyte, or mineral disturbances (such as decreased potassium levels)
• Complications of intra-abdominal surgery
• Decreased blood supply to the abdominal area (mesenteric artery ischemia)
• Injury to the abdominal blood supply
• Intra-abdominal infection
The Difference between Paralytic Ileus and
Obstructive Ileus

Paralytic Ileus Obstructive Ileus

• Bowel sounds minimal • Bowel sounds hyperactive


• Air Fluid level provides • Air fluid level provides a
line up stepladder

• Not accompanied by a • Accompanied by a


paroxysmal colicky paroxysmal colicky
abdominal pain abdominal pain
Diagnostic approach
• Sign & symptons:
1. nausea and vomiting
2. Cramps
3. bloating
• Physical examination
1. Intensified (hyperactive) bowel sounds  in early phase
2. in the late phase, bowel damage can cause paralysis without any peristaltic
activity
• Work up
Lab  no spesific lab test for the ileus paralytic, should check
1. Electrolytes (hypokalemia may indicate functional ileus)
2. Renal function tests (these may suggest renal failure due to fluid shifts)
Imaging
1. Abdominal USG
2. Abdominal plain films
3. Abdominal CT-scan  assessment of the
degree of severity, precise localization, and
determination of the cause along with the
detection of potential complications
(ischemia, perforation).

CT of a patient with mechanical small-bowel ileus, showing


prestenotic dilatation of the small bowel (thick arrows)
Treatment
• Initial treatment
1. Intravenous fluid to replace volume deficits and correct any electrolyte or
acid–base disturbances
2. Patients who are vomiting should undergo placement of a nasogastric tube
for gastrointestinal decompression

• After initial treatment and completion of the diagnostic evaluation, it must


be determined whether the patient should be taken to surgery
Diverticulosis
https://www.ncbi.nlm.nih.gov/books/NBK430771/
Definition & etiology
• is a clinical condition in which multiple sac-like protrusions (diverticula)
develop along the gastrointestinal tract
• E/:
1. the exact cause of these abnormalities is unknown
2. peristalsis abnormalities (e.g., intestinal spasms)
3. intestinal dyskinesia, or high segmental intraluminal pressures
Risk factor
• diet low in fiber and high in red meat
• obesity or a larger waist circumference
• Smokers
• Medications associated with an increased risk of diverticular bleeding
(NSAIDS, steroid)
Pathophysiology
• Diverticula occur in weaker portions of the colonic
wall where the vasa recta infiltrate the circular
muscular layer
• mucosa and submucosa herniating through a defect
or weakness in the muscularis layer, covered
externally only by serosa
• colonic motility (e.g., intestinal spasms or
dyskinesis) resulting in exaggerated segmental
muscle contractions, elevated intraluminal pressures,
and separation of the colonic lumen into chambers
• Connective tissue disorders may additionally predispose an individual to the
formation of colonic diverticula
• Diverticula are prone to bleeding due to the proximity of the vasa recta to the
intestinal lumen as a result of herniation of the mucosa and submucosa through the
muscularis layer.
• diverticula formation  the vasa recta become separated from the intestinal lumen by
a layer of mucosa alone  exposed to a greater amount of injury  results in
eccentric intimal thickening, thinning of the media, and ultimately segmental
weaknesses along these arteries which predispose the vasa recta to rupture and
bleeding into the intestinal lumen
Diagnostic approach
• Sign & symptons
1. Most of them asimptomatic
2. unexplained abdominal pain or cramping
3. alterations in bowel habits
4. blood in the stool. Any bleeding associated with diverticulosis is painless.
5. A diagnosis of diverticulosis is suspected when a patient presents with a
history of painless rectal bleeding or unexplained abdominal pain or cramping,
or alterations in bowel function.
• Work up
1. confirmed by colonoscopy or an x-ray following a barium enema
2. if presents with extreme abdominal pain  the choice is typically a CT
of the abdomen to avoid the risk of intestinal rupture in the setting of
intestinal infection or inflammation.
3. Colonoscopy  identify source of bleeding
Treatment
• aimed at reducing intestinal spasms which may be achieved by increasing
fiber and fluids in the diet.
• Most bleeding associated with diverticulosis is self-limiting and does not
require intervention
• some cases  endoscopic, radiologic, or surgical intervention may be
required to stop persistent bleeding
• case of a giant diverticulum, with an increased risk of infection and rupture,
surgery is more likely to be considered.
Complications
1. rectal bleeding called diverticular bleeding
2. diverticular infection, called diverticulitis
• Divetticulitis :
1. An abscess, which occurs when pus collects in the pouch.
2. An abnormal passageway (fistula) between sections of bowel or the
bowel and bladder.
Prevention
• Exercise regularly
• Eat more fiber
• Drink plenty of fluids
Umbilical infection
Definition & etiology
• infection of the umbilical stump
• occurring primarily in the neonatal period
• E/:
1. umbilicus becomes colonized with many different types of bacteria  (+)
gram microorganism
2. Aerobic bacteria are present in approximately 85% of infections predominated
by Staphylococcus aureus, group A Streptococcus, Escherichia coli
Risk factor
• maternal chorioamnionitis
• prolonged rupture of membranes
• low birth weight
• umbilical vessel catheterization.
Pathophysiology
• The umbilical cord stump then gradually dries and typically falls off
within 5 to 15 days  Both skin and enteric bacteria may colonize the
devitalized tissue of the stump  infection
Diagnosic approach
• Sign & symptons :
1. purulent drainage or be bleeding from the umbilical cord stump
2. Early  may have superficial cellulitis, if untreated  involve the entire abdominal wall
3. Lethargy
4. Fever
• Examination :
1. palpation  tenderness
2. Inspection  Erythema and induration of the umbilicus and surrounding tissues
• Work up
1. complete blood count and culture
2. cultures of any purulent material from the umbilical stump should be
sent prior to initiation of antibiotics if possible
Treatment
• Broad spectrum parenteral antibiotics
1. Antibiotic coverage should be directed against both gram-positive and
gram-negative organisms
2. antistaphylococcal penicillin and an aminoglycoside antibiotic is
recommended for uncomplicated omphalitis
3. Intravenous antimicrobial therapy + clindamycin or metronidazole
Complications
• Sepsis  can progress to septic shock and death
• Peritonitis
• Intestinal gangrene
• septic umbilical arteritis
• portal vein thrombosis
Prognosis
• Good if diagnosic immediately
• Poor if complicated infection
POTASIUM
IMBALANCE
Potassium Imbalance
• Potassium  intracellular cation , for nerve & muscle cell, regulated by a
pump called sodium potassium adenosine triphosphatase (ATPase).
• Excretion via kidney.
• Evaluation of serum potassium must consider the effects of
changes in serum pH.
• Serum pH falls  serum potassium rises, because potassium
shifts from the cellular to the vascular space.
• Serum pH rises  serum potassium falls , because potassium
shifts from the vascular space into the cells.
• Hyperkalemia  serum potassium concentration >5 mEq/L, it
is moderate (6 to 7 mEq/L) and severe (>7 mEq/L)
• Hyperkalemia is most commonly seen in patients with end-
stage renal disease.
• Signs and symptoms of hyperkalemia include: weakness,
ascending paralysis, and respiratory failure.
• Hypokalemia  serum potassium level <3.5 mEq/L.
• The most common causes of low serum potassium: gastrointestinal loss
(diarrhea, laxatives), renal loss (hyperaldosteronism, severe hyperglycemia,
potassium-depleting diuretics, carbenicillin, sodium penicillin, amphotericin
B), intracellular shift (alkalosis or a rise in pH), and malnutrition.
• Symptoms of mild hypokalemia are weakness, fatigue, paralysis, respiratory
difficulty, constipation, paralytic ileus, and leg cramps
Signs and symptoms
• The symptoms of hypokalemia are nonspecific and predominantly are related to
muscular or cardiac function. Complaints may include the following:
• Weakness and fatigue (most common)
• Muscle cramps and pain (severe cases)
• Worsening diabetes control or polyuria
• Palpitations
• Psychological symptoms (eg, psychosis, delirium, hallucinations, depression)
If the urine potassium level is less than 20 mEq/L, consider the following:
• Diarrhea and use of laxatives
• Diet or total parenteral nutrition (TPN) contents
• The use of insulin, excessive bicarbonate supplements, and episodic
weakness

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