• In all patients with shock, HR, BP, and

oxyhemoglobin saturation are continuously

monitored
 Obstructive Shock
• the central venous pressure may be elevated
but the TTE or TEE may show reduced left
ventricular filling,

• Pericardiocentesis or window for tamponade,

• chest tube placement for tension pneumothorax,
• catheter-directed thrombolytic therapy for massive pulmonary
embolism can be life-saving in cases of obstructive shock.

Current
• TEE is a test that uses sound waves to make
pictures of your heart’s muscle and chambers,
valves and outer lining (pericardium), as well
as the blood vessels that connect to your
heart.
• Cardiac Tamponade
– is most commonly identified in penetrating
thoracic trauma, (but it can occur as the result of blunt injury)
– Tachycardia, muffled heart sounds, and dilated, engorged
neck veins with hypotension resistant to fluid therapy
suggest cardiac tamponade.
– Tension pneumothorax can mimic cardiac tamponade, but
it is differentiated from the latter condition by the findings of
• absent breath sounds, tracheal deviation, and a
hyperresonant percussion note over the affected
hemithorax.
– best managed by thoracotomy.
• Pericardiocentesis may be used as a temporizing
 Cardiac Tamponade
• Airway: May have compromised airway if level of
consciousness is decreased
• Breathing: Increased work of breathing and
respiratory rate; respiratory distress
• Circulation: Tachycardia, decreased peripheral
pulses, jugular vein distention, poor capillary refill,
muffled heart sounds, narrow pulse pressure
• Disability: Decreased level of consciousness
• Exposure: cool extremities
• Tension pneumothorax
• usually occurs in the setting of penetrating trauma, lung
infection, cardiopulmonary resuscitation, or positive-pressure
mechanical ventilation.
• In tension pneumothorax, the pressure of air
in the pleural space exceeds ambient pressure
throughout the respiratory cycle.
• should be suspected in the presence of marked
tachycardia, hypotension, and mediastinal or
tracheal shift
• chest radiographs show a large amount of air in the
affected hemithorax and contralateral shift of the
mediastinum.
 Pulmonary Embolism
• Large thrombi lodge artery pulmo
• The classic presentation : the abrupt onset of
pleuritic chest pain, shortness of breath, and
hypoxia
• pulmonary embolism is a complication of
venous thromboembolism, most
commonly deep venous thrombosis
• Clinical signs and symptoms for pulmonary
embolism are nonspecific → CT Angiography
• Thrombolytic therapy
 Peritonitis
• Peritonitis is an inflammation of the
peritoneum; it may be localized or diffuse in
location, acute or chronic in natural history,
and infectious or aseptic in pathogenesis.
• When no intraabdominal source is identified,
infectious peritonitis is called primary or
spontaneous.
• The conditions that most commonly result in
the introduction of bacteria into the
peritoneum are ruptured appendix, ruptured
diverticulum, perforated peptic ulcer,
incarcerated hernia, gangrenous gall bladder,
volvulus, bowel infarction, cancer,
inflammatory bowel disease, or intestinal
obstruction.
 Types of Peritonitis
• Spontaneous peritonitis
– an infection that develops in the peritoneum
– Caused by
• Liver disease with cirrhosis
– Such disease often causes a buildup of abdominal fluid (ascites)
that can become infected.
• Kidney failure getting peritoneal dialysis.
– This technique, which involves the implantation of a catheter into
the peritoneum, is used to remove waste products in the blood of
people with kidney failure.
– It's linked to a higher risk of peritonitis due to accidental
contamination of the peritoneum by way of the catheter.
 Types of Peritonitis
• Secondary peritonitis
– which usually develops when an injury or infection in the
abdominal cavity allows infectious organisms into the peritoneum
– Caused by
• A ruptured appendix, diverticulum, or stomach ulcer
• Digestive diseases such as Crohn's disease and diverticulitis
• Pancreatitis
• Pelvic inflammatory disease
• Perforations of the stomach, intestine, gallbladder, or appendix
• Surgery
• Trauma to the abdomen, such as an injury from a knife or gunshot wound
• acute abdominal pain and tenderness, usually with fever
• widespread inflammation and diffuse abdominal tenderness and
rebound.
• Tachycardia, hypotension, and signs of dehydration are common.
• Leukocytosis and marked acidosis are common laboratory findings.
• Free air under the diaphragm is associated with a perforated viscus.
• CT and/or ultrasonography can identify the 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.
 Treatment
• Antibiotic to treat infection
• Emergency surgery
– if peritonitis has been caused by conditions such
as appendicitis, a perforated stomach ulcer, or
diverticulitis.
 Appendicitis
• The appendix is a small, tube-like organ attached to the first
part of the large intestine, also called the colon.
• It is located in the lower right area of the abdomen. It has no
known function. A blockage inside of the appendix causes
appendicitis
 Epidemiology
• Peak incidence : ages 10 – 30 years
• Most common acute surgical condition of
abdomen
• 250.000 cases / year in USA
 Etiology
• Obstuction, by:
– Fecalith
– Enlarged lymphoid follices, associated with a
variety of inflammatory and infectious disorders
including Crohn disease, gastroenteritis,
amebiasis, respiratory infections, measles, and
mononucleosis
– Worms (pinworms, Ascaris, and Taenia)
– Viral infections ( measles )
– Tumors
 Pathophysiology
• Appendix obstruction
• Bacterial multiply and invade appendicitis
• Inflamation of appendix
• Rupture of primary appendiceal abcess may
go to bladder,smallintestine,sigmoid or secum
 Classification
• Acute : manifestation of chron’s disease
• Chronic : tuberculosis,amebiasis ‘appendiceal
inflammation is not usually the cause of
prolonged abdominal pain of weeks or moths
duration .
• Recurrent acute appendicitis
 Symptoms
• wake up at night
• is new and unlike any pain felt before
• gets worse in a matter of hours
• gets worse when moving around, taking deep breaths,
coughing, or sneezing
• loss of appetite
• Nausea
• Vomiting
• constipation or diarrhea
• a low-grade fever that follows other symptoms
• the feeling that passing stool will relieve discomfort
 Clinical SIGNS
• Tenderness (Maximal
at the Mc Burney’s
p.)
• Rowsing Sign
• Iliopsoas Sign
• Obturator Sign
 Botulism
• Botulism is an acute neurologic disorder that
causes potentially life-threatening
neuroparalysis due to a neurotoxin produced
by Clostridium botulinum.
 Sign and Symptomps
• More than 90% of patients with botulism have 3-5
of the following signs or symptoms:
• Nausea
• Vomiting
• Dysphagia
• Diplopia
• Dilated/fixed pupils
• Extremely dry mouth unrelieved by drinking fluids
• The autonomic nervous system is also involved in
botulism, with manifestations that include the
following:
• Paralytic ileus advancing to severe constipation
• Gastric dilatation
• Bladder distention advancing to urinary retention
• Orthostatic hypotension
• Reduced salivation
• Reduced lacrimation
 Diagnosis
• A mouse neutralization bioassay confirms
botulism by isolating the botulinum toxin.
Toxin may be identified in the following:
• Serum
• Stool
• Vomitus
• Gastric aspirate
• Suspected foods
• Meticulous airway management - Of paramount importance, since
respiratory failure is the most important threat to survival in
patients with botulism
• Nasogastric tube feeding can be used for nutritional
supplementation
• Foley catheter - Often used to treat bladder incontinence; the
catheter must be monitored conscientiously and changed regularly
• Antibiotic therapy - Useful in wound botulism, but has no role in
foodborne botulism
• Magnesium salts, citrate, and sulfate should not be administered,
because magnesium can potentiate the toxin-induced
neuromuscular blockade.
 Shock
• Shock is the clinical syndrome that results from
inadequate tissue perfusion.
• The hypoperfusion-induced imbalance between the
delivery of and requirements for oxygen and substrate
leads to cellular dysfunction.
• This leads to a vicious cycle in which impaired perfusion is
responsible for cellular injury that causes maldistribution
of blood flow, further compromising cellular perfusion;
the latter ultimately causes multiple organ failure (MOF)
and, if the process is not interrupted, leads to death.
 Shock
• MAP = CO x SVR
• O2 saturation
 Hypovolemic Shock
• This most common form of shock results either
from the loss of red blood cell mass and plasma
from hemorrhage or from the loss of plasma
volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible losses.
• The normal physiologic response to hypovolemia is
to maintain perfusion of the brain and heart while
attempting to restore an effective circulating blood
volume.
 Infusion Rates
Access Gravity Pressure

18 g peripheral IV 50 mL/min 150 mL/min

16 g peripheral IV 100 mL/min 225 mL/min
14 g peripheral IV 150 mL/min 275 mL/min
8.5 Fr CV cordis 200 mL/min 450 mL/min
• Primary Survey: A B C D E
• Secondary Survey
• Dugaan syok sepsit et causa peritonitis
 Sepsis
• Two or more of SIRS criteria
• Temp > 38 or < 36 C
• HR > 90
• RR > 20
• WBC > 12,000 or < 4,000
• Plus the presumed existence of infection
• Blood pressure can be normal!
 Septic Shock
• Sepsis (remember definition?)
• Plus refractory hypotension
• After bolus of 20-40 mL/Kg patient still has one of
the following:
• SBP < 90 mm Hg
• MAP < 65 mm Hg
• Decrease of 40 mm Hg from baseline
 Septic Shock
• Clinical signs:
• Hyperthermia or hypothermia
• Tachycardia
• Wide pulse pressure
• Low blood pressure (SBP<90)
• Mental status changes
• Beware of compensated shock!
• Blood pressure may be “normal”
 Treatment Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.
 Treatment of Sepsis

• Antibiotics- Survival correlates with how quickly the

correct drug was given
• Cover gram positive and gram negative bacteria
• Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or
• Imipenem 1 gram IV
• Add additional coverage as indicated
• Pseudomonas- Gentamicin or Cefepime
• MRSA- Vancomycin
• Intra-abdominal or head/neck anaerobic infections- Clindamycin
or Metronidazole
• Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
• Neutropenic – Cefepime or Imipenem
 Persistent Hypotension

• If no response after 2-3 L IVF, start a

vasopressor (norepinephrine, dopamine,
etc) and titrate to effect
• Goal: MAP > 60
• Consider adrenal insufficiency:
hydrocortisone 100 mg IV
 Anaphylactic Shock

• Anaphylaxis – a severe systemic

hypersensitivity reaction characterized by
multisystem involvement
• IgE mediated
• Anaphylactoid reaction – clinically
indistinguishable from anaphylaxis, do not
require a sensitizing exposure
• Not IgE mediated
 Anaphylactic Shock

• What are some symptoms of anaphylaxis?

• First- Pruritus, flushing, urticaria appear

• Next- Throat fullness, anxiety, chest tightness,

shortness of breath and lightheadedness

• Finally- Altered mental status, respiratory distress

and circulatory collapse
 Anaphylactic Shock
• Risk factors for fatal anaphylaxis
• Poorly controlled asthma
• Previous anaphylaxis
• Reoccurrence rates
• 40-60% for insect stings
• 20-40% for radiocontrast agents
• 10-20% for penicillin
• Most common causes
• Antibiotics
• Insects
• Food
 Anaphylactic Shock

• Mild, localized urticaria can progress to full anaphylaxis

• Symptoms usually begin within 60 minutes of exposure
• Faster the onset of symptoms = more severe reaction
• Biphasic phenomenon occurs in up to 20% of patients
• Symptoms return 3-4 hours after initial reaction has cleared
• A “lump in my throat” and “hoarseness” heralds life-
threatening laryngeal edema
 Anaphylactic Shock- Diagnosis

• Clinical diagnosis
• Defined by airway compromise, hypotension, or
involvement of cutaneous, respiratory, or GI
systems
• Look for exposure to drug, food, or insect
• Labs have no role
 Anaphylactic Shock- Treatment
• ABC’s
• Angioedema and respiratory compromise require
immediate intubation
• IV, cardiac monitor, pulse oximetry
• IVFs, oxygen
• Epinephrine
• Second line
• Corticosteriods
• H1 and H2 blockers
 Anaphylactic Shock- Treatment

• Epinephrine
• 0.3 mg IM of 1:1000 (epi-pen)
• Repeat every 5-10 min as needed
• Caution with patients taking beta blockers- can cause severe
hypertension due to unopposed alpha stimulation
• For CV collapse, 1 mg IV of 1:10,000
• If refractory, start IV drip
 Anaphylactic Shock - Treatment
• Corticosteroids
• Methylprednisolone 125 mg IV
• Prednisone 60 mg PO
• Antihistamines
• H1 blocker- Diphenhydramine 25-50 mg IV
• H2 blocker- Ranitidine 50 mg IV
• Bronchodilators
• Albuterol nebulizer
• Atrovent nebulizer
• Magnesium sulfate 2 g IV over 20 minutes
• Glucagon
• For patients taking beta blockers and with refractory hypotension
• 1 mg IV q5 minutes until hypotension resolves