GROUP 10

 Tutor : dr. Zita Atzmardina

 Anggota :
1. Alexander Kevin (405120108)
2. Olga Adhitya (405120112)
3. Desika Santi (405120216) (secretary)
4. Gilda (405130035)
5. Nicole Nastassja K. (405130043)
6. Ryan Juliansyah (405130048) (leader)
7. Dicky Chandra (405130122)
8. Kartika Sutanto (405130146) (writer)
9. Dwi Ariane Caesaria (405130148)
10. Vannesa Lam (405130152)
11. Vikas Indru M. (405130189)
12. Ahmad Fathul Adzmi (405130213)
 FOURTH PROBLEM
MY STOMACH BURN
Male, 46 years old, was brought to emergency department by his family for feeling exhausted
and very drowsy since 6 hours before. The patient has been defecating black watery stools
since 3 days ago, several times a day, and has vomited around 2 glasses(@200ml) of
blackish blood since than. The patient vomited every time he eats or drinks and he has been
feeling shivery. For the past one year, the patient had been taking jamu and painkiller (
sodium diclofenac) form a local store to treat his right leg’s pain. The patient worked as a
bartender and had a habit of drinking alcohol since 20 years ago. There is also a history of
liver malignancy on his father part of family .
On initial examination, he appears to be apathetic, with his blood pressure of 80 per
palpation, heart rate of 120 beats per minute with weak palpation, respiratory rate of 20
breaths per minute , temperature of 38ºC, and oxygen saturation of 97 %. His conjunctivae
are pale, his sclera are not icteric in color, his jugular venous pressure is 5 - 1cm H2O and
there aren’t any paresis on his cranial nerve examination. His lung examination is within
normal limits, the first and second heart sounds are normal, without any gallop, but systolic
murmurs is heard. His abdomen is a bit bloated, with an enlarged spleen (schufner 1 ). His
palmar are erythematous. On his right foot’s first metatarsophalangeal joint is seen an
erythematous tophus. On his intial laboratory examination, his hemoglobin is 5.6 g’/dl,
hematocrit is 16.8 %, leukocyte is 17.000/ μL, thrombocyte is 142.000/ μL, MCV of 84 fl,
MCH of 38 pg/cell,non- reactive Hbsag, and reactive anti – HBs.
The attending ED physician started blood transfusion as an initial treatment for
this patient. After the third pack, the patient’s fever became worse, 40. he also
feels suffocated. His respiratory rate was increased to 25 breaths perminuts,
oxygen saturation to 88 % ,JVP to 5 + 0 cm H2O, and there are soft crackles in
the base of both of his lungs. His blood gas analysis results are : PH 7.32, pCo
28.8 mmHg,pO2 68 mmHg, HCO3 16 mmol/l, and sat 89%.
Discuss this case, assess the patient, and plan the proper treatment for this
patient while considering every possibilties!
 …
LEARNING OBJECTIVES ??
!!!
1. Identify Gastrointestinal Bleeding
2. Identify Electrolyte Disorders and Acid-
Base Disorders
MATERI
3. Identify Blood transfusion reaction
4. Identify pulmonary edema
5. Identify anemia Disorders
6. Identify pathophysiology according to
the problem
LO 1
IDENTIFY GASTROINTESTINAL BLEEDING
IDENTIFIKASI UPPER GI BLEEDING
 Hematemesis is vomitus of red blood or “coffee-grounds” material.
 Melena is black, tarry, foul-smelling stool.
 Hematochezia is the passage of bright red or maroon blood from the rectum.
 Finally, patients may present only with symptoms of blood loss or anemia such
as lightheadedness, syncope, angina, or dyspnea.

Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL, Loscalzo J, editors. Harrison’s principle of internal medicine. 18th ed. New York: McGraw-Hill 2011.
GASTROINTESTINAL
BLEEDING

Rosen’s Emergency Medicine. Concept and clinical practice. 8th Ed.

John A. M, MD, dkk. Rosen’s Emergency Medicine Concepts and Clinical Practice. 8th Edition. Volume 1. Philadelphia: Mosby Elsevier;
2012.
 PEPTIC ULCER

 Painful sores or ulcers in the lining of the stomach or the duodenum.

 An ulcer is the end result of an imbalance between digestive fluids in the stomach
and duodenum.
 Most ulcers are caused by an infection with a type of bacteria called Helicobacter
pylori
 Risk factors:
 Use of NSAIDs
 Excess acid production from gastrinomas, tumors of the acid producing cells of the stomach that
increases acid output (seen in Zollinger-Ellison syndrome)
 Excessive drinking of alcohol
 Smoking or chewing tobacco
 Serious illness
 Radiation treatment to the area

https://www.nlm.nih.gov/medlineplus/ency/article/000206.htm
http://www.webmd.com/digestive-disorders/digestive-diseases-peptic-ulcer-disease?page=2
 SIGN AND SYMPTOMS
 An ulcer may or may not have symptoms.
When symptoms occur, they may include:  “alarm” symptoms could be signs of a
 A gnawing or burning pain in the middle or serious problem
upper stomach between meals or at night  bleeding—when acid or the peptic ulcer
 Bloating breaks a blood vessel
 Heartburn  perforation—when the peptic ulcer burrows
 Nausea completely through the stomach or
duodenal wall
 Emergency Symptoms
 obstruction—when the peptic ulcer blocks
 sharp, sudden, persistent, and severe
the path of food trying to leave the stomach
stomach pain
 bloody or black stools
 bloody vomit or vomit that looks like coffee
grounds
 Diagnose :
 Anamnese : history of NSAID drug user, smokers, alcoholic, family
history of peptic ulcer
Gastric ulcer Duodenal ulcer
Pain occurs after eating Pain occurs while hungry
and relieve with food or
drink (Hunger pain food
relief)
Pain in the left side of Pain in the right side of
midline of the body midline of the body

 Physical exam :
 To find out the complications (such as peritonitis, retention of liquid in gaster,
bleeding)
 Investigation :
 Laboratory
 Barium meal contrast radiograft
 EGD
 Tests for H. pylori (rapid test urease, urea breath test, fecal antigen testing,
serology test)
TREATMENT
 PERFORATION
 Gastrointestinal perforation is a hole
that develops through the wall of the
esophagus, stomach, small
intestine, large bowel, rectum, or
gallbladder.
 Sign and Symptoms
 Nausea
 vomiting
 Etiology
 Penetrating injury to the lower chest
or abdomen (eg, knife injuries)
 Blunt abdominal trauma to the
stomach
 Ingestion of aspirin, nonsteroidal anti-
inflammatory drugs (NSAIDs), and
steroids

 anorexia
 Presence of a predisposing condition
 Bowel sounds are quiet to
 Bowel injuries associated with
absent endoscopy
 Endoscopic biliary stent
 severe stomach pain
 Intestinal puncture as a complication
 Chills
of laparoscopy
 fever
 Bacterial infections
 Inflammatory bowel disease
TREATMENT
 The mainstay of treatment for intestinal perforation is surgery. Emergency
medical care includes the following steps:
 Establish intravenous access, and initiate crystalloid therapy in patients with clinical
signs of dehydration or septicemia.
 Do not give anything by mouth.
 Start intravenous administration of antibiotics to patients with signs of septicemia.
 For a perforated duodenal ulcer,may include:
 a highly selective vagotomy, a truncal vagotomy and pyloroplasty, or vagotomy and
antrectomy.
 For a perforated gastric ulcerdepends on the patient's condition:
 If the patient is moribund, the ulcer is best excised by grasping it with multiple Allis
clamps and using a GIA-60 linear stapler. Or,can be excised with electrocautery
 In a stable patient, the ulcer is excised and sent for frozen section analysis to exclude
malignancy
ESOPHAGEAL VARICES
 Approximately 5–15% of cirrhotics per
year
 Grade 1 – Small, straight
Several factors predict the risk of bleeding: esophageal varices
 including the severity of cirrhosis  Grade 2 – Enlarged, tortuous
(Child’s class, MELD score); esophageal varices
 the height of wedged-hepatic vein
pressure
occupying less than one third
 the size of the varix
of the lumen
 the location of the varix  Grade 3 – Large, coil-shaped
 certain endoscopic stigmata esophageal varices
 red wale signs
occupying more than one
 hematocystic spots, diffuse erythema,
bluish color, cherry red spots, white-
third of the lumen
nipple spots
 Patients with tense ascites
DIAGNOSIS

 endoscopy.
 Abdominal imaging

 computed tomography (CT) or MRI

 interventional radiologic
 normal wedged-to-free gradient is 5 mmHg
(patients with a gradient >12 mmHg are at risk
for variceal hemorrhage).
divided into two main categories:
 (1) primary prophylaxis
 (2) prevention of rebleeding once there has been an
initial variceal hemorrhage.

Primary:
 routine screening by endoscopy of all patients with
cirrhosis.
 nonselective beta blockade
 variceal band ligation.
 Endoscopic variceal ligation (EVL)
PREVENTION OF RECURRENT BLEEDING

 repeated variceal band ligation until varices are

obliterated
 Beta blockade

 Nonselective beta blockade  prevent further

bleeding from portal hypertensive gastropathy
once varices have been obliterated.
 TIPS  less common
ACUTE BLEEDING TREATMENT
 repeated variceal band ligation until varices are obliterated.
 fluid and blood-product replacement
 vasoconstricting agents (somatostatin or octreotide 50–100 μg/h by
continuous infusion)
 Balloon tamponade (Sengstaken-Blakemore tube or Minnesota tube) 
patients who cannot get endoscopic therapy immediately or who need
stabilization prior to endoscopic therapy.
 Endoscopic intervention  first-line
 variceal injection therapy (sclerotherapy) as initial therapy  bleeding is
vigorous.
 Variceal band ligation (should be repeated until obliteration of all varices is
accomplished)
 transjugular intrahepatic portosystemic shunt (TIPS)  bleeding continues
from gastric varices
 Surgical esophageal transsection (rare and poor outcome)
STRESS ULCER / STRESS INDUCED GASTRITIS

 Mucosal erosions and superficial hemorrhages in patients who

are critically ill or in those who are under extreme physiologic
stress, resulting in minimal-to-severe gastrointestinal (GI) blood
loss
 Etiology: massive burn injury, head injury associated with
raised intracranial pressure, sepsis and positive blood culture
results, severe trauma and multiple system organ failure
Diagnosis :
 treatment:
 Coffee ground vomitus
 Sucralfate: Primary agent for
 Melena prophylaxis
 Histamine 2 (H2) receptor blockers (eg,
 Hematemesis (in
ranitidine, famotidine, cimetidine,
extreme cases) nizatidine)
 Orthostasis (unusual)  PPI (eg, esomeprazole, pantoprazole)
 Hematocrit

 Coagulation profile

 Nasogastric tube and

lavage
 Endoscopy
 GASTRIC CANCER
 Uncontrolled proliferation of the cells in the stomach
 Classification:
 Intestinal
 Diet
 Smoking
 Helicobacter pylori infection
 Previous gastric surgery
 Pernicious anemia
 Adenomatous polyps
 Chronic atrophic gastritis
 Radiation exposure

 Diffuse

http://emedicine.medscape.com/article/278744-clinical
 Signs and Symptoms  PE:
 Indigestion  palpable enlarged stomach
 Nausea or vomiting with succussion splash
 Dysphagia  Hepatomegaly
 Postprandial fullness  periumbilical metastasis
 Loss of appetite (Sister Mary Joseph nodule)
 Melena or pallor from  enlarged lymph nodes
anemia  Examination:
 Hematemesis  Endoscopy
 Weight loss  Histology
 Biopsy
 Cancer Antigen
 Complication
 Pathologic peritoneal and
pleural effusions
 Obstruction of the gastric
outlet, gastroesophageal
junction, or small bowel
 Bleeding in the stomach
from esophageal varices or
at the anastomosis after
surgery
 Intrahepatic jaundice
caused by hepatomegaly
 Extrahepatic jaundice
 Inanition from starvation or
cachexia of tumor origin
 Prevention
 Increased consumption of
fresh fruits and vegetables
(vit C)
 Decreased intake of salt
 Decreased contamination of
food by carcinogenic
compounds arising from the
decay of unrefrigerated meat
products
GASTROINTESTINAL BLEEDING

Rosen’s Emergency Medicine. Concept and clinical practice. 8th Ed.

LO 2
IDENTIFY ELECTROLYTE DISORDERS AND
ACID-BASE DISORDERS
 HIPONATREMIA

 Defined as Na plasma level <135

mEq/L, severe hiponatremia when
the concentration of plasma Na
<120 mEq/L
 Acute hiponatremia: last for <48
hours, there are a severe
symptoms such as seizure and LOC
 Chronic hiponatremia: last for >48
hours, there are a mild symptoms
such as fatigue
Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al., editors. Harrison’s principle of internal medicine. 18th
ed. USA: The McGraw-Hill Medical; 2012.
Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis & treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
ACID-BASE DISORDERS
 normally between 7.36 and 7.44.
 Serum pH is determined by the relative concentrations of bicarbonate
(HCO3 −) and carbon dioxide (Paco2)
 Acidosis that lowers HCO3 − or raises Paco2 (acidemia, pH is below 7.36)
 alkalosis  raises HCO3 − or lowers Paco2 (alkalemia, serum pH is above
7.44)
 Bicarbonate concentration  kidneys
 Paco2  lung ventilation.
 Uncommonly, the acid-base disorder is severe enough  acidemia or
alkalemia itself is dangerous;
 serum pH below 6.7 or higher than 7.6  unsustainable  cause cardiac
hypocontractility and irritability, seizures, cerebral edema, and a variety of
metabolic disturbances.
RESPIRATORY ACIDOSIS

 hypoventilation 
inappropriately
elevated Paco2 and
resulting acidemia.
RESPIRATORY ALKALOSIS
 increased minute ventilation  decreased Paco2 and
subsequent increase in serum pH.
 associated with hysterical hyperventilation;
 respiratory alkalosis  classically complain of lip and
extremity paresthesias and may also experience muscle
cramps and lightheadedness or even syncope ( as well
as hypocalcemia  carpopedal spasm)
 Response  cellular secretion of H+ in exchange for K+;
 if respiratory alkalosis persists, the kidneys excrete
bicarbonate and retain chloride compensatory
metabolic acidosis with reduced serum HCO3 −,
hypokalemia, and hyperchloremia.
management  hypocapnia symptoms can be relieved in patients with psychological
hyperventilation by reassurance.
The technique of using a paper bag  rebreathing
METABOLIC
ACIDOSIS
 defined by a reduced serum
bicarbonate concentration.
 Etiology: acids are added
(either by intrinsic processes
or from exogenous sources),
acid excretion is impaired, or
there is inappropriate loss of
alkali.
 Divided: normal anion gap
and elevated anion gap
 The causes of elevated anion
gap  remembered by the
mnemonic MUDPILES
DIABETIC KETOACIDOSIS.
 defined by hyperglycemia, ketonemia, and acidemia.
 type 1 insulin-dependent diabetics or type 2 non–insulin-dependent
diabetics.
 Manifestation: progressive polyuria, polydipsia, and malaise, but
diabetic ketoacidosis may be manifested atypically with chief
complaints of vomiting, abdominal pain, or altered mental status.

Management:
 identification of the precipitant is a management priority.
 intravenous fluids
 insulin therapy
 careful attention to and replacement of electrolytes, particularly
potassium.
ALCOHOLIC KETOACIDOSIS
 elevated anion gap metabolic acidosis (mistaken for the more common
diabetic ketoacidosis)
 long-standing ethanol user abruptly stops drinking; malnutrition and
dehydration.
 may demonstrate a high anion gap, but a mixed acid-base disorder can be
due to concomitant ethanol withdrawal, which may cause a respiratory
alkalosis, and vomiting  metabolic alkalosis.
 symptoms of vomiting, abdominal pain, dehydration, altered mental status,
prostration, and lethargy; however, alcoholic ketoacidosis patients generally
do not demonstrate hyperglycemia or glycosuria.

 Urine dipsticks detect acetoacetate but not β-hydroxybutyrate;

 The treatment is dextrosecontaining fluids; insulin is contraindicated

RENAL FAILURE

 Any condition that reduces glomerular filtration

rate  unmeasured anions such as sulfate,
phosphate, urate, and hippurate  elevated
anion gap metabolic acidosis.

Management:
 sodium bicarbonate (bridge to renal
replacement therapy when uremia-associated
metabolic acidosis is severe).
IRON
 cause of metabolic acidosis
 prominent vomiting and other gastrointestinal symptoms
from gastric irritation, followed by systemic toxicity that
includes myocardial depression, liver injury, and lactic
acidosis from cellular mitochondrial poisoning.

 A plain radiograph of the abdomen  evidence of an

iron ingestion while serum iron concentration is
determined.
 Treatment  fluid resuscitation, gastrointestinal
decontamination, and chelation with deferoxamine.
 NORMAL ANION GAP METABOLIC ACIDOSIS

 less likely to be
immediately
dangerous or caused
by an imminently
dangerous condition
 caused by gastric loss
of bicarbonate in the
setting of diarrhea.
PHYSIOLOGIC COMPENSATION
 the extracellular bicarbonate–carbonic acid system and
intracellular protein buffers.
 Medullary chemoreceptors augment alveolar ventilation to blow
off carbon dioxide correcting serum pH.
 In severe metabolic acidosis (pH < 7.1), hyperventilation
Kussmaul’s respirations
 In cases of prolonged metabolic acidosis  the kidney
generates a compensatory aciduria by secreting H+ and
retaining HCO3 −.
MANAGEMENT

Theoretic harms of using intravenous sodium bicarbonate to correct

acidemia include the following:
• Paradoxical CNS acidosis.
• Hypokalemia (which can cause respiratory muscle weakness, impairing
respiratory compensation), hypocalcemia, hypernatremia
• Volume overload
• Hyperosmolality
• Overshoot alkalosis Many authors question the utility of bicarbonate
therapy even in cases of severe acidemia, given these potential harms and
the absence of demonstrated benefit.
METABOLIC ALKALOSIS
 the loss of H+ or
retention of HCO3 −
 consequence of
prolonged vomiting
or nasogastric
suction or as a
compensation for
chronic respiratory
acidosis.
MIXED DISORDERS
 A simple acid-base disorder is a combination of a
primary disturbance and subsequent
compensation.
 occur when two or more primary acid-base lesions
coincide.
 These simultaneous conditions may push the
serum pH in the same or opposite directions, and
each will generate its own compensatory
responses
 mixed disorders may therefore be difficult to
recognize by either clinical or laboratory features.
KOMPENSASI ASIDOSIS RESPIRATORIK

http://www.austincc.edu/apreview/EmphasisItems/Electrolytefluidbalance.html
KOMPENSASI ALKALOSIS RESPIRATORIK

http://www.austincc.edu/apreview/EmphasisItems/Electrolytefluidbalance.html
KOMPENSASI ASIDOSIS METABOLIK

http://www.austincc.edu/apreview/EmphasisItems/Electrolytefluidbalance.html
KOMPENSASI ALKALOSIS METABOLIK

http://www.austincc.edu/apreview/EmphasisItems/Electrolytefluidbalance.html
LO 3
IDENTIFY BLOOD TRANSFUSION REACTION
BLOOD TRANSFUSION
Blood Banking
 Blood collection bags contain anticoagulant preservative of citrate,
phosphate, dextrose, and adenine (CPDA-1), ensuring a shelf life of 35 days
and hematocrit of 70 to 80% for PRBCs.
 Addition of solutions for nutrients (Adsol, Nutricel, Optisol) extend maximum
storage to 42 days and lowering viscosity making infusion easier
 Storage can impair red cell function
 Blood is kept at temp of 1-6 °C (cell metabolism continues)
 Decrease in pH and level of 2,3-diphosphoglycerate, cell becomes more
spherical and rigid, increasing resistance to capillary flow. [these changes are
reversed few minutes after infusion]
 Potassium cell leakage
Immune-Mediated Adverse Effect
Acute
Intravascular Hemolytic Transfusion Reaction
• Result from ABO incompatibility  intravascular destruction of transfused red cells 
hemoglobinemia and hemoglobinuria
• Onset is immediate
• Symptoms: fever, chills, headache, nausea, vomiting, sensation of chest restriction, joint or lower
back pain, burning sensation at the site of infusion
• Treatment: stop transfusion immediately, initiate vigorous crystalloid therapy

Febrile Transfusion
• 1oC or greater temperature elevation
• Result from the reaction of antileukocyte antibodies
• Treatment: symptomatic w/ analgesics, antipyretics, antihistamine

Allergic Reactions (urticaria to anaphylaxis)

• Urticaria or hives
• Attributed to an allergic, antibody-mediated response to a donor’s plasma proteins
• Treatment: antihistamine

Transfusion-Related Acute Lung Injury

• Might result from a reaction between transfused antibodies and leukocytes in the recipient, as well as
effects of biologically active factor that accumulate in store blood
• Occur within 6 hours after a transfusion
• Clinical Findings: noncardiogenic pulmonary edema, dyspnea, hypoxemia, bilateral infiltrates on chest
radiograph
• Treatment: stop transfusion, notify blood bank, provide respiratory support
Immune-Mediated Adverse Effects
Delay
Extravascular Hemolytic Transfusion Reaction
• Caused by an anamnestic response in patient previously sensitized to red cell
antigens by transfusion, pregnancy or transplant
• Repeat exposure from transfusion  antibody level rise  extravascular
hemolysis
• Patient may have fever, anemia, and jaundice
Transfusion-Associated Graft-versus-Host Disease
• Transfused lymphocytes proliferate and attack the recipient
• Mortality > 90% , rare
• Symptoms: fever, erythematous rash, diarrhea,  liver enzymes,
pancytopenia
• Treatment: bone marrow transplant
• Prevention gamma irradiation of all cellular components
Non-Immune-Mediated Adverse Effects
Acute
Circulatory Overload
• Chronically anemic, normovolemic elderly patients are at greatest risk for
developing CHF with rapid infusion of blood
• Prevention: slow transfusion and administering diuretics
Bacterial Contamination
• Most commonly w/ Yersinia enterocolitica
• During and after transfusion, patient may develop rigors, vomiting, abdomen
cramps, fever, shock, renal failure, DIC
• Management: stop transfusion, obtain blood culture, initiate broad-spectrum
Antibiotics and hemodynamic support
Chronic
Risk of Transfusion –Transmitted Viruses
• Hepatitis C, HIV infection, Hepatitis B, CMV
MANAGEMENT
 Whole blood: rarely used
 Packed Red Blood Cells: Helps with Oxygen delivery at micro
vascular level  improve intracellular oxygen consumption
 FOCUS trial: Hb ≤ 8g/dL
 American Society of Anesthesiologists: Hb ≤ 6g/dL – transfusion, 6-10
careful monitoring
 Eastern Association for the Surgery of Trauma and the American College
of Critical Care Medicine : Hb ≤ 7g/dL
 Most physicians will transfuse: if ongoing severe hemorrhage & unstable
vital signs, occasionally with hold transfusion even when Hb is less than
6 in young, healthy, asymptomatic patient at low risk for further
bleeding.
 Artificial oxygen carriers : still being developed
LO 4
IDENTIFY PULMONARY EDEMA
PULMONARY EDEMA
 a condition caused by
excess fluid in the lungs.
This fluid collects in the
numerous air sacs in the
lungs, making it difficult
to breathe.
 Class/: cardiogenic or
non-cardiogenic
 Cardiogenic : heart failure /
congestive heart failure.
 Non : pneumonia, ARDS,
trauma, drugs intoxication,
or kidney failure.
 Sign n symptoms :
 Shortness of breath
 Dyspnea that worsens when
lying down
 Coughing up blood
 Proxysmal nocturnal
dyspnea
 Chest pain (cardiogenic)
 Wheezing
 Swelling in lower extremities
 Fatigue
 Sweating
 Anxiety or restlessness
 Xray cardiogenic:
 enlarged cardiac silhouette, pleural effusions
 X-ray: peribronchial thickening, prominent vascular markings in
the upper lung zones and Kerley B lines  patchy alveolar filling/
perihilar alveolar infiltrate diffuse
 Xray noncardiogenic:
 Pulmonary edema, heart size is normal, no pleural effusions
 Hyaline membranes in the alveoli, diffuse alveolar infiltrates and
inflammation  pulmonary fibrosis
 Hypoxemia of cardiogenic: V/Q mismatch and responds to
the administration of supplemental oxygen
 Hypoxemia of noncardiogenic: intrapulmonary shunting and
persists despite high concentrations of inhaled O2
Radiograph shows acute pulmonary edema in a patient known to have ischemic cardiomyopathy. Findings are
Kerley B lines (1mm thick and 1cm long) in the lower lobes and Kerley A lines in the upper lobes.

http://emedicine.medscape.com/article/360932-overview
 Treatment:
 MI protocols and coronary artery reperfusion therapy
 Oxygenation and Ventilation  Positive-Pressure
Ventilation (mask/ETT)
 Loop diuretics: furosemide, bumetanide, and
torsemide (reduce preload)
 furosemide should be ≤0.5 mg/kg  renal patient/chronic
diuretic use/hypervolemia: 1 mg/kg
 Nitrates Nitroglycerin and isosorbide dinitrate:
venodilators & vasodilate coronary
 Sublingual nitroglycerin (0.4 mg × 3 every 5 min)
 IV nitroglycerin (5–10 μg/min)
 IV nitroprusside (0.1–5 μg/kg per min)
 Morphine: 2-4mg IV boluses
 Angiotensin-Converting Enzyme (ACE) Inhibitors
 Other Preload-Reducing Agents IV: recombinant brain
natriuretic peptide (nesiritide)
 Physical Methods: (Reduction of venous return) without
hypotension: sitting position with the legs dangling along the
side of the bed
 Inotropic and Inodilator Drugs: dopamine and dobutamine,
milrinone(inodilator) (50 μg/kg followed by 0.25–0.75 μg/kg
per min)
 Digitalis Glycosides
 Intraaortic Counterpulsation IABP
LO 5
IDENTIFY ANEMIA DISORDERS
 ANEMIA
 Anemia is an absolute decrease
in the number of circulating Common Sites of Blood Loss
RBCs
Trauma
 In emergency medicine, anemia
is divided into 2 broad categories Plural, Peritoneal, Pelvic, and
Retroperitoneal spaces
 Emergent, having immediate life-
threatening complications Non traumatic
 Nonemergent, with less imminent
danger to the patient Patients receiving anticoagulants, the
Gastrointestinal tract, retroperitoneal
space, uterus, and adnexa

Other: Hemolytic conditions

ANCILLARY EVALUATION
 Complete blood count with leukocyte differential
 Reticulocyte count
 Peripheral smear
 RBC indices
 Mean corpuscular volume (MCV) mean corpuscular hemoglobin (MCH), and mean
corpuscular hemoglobin concentration (MCHC).
DIAGNOSTIC FINDINGS IN EMERGENT ANEMIA

Clinical Features Ancillary evaluation

 Blood loss  IV lines are placed to assess
  BP, postural
hypotension,
lightheadedness, HR,
RR
 Complaints of thirst,
altered mental status, 
urine output
 Patient’s age, concomitant
illness, and underlying
hematologic, cerebral, and
cardiovascular status also
influence the clinical
findings
initial laboratory tests:
 CBC and peripheral smear
 Blood sample for type and
crossmatch
 Prothrombin time
 PTT
 Glucose level
 Creatinine level
 Urinalysis for free hemoglobin
 Clotting and unclotted blood
samples for later testing
DIAGNOSTIC FINDINGS IN NONEMERGENT
ANEMIA
Clinical Features Ancillary evaluation
 Usually seen in  CBC with leukocyte
ambulatory patients differential
complaining of fatigue  Reticulocyte count
and weakness  Peripheral smear
 Irritability, headache,
 RBC indices including
postural dizziness, MCV, MCH, MCHC
angina, exercise
tolerance, shortness of
breath
MANAGEMENT
1. Type and crossmatch blood in patients with anemia and ongoing blood
loss so that it’s available for transfusion
2. Consider immediate transfusion of packed RBCs in symptomatic patients
who are hemodynamically unstable and have evidence of tissue hypoxia
3. Admit patients with anemia and ongoing blood loss for further evaluation
and treatment. Admit patients with chronic anemia or newly diagnosed
anemia with unclear etiology if they are hemodynamically unstable,
hypoxic, acidotic, or demonstrate cardiac ischemia.
4. Consider hematology consultation to assist in evaluation of those patients
with anemia of unclear etiology, anemic patients with concomitant
abnormalities of platelets and white blood cell counts, and patients with
suspected bleeding disorders.

 Excerpt From: David M. Cline. “Tintinalli's Emergency Medicine Manual.”

iBooks.
LO 6
IDENTIFY PATHOPHYSIOLOGY ACCORDING TO
THE PROBLEM
CONCLUSION
 The patient has been defecating black watery stools and vomited around 2
glasses(@200ml) of blackish blood patient Gastrointestinal Bleeding
suspect Esophageal Varices, Peptic Ulcers
 hemoglobin is 5.6 g’/dl, MCV of 84 fl, MCH of 38 pg/cell  anemia
 The patient’s fever became worse, 40 , respiratory rate was increased to 25 breaths
perminuts, oxygen saturation to 88 % ,JVP to 5 + 0 cm H2O, and there are soft
crackles in the base of both of his lungs because Blood transfusion reaction
 His blood gas analysis results are : suspect partially compensated metabolic acidosis
 PH 7.32  acidosis
 pCo 28.8 mmHg 
 pO2 68 mmHg
 HCO3 16 mmol/l, and 
SUGGESTION

 Volume replacement
 endoscopy is the criterion standard in
diagnosing and therapy
 Need imaging modalities such as CT scanning,
MRI, and Barium are also performed for a more
complete evaluation.
REFERENCES
 Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al.,
editors. Harrison’s principle of internal medicine. 18th ed. USA: The
McGraw-Hill Medical; 2012.
 Papadakis MA, McPhee SJ, Rabow MW. Current medical diagnosis &
treatment. 54th ed. New York: Mc-Graw Hill Education; 2014.
 Rosen’s Emergency Medicine, 8th Ed.