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 SHOCK
• Circulatory insufficiency that create an
imbalance between tissue oxygen supply
(delivery) and oxygen demand (consumption).
• Classification:
– Hypovolemic Shock
– Cardiogenic Shock
– Distributive (Neurogenic Shock and Anaphylactic
Shock)
– Obstructive Shock

Tintinalli’s emergency medicine manual. 7th Edition

CLASSIFICATION

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.67-74.

 Pathophysiology

Harrison’s principles of internal medicine. 16th Ed. USA: McGraw-Hill Companies; 2005. p. 1745
Harrison’s principles of internal medicine. 16th Ed. USA: McGraw-Hill Companies; 2005. p. 1747
Harrison’s principles of internal medicine. 16th Ed. USA: McGraw-Hill Companies; 2005. p. 1748
Harrison’s principles of internal medicine. 16th Ed. USA: McGraw-Hill Companies; 2005. p. 1748
Rosen’s Emergency Medicine. 8th ed. 2016.
Elsevier. p.67-74.
 Hipovolemic Shock
– results from a rapid reduction in blood volume →
baroreceptor activation → vasoconstriction, slight↑
diastole BP  narrowing of the pulse pressure
progresses  decrease in ventricular filling and CO 
reduction in systolic BP
– Cardiovascular response to hemorrhage can vary
with underlying cardiopulmonary status, age, and
presence of ingested drugs.
– Responses of HR and BP are notoriously variable in
hemorrhage, so no firm conclusion can be made at
the bedside about the presence or absence of
hemorrhagic shock simply by evaluating HR and BP.

Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.67-74.

 Etiology of Hypovolemic shock
• Hemorrhage • Loss of extracellular fluid
– GI bleed – Vomiting, dehidration,
– Trauma diarrhea
– Aggressive treatment of
– Massive hemoptysis diuretics
– Post-partum bleeding – Diabetes insipidus
• Loss of plasma – Adrenal insufficiency
– Pancreatitis
– Severe burns
– Skin desquamation
Wijaya IP. Syok Hipovolemik. Dalam: Buku Ajar Ilmu Penyakit Dalam. Edisi VI. Jilid III. Jakarta: Interna Publishing; 2014.
Pathophysiology of Hypovolemic Shock
Decreased intravascular volume

Decreased venous return

Decreased ventricular filling

Decreased stroke volume

Decreased cardiac output

Inadequate tissue perfusion

 Classification of Hemorrhage
Class
Parameter I II III IV
Blood loss (mL) < 750 750 – 1500 1500 – 2000 > 2000
Blood loss (%) < 15 15 – 30 30 – 40 > 40
Heart rate (bpm) < 100 >100 >120 > 140
Blood pressure Normal Orthostatic Hypotension Severe
hypotension
Pulse pressure Normal/   
Respiratory rate < 20 20 – 30 30 – 40 > 35
Urine output > 30 20 – 30 5 – 15 Negligible
(mL/hr)
CNS Symptoms Normal Anxious Confused Lethargic
Fluid replacement Crystalloid Crystalloid Crystalloid + Crystalloid +
blood blood
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003/table/T1/
Clinical Signs of Hypovolemic Shock

Harrison’s principles of internal medicine. 16th Ed. USA: McGraw-Hill Companies; 2005. p. 1749
Rosen’s Emergency Medicine. 8th ed. 2016.
Elsevier. p.67-74.
Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier. p.67-74.
• Treatment :
– Initial resuscitation
– Rapid infusion of isotonic saline or Ringer’s lactate
– Infusion of 2–3 L of salt solution over 20–30 min
– Massive transfusion (FFP and platelets) approaching a 1:1
ratio of PRBC/FFP
– Extreme emergencies  type-specific or O-negative PRBCs
– Inotropic  norepinephrine, vasopressin, or dopamine
– ↑ MAP  Naloxone bolus 30 mcg/kg in 3-5 min, increased
to 60 mcg/kg with dextrose 5% in 1 hour

Kasper DL, Hauser SL, Jameson JL, Fauci AS, Longo DL, Loscalzo S, editors. Harrison’s Principles of Internal Medicine. 19th ed.
McGrawHill; 2015.
Wijaya IP. Syok Hipovolemik. Dalam: Buku Ajar Ilmu Penyakit Dalam. Edisi VI. Jilid III. Jakarta: Interna Publishing; 2014.
 SEPTIC SHOCK
Septic shock can be produced by infection with any microbe, although in one
half / more of cases of septic shock, no organism is identified.

Mediators  lipopolysaccharide (in the outer cell membrane of gram (-)

bacteria).
Gram- 1. Patients treated at home for chronic immunocompromising
positive diseases with indwelling catheters  portals of entry into the
sepsis vascular space for Staphylococcus aureus & coagulase-
negative staphylococci.
2. Community-acquired infections caused by antibiotic-resistant
gram-positive organisms has greatly increased (including
infections caused by S. aureus, Streptococcus pneumoniae,
and Streptococcus pyogenes).

3 effect • Relative hypovolemia

• Cardiovascular depression Rosen’s
• Induction of systemic inflammation
Rosen’s emergency medicine: concept and clinical practice,
8th ed. p.70
 SEPTIC SHOCK (2)
•Septic shock often causes absolute hypovolemia from gastrointestinal volume
losses, tachypnea, sweating, and decreased ability to drink during development of
the illness.
•Sepsis also induces capillary leak, which leads to relative loss of intravascular
volume into third spaces
3 effect • Relative hypovolemia
• Cardiovascular depression
• Induction of systemic inflammation
Treatments •Establishing adequate ventilation to correct hypoxia and acidosis
and to reduce systemic oxygen consumption and left ventricular
work
•Achieve adequate ventricular filling
•Eradicate the infection with antimicrobial therapy and surgical
drainage (if necessary)

Rosen’s emergency medicine: concept and clinical practice, 8th ed. p.68
Rosen’s emergency medicine: concept and clinical practice,
8th ed. p.69
Rosen’s emergency medicine: concept
and clinical practice, 8th ed. p.72
Rosen’s emergency medicine:
concept and clinical practice,
8th ed. p.73
 Cardiogenic Shock
• Definition : Cardiogenic shock results when
more than 40% of the myocardium becomes
necrosed from ischemia, inflammation, toxins,
or immune destruction.
• Etiology : The primary cause of cardiogenic
shock is pump failure.
• Produces same circulatory and metabolic
alterations that are observed with
hemorrhagic shock.
Patophysiology :
• Infection, hemorrhage, vasodilatory drug
overdose  secondary makes impaired
baseline cardiac function  contribute to the
development of circulatory shock
• Severe left ventricular dysfunction 
cardiogenic shock.
• Acute massive pulmonary embolism 
obstruction of the pulmonary vasculature 
right ventricular overload  left ventricular
filling  shock cardiogenic
• Hypoxemia, together with coronary
hypoperfusion from arterial hypotension, and
 Diagnosis
In general, patients in shock exhibit a stress
response: They are ill appearing, pale, often
sweating, usually tachypneic or grunting, and often
with a weak and rapid pulse

Empiric Criteria for Diagnosis of Circulatory Shock

• Ill appearance or altered mental status
• Heart rate >100 beats/min
• Respiratory rate >22 breaths/min or PaCO2 <32
mm Hg
 Diagnosis
Criteria for Cardiogenic Shock
• Cardiac failure
Clinical evidence of impaired forward flow of
the heart, including presence of dyspnea,
tachycardia, pulmonary rales, peripheral
edema, or cyanosis
• Cardiogenic shock
Cardiac failure plus four criteria in empiric
criteria
Echocardiography
 Clinical Management
• Ameliorate increased work of breathing;
provide oxygen and positive end-expiratory
pressure (PEEP) for pulmonary edema
• Begin inotropic support; dobutamine (5p-
g/kg/min) is common empiric agent
• Seek to reverse the insult (e.g., initiate
thrombolysis, arrange percutaneous
transluminal angioplasty, or administer
charcoal for drug overdose)
• Consider intra-aortic balloon pump
 Cardiogenic shock
• Characterized by systemic hypoperfusion due
to severe depression of the cardiac index and
sustained systolic arterial hypotension despite
an elevated filling pressure
• The most common etiology is severe left
ventricular dysfunction  pulmonary
congestion and or systemic hypoperfusion

Harrison’s Principles of Internal Medicine 19th edtion p.1759

Harrison’s Principles of Internal Medicine
19th edtion p.1760
Harrison’s Principles of Internal
Medicine 19th edtion p.1759
• Patient profile : • Clinical findings :
– Dyspnea and appear
– Older age pale, mental status may
– Female be altered
– Pulse is typically weak
– Prior MI and rapid or severe
– Diabetes bradycardia
– Tachypnea and jugular
– Anterior MI location venous distention may
– Extensive coronary be present
artery stenoses

Harrison’s Principles of Internal Medicine 19th edtion p.1759-60

• Diagnosis : • Laboratory findings :
– Lactic acid level is elevated
– Focused history and – ABG  hypoxemia and anion
PE gap metabolic acidosis
– Cardiac markers are typically
– Blood specimens markedly elevated
– ECG and chest x-ray • Chest roentgenogram :
– Pulmonary vascular
congestion and often
pulmonary edema
– Heart size is normal

Harrison’s Principles of Internal Medicine 19th edtion p.1760

.
Rosen’s Emergency Medicine. 8th ed. 2016. Elsevier.
Harrison’s Principles of Internal Medicine
19th edtion p.1761
• Management :
– Ameliorate increased work of breathing; provide
oxygen and positive end expiratory pressure
(PEEP) for pulmonary edema
– Vasopressor or inotropic support
– Seek to reverse the insult
– Consider intra aortic balloon pump
counterpulsation for refractory shock

Rosen’s Emergency Medicine 7th edition p.39

 Neurogenic Shock
• Autonomic dysfunction due to spinal cord
injury (blunt or penetrating trauma) that
causes hypotension and bradycardia

Greenberg
 Pathophysiology
• Injury to the spinal cord disorders 
disruption of the sympathetic autonomic
outflow (the signal comes from the gray cornu
lateralis)
• Decrease tone adrenergic  inability to
improve the performance of cardiac inotropic,
poor constriction of peripheral vascularity
• Vagal tone which does not experience
resistance  hypotension and bradycardia
• peripheral vasodilatation  warm skin and
 Treatment
• Hypotension  crystalloid IV fluid
• Pressor drugs (dopamine and dobutamine) if
response to IV fluids is suboptimal
• bradycardia  atropine
• traumatic spinal cord injury  corticosteroids
(methylprednisolone  blunt injury)
• Evaluation of neurological and neurosurgical
emergencies
 Acute abdomen
• The majority of emergency cases
• Causes vary, from self-limiting to a life-
threatening illness
• Give parenteral opioid analgesic to relieve
pain when its too hurt

Source: Macleod Pemeriksaan Klinis Edisi 13, Elsevier

 Abdominal Pain, Acute
Source of pain:
• Intra-abdominal
• Extra-abdominal

 Most common: gastrointestinal

tract & genitourinary tract

Abdominal pain (pain pathways)

• Visceral pain
• stomach, duodenum, liver, pancreas  upper abdominal pain
• small bowel, proximal colon, appendix  periumbilical abdominal pain
• distal colon, genitourinary tract  lower abdominal pain
• Somatic pain
• Irritation of the parietal peritoneum
• Referred pain
• Pain felt at a distance from its source 39

Rosen’s emergency medicine. 8th ed.

 Abdominal Pain
Visceral Somatic Reffered

Source: rosen’s emergency medicine

Right Upper Quadrant Pain

http://www.aafp.org/afp/2008/0401/p971.html
Right Lower Quadrant Pain

http://www.aafp.org/afp/2008/0401/p971.html
Left Lower Quadrant Pain

http://www.aafp.org/afp/2008/0401/p971.html
Emergent vs Less Emergent
Sabiston Textbook Of Surgery 19th Edition
Sabiston Textbook Of
Surgery 19th Edition
Sabiston Textbook Of
Surgery 19th Edition
Sabiston Textbook Of
Surgery 19th Edition
Intususeption
 Intususeption
• Intussusception is a process in which a segment of intestine
invaginates into the adjoining intestinal lumen, causing bowel
obstruction.
• Because intussusception seems to occur more often in the fall
and winter and because many children with the problem also
have flu-like symptoms  some suspect a virus may play a role
in the condition,  Sometimes, a lead point can be identified as
the cause of the condition — most frequently the lead point is a
Meckel's diverticulum (a pouch in the lining of the small
intestine).
• In adults, intussusception is usually the result of a medical
condition or procedure, including:
 A polyp or tumor
 Scar-like tissue in the intestine (adhesions)
 Weight-loss surgery (gastric bypass) or other surgery on the
intestinal tract http://emedicine.medscape.com/article/93070
8-overview#a6
 Inflammation due to diseases such as Crohn’s disease
 History
• The patient with intussusception is
usually an infant, often one who
has had an upper respiratory
infection, who presents with the
following symptoms:
• Vomiting
• Abdominal pain: Pain in
intussusception is colicky, severe,
and intermittent
• Passage of blood and mucus:
Parents report the passage of
stools  that look like currant
jelly (a mixture of mucus, sloughed
mucosa, and shed blood; diarrhea)
can also be an early sign of
intussusception
• Lethargy
• Palpable abdominal mass
 Diagnosis
• colonoscopy
• Imaging studies used in the
diagnosis of intussusception
include the following:
• Radiography: Plain abdominal
radiography reveals signs that
suggest intussusception in only
60% of cases
• Ultrasonography: Hallmarks of
ultrasonography include the
target and pseudokidney signs
• Contrast enema: This is the
traditional and most reliable way
to make the diagnosis of
intussusception in children
 Management
• Nonoperative reduction
• Therapeutic enemas include the
following:
• Hydrostatic: With barium or water-
soluble contrast
• Pneumatic: With air insufflation; this is
the treatment of choice in many
institutions, and the risk of major
complications with this technique is
small
• Surgical reduction
• Traditional entry into the abdomen is
through a right paraumbilical incision.
• If manual reduction is not possible or
perforation is present, a segmental
resection with an end-to-end
anastomosis is performed.
• Laparoscopy
 Differential Considerations
• The differential diagnosis includes other
causes of bowel
• obstruction.
 Initial care
• When your child arrives at the hospital,
the doctors will first stabilize his or her
medical condition. This includes:
• Giving your child fluids through an
intravenous (IV) line
• Helping the intestines decompress by
putting a tube through the child's nose
and into the stomach (nasogastric tube)
Rosen_&#039;s Emergency Medicine - Concepts and Clinical
Practice (8th Ed.)
http://emedicine.medscape.com/article/930708-
overview#a6
 Intestinal Perforation
• Upper-bowel perforation can be described as either free or
contained. Free perforation occurs when bowel contents spill freely
into the abdominal cavity, causing diffuse peritonitis (eg, duodenal
or gastric perforation). Contained perforation occurs when a full-
thickness hole is created by an ulcer, but free spillage is prevented
because contiguous organs wall off the area (as occurs, for example,
when a duodenal ulcer penetrates into the pancreas).
• Lower-bowel perforation (eg, in patients with acute diverticulitis or
acute appendicitis) results in free intraperitoneal contamination.
 Radiography Ultrasound
• Free air trapped in the • Localized gas collection related
subdiaphragmatic locations - If the to bowel perforation may be
quantity of free air is great enough, its detectable, particularly if it is
presence can be visualized on the
associated with other
supine radiograph of the abdomen,
allowing clear definition of the inner and
ultrasonographic abnormalities
outer surface of the wall of the bowel (eg, thickened bowel loop).
• Visible falciform ligament - The ligament The site of bowel perforation
may appear as an oblique structure can be detected by
extending from the right upper quadrant ultrasonography (eg, gastric vs
toward the umbilicus, particularly when duodenal perforation,
large quantities of gas are present on perforated appendicitis vs
either side of the ligament perforated diverticulitis).
• Air-fluid level - This is indicated by the Ultrasonograms of the
presence of hydropneumoperitoneum or abdomen can also provide
pyopneumoperitoneum on erect
rapid evaluation of the liver,
radiographs of the abdomen
spleen, pancreas, kidneys,
ovaries, adrenals, and uterus.
 CT Scan Abdomen
• CT of the abdomen can be a valuable
investigative tool, providing differential
morphologic information not obtainable with
plain radiography or ultrasonography.
• CT scans may provide evidence of localized
perforation (eg, perforated duodenal ulcer)
with leakage in the area of the gallbladder and
right flank with or without free air being
apparent. They may show inflammatory
changes in the pericolonic soft tissues and focal
abscess due to diverticulitis (may mimic
perforated colonic carcinoma). CT scans may
not provide definitive radiographic evidence of
perforated Meckel diverticulitis.
Laboratory
• A complete blood count (CBC) may
reveal parameters suggestive of
infection (eg, leukocytosis), though
leukocytosis may be absent in elderly
patients.
• Elevated packed blood cell
volume suggests a shift of
intravascular fluid.
• Blood culture for aerobic and
anaerobic organisms is indicated.
• Findings from liver function and renal
function tests may be within
reference ranges (or nearly so) if no
preexisting disorder is present.
 Treatment
• The mainstay of treatment for intestinal
perforation is surgery.
• Surgery for intestinal perforation is
contraindicated in the presence of general
contraindications to anesthesia and major
surgery, such as severe heart failure, respiratory
failure, or multiorgan failure. It is also
contraindicated if the patient refuses the
operation and no evidence of generalized
peritonitis exists.
• Surgery is contraindicated if a contrast meal

Postoperative Care
Intravenous replacement therapy
• The aim of intravenous replacement
therapy is to maintain intravascular
volume and hydrate the patient. Monitor
by CVP measurement and urinary output.
Nasogastric drainage
• Perform nasogastric drainage
continuously until drainage becomes
minimal. At that stage, the nasogastric
tube may be removed.
Antibiotics
• Continue administration of the antibiotics
commenced preoperatively unless the
results of cultures taken at the time of the
operation reveal that the causative
organisms are resistant to them.
• The goal of antibiotic therapy is to
achieve levels of antibiotics at the site of
infection that exceed the minimum
inhibitory concentrations for the
pathogens present.
• In the presence of intra-abdominal
infections, gastrointestinal function is
often impaired; therefore, oral antibiotics
are not efficacious, and intravenous
antibiotics are recommended.
• If no obvious improvement in the patient's
condition occurs within 2-3 days, consider
the following possibilities:
- The initial operative procedure was
inadequate.
- Complications have occurred.
- A superinfection has occurred at a
new site.
- The dose of antibiotic is inadequate.
- The antibiotics used do not provide
adequate coverage for anaerobes
and gram-negative organisms.
Analgesics
• such as intravenous morphine, should be
given continuously or in small doses at
frequent intervals.
 Peritonitis
• inflammation of the peritoneum — a silk-like
membrane that lines your inner abdominal wall
and covers the organs within your abdomen -
• life-threatening event that is often accompanied
by bacteremia and sepsis syndrome

• Peritonitis is caused by a collection of blood,

body fluids, or pus in the abdomen (intra-
abdominal abscess).

Types of peritonitis are:

 Primary (spontaneous) bacterial
peritonitis
• Usually caused by single organism
• Etiology
– Occurs most commonly in conjunction with
cirrhosis of the liver (frequently the result of
alcoholism)
– Metastatic malignant disease
– postnecrotic cirrhosis
– chronic active hepatitis & acute viral hepatitis
– congestive heart failure
– systemic lupus erythematosus
• Clinical manifestation
– Fever (80%)
– Acites  predates infection
– Abdominal pain, an acute onset of symptoms, and
peritoneal irritation (physical examination)
– Nonlocalizing symptoms  malaise, fatigue, or
encephalopathy

• Other examination
– >250 PMNs/L is diagnostic for PBP
– Blood culture
• enteric gram-negative bacilli (Escherichia coli)  most commonly
encountered
• gram-positive organisms (streptococci, enterococci, or even
pneumococci)  sometimes found
• Treatment
– Third-generation cephalosporins (cefotaxime 2 g q8h,
administered IV)  initial coverage in moderately ill
patients
– Broad-spectrum antibiotics, such as penicillin/β-
lactamase inhibitor combinations
(piperacillin/tazobactam 3.375 g q6h IV for adults with
normal renal function); ceftriaxone (2 g q24h IV)
• Prevention
– Up to 70% of patients experience a recurrence within
1 year
– Antibiotic prophylaxis reduces this rate to <20%
 Secondary peritonitis
• bacteria contaminate the peritoneum as a result
of spillage from an intraabdominal viscus 
chemical irritation and/or bacterial
contamination
• Found almost always constitute a mixed flora in
which
– facultative gram-negative bacilli
– anaerobes predominate, especially when the
contaminating source is colonic
• Early death in this  gram-negative bacillary
sepsis and to potent endotoxins circulating in the
• Clinical manifestation
– local symptoms may occur in secondary
peritonitis, ex:
• Epigastric pain from a ruptured gastric ulcer
• Appendicitis  vague, with periumbilical discomfort
and nausea; number of hours  pain localized right
lower quadrant
– lie motionless
– knees drawn
– Coughing and sneezing
• Physical examination
• Treatment
– antibiotics aimed particularly at aerobic gram-
negative bacilli and anaerobes
– penicillin/β-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q4–6h IV); cefoxitin (2
g q4–6h IV)
– Patients in the intensive care unit  imipenem
(500 mg q6h IV), meropenem (1 g q8h IV), or
combinations of drugs, such as ampicillin plus
metronidazole plus ciprofloxacin
– Surgical intervention + antibiotics (bacteremia) 
 Acute appendicitis
• Defined as an inflammation of the inner lining of
the vermiform appendix that spreads to its other
parts.

Position:
• It originates 1.7-2.5 cm below the terminal
ileum, dorsomedial location (most common)
from the cecal fundus, directly beside the ileal
orifice, or as a funnel-shaped opening (2-3% of
patients).
• The appendix has a retroperitoneal location in
65% of patients and may descend into the iliac
 Etiology
• lymphoid hyperplasia
• infections (more common during childhood and
in young adults) :
bacteria : Yersinia specieses, tuberculosis
parasites : Schistosomes species,
pinworms, Strongyloides stercoralis
Fungal : actinomycosis,
Mycobacteria species, Histoplasma species virus :
adenovirus, cytomegalovirus
• fecal stasis and fecaliths (more common in elderly
patients)
• foreign bodies : shotgun pellet, intrauterine
 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
• pain is mild, often cramping (usually lasting 4–6 h)
• As inflammation spreads to the parietal peritoneal
surfaces  pain becomes somatic, steady, more
severe and aggravated by motion or cough
• Nausea and vomiting
 Physical findings
• McBurney's sign, bloomberg sign, rovsing sign,
psoas sign, obturator sign
• The temperature is usually normal or slightly
elevated [37.2°–38°C, >38.3°C  perforation
• Rigidity and tenderness  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 diarrhea, vomiting, and
abdominal pain, fever
 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  carcinoma of the
cecum (elderly individuals)
• if the appendix lies close to the right ureter or
bladder  urine may contain a few white or red
blood cells without bacteria
 Treatment

• appendectomy as soon as the patient can be prepared

• 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  resolution of symptoms within 1 week
– Interval appendectomy can be performed safely 6–12 weeks later

Antibiotics are selected to provide coverage for aerobic and anaerobic

organisms:
• Ampicillin/sulbactam
• Clindamycin
• gentamicin
• Cefoxitin
• Cefotetan
• Piperacillin/tazobactam
• Ticarcillin/clavulanate
• Imipenem/cilastatin
 hernia
• With nearly 10% of the population
developing some sort of hernia during
their lifetime, this is among the most
common of surgical problems.
• Hernias are classified by anatomic
location, hernia contents, and the status
of those contents (e.g., reducible,
strangulated, or incarcerated)
• A hernia is called reducible when the
hernia sac itself is soft and easy to
replace back through the hernia neck
defect.
• A hernia is incarcerated when it is firm, often
painful, and nonreducible by direct manual
pressure.
• Strangulation develops as a consequence of
incarceration and implies impairment of
blood flow (arterial, venous, or both).
• A strangulated hernia presents as severe,
exquisite pain at the hernia site, often with
signs and symptoms of intestinal obstruction,
toxic appearance, and, possibly, skin changes
overlying the hernia sac.
• A strangulated hernia is an acute surgical
emergency.
 Inguinal Hernia
• 75% hernia  most common
• Male > female ; inguinal hernia = most common hernia
in women
• Inguil hernia  groin mass
• The mass may become larger or the patient may have
begun to develop symtops of incarceration or
strangulation
• DD = hidradenitis, abscess, sebaceous cyst, lymphoma,
hydrocele, varicocele, femoral hernia, and femoral
aneurysm
• Direct inguinal hernia = weakness in the transversalis
Tintinalli
Tintinalli
Ventral and incisional hernias Umbilical hernia
• Ventral hernias develop as a result of a
defect in the anterior abdominal wall and
• The adult form of umbilical hernia is largely
can be either spontaneous or acquired. acquired and due to medical conditions that
• They are typically characterized by their increase intra-abdominal pressure, including
anatomic location as epigastric, umbilical, ascites, pregnancy, and obesity.
incisional, or hypogastric
• Incisional hernias account for up to 20% • Although strangulation is unusual in most
of all abdominal wall hernias. patients, those with chronic ascites (i.e.,
• They are often the result of excess wall cirrhotics) are at risk for umbilical hernia
tension or inadequate wound healing.
• They are also associated with surgical
strangulation, rupture, and death from
wound infections. peritonitis.
• Risk factors for the development of
incisional hernias include obesity age,
wound infection, and medical conditions
(i.e., chronic obstructive pulmonary
disease) that increase intra-abdominal
pressure.
• Incisional hernias can become quite large
and produce symptoms varying from
discomfort to extrusion of abdominal
contents to incarceration and
strangulation.
• Despite primary repair, the recurrence
rate can be as high as 50%.

Tintinalli
Obturator hernia
• Obturator hernia = bowel
herniation through the obturator
canal and nearly always presents as
either partial or complete bowel
obstruction
• Typical patient = elderly frail female
with signs and symptoms of
intestinal obstruction
• Diagnosis is made by CT Scanning
of the abdomen and pelvis
• It’s important to properly diagnose
this hernia given its high
complication rate reported as
perforation in >50% of cases and
mortality approaching 20%
Richter hernia
• Richter hernia involves only the antimesenteric
border of the intestine and only involves a
portion of the wall circumference.
• The Richter hernia presents differentially from
a traditional incarcerated/strangulated hernia,
as it often presents without vomiting or
intestinal obstruction due to the incomplete
involvement of the circumference of the
intestine.
• Thus, the Richter hernia more often leads to
strangulation and gangrene than other more
standard hernias.
• Surgical repair is indicated when diagnosed
Tintinalli
Tintinalli
Diagnosis Treatment
• The dynamic abdominal sonography
for hernia examination has good • If the hernia is easily reducible on physical
results in the hands of surgeons as examination, then refer the patient for elective
compared to CT for the diagnosis of outpatient surgical repair.
hernia
• Strangulated bowel, by definition,
• If the hernia is exquisitely tender and is
has vascular compromise. associated with systemic signs and symptoms,
• In the natural history of an such as intestinal obstruction, toxic appearance,
incarcerated hernia, the thin-walled peritonitis, or sepsis, then assume hernia
veins and lymphatics become
compressed and compromised strangulation.
before the thick-walled arterial • Consult general surgery immediately.
supply • Administer broad-spectrum IV antibiotics, such
• Doppler US can detect the arterial
flow to the loop of bowel but is
as cefoxitin, provide fluid resuscitation and
usually not sensitive enough to adequate narcotic analgesia, and obtain
detect venous flow and cannot preoperative laboratory studies.
detect lymphatic flow. Thus, Doppler • If the hernia is incarcerated but the patient does
US can be insensitive for
strangulation not yet show signs of strangulation, then make
• CT is the best-performing one or two attempts at reduction in the ED.
radiographic test for hernia diagnosis
and can identify uncommon hernia
types (e.g., Spigelian or obturator) as
well as demonstrate incarceration
and strangulation

Tintinalli’s