Pemicu 1 KGD: Muhammad Fahmi Rosyadi 405140220

Pemicu 1 KGD
Muhammad Fahmi Rosyadi

405140220
SHOCK
Define, classify, etiologies, diagnose
(S&S, lab, Radiology), management
LI 1
Shock
• The clinical syndrome results from inadequate tissue perfusion.
Irrespective of cause:
Harrison’s Principle of Internal Medicine, 19th edition

Ssx & signs
• Hypotension = systolic BP ≤ 90 mmHg or
mean arterial pressure (MAP) of < 60–65 mm
Hg
– Must be evaluated relative to the patient’s normal
blood pressure.
– A drop in systolic pressure of > 10–20 mm Hg or
an increase in pulse of > 15 beats per minute
with positional change suggests depleted
intravascular volume.
CURRENT Medical Diagnosis & Treatment 2017

• However, blood pressure is often not the best indicator of
end-organ perfusion because compensatory mechanisms:
– increased HR
– increased cardiac contractility
– Vasoconstriction
can occur to prevent hypotension.
• Hypotension  cool or mottled extremities & weak or
thready peripheral pulses.
• Splanchnic vasoconstriction  oliguria, bowel ischemia,
hepatic dysfunction  ultimately result in multi-organ failure.
• Mentation may be normal or patients may become restless,
agitated, confused, lethargic, or comatose as a result of
inadequate perfusion of the brain.

Lab & imaging
• Blood specimens should be evaluated for:
– complete blood count,
– electrolytes,
– glucose,
– arterial blood gas determinations,
– coagulation parameters,
– lactate levels,
– typing and cross-matching
– bacterial cultures.
• An electrocardiogram & chest radiograph should also
be part of the initial assessment.

General Principles of Shock management
• Overall goal = improve O2 delivery or utilization  prevent cell & organ injury
• Effective th/ = treat underlying etio, restore adeq perfusion, monitoring,
comprehensive supportive care
• Restore perfusion = adeq BP, increase CO, and/or optimize O2 content of blood
(decrased O2 demand when possible)
Component Intervention
BP (min achieve >=65 mmHg Fluids, vasopressor or vasodilator agents
MAP)
CO
1. Preload 1. Fluids, vasodilator agents (only if BP adeq)
2. Contractility 2. Inotropic agents
3. Afterload 3. Vasopressor or vasodilator agents
O2 content
1. Hb (oxyHb saturation 1. Blood transfusion
recommended >=95%) 2. Supplemental O2, mechanical ventilation
2. Hb saturation 3. Mech ventilation, sedation, analgesia, antipyretics
3. O2 demand
Society of Critical Medicine: Fundamental Critical Care Support. 4th ed. 2007
• Monitoring
– To determine appropriate interventions & assess response
to intervention
– Cont. ECG  assess HR & rhythm
– BP best monitored w/ arterial catheter (inacurracy of non-
invasive devices)
– Pulse-oximetry routinely monitored  ensure adeq oxyHb
saturation
– Central Venous Pressure  indicator of right ventricular
preload
– Urinary catheter should be inserted  monitor urine
output (renal perfusion); suggested goal 0,5-1 mL/kg/h
– Lactate [] measured initally  monitored at some intervals
• (N) or << [] = improved O2 balance
• Fluid th/  Initial th most forms of shock = replace intravasc vol
– Physical exam = valuable info
• Distended neck veins = high ventricular filling pressure
• Clear lung fields & flat neck veins = inadeq preload in hypotensive pts
– IV vol def (x anemic)  crystalloid or colloid sol
• Crystalloid less expensive than coloids; includes: (boluses of 500-1000 ml)
– Ringer lactate
– Normal saline
Dextrose 5% in water (x) offer any expansion of IV vol due t quick distribution
throuout body fluid compartments
• Colloid sol: (titrated boluses of 300-500 ml)
– Hetastarch, albumin, gelatins
Smaller bolus # = for pts suspected or known cardiogenic shock
– Packed RBC indicated to >> O2 carrying capacity in pts w/ signif bleed or anemia
– Critically ill pts; Hb [] 7-9 mg/dL = adeq after stabilization
– FFP (fresh frozen plasma) = only for correction of coagulopathy, not for vol replacement
• Vasoactive agents
– Medications w/: vasopressors, inotropic, vasodilator
• Dopamine (three effects)
– Low rate infusion 2-3 ug/kg/min = modest inotropic & chronotropic
– Intermediate 4-10 ug/kg/min = primarily inotropic & losses effect on kidney
– Higher rate >=10 ug/kg/min = signif a-agonist effect  dose related
vasoconstriction
– >= 25 ug/kg/min = no advantage over NE (> vasopressor effect)
– AE = arrythmias & tachycardia
• NE (a-adrenergic vasopressor, B-adrenergic, inotropic,
chronotropic) starts at 0,05 ug/kg/min  titrated to desired
effects
• Epinephrine (a & B-adrenergic; potent inotropic & chronotropic;
higher dose: vasopressor) start at 0,1 ug/kg/min  titrated
• Vasopressin (V1 rec  vasoconstriction  >> BP  << CO) 0,01-
0,04 units/min
• Dobutamin (B adrenergic agonist + inotropic effect) doses of 5 – 20
ug/kg/min  >> CO  MUST BE (+) TO HYPOTENSIVE PTS
Specific forms of
shock
Classification

Essentials of Pathophysiology: Concepts of Altered Health States, 2011
Hypovolemic Shock
• Results from decreased intravascular volume
secondary to loss of blood (hemorrhagic) or fluids
and electrolytes (non hemorrhagic)
– Etiology may be suggested by the clinical setting (eg,
trauma) or Sign & symptoms of blood loss (eg,
gastrointestinal bleeding) or dehydration (eg, vomiting or
diarrhea).
• Compensatory vasoconstriction may transiently
maintain the blood pressure but unreplaced losses
of >15% of the intravascular volume  hypotension
& progressive tissue hypoxia.
S&S of Hypovolemic Shock
• Evident when signs of hypoperfusion:
– oliguria,
– altered mental status,
– cool extremities
• Jugular venous pressure is low, there is a narrow
pulse pressure  indicative of reduced stroke
volume.
• Dx is more difficult when the source of blood
loss is occult: GI tract, or when plasma volume
alone is depleted.
• After acute hemorrhage, Hb & Ht # do not
change until compensatory fluid shifts have
occurred or exogenous fluid is administered.
• Thus, an initial normal hematocrit does not
disprove the presence of significant blood loss.
suggest the presence of hypovolemia:
• Plasma losses  hemoconcentration
• free water loss  hypernatremia

• Essential to distinguish between hypovolemic
and cardiogenic shock
– both may respond to volume initially, definitive
therapy differs significantly.
• Both forms are associated with a reduced cardiac
output and a compensatory sympathetic
mediated response = tachycardia & elevated
systemic vascular resistance.
• However, the findings in cardiogenic shock of
jugular venous distention, rales, and an S3 gallop
distinguish it from hypovolemic shock and signify
that ongoing volume expansion is undesirable
and may cause further organ dysfunction.
Treatment of Hypovolemic Shock
• Initial resuscitation = rapid re-expansion of
circulating intravascular blood volume + control
ongoing losses  Stroke volume & cardiac output
rise with the increase in preload.
• After resuscitation, the compliance of the
ventricles may remain reduced due to increased
interstitial fluid in the myocardium. Therefore,
elevated filling pressures are frequently required
to maintain adequate ventricular performance.

Treatment
• Directed toward correcting or controlling the
underlying cause and improving tissue perfusion.
• Ongoing loss of blood must be corrected, such as in
surgery.
• Oxygen is administered to increase oxygen delivery to
the tissues.
• Medications usually are administered intravenously.
• Frequent measurements of heart rate and cardiac
rhythm, blood pressure, and urine output are used to
assess the severity of circulatory compromise and to
monitor treatment.

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition
Cardiogenic shock
• Results from cardiac failure with the resultant inability of the heart to
maintain adequate tissue perfusion.
• The clinical definition = evidence of tissue hypoxia due to decreased
cardiac output (cardiac index < 2.2 L/min/m2 ) in the presence of
adequate intravascular volume.
• most often caused by myocardial infarction
– but can also be due to:
• cardiomyopathy,
• myocardial contusion,
• valvular incompetence or stenosis
• arrhythmias.
• Patient profile:
– In patients with acute MI, older age, female sex, prior MI, diabetes, and
anterior MI location are all associated with an increased risk of CS.
– Shock associated with a first inferior MI  prompt a search for a mechanical
cause.
– Reinfarction soon after MI increases the risk of CS.
S&S of Cardiogenic shock
• Signs of global hypoperfusion with oliguria, altered mental status, and
cool extremities.
• Jugular venous pressure is elevated
• there may be evidence of pulmonary edema with respiratory compromise
in the setting of left-sided heart failure.
• A transthoracic echocardiogram (TTE) or a transesophageal
echocardiogram (TEE) is an effective diagnostic tool to differentiate
hypovolemic from cardiogenic shock.
– In hypovolemic shock, the left ventricle will be small because of
decreased filling, but contractility is often preserved.
– Cardiogenic shock results from cardiac failure with a resultant
decrease in left ventricular contractility.
– In some cases, the left ventricle may appear dilated and full because
of the inability of the left ventricle to eject a sufficient stroke volume
Treatment
• Improving cardiac output
• Reducing the workload and oxygen needs of the myocardium,
• Increasing coronary perfusion
• Fluid volume must be regulated within a level that optimizes the filling
pressure and stroke volume.
• Pulmonary edema and arrhythmias should be corrected or prevented to
increase stroke volume and decrease the oxygen demands of the heart.
• Coronary artery perfusion is increased by promoting coronary artery
vasodilation, increasing blood pressure, decreasing ventricular wall
tension, and decreasing intracardiac pressures.

• The goal of pharmacologic treatment = increase cardiac
contractility without increasing heart rate.
• Dopamine and dobutamine are the most commonly used
inotropic agents.
– Initially, dopamine is the drug of choice because it acts as
an inotrope as well as a vasoconstrictor.
– Dobutamine, an inotrope with arterial dilator properties,
can be used in persons with less severe hypotension.
– Catecholamines, such as norepinephrine, increase cardiac
contractility but must be used with extreme caution
because they also result in arterial constriction and
increased heart rates, which worsens the imbalance
between myocardial oxygen supply and demand.

Obstructive Shock
• Circulatory shock that results from mechanical
obstruction of the flow of blood through the
central circulation (great veins, heart, or
lungs)
– Cardiac tamponade
– tension pneumothorax
– massive pulmonary embolism (freq cause)
cause an acute decrease in cardiac output resulting
in shock.

S&S of obstructive shock
• The primary physiologic result of obstructive
shock is elevated right heart pressure due to
impaired right ventricular function. Signs of
RH failure:
– elevation of Central venous pressure
– jugular venous distention
• Pressures are increased despite impaired
venous return to the heart.

Treatment of Obstructive Shock
• Focus on correcting the cause of the disorder,
frequently with surgical interventions:
– pulmonary embolectomy
– pericardiocentesis (i.e., removal of fluid from the
pericardial sac) for cardiac tamponade
– insertion of a chest tube for correction of a tension
pneumothorax or hemothorax.
• Severe or massive pulmonary embolus: fibrinolytic
drugs may be used to break down the clots causing
the obstruction.

relaxation of vascular
smooth muscle

The emergency management of patients with cardiogenic shock,
acute pulmonary edema, or both is outlined.
• *Furosemide:
– <0.5 mg/kg for new-onset acute pulmonary edema without
hypervolemia;
– 1 mg/kg for acute on chronic volume overload, renal insufficiency.
– *Indicates modification from published guidelines.
– ACE, angiotensin-converting enzyme; BP, blood pressure; MI,

myocardial infarction.
– (Modified from Guidelines 2000 for Cardiopulmonary Resuscitation

and Emergency Cardiovascular Care. Part 7:The era of reperfusion:
Section 1: Acute coronary syndromes (acute myocardial infarction).
The American Heart Association in collaboration with the International
Liaison Committee on Resuscitation. Circulation 102:I172, 2000.)
Distributive Shock
(Septic Shock, Anaphylactic Shock)
• The reduction in systemic vascular resistance results in
inadequate cardiac output and tissue hypoperfusion despite
normal circulatory volume (normovolemic shock).
• Characterized by:
– loss of blood vessel tone,
– enlargement of the vascular compartment,
– displacement of the vascular volume away from the heart and central
circulation.
• In distributive shock, the capacity of the vascular
compartment expands to the extent that a normal volume of
blood does not fill the circulatory system

• 2 main causes of loss of vascular tone:
– a decrease in the sympathetic control of vasomotor tone
– release of excessive vasodilator substances.
Others:
– complication of vessel damage resulting from prolonged and severe
hypotension due to hemorrhage (irreversible or latephase hemorrhagic
shock)
– Sepsis, anaphylaxis, systemic inflammatory response syndrome (SIRS)
produced by severe pancreatitis or burns
– traumatic spinal cord injury,
– acute adrenal insufficiency
• There are 3 shock states that share the basic circulatory pattern
of distributive shock:
– neurogenic shock,
– anaphylactic shock,
– septic shock.

S&S of distributive shock
• Signs:
– Hyperdynamic heart sounds,
– warm extremities initially,
– wide pulse pressure indicative of large stroke volume.
• The echocardiogram may show a hyperdynamic left
ventricle.
• Fluid resuscitation may have little effect on blood pressure,
urinary output, or mentation.
• Septic shock is diagnosed = clinical evidence of infection in
the setting of persistent hypotension + organ hypoperfusion:
– lactic acidosis, decreased urinary output, or altered mental status
despite adequate volume resuscitation.
• Neurogenic shock is diagnosed when there is evidence of
central nervous system injury and persistent hypotension
despite adequate volume resuscitation.
Septic Shock
• Sepsis is the most common cause of distributive shock and
carries a mortality rate of 20–50%.
• Sepsis is defined as the presence of infection (either
documented or suspected) + systemic manifestations of
infection.
• Septic shock is diagnosed when hypotension from sepsis
persists despite adequate fluid resuscitation.
• The most common cause of septic shock in hospitalized
patients is infection with gram-negative organisms;
polymicrobial infections are almost as likely.
– The incidence of sepsis from fungal organisms is increasing but remains
less than that for bacterial infections.
• Risk factors for septic shock = bacteremia, extremes of age,
diabetes, cancer, immunosuppression, and history of a recent
invasive procedure.
• Systemic inflammatory response syndrome (SIRS)
– Defined as a systemic response to a nonspecific infectious or
noninfectious insult—such as from burns, pancreatitis, an
autoimmune disorder, ischemia, or trauma—the presence of
2 or more of the following clinical criteria help establish the
diagnosis of SIRS:
– (1) body temperature > 38o C (100.4o F) or < 36o C (96.8o F)
– (2) heart rate > 90 beats per minute
– (3) respiratory rate more than 20 breaths per minute or
hyperventilation with an arterial carbon dioxide tension
(Paco2) > 32 mm Hg
– (4) abnormal white blood cell count (> 12,000/mcL or <
4000/mcL or > 10% immature (band) forms).
– When a source of infection is confirmed, SIRS is categorized
as sepsis.

• Septic shock, which is the most
common type of vasodilatory shock, is
associated with the systemic response
to severe infection
The nomenclature related to sepsis and
septic shock has been evolving.
• Sepsis = suspected or proven infection
plus the clinical manifestations of what
has been termed the systemic
inflammatory response (e.g., fever,
tachycardia, and elevated white blood
cell count [leukocytosis]).
• Severe sepsis = sepsis plus evidence of
sepsis-induced organ dysfunction or
tissue hypoxia (e.g., hypotension,
hypoxemia, oliguria, metabolic
acidosis, thrombocytopenia)
• Septic shock = severe sepsis with
hypotension, despite fluid
resuscitation.
Manifestation
• Sepsis and septic shock are typically manifested by hypotension and
warm, flushed skin.
• Septic shock often presents with a decrease in systemic vascular
resistance.
• There is hypovolemia due to arterial and venous dilatation, plus leakage
of plasma into the interstitial spaces.
• Abrupt changes in cognition or behavior are due to reduced cerebral
blood flow and may be early indications of septic shock.
• Fever and increased leukocytes are present.
• An elevated serum lactate or metabolic acidosis indicates anaerobic
metabolism due to tissue hypoxia or cellular dysfunction and altered
cellular metabolism.
• Tissue hypoxia produces continued production and activation of
inflammatory mediators, resulting in further increases in vascular
permeability, impaired vascular regulation, and altered hemostasis

Treatment of sepsis & septic shock
• Focuses on control of the causative agent and support of the
circulation
• The administration of antibiotics that are specific for the infectious
agent is essential.
– However, antibiotics do not treat the inflammatory response to the
infection
• Cardiovascular status supported to increase oxygen delivery to the
cells and prevent further cellular injury.
• Swift and aggressive fluid administration is needed to compensate
for third spacing.

Textbook of Adult Emergency Medicine E-Book
• Equally aggressive use of vasopressor agents, such as
norepinephrine or dopamine, is needed to counteract the
vasodilation caused by inflammatory mediators.
• Persons with severe sepsis and hyperglycemia should receive
intravenous insulin therapy to maintain their blood glucose
levels at a target level of less than 150 mg/dL, based on
frequent measurement of blood glucose levels.
• Ongoing assessment of CVP, central or mixed venous oxygen
saturation, mean arterial pressure, urinary output, and
laboratory measurements of serum lactate, base deficit, and
pH are used to evaluate the progression of sepsis and
adequacy of treatment

Recent advances in the treatment of sepsis = recombinant
human activated protein C (rhAPC).
• 45–48 rhAPC is a naturally occurring anticoagulant factor that
acts by inactivating coagulation factors Va and VIII.
• In addition to its anticoagulant actions, rhAPC has direct anti-
inflammatory properties: inhibiting the production of
cytokines by monocytes and blocking cell adhesion.
• It also has antiapoptotic actions that may contribute to its
effectiveness.
• rhAPC is not recommended for use in children or adults with
risk for bleeding.

https://www.mdanderson.org/documents/for-physicians/algorithms/clinical-management/clin-management-sepsis-management-adult-web-algorithm.pdf
Anaphylactic Shock
• Anaphylaxis = clinical syndrome that represents the most
severe systemic allergic reaction.
• Anaphylactic shock results from an immunologically
mediated reaction (IgE) in which vasodilator substances
(histamine) are released into the blood  vasodilation of
arterioles and venules along with a marked increase in
capillary permeability.
• The vascular response in anaphylaxis is often accompanied
by life-threatening laryngeal edema and bronchospasm,
circulatory collapse, contraction of gastrointestinal and
uterine smooth muscle, and urticaria (hives) or angioedema

• Most frequent causes of anaphylactic shock are reactions to
medications, such as penicillin; foods, such as nuts and
shellfish; and insect venoms (most common cause is stings
from insects of the order Hymenoptera (i.e., bees, wasps, and
fire ants))
• Latex allergy causes life-threatening anaphylaxis in a growing
segment of the population. Health care workers and others
who are exposed to latex are developing latex sensitivities
that range from mild urticaria, contact dermatitis, and mild
respiratory distress to anaphylactic shock.
• Children with spina bifida also are at extreme risk for this
serious and increasingly common allergy.

• The onset and severity depend on = sensitivity of the person and the
rate and quantity of antigen exposure.
• S&S of impending anaphylactic shock =
– abdominal cramps;
– apprehension/anxiety;
– warm or burning sensation of the skin, itching, and urticaria (i.e., hives);
– coughing, choking, wheezing, chest tightness, and difficulty in breathing.
• After blood begins to pool peripherally  precipitous drop in blood
pressure ; pulse becomes so weak that it is difficult to detect.
• Life-threatening airway obstruction may ensue as a result of laryngeal
angioedema or bronchial spasm.
• Anaphylactic shock often develops suddenly; death can occur within
minutes unless appropriate medical intervention is promptly instituted.

Treatment of Anaphylaxis
• Immediate discontinuation of the inciting
agent or institution of measures to decrease
its absorption (e.g., application of ice to the
site of an insect bite)
• Close monitoring of cardiovascular and
respiratory function, maintenance of
respiratory gas exchange, cardiac output, and
tissue perfusion.
• Epinephrine is given  constricts blood
vessels and relaxes the smooth muscle in the
bronchioles  restore cardiac and respiratory
function.
• Other treatment measures =
– administration of oxygen,
– antihistamine drugs,
– corticosteroids.
– The person should be placed in a supine
position, because the sitting position can
produce a severe decrease in venous return.
Advanced pediatric life support AU
Neurogenic Shock
• Caused by decreased sympathetic control of blood
vessel tone due to a defect in the vasomotor center in
the brain stem or the sympathetic outflow to the blood
vessels.
• Spinal shock = neurogenic shock that occurs in persons
with spinal cord injury
• Output from the vasomotor center can be interrupted by
brain injury, the depressant action of drugs, general
anesthesia, hypoxia, or lack of glucose (e.g., insulin
reaction).
• Fainting due to emotional causes is a transient form of
impaired sympathetic outflow.

• Many general anesthetic agents can cause a
neurogenic shocklike reaction, especially during
induction, because of interference with sympathetic
nervous system function.
• Spinal anesthesia or spinal cord injury above the
midthoracic region can interrupt the transmission of
outflow from the vasomotor center.
• In contrast to other shock states due to the loss of
blood volume or impaired cardiac function, the heart
rate in neurogenic shock often is slower than
normal, and the skin is dry and warm.
• This type of distributive shock is rare and usually
transitory.
ACUTE ABDOMEN
Define, Etiologies, Diagnose,
Management
LI 2
• Abdominal pain = 5-10% all emergency
department visits
• Freq arises from pathologies in GI &
Genitourinary systems
– However may result from CV, pulmo, metabolic,
infective and toxic causes
• Special considerations: elder,
immunocompromised, women on
childbearing age, children  avoid miss dx
and poor outcomes
Abdominal pain may result from
• Visceral pain
– Pain poorly localized, colicky, intermittent & recurrent in nature.
– Stimulation of autonomic nerves investing the visceral peritoneum
causes visceral pain
• e.g. when hollow organs are distended, or when capsules covering solid
organs are stretched.
– Visceral pain localizes to the abdominal region that correlates with the
embryonic segments of the viscera:
• Foregut: (stomach, duodenum, liver, biliary tract, pancreas) localize to the
upper abdomen
• Midgut: (small bowel, proximal colon, appendix) localize to the
periumbilical region
• Hindgut: (distal colon, genitourinary tract) localize to the lower abdomen.
• Somatic pain:
– Pain is well localized, often constant and intense.
– Results from local irritation of the parietal peritoneum.
– Localized more specifically to the area of pathology
however, important to recognize that the area of pain does not always correspond
to the supposed anatomic location of the underlying pathology
e.g. acute appendicitis may present as suprapubic or flank pain.
• Referred pain:
– Pain felt at a distance from the site of origin.
– Occurs because afferent pain fibres from areas of high sensory input (e.g. the
skin) enter the spinal cord at the same level as nociceptive fibres from an area
of low sensory input (e.g. the viscera).
– The brain, being more used to pain signals from the skin, wrongly interprets the
pain signal from the viscera as that from the dermatome.
Causes of abdominal pain
Generalized diffuse pain

that is poorly localized
may be due to benign
causes (e.g.
gastroenteritis,
constipation and
menstrual
cramps) or from life-
threatening conditions =
Clinical features: Vital signs and
general condition
• During triage a rapid assessment is made by looking at
the patient’s general condition as well as vital signs.
• Obviously ill patients, those in severe pain or with
abnormal vital signs should be given priority.
• However, one cannot rule out life-threatening causes
of abdominal pain by the absence of abnormal vital
signs.
– It has been estimated that up to 7% of patients with
normal vital signs may have an underlying life-threatening
process, and this percentage increases in the elderly.
• Tachycardia may be absent in patients with
autonomic dysfunction, in the elderly, and in
patients on medications that may blunt the
cardiac response to illness or volume loss.
• The elderly, the immunocompromised, or
those in severe septic shock may sometimes
not mount a febrile response.
– Even in the immunocompetent, fever may not
always accompany acute inflammatory conditions
Patient demographics and
background history
• Key questions in the background history are:
– Previous abdominal surgery
– Use of tobacco, alcohol, or recreational drugs
– Chronic illness, e.g. diabetes mellitus, hypertension, coronary
artery disease, human immunodeficiency infection, systemic
lupus erythematosus
– Vascular, thrombotic and embolic risks e.g. atrial fibrillation,
vasculitis, peripheral vascular disease
– Medication history, e.g. use of nonsteroidal anti-inflammatory
drugs, pain medications, antibiotics, steroids, anticoagulants
– History of recent trauma
For women of childbearing age it is important to ascertain the presence or absence of
pregnancy
Pain attributes
Severity of pain:
• experienced is dependent on a number

of factors in addition to the underlying
pathology, and is not always
commensurate with the severity of the
underlying illness.
• The elderly in particular often have a
diminished sense of pain.
• Nonetheless, patients in severe pain
should be assessed early and given pain
relief.
• Pain scores may be used to record and
monitor progress.
Character of pain:
• Colicky abdominal pain results usually

from obstruction of a hollow viscus.
• Constant non-colicky pain usually
denotes an inflammatory or vascular
process.
Precipitating and relieving factors:
• Pain from peritonitis worsens with movement, deep

breathing, coughing or sneezing.
• Pain from peptic ulcer disease classically increases with
hunger and decreases with food, antacid or milk.
• Pain from biliary colic tends to occur after full or fatty
meals.
• Pain from acute pancreatitis classically worsens with
supine posture and is relieved by sitting up.
Recurrent episodes of abdominal pain:
• This suggests chronic recurrent conditions, e.g. peptic

ulcer, biliary colic, renal colic, diverticulitis.
• Mesenteric ischaemia and testicular torsion may also
present with recurrent episodes
Associated symptoms
• Constitutional symptoms, e.g. fever, chills, rigors, weight loss, arthralgia.
• Gastrointestinal tract symptoms, e.g. anorexia, nausea, vomiting,
diarrhoea, constipation.
– Nausea and vomiting are non-specific symptoms which may result from intra-
and extra-abdominal causes.
• However, feculent vomitus is highly indicative of intestinal obstruction.
• Vomiting of fresh or altered blood, as well as the passage of black tarry
stools, indicates gastrointestinal haemorrhage.
• Failure to pass stools and flatus over a 24–48-hour period suggests
possible intestinal obstruction.
• Genitourinary tract symptoms, e.g. dysuria, frequency, urgency,
haematuria, suggest urinary tract pathologies.
• A purulent discharge from the vagina suggests possible pelvic
inflammatory disease.
Physical Examination:
• Consider the general condition & vital signs of the patient.
• Drowsy or unwell, abnormal vital signs  urgent attention.
• Posture of the patient may give a clue to the possible
underlying disease.
– Patients with renal colic typically roll about in pain
– Those with peritonitis lie still to avoid movements that might
aggravate the pain.
• Inspect for pallor, jaundice, hydration status, enlarged lymph
nodes, and signs of chronic liver or renal disease.
Rectal Examination Examine hernial orifices
• This is useful in cases of • All hernias should be
gastrointestinal examined for signs of
haemorrhage, perianal or strangulation.
perirectal diseases, stool • Hernias are most commonly
impaction, prostatic present in the inguinal or
pathologies and rectal femoral area, along the
foreign bodies. midline, or arising from old
surgical scars.
Laboratory
Examination
Imaging
Plain X rays Ultrasound CT
• A place for plain X-rays as a • Ultrasound does not • Modality of choice for
first-line investigation in involve ionizing radiation, evaluation of
patients with: rapid, non-invasive, may abdominal pain in the
– suspected bowel be performed at the non-obstetric patient
obstruction bedside. • Detailed visualization of
– bowel perforation • Ideal evaluation tool in intra-, extra- and
– foreign body unstable patients or those retroperitoneal
who are pregnant. structures.
• A 3-view series comprising the
upright chest, supine & • Ultrasound is operator • Identifies the exact site
upright abdominal dependent and of disease, impact on
radiographs recommended. appropriate training is the surrounding
necessary to ensure structures, guiding
• X-ray findings for bowel
competence. further management.
obstruction and perforation
are fairly specific but not • The sensitivity of • With or without IV &
sensitive ultrasound may also be oral contrast agents.
reduced by technical
– they help to establish, but
limitations (e.g. obesity,
not exclude, these
bowel gas, subcutaneous
diagnoses.
emphysema).
• Bedside emergency US examination significantly for diagnosis &
management of life-threatening conditions:
Abdominal aortic aneurysm (AAA): Ectopic pregnancy:
screening tool (aortic diameter >3 • (+)ve pregnancy test, empty uterus
cm), especially when the patient is not (especially in the presence of free
suitable for transfer to a CT facility. intraperitoneal fluid) implies ectopic
pregnancy until proven otherwise.
• Hypotensive symptoms suggestive • Ultrasound findings: detect adnexal mass,
of rupture (abdominal pain, extrauterine gestational sac, extrauterine
backache or flank pain) = indication blood clots & interstitial ectopic pregnancy.
for urgent intervention. • Transvaginal ultrasound is more sensitive
Haemoperitoneum (abdominal
trauma)
• The focused abdominal sonogram for
trauma (FAST) examination is now First choice for suspected
considered to be an essential evaluation gallbladder disease
in unstable patients who have sustained
abdominal trauma.
• (+) free intraperitoneal fluid
• In the emergency setting, CT is useful for:
– Assessment in abdominal trauma.
– Detection of inflammatory lesions (e.g. appendicitis,
pancreatitis, diverticulitis, abscesses).
– Detection of neoplastic lesions.
– Evaluation of vascular pathology (e.g. aortic aneurysm,
aortic dissection, mesenteric ischaemia).
– Detection of intra-abdominal and retroperitoneal bleed or
abscesses.
– Detection of pneumoperitoneum, obstruction of hollow
organs, and abnormal calcifications, e.g. ureteric calculi.
– Assessment of the kidneys and urinary tracts.
Diagnosis of Acute Abdominal Pain in Older Patients. American Family Physician. 2006
Diagnosis of Acute Abdominal Pain in Older Patients. American Family Physician. 2006
(CAD = coronary artery disease; ECG = electrocardiography; UTI = urinary tract infection; MI = myocardial infarction; CHF = congestive heart
failure; PE = pulmonary embolism; SBO = small bowel obstruction; LBO = large bowel obstruction; RUQ = right upper quadrant; AAA = abdominal
aortic aneurysm; RLQ = right lower quadrant; CT = computed tomography.)
General management
Resuscitation Symptom relief Antibiotics
• Prompt resuscitation • Pain relief should be • Antibiotics are

should take instituted as early as indicated in suspected
precedence over possible for patients intraabdominal sepsis.
diagnosis in unstable presenting with The antibiotics used
patients. abdominal pain. should cover Gram-
• Patients may be in • Relieving pain does negative aerobes as
shock as a result of not mask signs of well as anaerobes.
blood loss, fluid loss, peritonism or obscure • Additional coverage
sepsis, or from the diagnosis. for Gram-positive
concurrent aerobes is required in
cardiovascular events. patients with
• Appropriate fluid spontaneous bacterial
therapy and inotropic peritonitis.
support should be
instituted early to
prevent further
deterioration and
end-organ
dysfunction
Treatment
Antibiotics are indicated for suspected
abdominal sepsis and peritonitis.
Endogenous gut flora cause abdominal

infections in the GI or GU tract.
In all intra-abdominal non-gynecologic

infections, coverage should minimally
be targeted at anaerobes and facultative
aerobic gram negatives.
An exception to this generalization is the

need to provide additional coverage
for gram-positive aerobes (e.g.,
Pneumococcus) in spontaneous (primary)
bacterial peritonitis.
Tintinalli Emergency Medicine. 8th edition

Common Problems in Acute Care Surgery. Moore L.J, turner KL, Todd SR. Springer: 2013
Common Problems in Acute Care Surgery. Moore L.J, turner KL, Todd SR. Springer: 2013
Esophageal Caustic Injury
• >> accidents = < 4 years of age or at 21 as suicide attempts.
• Caustic agents = acidic or alkaline
– Common alkali-containing caustic agents:
• household bleaches, drain openers, toilet bowel cleaners,
dishwashing agents and detergents.
– Acid-containing agents:
• toilet bowl cleaners, anti-rust compound, swimming pool cleaners,
vinegar, formic acid used in the rubber tanning industry and other
similar acids
• Substances with extremes of pH ( <2 or >12) = very corrosive; create
severe injury & burns in UGIT
• Locations most seriously affected = esophagus and stomach
– Corrosive material often remains in these areas for a longer period of
time. However, injuries can also occur in any area in contact with the
caustic agents (oral mucosa, pharyngeal area, upper airways, and
duodenum)
Management of esophageal caustic injury. World J Gastrointest Pharmacol Ther. 2017 May 6; 8(2): 90–98.
tends to be consumed
Acids, have a pungent
in smaller amounts and
odor and an unpleasant
are swallowed rapidly
taste.
after ingestion
Alkaline: colorless,
relatively tasteless, amount ingested
more viscous, less tends to be more
marked odor
reacts with tissue converted to acid
proteins proteins
transformed into
react with proteins
proteinases and
and fats
soaps
coagulum prevents the
coagulation necrosis corrosive agent from
spreading transmurally
liquefactive deeper penetration

necrosis into tissues
reducing the incidence

of full thickness injury
Healing process typically
begins 3 weeks after
Mucosal injury begins
within minutes of
ingestion: tensile strength
Continue next several of esophageal and/or
caustic ingestion:
days ~4 to 7 d later:
necrosis &
mucosal sloughing,
gastric tissues is the lowest.
hemorrhagic
bacterial invasion, • If the ulcerations extend well
congestion secondary
granulation tissue and beyond the muscularis layer, the
to the formation of
collagen deposition wall becomes vulnerable to
thrombosis in the small
vessels perforation
• Avoiding endoscopy b/w 5th and
the 15th day after caustic
ingestion
By the 3rd week: Lower esophageal

scar retraction; may stricture formation sphincter pressure
continue for a few occurs. impaired in the
more months process
increased frequency further aggravates

accelerates the
and severity of acid existing mucosal
stricture formation
reflux injury
• The severity of injury depends on several
aspects:
– Concentration of the substance
– amount ingested
– length of time of tissue contact
– pH of the agent
Solid materials easily adhere to the mouth and
pharynx  greatest damage to these regions.
Liquids pass through the mouth & pharynx more
quickly consequently  maximum damage in the
esophagus and stomach
Clinical Presentation
• diverse and do not always correlate with the degree of
injury.
• Symptoms mainly depend on the location of damage.
– Hoarseness and stridor are signs that are highly suggestive
of an upper respiratory tract involvement, particularly the
epiglottis and larynx. Presence of these findings may signal
a potentially life-threatening respiratory event
– The upper gastrointestinal tract, on the other hand, may
present as dysphagia or odynophagia for esophageal injury
and hematemesis or epigastric pain for gastric involvement
Complications
• Short-term = perforation and death.
– Perforation of the esophagus or stomach can occur at any time during
the first 2 to 3 wk of ingestion.
– A sudden worsening of symptoms or an acute deterioration of a
previously stable condition should warrant a thorough investigation to
rule out the possibility of a perforated viscus
• Chronic = stricture formation, gastric outlet obstruction and malignant

transformation.
– Patients with esophageal strictures usually complain of dysphagia and
substernal pressure, and may become symptomatic 3 wk or later after
ingestion.
– Symptoms of early satiety, post-prandial nausea or vomiting, and
extreme weight loss suggest gastric obstruction. The latter commonly
occurs in the first 5 to 6 wk of ingestion
Zargar classification
A: Zargar Grade 0: Normal mucosa; Management of
B: Zargar Grade I: Edema and erythema of the mucosa; esophageal caustic
injury. World J
C: Zargar Grade IIA: Hemorrhage, erosions, blisters, superficial ulcers; Gastrointest Pharmacol
D: Zargar Grade IIB: Circumferential bleeding, ulcers. Exudates; Ther. 2017 May 6; 8(2):
E: Zargar Grade IIIB: Focal necrosis, deep gray or brownish black ulcers; 90–98.
F: Zargar Grade IIIB: Extensive necrosis, deep gray or brownish black ulcers.
Intussusception
• 1 segment of bowel (intussusceptum) • Aged 5–12 mo = periods of screaming,
slides inside the adjacent segment vomiting, blood in the faeces (‘redcurrant
jelly’) & drawing up of the legs. Child is
• >> early childhood (95%)
pale
• Occurs mainly at the ileocaecal valve • Sausage-shaped mass on palpation of
(ileocolic intussusception) abdomen.
• Males: females 2:1. • Peritonitis & gangrene may occur w/in 24
• Aetiology is unclear: hrs untreated.
– may be related to an adenovirus • A barium enema may resolve the
intussusception by forcing the invaginated
causing enlargement of lymphatic
segment back with hydrostatic pressure.
tissue in the intestinal wall  Alternatively, surgery may be required.
protrudes into the lumen; pushed
into the adjacent section by
peristalsis.
– Some cases = polyp (Peutz–Jeghers
polyps), Meckel’s diverticulum or
carcinoma may project into the
lumen and be pushed along in a
similar way
(Crash course) Megan Griffiths_ Rusheng Chew-Gastrointestinal system-Elsevier, Mosby
Appendicitis
• It is a blind-ending sac and so may become inflamed
(appendicitis) if obstructed, e.g. by faecoliths, which are small,
hard masses of faeces.
• Peak age: adolescence & young adulthood
• No typical radiation
• Quality: initially dull  severe
• RLQ pain; migrate from periumbilical area
• Pain before vomiting
• Anorexia, vomiting, fever, elevated WBC
• CT scan preferred
• Complication: perforation, abscess
• This requires surgical removal of the appendix to prevent
rupture and peritonitis.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th edition
Abscess of Appendix
Inflamed appendix
may become
surrounded by appendix mass
adjacent small
bowel & omentum
generalized
peritonitis or local
perforate
adhesion 
appednix abscess
• Ssx (+) in 48 hrs = truly

appendicitis
• Appendix mass enlarges 
tempt fails to settle 
abscess dev
• Pts: toxic + tachycarida
• Req surgical drainage &
appendicectomy or
percutaneous insertion of
drain under US control Churchill's Pocketbook of Surgery E-Book
Imaging
• US = first investigation advised to evaluate a
suspected appendicular pathology.
– Findings of an appendicular abscess include:
• Fluid collection (hypoechoic) in the appendicular region
• may be well circumscribed and rounded or ill-defined
and irregular in appearance
• Appendix may be visualised within the mass
• CT
– Fluid collection is seen in the appendicular region
with or without air within.
– Appendicolith may be visualized.
https://radiopaedia.org/articles/appendicular-abscess
Peptic ulcer
• Arise when damaging factors: • Epigastric pain = main presenting
– gastric secretions, symptom,
– overwhelm the natural protection – Endoscopy and tests for the
of the mucosal lining of the presence of H. pylori being the
gastrointestinal tract. usual investigations when peptic
• Result from: ulcer disease is suspected.
– decrease in protective factors • Th/:
– increase in damaging factors – proton pump inhibitors for at least
2 months
– Both
– triple therapy for the eradication
• 2 main types of peptic ulcers: duodenal of H. pylori if necessary.
ulcers and gastric ulcers (especially at
the junction of the antrum and the – If possible, patients are advised to
body). stop taking NSAIDs or use the
lowest dose possible for symptom
– Other sites: distal oesophagus, esp control.
Barrett’s oesophagus, Meckel’s
diverticulum and where
gastroenterostomy performed.
• >> incidence 45 years.
• Both duodenal and gastric ulcers are
common in the elderly.
Duodenal ulcers Gastric ulcers
• Duodenal ulcers (DU) are two to • Seventy per cent of GU are associated
three times more common than with H. pylori, with the rest mainly
gastric ulcers (GU), occurring in associated with NSAID treatment.
about 15% of the population. • Gastric ulcers may also occur in response
• Approximately 90% of DU are to acute gastritis or extreme hyperacidity,
associated with H. pylori. as in Zollinger–Ellison syndrome.
• Classically the epigastric pain is • The epigastric pain is characteristically
said to be relieved by food or associated with food.
antacids, and exacerbated by • Zollinger–Ellison syndrome is a rare
hunger. condition due to gastrin-secreting
pancreatic adenomas causing excess acid
production. It can lead to acute ulcers in
the antrum, duodenum and, in severe
cases, the jejunum.

Peritonitis
• Generalized: manifests classic signs of tenderness, guarding, rebound
tenderness, rigidity
• The abdomen may be distended
• Bowel sounds may be absent
• Bowel contents, bile, urine, and blood are irritant to the peritoneum and
generalized peritonitis can be due to
– a perforated viscus
– mesenteric ischemia
– strangulation of the bowel secondary to an internal or external hernia,
or a volvulus
– an intraperitoneal bleed
– rupture of a localized abscess into the general peritoneal cavity.
• Free intraperitoneal gas is not always present on chest X-ray 
particularly true of appendicular and gallbladder perforations.
• Laparotomy necessary after adequate resuscitation
Textbook of Clinical Gastroenterology and Hepatology (2nd Edition)

Incarcerated Hernia
• Contents of hernia sac cannot be reduced into
abdominal cavity
• Contained structures, include:
– Small bowel
– Appendix
– Omentum
– Colon
– Meckel diverticulum (rarely)
– In girls: ovary, fallopian tube or both
– Rarely: uterus in infants can also be pulled into sac
• Strangulated hernia: tightly constricted in its passage through
inguinal canal  hernia contents become ischemic or
gangrenous
• Incarceration may be tolerated in adults for years
• Most non-reducible inguinal hernias in children rapidly
progress to strangulation w/ potential infarction of hernia
contents (if not treated)
Herniated viscera impaired

passes through Inguinal canal external ring lymphatic &
internal ring venous drainage
total occlusion of further increase

swelling of
arterial supply to compression in
herniated viscera
trapped viscera inguinal canal
• Testis is also at risk of ischemia due to
compression of spermatic cord structures by
strangulated hernia
• In girls: herniation of ovary at risk of
strangulation & torsion
Symptoms of incarcerated hernia
• Irritability • Fever
• Pain in the groin & abdomen • Signs of intestinal obstruction
• Abdominal distension • Testes maybe swollen or normal &
• Vomiting hard on affected side
• Tense, non fluctuant mass in – venous congestion resulting from
inguinal region compression of spermatic veins
& lymphatic channels at inguinal
– Can extend down to scrotum & ring by tightly strangulated
labia majora hernia mass
• Mass is well defined, may be • Abdominal radiographs:
tender, does not reduce
features of partial or complete
• Onset of ischemic changes  pain intestinal obstruction; gas w/in
intensifies  vomiting becomes incarcerated bowel segments
bilious is feculent
may seen below inguinal
• Blood noted in stools ligament or w/in scrotum
• Mass: tender often edema &
erythema overlying skkin
Nelson textbook of pediatrics (2011)

Biliary Colic
• F > M; < 60 yo
• RUQ > epigastric pain
• Radiates to right subcapsular area
• Initially colicky - continuous  resolves <6 hr
• Bloating & dyspepsia
• Lab: suspect common bile duct stone if >>
bilirubin
• US imaging
• Complications: cholecystitis
Upper & Lower
GASTROINTESTINAL BLEEDING
Define, etiologies, diagnose, explain
management
LI 3
Gastrointestinal bleeding
Upper GIB (UGIB) ~1.5–2 times >> lower GIB (LGIB)
Hematemesis, vomitus of red blood or “coffee-
grounds” material;
Overt GIB is
Melena, black, tarry, foul-smelling stool;
manifested by:
Hematochezia, passage of bright red or maroon

GIB = overt or occult blood from the rectum.
bleeding.
Identification: patients (+) ssx of blood loss or
anemia: lightheadedness, syncope, angina, or
Occult GIB: absence
dyspnea; or when routine diagnostic evaluation
of overt bleeding.
reveals iron deficiency anemia or a positive fecal
occult blood test.
UGIB
GIB categorized by
LGIB
the site of bleeding
obscure GIB if the

source is unclear.
UGIB
• Common medical emergency; carries substantial mortality.
Mortality rate still ranges from 15% to 50%
• Upper endoscopy = standard diagnostic & therapeutic tool
– Defines cause of bleeding & provides prognostic information, more
importantly, therapies carried out during endoscopy improve patients’
outcomes.
– Should be performed by medical or surgical gastroenterologists with
expertise in therapeutic endoscopy; performed in a unit supported by
appropriate staff, monitoring and resuscitation equipment.
• Stratification of the patients into low- or high-risk groups aids
in formulating a clinical management plan and early
endoscopy with aggressive post-hemostasis care should be
provided in high risk patients.

• A preliminary assessment of risk based on
several clinical factors aids in the resuscitation
as well as the rational triage of the patient.
• Clinical predictors of increased risk of
rebleeding and death:
– Age >60 years
– comorbid illnesses
– systolic blood pressure <100 mm Hg
– pulse >100 beats/min
– bright red blood in the nasogastric aspirate or on
rectal examination.

1. High risk 2. Low to moderate risk
• Patients with active bleeding • All other patients are admitted to

• Hematemesis or bright red blood a step-down unit or medical ward
on nasogastric aspirate after appropriate stabilization for
• Shock further evaluation and treatment.
• persistent hemodynamic • Patients without evidence of
derangement despite fluid active bleeding undergo
resuscitation nonemergent endoscopy usually
within 24 hours.
• serious comorbid medical illness,
or evidence of advanced liver
disease require admission to ICU.
• After adequate resuscitation,
endoscopy should be performed
within 2-24 hours in most patients
but may be delayed in selected
patients with serious
comorbidities (eg, acute coronary
syndrome) who do not have signs
of continued bleeding.
UGIB Sign & Symptoms
• Hematemesis = vomiting of blood or blood clots
– Fresh hematemesis is often a reliable sign signifying ongoing or active
bleeding.
– Occasionally, vomiting of swallowed blood from hemoptysis or
bleeding from the upper aero-digestive tract, e.g., nasopharynx, can
confuse the diagnosis.
– Coffee ground vomiting is also a classic sign of upper gastrointestinal
bleeding  indicates a less severe bleedVomitus + oxidized iron
within heme mol (RBCs) after exposure to gastric acid.
• Melena = passage of dark, tarry stool with a characteristic pungent
smell.
– Occurs when hemoglobin is converted to hematin or other
hemochromes by bacterial degradation.
– This can be produced experimentally by the ingestion of as little as
100–200mL of blood.

• Blood absorbed by the small intestine  raised blood urea 
Raised BUN: creatinine ratio aid the diagnosis of UGIB.
– Some of this azotemia is probably secondary to
hypovolemia.
• >> volume of UGIB  hematochezia (passage of fresh blood
per rectum).
• << volume of bleeding (but sufficient to supply enough
hemoglobin for degradation & colonic motility sufficiently
slow)  bleeding from the small bowel or proximal colon
cause melena.
• Small bowel bleeding is however uncommon. Bleeding from
colonic sources, e.g. tumors
– slow (e.g. tumors) anemia or hemoccult positive stool
– rapid, (e.g. diverticular disease)  hematochezia.

Initial Management
• Resuscitation = 1st priority in the management of patients
with UGIB.

• Impaired mental status, their airways should be
protected and often orotracheal intubation is
required prior to endoscopy.
• A urinary catheter is useful, especially in those with
hemodynamic compromise, to detect oliguria.
• A central venous catheter is useful for monitoring
volume replacement, particularly in those with
incipient heart failure.
• Physical examination may reveal stigmata of chronic
liver disease that may call for specific treatments
such as vasoactive drugs, antibiotics, and drugs to
prevent encephalopathy
Causes of UGIB
UGIB categorized
Variceal Non-variceal bleeding.
Others
Peptic Non- (uncommo
Patients ulcers steroidal
suffering from n):
remain the antiinflam
variceal bleeding commones matory
have increased t cause drugs or
over the past accounting Mallory- Vascular
aspirin use Neoplasms
decade for 27% of Weiss tear abnr
accounting for cases.
8% of those
presenting with common in
acute upper GIB. the elderly.
Helicobacter
pylori infection is
less prevalent in
bleeding peptic
ulcers compared
to uncomplicated
peptic ulcers.


Peptic Ulcer
The endoscopic appearances of bleeding peptic ulcers can be categorized into:

• actively bleeding (Forrest I),
• ulcers that exhibit stigmata of recent bleeding (nonbleeding visible vessel defined as
protuberant discoloration (II a)
• an adherent clot (II b),
• flat pigmentations (II c)),
• Clean base ulcer (Forrest III)
Portal Hypertension

Esophagogastric varices
• Bleeding often severe and mortality from the first bleeding is
often high
• Overall prognosis dependent on the severity of liver disease
as indicated by the Child-Pugh grading.
• (+) features suggesting chronic liver disease
– e.g. alcohol use, ascites and jaundice  alert the possibility of a
variceal bleed.
• It calls for specific treatments of prophylactic broad spectrum
antibiotics and vascoactive drugs.
– Emergency endoscopic treatment is often associated with transient
bacteremia

• (+) prophylactic AB << incidence of sepsis: bacterial
peritonitis; shown to improve survival
• Early administration of a vasoactive drug: vasopressin or
its analog or somatostatin or its analogs << portal venous
BF & variceal pressure  subsequent endoscopic
treatment easier.
– continued 2–5 days after endoscopic control to prevent
recurrent bleeding
• Massive bleeding, passage of a Sengstaken Blakemore
tube (with orotracheal protection of the airway) is
necessary.
– In up to 30% of cirrhotic patients presenting with UGIB, the
bleeding source is non-variceal.
– In those with massive bleeding and often obtunded mental
state from shock or encephalopathy, an orotracheal tube is
required prior to endoscopy.
• Band ligation is the endoscopic treatment of choice for
esophageal varices.
– When compared to endoscopic sclerotherapy, band ligation
is associated with less local complications such as
mediastinitis, esophageal strictures  faster eradication of
esophageal varices

• Gastric varices = continuity with esophageal varices or occur
in isolation.
• Isolated fundal varices are associated with high risk of
recurrent bleeding and death.
• In the control of acute bleeding from isolated fundal varices,
histoacryl glue injection appears to be the only effective
method.
• Many would consider a transjugular intrahepatic
portosystemic shunt (TIPS) or early shunt surgery as an
alternative, especially after initial control with glue injection.
• In those patients where endoscopic therapy fails, a
Sengstaken-Blakemore tube can tamponade bleeding in
about 90% of cases; however, following deflation of the
balloons, recurrent bleeding occurs in about 50% of cases.

Other causes
• Mallory-Weiss Tears (5-10% cases UGIB)
– Lacerations of the gastroesophageal junction
– History of heavy alcohol use or retching.
– < 10% have continued or recurrent bleeding.
– Fresh hematemesis that occurs after emesis is typical of a Mallory-Weiss tear.
– The condition is often self-limiting and carries an excellent prognosis.
• Gastric Neoplasms (1%)
• Erosive gastritis (<5%)
– Superficial process; unusual to cause severe bleeding; common results:
chronic blood loss
– Due to NSAIDs, alcohols, severe medical or surgical illnesses (Stress-related
mucosal disease)
• Erosive Esophagitis
– Due to chronic G-E reflux
– Rarely cause significant UGIB esp pts who are bed bound long-term
• Vascular anomalies (7%)
Found throughout the GIT & may be the source of chronic or acute
gastrointestinal bleeding.
Angioectasias (angiodysplasias) Telangiectasias
Most common • small, cherry red lesions caused by dilation
• 1-10 mm distorted, aberrant submucosal of venules that may be part of systemic
vessels caused by chronic, intermittent conditions (hereditary hemorrhagic
obstruction of submucosal veins. telangiectasia, CREST syndrome) or occur
sporadically.
• (+) bright red stellate appearance
• Occur throughout the gastrointestinal tract
(esp right colon)
The Dieulafoy lesion Gastric vascular ectasia (GAVE) or

• aberrant, large-caliber submucosal artery, “watermelon stomach”
most commonly in the proximal stomach • characterized by the presence of linear red
that causes recurrent, intermittent streaks radiating from the pylorus.
bleeding
• Treatment is often difficult. Thermal
ablative techniques appears to be the most
effective option, although repeated
sessions may be required
Prognosis
• Despite advances in medical management, the mortality rate of patients
suffering from upper gastrointestinal bleeding remains high and depends
on the underlying pathology.
• In patients with non-variceal bleeding, a mortality rate up to 15% has been
reported.
• A number of studies have identified independent predictors for mortality
and these include age, comorbidities, shock at presentation, in-hospital
bleeders and presence of rebleeding
• In acute variceal hemorrhage, the risk of mortality can be up to 50% and
the risk of mortality is strongly dependent on pre-existing liver function
and the severity of cirrhosis
• The recognition of these predictors may help select patients who are most
at risk and may benefit from intensive post-hemostasis care.

LGIB
• Acute lower gastrointestinal (LGI) bleeding, defined
as bleeding from a site distal to the duodenum
(most commonly the colon)

Diverticulosis
• Most common colonic cause for patients
hospitalized with severe hematochezia.
• It originates frequently (about 50%) from the
right half of the colon (at or proximal to the
splenic flexure).
• Actively bleeding colonic diverticula have
been treated with epinephrine injection,
multipolar probe coagulation (MPEC) and
metallic clips.

Internal Hemorrhoids
• The most common cause of colonic bleeding in ambulatory
outpatient adults.
• Most internal hemorrhoid bleeding is self-limited, and manifested
by bright red blood on the toilet tissue.
• Medical therapy = fiber supplementation, stool softeners, rectal
suppositories and sitz baths.
• 2nd most common cause of severe hematochezia in patients
hospitalized with presumed colonic hemorrhage
• Prior to assuming that severe hematochezia is from more proximal
lesions, the anal canal should always be examined by rigid slotted
anoscope. If that is not diagnostic, try turnaround in the rectum
with a flexible sigmoidoscope to identify internal hemorrhoids.
• rubberband ligation for emergency hemostasis of bleeding internal
hemorrhoids usually used
Focal ulcers or colitis
• Focal ulcers proximal to the sigmoid colon are
an uncommon cause of severe colonic
hemorrhage
• Bleeding colonic ulcers were caused by:
– recent polypectomy with ulceration, inflammatory
bowel disease (IBD), ischemic ulcers or infectious
colitis (such as pseudomembranous colitis or
cytomegalovirus – CMV – ulcers)

Rectal Ulcer
• may be a cause of severe lower GI
hemorrhage, especially in elderly or
debilitated patients with constipation, who
are often confined to bed.
• The ulcers may be either solitary or multiple,
and associated with fecal impaction, rectal
prolapse, ischemia or trauma

Colonic tumors
• Cancer or stromal tumors, occasionally
present with hematochezia and may occur
anywhere in the rectum or colon.
• Overt bleeding suggests that the lesion has
ulcerated into underlying vessels, usually an
artery.

Colonic angiodysplasia
• Bleeding colonic angiodysplasias most often occur in the right
colon and are usually multiple or diffuse
• may be associated with advanced age and medical
conditions such as chronic renal insufficiency, cirrhosis,
valvular heart disease, and collagen vascular disorders.
• Bleeding from angiodysplasia is usually mild to moderate and
is self-limited.
• Such bleeding is usually intermittent and usually presents
with slow GI bleeding and chronic iron deficiency anemia.
• The main risk of endoscopic coagulation of angiodysplasia is
severe, delayed bleeding and post-coagulation syndrome

Capsule endoscopy: record
images of the digestive tract
for use in medicine. The
capsule is the size and shape
of a pill and contains a tiny
camera. After a patient
swallows the capsule, it takes
pictures of the inside of the
gastrointestinal tract.
Scintigraphy: A diagnostic test
in which a two-dimensional
picture of a body radiation
source is obtained through the
use of radioisotopes

Emergency surgery
• Considered for patients with:
1. Hypotension or shock, despite resuscitative
efforts;
2. Continued bleeding with transfusion of six or
more units of blood and no diagnosis by
emergency endoscopy (push enteroscopy,
colonoscopy, and anoscopy);
3. Severe active bleeding cannot be controlled
by colonoscopy or angiography.

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Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Harrison’s Principle of Internal Medicine, 19th edition

– ACE, angiotensin-converting enzyme; BP, blood pressure; MI,

– (Modified from Guidelines 2000 for Cardiopulmonary Resuscitation

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Essentials of Pathophysiology: Concepts of Altered Health States, 2011

Generalized diffuse pain

• experienced is dependent on a number

• Colicky abdominal pain results usually

• Pain from peritonitis worsens with movement, deep

Recurrent episodes of abdominal pain:

• This suggests chronic recurrent conditions, e.g. peptic

• Prompt resuscitation • Pain relief should be • Antibiotics are

Endogenous gut flora cause abdominal

In all intra-abdominal non-gynecologic

An exception to this generalization is the

Tintinalli Emergency Medicine. 8th edition

liquefactive deeper penetration

reducing the incidence

By the 3rd week: Lower esophageal

increased frequency further aggravates

• Chronic = stricture formation, gastric outlet obstruction and malignant

• Ssx (+) in 48 hrs = truly

(Crash course) Megan Griffiths_ Rusheng Chew-Gastrointestinal system-Elsevier, Mosby

Textbook of Clinical Gastroenterology and Hepatology (2nd Edition)

Herniated viscera impaired

total occlusion of further increase

Nelson textbook of pediatrics (2011)

Hematochezia, passage of bright red or maroon

obscure GIB if the

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition

CURRENT Medical Diagnosis & Treatment 2017

• Patients with active bleeding • All other patients are admitted to

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition

Variceal Non-variceal bleeding.

CURRENT Medical Diagnosis & Treatment 2017

Textbook of Clinical Gastroenterology and Hepatology, 2nd edition