CASE

STUDIES ON
MAJOR
CONCEPTS
EMERGENCY AND TRAUMA
 PEPTIC ULCER
By: ALCE
Case Scenario – S.K., a 51-year-old roofer, was admitted to the hospital 3 days ago after falling 15 feet from a
roof. He sustained bilateral fractured wrists and an open fracture of the left tibia and fibula. He was taken to
surgery for open reduction internal fixation (ORIF) of all of his fractures. He is recovering in your orthopedic unit.
You have instructions to begin getting him out of bed and into the chair today. When you enter the room to get
S.K. into the chair, you notice that he is agitated and dyspneic. He says to you, “My chest hurts really badly. I
can't breathe.”
You auscultate S.K.'s breath sounds. You find that they are diminished in the left lower lobe (LLL). S.K. is
diaphoretic and tachypneic and has circumoral cyanosis. His apical pulse is irregular and 110 beats/min.
The physician orders the following: arterial blood gases (ABGs), chest x-ray (CXR), ECG, and a helical (spiral)
CT of the lungs.
ABGs pH 7.49 PaCO2 30.6 mm Hg PaO2 52 mm Hg HCO3 24.2 mmol/L SaO2 83% A-a oxygen gradient 32
mm Hg
Pathophysiology

The mechanism of occurrence of PUD results from an imbalance between gastric mucosal protective and destructive
factors. Risk factors predisposing to the development of PUD:
- H. pylori infection
- NSAID use
- First-degree relative with PUD
- Emigrant from a developed nation
- African American/Hispanic ethnicity
With peptic ulcers, there is usually a defect in the mucosa that extends to the muscularis mucosa. Once the protective
superficial mucosal layer is damaged, the inner layers are susceptible to acidity. Further, the ability of the mucosal cells to
secrete bicarbonate is compromised.
H. pylori is known to colonize the gastric mucosa and causes inflammation. The H. pylori also impairs the secretion of
bicarbonate, promoting the development of acidity and gastric metaplasia.
Concept Map

Risk
Risk Factors
Factors

••Smoking
Smoking
••Drink
Drink alcohol
alcohol
••Untreated
Untreated stress
stress
••Spicy
Spicy foods
foods

Signs
Signs and
and Symptoms
Symptoms

Types:
Types: ••Burning
Burning stomach
stomach painpain
Gastric
Gastric ••Feeling
Feeling of
of fullness,
fullness, bloating
bloating or
or
belching
belching
Duodenal
Duodenal ••Intolerance
Intolerance toto fatty
fatty foods
foods
••Heartburn
Heartburn
••Nausea
Nausea

Peptic
Ulcer
 BEE STING
By: ADUNA
A 12-year-old boy is brought to the emergency department with a chief complain of localized pain, swelling and starting to feel like he’s short out of
breath after being stung by a bee.
Chief complain: localized pain, swelling and shortness of breath
Past: His father has hypertension while his mother has diabetes. Client is a student and he plays with their dogs on their yard after school. He
takes multivitamins everyday and does not have any serious illness.
Present: He had been well until he was stung on his right forearm while playing in the yard. He initially complained of localized pain and swelling.
Fifteen minutes later, he began to complain of shortness of breath. His parents observed him to be wheezing. He also said that he felt very weak
and dizzy. His parents brought him immediately to the local emergency department.
Lab: VS T 37.1, P 120, R 39, BP 69/45. He is in mild respiratory distress. He is drowsy and pale, but awakens when you talk to him. He has
generalized urticaria. He has no conjunctival edema. His lips and tongue are not swollen. His voice sounds normal. Heart tachycardic without
murmurs. His lung examination shows mild wheezing and fair aeration with minimal retractions. His abdomen is soft and non-tender. His face is
moderately pale. The bee sting site on his right forearm is unremarkable with no foreign body seen.
Pathophysiology

Antigen exposure attacks B cell. Then there will be a release of IgE antibody. IgE antibody binds to
surface of mast cells and basophils. Calcium influx into mast cells and basophils. There will be
release of chemical mediators like histamine and this can have effects to the lungs, heart and skin
therefore leading to anaphylaxis. (Reference: Incidence of anaphylaxis in the emergency department
of general hospital in Milan, Pastorello EA, Rivolta F, Bianchi M. 2001).
Concept Map
 POST PARTUM HEMORRHAGE
By: BAYAUA

Case Scenario: A 29-year-old female (G1P1) is readmitted two weeks post–vaginal delivery due to increased vaginal bleeding. She
reports that the bleeding began on the tenth day after delivery and has increased in severity each subsequent day. The delivery
was uncomplicated with minimal blood loss and the patient did not receive any epidural anesthesia. She has taken 200 mg of
ibuprofen daily since delivery. The patient reports a medical history of iron deficient anemia due to menorrhagia.
History Of Present Illness: She reports that the bleeding began on the tenth day after delivery and has increased in severity each
subsequent day. The delivery was uncomplicated with minimal blood loss and the patient did not receive any epidural anesthesia.
She has taken 200 mg of ibuprofen daily since delivery. The patient reports a medical history of iron deficient anemia due to
menorrhagia.
Family History: She is adopted and does not know her family history.
Pathophysiology

Uterine atony, or diminished myometrial contractility, accounts for

80% of postpartum hemorrhage. The other major causes include
abnormal placental attachment or retained placental tissue,
laceration of tissues or blood vessels in the pelvis and genital
tract, and maternal coagulopathies.
Concept Map

A 29-year-old female (G1P1)

is readmitted two weeks
post–vaginal delivery due to
increased vaginal bleeding.

She reports that

the bleeding POST-PARTUM She has taken
began on the HEMORRHAGE 200 mg of
tenth day after ibuprofen daily
delivery and has since delivery.
increased in
severity each
subsequent day

The delivery was

uncomplicated with
minimal blood loss
and the patient did
not receive any
epidural anesthesia
 CRUSH SYNDROME
By: BERNABEO

Case Scenario: A 60-year-old man presents to the emergency room after an earthquake. His right leg had been
trapped under his truck for an hour. After he was extracted, he was rushed to the emergency room, where aggressive
fluid hydration was started. There is no penetrating injury. On physical exam, there is a large ecchymosis and
abrasion on the right thigh. The right thigh is severely tender to palpation and the muscles feel tense. Laboratory
evaluation reveals hyperkalemia and significantly elevated creatine kinase. He is immediately started on intravenous
fluids and calcium gluconate.

History of Present Illness His right leg had been trapped under his truck for an hour due to earthquake.
Pathophysiology

Traumatic rhabdomyolysis, as it pertains to crush syndrome, results when muscle mass is compressed, causing direct
injury to muscle fibers. As the tissue is compressed, it is deprived of blood flow and becomes ischemic, eventually leading
to cellular death. The time to injury and cell death varies with the crushing force involved; however, skeletal muscle can
often tolerate ischemia for up to 2 hr without permanent injury. In the 2- to 4-hr range, some reversible cell damage occurs,
and by 6 hr irreversible tissue necrosis generally sets in
Concept Map:

SIGNS & SYMPTOMS RISK FACTORS

Skin injury and

swelling
Hypotension Wound infection
 
Type of injury
 
Paralysis and
paresthesia
Renal failure
  

  hemodialysis
Compartment
Hypothermia
syndrome
 
 

Acute lung injury /

ARDS
hypovolemic shock
 
 COVID
By: COCUSA

A 25 year old women who was taken to the emergency department, was complaining of having a fever, loss of taste and smell
for 5 days. The doctor suspected that it is Covid-19 as the patient is showing its common symptoms. The doctor immediately
request for a swab test. While waiting for the result, they admitted the patient as a PUI (Person Under Investigation) in a facility
area located at the hospital. Her vital signs: temp : 39.6 BP: 130/100 Pulse Rate: 110 RR: 25 and No Family history. When the
result came and they confirmed that the patient is positive from the virus, they transferred the patient in a covid patients
isolation facility.
Pathophysiology

Coronaviruses are large, enveloped, single-stranded RNA viruses found in humans and other mammals, such as dogs, cats, chicken,
cattle, pigs, and birds. Coronaviruses cause respiratory, gastrointestinal, and neurological disease.
which typically cause common cold symptoms in immunocompetent individuals. SARS-CoV-2 is the third coronavirus that has caused
severe disease in humans to spread globally in the past 2 decades.
The first coronavirus that caused severe disease was severe acute respiratory syndrome (SARS), which was thought to originate in
Foshan, China, and resulted in the 2002-2003 SARS-CoV pandemic. The second was the coronavirus-caused Middle East respiratory
syndrome (MERS), which originated from the Arabian peninsula in 2012.
 
SARS-CoV-2 has a diameter of 60 nm to 140 nm and distinctive spikes, ranging from 9 nm to 12 nm, giving the virions the appearance
of a solar corona .Through genetic recombination and variation, coronaviruses can adapt to and infect new hosts. Bats are thought to
be a natural reservoir for SARS-CoV-2, but it has been suggested that humans became infected with SARS-CoV-2 via an intermediate
host, such as the pangolin
Concept Map
Most common symptoms:
Fever
dry cough
tiredness

Less common symptoms: COVID 19

aches and pains
sore throat
diarrhea
conjunctivitis
headache
loss of taste or smell
a rash on skin, or discolouration of
fingers or toes
Serious symptoms:
difficulty breathing or shortness of breath
chest pain or pressure
loss of speech or movement
Risk Factors:
Obesity
Age
Smoking
Alcohol
Physical Inactivity
Pollution
 ASPIRATION PNEUMONIA
By: DELA CRUZ

Case Scenario: G. is a 92 years old female come to the ER loss of consciousness, lack ability of breathing, from
ER transfer direct to ICU then after approximately one week she transmitted into EAMC.
History of Past Illness: She has history of old CVA, DVT, HTN, DM, Stroke, secondary epilepsy and bedridden.
Family History: Her sister has a HTN , DM.
History of Present Illness: Patient had loss of consciousness, lack ability of breathing, from ER transfer direct to
ICU then after approximately one week she transmitted into EAMC.
Pathophysiology

In normal healthy adults, the mucociliary mechanism and alveolar macrophages act as defenses in clearing micro
aspirations from the oropharyngeal secretions. The pathological process of aspiration pneumonia occurs when the
normal defense mechanisms fail in a predisposed individual. The entry of fluid into the bronchi and alveolar space
triggers an anti-inflammatory reaction with the release of proinflammatory cytokines, tumor necrosis factor-alpha, and
interleukins. Inoculation of organisms of common flora from the oropharynx and esophagus results in the infectious
process. Mendelson first studied the pathophysiology of aspiration pneumonitis by inducing gastric contents in the
rabbit’s lung and comparing it to 0.1 N hydrochloric acid. Later studies conducted in rats using diluted hydrochloric acid
demonstrated the biphasic response with the initial corrosive phase by acidic pH followed by a neutrophil-mediated
inflammatory response. Inoculation of normal oropharyngeal flora in the aspirate results in the infectious process and
results in aspiration pneumonia. If the bacterial load of aspirate is low normal host defenses will clear the secretions and
prevent infection.
Concept Map

Signs and Symptoms Risk Factors

Chest pain Being less alert due to medicines,

Coughing up foul-smelling, illness, surgery, or other reasons
greenish or dark phlegm
Receiving medicine to put
Fatigue you into a deep sleep for
surgery (general anesthesia)
Fever
Poor gag reflex in people who
Shortness of breath
ASPIRATION are not alert (unconscious or
PNEUMONIA semi-conscious) after a stroke
Wheezing
or brain injury
Excessive sweating
Drinking large
Problems swallowing amounts of alcohol 

Confusion Old age  Coma Problems with swallowing

 STAB WOUND
By: MUNGCAL

Case Scenario: A male of about 27 years old, was brought to the casualty department of Dhaka Medical College
Hospital (DMCH) with an injury on the left thigh on 29/08/2007 around 7 PM. According to his statement on the way
to home by a rickshaw, he was attacked by a group of snatchers. One of them within a short period of time put a
sharp pointed knife on his left thigh and snatched his moneybag. At that time the victim protested and was stabbed
on the front of the left thigh. The people from near by rushed to the spot and the assailants fled away. Then he was
brought to the emergency department of DMCH.
 
History of Present Illness: On examination one punctured wound was found on left mid thigh anteriorly. The wound
was measuring about 1′′x0.5′′x muscle depth. No major blood vessel was injured. The emergency medical officer
stitched the wound after proper toileting, prescribed medicine and advised to come after one week for stitch off.
Pathophysiology
 
As a projectile passes through tissue, it decelerates and transfers
kinetic energy to the tissue. Increased velocity causes more damage
than mass. Kinetic energy increases with the square of the velocity.
The space left by tissue that is destroyed by the penetrating object
forms a cavity, and this is called permanent cavitation. In addition to
damage to the tissues they contact, medium- and high-velocity
projectiles result in a secondary cavitation injury as the object enters
the body, it creates a pressure wave forcing tissue out of the way,
creating a cavity. The tissues move back into place, eliminating the
cavity, but the cavitation has already done considerable damage.
The characteristics of the damaged tissue determine the severity of the
injury: the denser the tissue, the greater the amount of energy
transmitted to it.
 Concept Map

SIGNS AND RISK FACTORS

DEFINITION
SYMPTOMS
 
Penetrating abdominal trauma is most commonly
caused by stabbing or gunshot wound. The most mild bleeding
commonly injured regions are the small bowel, large drainage of Racial
bowel, liver, and intra-abdominal vasculature. Over the pus
past few years, the management of patients with
penetrating abdominal has changed. This activity infection
reviews the pathophysiology and management of redness of the Sex
penetrating abdominal trauma and highlights the role of skin
the interprofessional team in managing this condition.
 VEHICULAR ACCIDENT
By: OMLANG
A 20-year-old, Hispanic female, 32 weeks pregnant, was brought to the emergency department (ED) in an ambulance by the
paramedics. She arrived in the ED immobilized on a flat board with a hard cervical collar in place. Juana was the driver of a
sedan involved in a single-vehicle collision. She stated she was driving at approximately 60 miles per hour on the highway and
suddenly lost control of the vehicle and crashed into a light pole. She also stated her head hit the windshield and shattered the
glass. She denied loss of consciousness. Upon her arrival in the ED, Juana was alert and oriented to person, place, and time
and had a Glasgow Coma Scale of 15/15. Her initial complaints were lightheadedness, weakness, left shoulder pain, and
severe abdominal cramping that started immediately following the car accident. She had a past medical history of sickle cell
disease and no previous pregnancies. Her lungs were clear bilaterally. Juana’s heart rate was 90 beats per minute (bpm), her
respiratory rate was 28, and her initial blood pressure (BP) was 130/80, and fetal pulse rate was 90. Once the cervical spine
films were taken and the flat board was removed, her BP reflected orthostatic changes of 100/60 and pulse of 120 bpm.
 CVA STROKE
By: ONIA

Case Scenario: Patient is a 62-year-old left-handed male, Filipino, married, Roman Catholic, known hypertensive for more than 10
years, maintained on Amlodipine 10mg and Atorvastatin 40mg. Patient was admitted due to loss of consciousness with high grade
fever.

History of Present Illness: 1 hour prior to admission, patient had sudden onset of right-sided weakness described as losing control of
what he was holding. This was also associated with sudden onset of loss of verbal output and loss of consciousness which prompted
immediate consult.

Vital Signs: BP: 150/100      HR: 139     RR: 137    Temp: 39.1 C     O2Sat: 88

Family History: HPN Maternal

Pathophysiology

Predisposing factors> vasoconstriction> blockage of the blood vessel>

lack of oxygen and nutrient supply> hypoxia> altered cerebral
metabolism> decreased cerebral perfusion> local acidosis> cytotoxic
edema> aneurysm rupture> stroke
Concept Map
CEREBRO VASCULAR ACCIDENT (STROKE)

SIGNS AND SYMPTOMS RISK FACTORS

- BALANCE: Loss of balance, headache - MODIFIABLE
dizziness - Blood pressure
- EYES: Sudden loss of vision in one or both - Cigarette smoking
eyes - Hyperlipidemia
- FACE: Drooping or uneven - Heart Disease
- ARM: Weakness - Diabetes Mellitus
- SPEECH: Difficulty speaking - Excessive Alcohol intake
- TIME: Call for an emergency on the onset of - Estrogen containing drugs
stroke - Polycythemia
- NON-MODIFIABLE
- Age/ Sex/ Race
TREATED WITH
- Previous vascular accident (MI,
- PHARMACOLOGICAL: Anti coagulants, Anti Stroke)
platelet therapy, Edema control (steroids, - Heredity
osmotic /loop diuretics), Anti hypertensives,
Seizure control (phenytoin), Thrombolytic
Agents (if blood clot)
- SURGICAL: Endarterectomy, Angioplasty and
Stents
- Lifestyle modification and diet
 
 HYPETENSIVE CRISIS
By: PANOPIO

Patient Killua is a 29 year old male presenting to the ED after being seen in clinic with a BP of 210/150.   Weight is
stable at 88 kg, height is 193 cm.  He reports new onset blurry vision for the past 3-4 days, nocturia ~3-4 times per
night X 2 weeks and frothy urine x 8 months. Denies edema, pain, nausea, or vomiting.
History of Present Illness: Chronic HTN, untreated. Arrived at the ED having a BP of 210/150 and reporting a new
onset of blurry vision for the past 3-4 days, nocturia: 3-4 times per night X 2 weeks and frothy urine x 8 months.
Family history: None
History of Past Illness: The patient had Hemolytic –Uremic Syndrome (HUS) as a child.
Chronic HTN, untreated.  Patient checks BP at local pharmacies, SBP usually ~180.
Pathophysiology
 H
By: PERENA
 GUN SHOT WOUND
By: SANTOS

Case Scenario: A 32-year-old man presents to the emergency department for treatment of a gunshot wound above the knee
on his left thigh. He reports having sustained the injury 1 hour earlier. The patient has no significant medical history and does
not have additional injuries. He is able to walk despite the injury.
His vital signs are normal except for an elevated pulse (110 bpm), which improved following the administration of fentanyl, and
high blood pressure (133/84 mm hg). Physical examination is normal except for an entrance wound noted on the upper outer
left thigh and an exit wound noted just above the knee. Distal neurovascular examination is intact, and there is no active
bleeding associated with the wound.
Complete blood count and metabolic panel are both ordered, and the results are normal. Radiographic examination of the
patient’s knee is obtained
History of Present Illness: The patient has no significant medical history and does not have additional injuries. He is able to
walk despite the injury.
Pathophysiology
 Concept Map

Sign & Symptoms

When cases of gunshot wound to the head arrive at the hospital,
aggressive treatment for resuscitation is required. The victim may
present with following abnormalities-
Brain Swelling
Brain Hemorrhage- Bleeding within brain or between skull and brain
Cerebral Ischemia- lack of blood supply to brain and
Risk factors
Although many youths desist in aggressive and antisocial
behavior during late adolescence, others are disproportionately
at risk for becoming involved in or otherwise affected by gun
violence. The most consistent and powerful predictor of future
violence is a history of violent behavior.

Increased Intracranial Pressure- Increased pressure within skull

resulting in displacement or compression of brain inside the skull.