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 Shock
•  clinical syndrome that results from inadequate
tissue perfusion
– Hypoperfusion / oxygen imbalance  cellular dysfunction
–  inflammatory mediators & release of damage-
associated molecular patterns  further compromise
perfusion
• functional and structural changes within the microvasculature
–  leads to a vicious cycle 
• maldistribution of blood flow
• further compromising cellular perfusion
• MOF
• Death

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Harrison's principles of internal medicine,
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• Classification of shock
– Hypovolemic
– Traumatic
– Cardiogenic
• Intrinsic
• Comprehensive
– Septic
• Hyperdinamic (early)
• Hypodinamic (late)
– Neurogenic
– Hypoadrenal

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Nelson’s pediatric, 19th edition
• Pathogenesis & organ response
– Micorcirculation
• CO <  vascular resistance >  maintain systemic
pressure  sustain adequate perfusion (brain & heart)
– Vasodilators (prostacyclin, NO, adenosine) VS vasoconstrictors
(nor-/epinephrine, angiotensin II, vasopressin, endothelin-1,
tromboxane A2)  maintain microcirculation
– If there is imbalance  SHOCK  derangement of cellular
metabolism  organ failure

• If MAP < 60 mmHg  organs falls & deteriorates

Harrison's principles of internal medicine,
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– Cellular response
• Transport of nutrients <  mitochondrial dysfunction and
uncoupling of oxidative phosphorylation  intracellular high-
energy phosphate <

• Hydrogen ion, lactate, other anaerobic metabolism product

(vasodilator metabolites) >  further hypotension and
hypoperfusion 
– homeostasis of calcium via membrane channels is lost  flooding of
calcium intracellularly + extracellular hypocalcemia
– Normal cellular transmembrane potential <  intracellular sodium and
water >  cell swelling interferes further with microvascular perfusion
– selective apoptotic (programmed cell-death) loss of cells

•  organ & immune failure

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– Neuroendocrine response
• Hypotension  vasomotor center > 
– Adrenergic >  norepinephrine >  peripheral and splanchnic
vasoconstriction  maintain central organ perfusion
– Vagal <  heart rate and cardiac output >

• Severe pain / stresses 

– ACTH >  cortisol >  peripheral uptake of glucose and amino
acids <, lipolysis >, gluconeogenesis >
– Glucagon >  gluconeogenesis >  blood glucose concentration
>

• Adrenergic discharge + perfusion of the juxtaglomerular

apparatus <
– Renin release >  angiotensin I  angiotensin II  aldosterone
>  maintenance of intravascular volume
– Vasopresin  vasoconstriction + water reabsorption >
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– Cardiovascular response
• Hypovolemia  preload <  SV <
– Compensatory mechanism to maintain CO: HR >

• Myocardial compliance <  ventricular end-diastolic volume

<  stroke volume < & filling pressure >  brain natriuretic
peptide >  sodium secretion >  relieve the pressure on
the heart

• Ventricular ejection <  systemic vascular resistance >

• Active venoconstriction (consequence of a-adrenergic
activity)  maintenance of venous return & ventricular
filling
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– Pulmonary response
• relative increase in pulmonary vascular resistance (septic shock),
exceed systemic vascular resistance  right heart failure
• Shock-induced tachypnea  tidal volume < & minute ventilation >
• Relative hypoxia & tachypnea  respiratory alkalosis
• Pain  functional residual capacity <  atelectasis

– Renal response
• e/ early aggressive volume repletion  serious complication of
shock and hypoperfusion
• Hypoperfusion  renal blood flow < + afferent arteriolar
resistance for diminished GFR > + aldosterone & vasopresin > 
conserve salt & water (urine <)

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– Metabolic derangements
• disruption of the normal cycles of carbohydrate, lipid,
and protein metabolism
– Oxygen  hepatic production of glucose >  pyruvate &
lactate >
– clearance of exogenous triglycerides < + hepatic lipogenesis >
 serum trygliceride concentration >
– protein catabolism >  negative nitrogen balance  muscle
wasting

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– Inflammatory response

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Nelson’s pediatric, 19 th edition
• Signs & symptoms

Nelson’s pediatric, 19 th edition

• DD

Buku saku pelayanan kesehatan anak di rumah sakit, WHO, 2009

Pocket book of hospital care for children, 2nd edition, WHO, 2013
• Monitoring & treament

Harrison's principles of internal medicine,

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Harrison's principles of internal medicine,
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Nelson’s pediatric 19 th edition
Nelson’s pediatric 19th edition
Nelson’s pediatric 19th edition
Nelson’s pediatric 19th edition
Buku saku pelayanan kesehatan anak di rumah sakit, WHO, 2009
Buku saku pelayanan kesehatan anak di rumah sakit, WHO, 2009
Pocket book of hospital care for children, 2nd edition, WHO, 2013
Pocket book of hospital care for children, 2nd edition, WHO, 2013
 Neurogenic shock
• Etiology
– Interruption of sympathetic vasomotor input after
• a high cervical spinal cord injury
• inadvertent cephalad migration of spinal anesthesia
• devastating head injury
–  arteriolar dilation + venodilation  pooling in the
venous system  venous return and cardiac output <

• Signs
– extremities are often warm

• Treatment
– Excessive volumes of fluid + norepinephrine or a pure -
adrenergic agent (phenylephrine) if hemorrhage has been
ruled out Harrison's principles of internal medicine,
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 Hypovolemic shock
• Etiology
– loss of red blood cell mass and plasma from
hemorrhage
– loss of plasma volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible losses

• Diagnosis
– signs of hemodynamic instability + obvious source of
volume loss
– Difficult diagnosis if the source of blood loss is occult
• GI tract, or when plasma volume alone is depleted

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• Sign & symptoms
– Severe  classic signs of shock
• blood pressure declines and becomes unstable even in
the supine position
• mental obtundation is an ominous clinical sign

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• Treatment
– Volume resuscitation  isotonic saline / Ringer's lactate
• 2–3 L of salt solution over 20–30 min
• severe traumatic brain injury (TBI)  small volumes of hypertonic
saline
– Continuing acute blood loss + Hb <= 10 g/dL  blood transf
– Administration of fresh-frozen plasma (FFP) and platelets,
packed red blood cells (PRBCs)
– Extreme emergencies  type-specific or O-negative packed red
cells
– norepinephrine, vasopressin, or dopamine may be required
• ONLY IF blood volume has been restored
– Supplemental oxygen + intubation

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 Sepsis & septic shock
• SIRS
– 2/more of
• fever (oral temperature >38°C) or hypothermia (<36°C)
• tachypnea (>24 breaths/min)
• tachycardia (heart rate >90 beats/min)
• leukocytosis (>12,000/L), leucopenia (<4,000/L), or >10% bands

• Sepsis
– SIRS that has a proven or suspected microbial etiology

• Septic shock
– Sepsis with hypotension (arterial blood pressure <90 mmHg
systolic, or 40 mmHg less than patient's normal blood pressure)
for at least 1 h despite adequate fluid resuscitation

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 Anaphylaxis shock
•  life-threatening response of a sensitized
human appears within minutes after systemic
exposure to specific antigen
– intense bronchospasm, vascular collapse, & shock
– Cutaneous manifestations
• pruritus and urticaria with or without angioedema
– GI manifestations
• nausea, vomiting, crampy abdominal pain, and diarrhea

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• Etiology
– antibiotics
• penicillins, cephalosporins, amphotericin B, nitrofurantoin,
quinolones
– pollen extracts
• ragweed, grass, trees
– nonpollen allergen extracts
• dust mites, dander of cats, dogs, horses, and laboratory animals
– Food
• peanuts, milk, eggs, seafood, nuts, grains, beans, gelatin in
capsules
– occupation-related products (latex rubber products)

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• Pathophysiology & manifestations
– differ in the time of appearance of symptoms and signs
• hallmark of the anaphylactic reaction is the onset of some
manifestation within seconds to minutes after introduction
– Laryngeal edema
• "lump" in the throat, hoarseness, or stridor
• feeling of tightness in the chest and/or audible wheezing
(bronchial obstruction)
• Secretions >, peribronchial congestion, submucosal edema, and
eosinophilic infiltration, and the acute emphysema (severe cases)
– diffuse erythema and a feeling of warmth
– Urticarial eruption + pruritus

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• Diagnosis
– onset of symptoms and signs within minutes after the
responsible material is encountered
– immunoassays using purified antigens
•  presence of specific IgE in the serum of patients with
anaphylactic reactions
– intracutaneous skin testing
•  elicit a local wheal and flare in response to the putative
antigen
– mast cell activation in a systemic reaction  tryptase
levels in serum >

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• Treatment
– 0.3 to 0.5 mL of 1:1000 (1 mg/mL) epinephrine SC or IM
• repeated doses as required at 5- to 20-min intervals for a severe
reaction
– if intractable hypotension occurs
• 2.5 mL epinephrine, diluted 1:10,000, at 5- to 10-min intervals IV
infusion + normal saline + vasopressor agents (dopamine)
– If hypoxia develops
• Oxygen alone via a nasal catheter or with nebulized albuterol +
endotracheal intubation or a tracheostomy
– Ancillary agents
• antihistamine diphenhydramine, 50-100 mg IM or IV
• aminophylline, 0.25-0.5 g IV

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Harrison's principles of internal medicine,
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Nelson’s pediatric, 19th edition
• Etiology

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• Pathophysiology

Nelson’s pediatric, 19 th edition

Nelson’s pediatric, 19 th edition
Nelson’s pediatric, 19th edition
• Clinical manifestations
– Hyperventilation
– Disorientation, confusion, and other manifestations of
encephalopathy
• in the elderly and in individuals with preexisting neurologic
impairment
– Cellulitis, pustules, bullae, or hemorrhagic lesions
• develop when hematogenous bacteria or fungi seed the skin or
underlying soft tissue/the effect of bacterial toxins
– Hypotension and DIC predispose to acrocyanosis and
ischemic necrosis of peripheral tissues
– nausea, vomiting, diarrhea, and ileus  acute
gastroenteritis

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• Clinical manifestations in children
– Primary
• fever, shaking chills, hyperventilation, tachycardia, hypothermia
• cutaneous lesions
– petechiae, ecchymoses, ecthyma gangrenosum, diffuse erythema
• changes in mental status
– confusion, agitation, anxiety, excitation, lethargy, obtundation, or coma
– Secondary
• hypotension, cyanosis
• symmetric peripheral gangrene (purpura fulminans)
• oliguria or anuria
• jaundice (direct hyperbilirubinemia)
• Signs of heart failure
– evidence of focal infection such as meningitis, pneumonia,
arthritis, cellulitis, or pyelonephritis
Nelson’s pediatric, 19th edition
• Laboratory findings
– Blood lactate levels > early
•  accumulation of lactate  metabolic acidosis (with increased
anion gap)
• increased glycolysis
• impaired clearance of the resulting lactate and pyruvate by the
liver and kidneys
– blood glucose concentration >
• Patients with DM
– Hypoglicemia
• impaired gluconeogenesis
• excessive insulin release on occasion
– Cytokine acute phase response
• inhibits the synthesis of transthyretin
• C-reactive protein, fibrinogen, and complement components >

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– leukocytosis with a left shift, thrombocytopenia,
hyperbilirubinemia, and proteinuria
– thrombocytopenia worsens
• prolongation of the thrombin time, decreased
fibrinogen, and the presence of d-dimers  suggesting
DIC
– levels of aminotransferases >, azotemia and
hyperbilirubinemia become more prominent
– Hyperventilation  respiratory alkalosis

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• Other examinations
– Chest radiograph
• normal or may show evidence of underlying
pneumonia, volume overload, or the diffuse infiltrates
of ARDS
– ECG
• Tachycardia & nonspecific ST–T-wave abnormalities

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• Major complications
– Cardiopulmonary
• Ventilation-perfusion mismatching  fall in arterial PO2 early
• generalized maldistribution of blood flow and blood volume and from
hypovolemia  Sepsis-induced hypotension
• Depression of myocardial function
– Adrenal insufficiency
• hypotension that is refractory to fluid replacement and requires
pressor therapy
– Renal complications
• Oliguria, azotemia, proteinuria, and nonspecific urinary casts
– Coagulopathy
• Thrombocytopenia & DIC
– Neurologic complications

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• Treatment
– Antimicrobial agents

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– Removal of the source of infections
• lungs, abdomen, and urinary tract
• Indwelling IV or arterial catheters should be removed

– Hemodynamic, Respiratory, and Metabolic Support

• IV fluids  1–2 L of normal saline over 1–2 h
• central venous pressure should be maintained at 8–12 cmH2O 
avoid pulmonary edema
• urine output (kept at >0.5 mL/kg per hour) with fluid
administration
• mean arterial blood pressure of >65 mmHg (systolic pressure >90
mmHg)
• Ventilator therapy
– If hypoxemia, hypercapnia, neurologic deterioration, or respiratory
muscle failure
• Erythrocyte transfusion if blood hemoglobin level <= 7 g/dL

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– General support
• nutritional supplementation
– reduce the impact of protein hypercatabolism
• Prophylactic heparinization to prevent deep venous
thrombosis
– If not have active bleeding or coagulopathy
• tight control of the blood glucose concentration in
recovery from critical illness
– insulin only if it is needed to maintain the blood glucose
concentration below 150 mg/dL
– must be monitored frequently (every 1–2 h) for hypoglycemia

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• Prognosis
– 20–35% of patients with severe sepsis and 40–
60% of patients with septic shock die within 30
days
– Others die within the ensuing 6 months
• result from poorly controlled infection,
immunosuppression, complications of intensive care,
failure of multiple organs, or the patient's underlying
disease

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• Prevention
– Most are complications of nosocomial infections
• reducing the number of invasive procedures
undertaken
• limiting the use (and duration of use) of indwelling
vascular and bladder catheters
• reducing the incidence and duration of profound
neutropenia (<500 neutrophils/ul)
• treating localized nosocomial infections

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ACUTE ABDOMEN
 Jenis nyeri perut
• Nyeri visceral
– Rangsangan pada organ atau struktur dalam
rongga perut.
– Peritoneum visceralesistem saraf
otonomtidak peka terhadap rabaan /
pemotongan
– Tidak dapat lokalisasi nyeri, sifat nyeri tumpul
• Nyeri somatic
– nyeri mudah terlokalisasi, sifat nyeri tajam.
– Diakibatkan adanya rangsang persarafan yang
mempersarafi peritoneum.
– Gesekan antara viscera yang meradang akan
menimbulkan rangsang peritoneum
parietaleperubahan intensitas nyeripasien
akan berusaha membatasi gerak/batuk agar
tidak bertambah nyeri
 Sifat nyeri
• Nyeri alih (referred pain )
– Terjadi jika suatu segmen persarafan melayani lebih dari satu daerah
– Diafragma yang berasal region leher dari C3-5 pindah kebawah saat masa
embryonalrangsangan pada diafragma akan menimbulkan nyeri di bahu
juga.
• Nyeri kolik
– Nyeri visceral akibat spase otot polos organ berongga, disebabkan karena
hambatan passase organ tersebut
– Nyeri timbul akibat hipoksia dinding saluran
– Kontraksi berjedasifat nyeri hilang timbul
• Nyeri pindah
– Contoh appendisitis
• Nyeri kontinu
– Dirasakan terus menerus akibat perangsangan pada peritoneum
parietale
Penyebab nyeri abdomen
 Intestinal Perforation
• Perforated Ulcer
– Perforated gastric/duodenal ulcer requires
immediate operative therapy
– Anterior gastric perforations cause peritonitis
– Posterior gastric and duodenal perforations may
not cause peritonitis, and after the acute episode
of pain, the leak may wall off, giving the
impression that the patient is improving
– Free air (80% of perforated ulcers)
 Etiology
• Helicobacter Pylori
• Smoking
• NSAIDs
Patophysiology
X-ray - diagnose
 Treatment
• Immediate surgery
• For a perforated duodenal ulcer,may include:
– a highly selective vagotomy, a truncal vagotomy and
pyloroplasty, or vagotomy and antrectomy.
• For a perforated gastric ulcerdepends on the
patient's condition:
– If the patient is moribund, the ulcer is best excised by
grasping it with multiple Allis clamps and using a GIA-
60 linear stapler. Or,can be excised with
electrocautery
– In a stable patient, the ulcer is excised and sent for
frozen section analysis to exclude malignancy
•  fibrous band of tissue; common cause of postoperative small
Adhesions
bowel obstruction after abdominal surgery; risk: 2-3%
• The majority of obstructions are associated with single adhesions
 occur at any time after the 2nd postoperative week
• Diagnostic
– Abdominal pain, constipation, emesis, and a history of intraperitoneal
surgery; nausea and vomiting quickly follow the development of pain
– Bowel sounds initially are hyperactive, and the abdomen is flat
– The bowel subsequently dilates  abdominal distention  bowel
sounds disappear
– Fever and leukocytosis are suggestive of necrotic bowel and peritonitis
– Plain radiographs  obstructive features; contrast studies  define
the cause
• Treatment
– Nasogastric decompression, intravenous fluid resuscitation, and
broad-spectrum antibiotics in anticipation of surgery
 Peritonitis
• Acute Peritonitis
– inflammation of the peritoneum
– Maybe localized or diffuse in location,acute and chronic in
natural history, and infectious or aseptic in pathogenesis
– infectious(primary peritonitis or spontaneus) and is usually
related to a perforated viscus (and called secondary peritonitis)
– Associated :
• with decreased intestinal motor activity
• resulting in distention of the intestinal lumen with gas and fluid
(adynamic ileus)
– Accumulation of fluid in the bowel and oral intake↓rapid
intravascular volume depletioncardiac, renal, and other
systems.
 2 Major Types
Primary
• Caused by the spread of an
infection from the blood &
lymph nodes to the
peritoneum.Very rare < 1%
• Usually occurs in people who
have an accumulation of fluid
in their abdomens (ascites).
• The fluid that accumulates
creates a good environment
for the growth of bacteria.
Secondary
• Caused by the entry of bacteria or
enzymes into the peritoneum from
the gastrointestinal or biliary tract.
• This can be caused due to an ulcer
eating its way through stomach
wall or intestine when there is a
rupture of the appendix or a
ruptured diverticulum.
• Also, it can occur due to an
intestine to burst or injury to an
internal organ which bleeds into
the internal cavity.
 Conditions Leading to Secondary
Perforations of bowel
•Trauma, blunt or penetrating
•Inflammation
Perforations or leaking of other organs
•Pancreas—pancreatitis
•Gallbladder—cholecystitis
•Appendicitis
•DiverticulitisBacterial Peritonitis •Urinary bladder—trauma, rupture
•Liver—bile leak after biopsy
•Peptic ulcer disease •Fallopian tubes—salpingitis
•Inflammatory bowel disease •Bleeding into the peritoneal cavity
•Iatrogenic
•Endoscopic perforation Disruption of integrity of peritoneal cavity
•Anastomotic leaks •Trauma
•Catheter perforation •Continuous ambulatory peritoneal dialysis
•Vascular (indwelling catheter)
•Embolus •Intraperitoneal chemotherapy
•Ischemia •Perinephric abscessIatrogenic—postoperative,
•Obstructions foreign body
•Adhesions
•Strangulated hernias
•Volvulus
•Intussusception
•Neoplasms
•Ingested foreign body, toothpick, fish bone
 SS
• acute abdominal pain and tenderness, usually with fever
• Bowel sounds are usually but not always absent.
• Tachycardia, hypotension, and signs of dehydration are
common
• Localized peritonitis is most common in uncomplicated
appendicitis and diverticulitis, and physical findings are
limited to the area of inflammation
• Generalized peritonitis is associated with widespread
inflammation and diffuse abdominal tenderness and
rebound.
• Rigidity of the abdominal wall is common in both localized
and generalized peritonitis
• Leukocytosis and marked acidosis are common
Clinical Features
laboratory findings.
• Plain abdominal films dilation of large and small
bowel with edema of the bowel wallFree air under
the diaphragm perforated viscus.
• CT and/or ultrasonography presence of free fluid or
an abscess.
• When ascites is present, diagnostic paracentesis with
cell count (>250 neutrophils/L is usual in peritonitis),
protein and lactate dehydrogenase levels, and culture
is essential.
• In elderly and immunosuppressed patients, signs of
peritoneal irritation may be more difficult to detect.
 Management
• Rehydration
• Correction of electrolyte abnormalities
• Antibiotics
• Surgical correction of the underlying defect
 Prognosis
• Mortality rates are <10% for uncomplicated
peritonitis associated with a perforated ulcer
or ruptured appendix or diverticulum in an
otherwise healthy person.
• Mortality rates of 40% have been reported for
elderly people, those with underlying
illnesses, and when peritonitis has been
present for >48 h.
 ACUTE APPENDICITIS
• Pathogenesis
– occur as a result of appendiceal luminal obstruction
• Obstruction is most commonly caused by a fecalith
• Enlarged lymphoid follicles associated with viral infections (e.g.,
measles)
• inspissated barium
• worms (e.g., pinworms, Ascaris, and Taenia)
• tumors (e.g., carcinoid or carcinoma)
– appendiceal ulceration
– Infection with Yersinia organisms may cause the disease
• Luminal bacteria multiply and invade the appendiceal wall  venous
engorgement and subsequent arterial compromise  gangrene and
perforation occur 
– slow: terminal ileum, cecum, and omentum (localized abscess); rapid:
perforation with free access to the peritoneal cavity
• Clinical manifestations
– abdominal discomfort and anorexia
– The pain is described as being located in the periumbilical
region initially and then migrating to the right lower
quadrant
• resulting from distention of the appendiceal lumen; pain is carried
on slow-conducting C fibers and is usually poorly localized in the
periumbilical or epigastric region
– In general, this visceral pain is mild, often cramping and
usually lasting 4–6 h
– As inflammation spreads to the parietal peritoneal
surfaces  pain becomes somatic, steady, and more
severe and aggravated by motion or cough
– Nausea and vomiting occur in 50–60% of cases
• Differential diagnosis
• Physical findings
– tenderness to palpation will often occur at McBurney's point
– Abdominal tenderness may be completely absent if a retrocecal or
pelvic appendix is present  tenderness in the flank or on rectal or
pelvic examination
• Referred rebound tenderness is often present and is most likely to be absent
early in the illness
– Flexion of the right hip and guarded movement by the patient are due
to parietal peritoneal involvement
– The temperature is usually normal or slightly elevated [37.2°–38°C
(99°–100.5°F)], >38.3°C (101°F)  perforation
– Rigidity and tenderness  more marked as the disease progresses to
perforation and localized or diffuse peritonitis
– Perforation is rare before 24 h after onset of symptoms, but the rate
may be as high as 80% after 48 h
– Any infant or child with diarrhea, vomiting, and
abdominal pain is highly suspect
– Fever is much more common in this age group
– abdominal distention is often the only physical finding

– In the elderly, pain and tenderness are often blunted

– the diagnosis is also frequently delayed and leads to a
30% incidence of perforation in patients over 70
– often present initially with a slightly painful mass (a
primary appendiceal abscess) or with adhesive
intestinal obstruction 5 or 6 days after a previously
undetected perforated appendix
• Laboratorium findings
– moderate leukocytosis of 10,000–18,000 cells/microL
is frequent
– Leukocytosis of >20,000 cells/microL  perforation
– Anemia and blood in the stool suggest a primary
diagnosis of carcinoma of the cecum, especially in
elderly individuals
– urine may contain a few white or red blood cells
without bacteria if the appendix lies close to the right
ureter or bladder
– Urinalysis is most useful in excluding genitourinary
conditions that may mimic acute appendicitis
• Radiographs
– opaque fecalith (5% of patients) is observed in the
right lower quadrant (especially in children)
– intestinal obstruction or ureteral calculus may be
present
– Ultrasound  an enlarged and thick-walled
appendix
– CT will include a thickened appendix with
periappendiceal stranding and often the presence
of a fecalith
• Treatment
– early operation and appendectomy as soon as the patient
can be prepared
– A different approach is indicated if a palpable mass is
found 3–5 days after the onset of symptoms  phlegmon
/ abscess
• broad-spectrum antibiotics, drainage of abscesses >3 cm,
parenteral fluids, and bowel rest usually show resolution of
symptoms within 1 week
• Interval appendectomy can be performed safely 6–12 weeks later
– antibiotics alone can effectively treat acute, nonperforated
appendicitis in 86% of male patients (higher recurrence
rate)
 Hernia
•  protursion of an organ or part of an organ
through a defect wall of the cavity containing
it, into an abnormal position
• Abdominal wall hernia
– Inguinal (direct or indirect)
– Femoral
– Umbilical & para-umbilical
– Incisional
– Ventral & epigastric
• Etiology
– Weakness in the abdominal wall
– Occur at the site of penetration of structures through the
abdominal wall
– The layers of the abdominal wall may be weakened
following a surgical incision
– Poor healing as a result of infection, hematoma formation
– Damage to the nerve  paralysis of abdominal muscles
– Increase of intra-abdominal pressure
• Chronic cough
• Constipation
• Urinary obstruction
• Pregnancy
• Abdominal distention with ascites
• Weak abdominal muscles
• Varieties
– Reducible hernia
• Can be replaced completely into the peritoneal cavity
• Presents as a lump that may disappear on lying down, not painful
• Examination: reveals a reducible lump with cough impulse
– Irreducible hernia
• Adhesions of its contents to the inner wall of the sac
• Painless, absence of cough impulse
– Strangulated hernia
• The hernia constricted on the neck of the sac  circulation is cut off
 perforation
• & gangrene
• Severe pain of sudden onset, colicky pain, vomitting, distention,
absolute constipation
• Examination: tender, tense hernia, overlying skin become inflamed,
noisy bowel sound
• (femoral, indirect inguinal, umbilical)
• Indirect inguinal hernia
Inguinal hernia
– Passes through the internal ring, along the canal in front of the
spermatic cord ; if large enough  emerges through the
external ring into scrotum
– Features
• Hernia doesn’t reach its full size until patient has been up & around a
little time; doesn’t reduce immediately when lies down
• Distinct tendency to strangulate
– Examination
• Can be felt in the mid-inguinal point
• Direct inguinal hernia
– Pushes its way directly forward through the posterior wall of the
inguinal canal
– Features
• Appears immediately on standing; disappearing at once when lies
down
• Treatment
– Herniotomy
• Patent processus vaginalis is ligated & hernial sac
excised at the age of about 1 year and adult
– Shouldice repair
• Excision of the sac & repair of the weakened inguinal
canal by plicating the transversalis fascia in the
posterior wall by nylon suture
– Lichtenstein repair
• Reinforcing the posterior wall with a nylon or
polypropylene mesh
 Femoral hernia
• Hernia passes through the femoral canal
• Clinical features
– Commonly in women (wider female pelvis)
– A non strangulated  globular swelling below &
lateral to the pubic tubercle; it enlarged on
standing, coughing, disappear when lies down
– Hernia enlargement  passes through the
saphenous opening in the deep fascia 
penetration of the great saphenous vein
 Richter’s hernia
• Occur in femoral sac, only part of the wall of
small intestine herniates through the defect
 strangulated
• Knuckle of bowel can become necrotic 
perforate  acute peritonitis
• Treatment
– Repaired with excision of the sac & closure of the
femoral canal because the danger of strangulation
• Exomphalos
– Failure of all part of the midgut to return to the abdominal
cavity in fetal life
– Bowel is contained within a translucent sac through a
defective anterior wall
– Untreated  rupture  fatal peritonitis (rupture may
occur during delivery)
– Treatment
• Surgical repair immediately
• Congenital umbilical hernia
– Result from failure of complete clossure of the umbilical
cicatrix
– Common in black children
– Treatment
• Not surgical repair (unless the hernia persist when the child is 2 yo

Umbilical hernia
 Para-umbilical hernia
• Acquired hernia that occurs just above or below
umbilicus
• Occurs in obese, multiparous, middle-aged
women
• Neck is narrow, prone to become irreducible or
strangulated
• Treatment
– Sac is excised and the edges of the rectus sheath are
overlapped above and below the hernia (Mayo’s
operation)
• Ventral hernia
– Exist as an elongated gap between the recti
– No treatment is required
• Epigastric hernia
– Consists of one or more small protursions through the defects in the
linea alba above umbilicus
– Contain only extraperitoneal fat, often surprisingly painful
– Treatment
• Suturing the defect
• Incisional hernia
– Occurs through a defect in the scar of a previous abdominal operation
– Wide neck, strangulation is rare
– Treatment
• Dissecting out and suturing the individual layers of abdominal wall
• If operation is inadviseable  abdominal belt

Ventral, epigastric, incisional hernia

GI BLEEDING