Oral Revalida Emergencies 2017 Script

ORAL
REVALIDA
EMERGENCIES
2016-2017

“Ars longa, vita brevis, occasio praeceps, experimentum periculosum, iudicium difficile.”
-Hippocrates

JMFV D2017, UST-FMS
UST-FMS Oral Revalida
Topics for Medical & Surgical Emergencies 2017

1. Basic Life Support p3

2. Acute Upper Airway Obstruction p100 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management)

3. Acute Asthma in Exacerbation p42 (Definition, Pathogenesis, Precipitating Factors, Clinical Manifestations,
Management)

4. Respiratory Distress Syndrome p77 (Definition, Incidence, Risk Factors, Pathophysiology, Clinical Manifestations,
Diagnosis, Prevention, Management, Prognosis)

5. Anaphylaxis p65 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management, Prevention)

6. Intestinal Obstruction in Children p97 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management)

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7. Diarrhea & Dehydration 5 ed p52 (Definition, Etiopathogenesis, Clinical Manifestations, Evaluation of
dehydration, Management)

8. Shock p21 (Definition, Types, Etiopathogenesis, Clinical Manifestations, Management)

9. Acute Abdomen p111 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management – at least 2
GI cases)

10. Acute Cholangitis p116 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

11. Gastrointestinal Bleeding p302 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

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12. Porto-systemic encephalopathy 5 ed p100 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management, Complications)

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13. Hypertensive Crisis 5 ed p144 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

14. Acute Heart Failure p123 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

15. Acute Myocardial Infarction p221 (Definition, Etiopathogenesis and types, Clinical Manifestations, Diagnosis,
Management)

16. Pulmonary Embolism p212 (Definition, Etiopathogenesis, Risk factors, Clinical Manifestations, Diagnosis,
Management)

17. Severe Asthma p208 (Definition, Etiopathogenesis, Clinical Manifestations, Management)

18. Hemoptysis p169 (Definition/classification, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

19. Pneumothorax p176 (Definition/classification, Risk factors Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management)

20. Acute Respiratory Failure p133 (Definition/types, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management)

21. Adrenal Crisis p115 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

22. DKA p158 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis/tests, Management, monitoring)

23. Thyroid Storm p163(Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis/tests, Management)

24. Uremia p192 (Definition, Etiopathogenesis, Clinical Manifestations, Procedures, Management)

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25. Rabies 5 ed p313 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

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26. Tetanus 5 ed (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

27. Increased ICP p237 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

28. Stroke p240 (Definition, Risk factors, Management)

29. Status Epilepticus p245 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

30. Spinal Cord Compression p248 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

31. Vaginal Bleeding in Pregnancy p269 (Causes, diagnosis, management)

32. Hypertension in Pregnancy p277 (Manifestations, diagnosis, management)

33. Gynecologic Emergencies p284 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management –
at least 2 emergencies)

34. Head Trauma p307 (Classification, Evaluation, Management)

35. Maxillofacial Injury p336 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management
according to site of injury)

36. Mechanical Intestinal Obstruction p345 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management for 1 type)

37. Spine Trauma p313 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

38. Thermal Burns p370/339 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

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39. Fractures 5 ed p229 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

40. Acute Urinary Retention p298 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

41. Ocular Trauma p402 (Causes, Clinical Manifestations, Management)

42. Foreign body in the esophagus/airway p441 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis,
Management)

43. Appendicitis p293 (Definition, Etiopathogenesis, Clinical Manifestations, Diagnosis, Management)

1. Basic Life Support: Cardiorespiratory Resuscitation p3

Basic Life Support is the foundation for saving lives following sudden cardiac arrest which continues to be a
leading cause of death in many parts of the world. Considering its multiple etiologies, the variety of
circumstances where it could occur & that it can happen to anyone - a universal strategy for successful
resuscitation is needed. The actions comprising this strategy are called the links in the “Chain of Survival”
which include:
I. Immediate recognition of cardiac arrest & activation of the Emergency Response System (EMS)
II. Early Cardiopulmonary Resuscitation (CPR)
III. Rapid defibrillation
IV. Effective Advanced Life Support (ALS)
V. Integrated post-cardiac arrest care

I. Immediate recognition of cardiac arrest & activation of the EMS.
• An adult is found unconscious, unresponsive or witnessed to have collapsed. Survey the scene &
ensure that it is safe
• Perform primary survey: Check for response by tapping on the shoulder and shouting,
“Hey, hey, are you okay?” x2 à No response
• “Activate the EMS and somebody get me an AED!”

II. Early CPR
• ABC à CAB
o Formerly sequenced as Airway-Breathing-Circulation or ABC, a change in the 2010 American
Heart Association Guidelines recommends the initiation of chest compressions before
ventilations thus the new sequence is CAB
o Chest compressions will be initiated sooner
o Critical initial elements of CPR are chest compressions and early defibrillation
• Extend the head to expose the neck. Take <10 seconds to feel for the pulse à No pulse à start CPR
• Compression
o Forceful rhythmic applications of pressure on the chest which create blood flow by increasing
intrathoracic pressure and directly compressing the heart which then generates blood flow and
oxygen delivery to the myocardium and brain
o “I will place the heel of one hand over the heel of the other on the patient’s sternal notch, then I
will position my shoulders over hands with elbows locked and arms straight”
o “I will then deliver High Quality chest compressions by
§ Pushing hard & fast delivering 100 compressions/min with a depth of at least 2in/5cm
and
§ I will Allow complete recoil of the chest after each compression to allow the heart to fill
completely”

• Airway
o “I will then start rescue breaths by mouth-to-mouth or bag-mask to provide oxygenation and
ventilation”
o “I will then open the airway by performing head tilt/chin lift maneuver or jaw thrust for
suspected victims of cervical spine injury (this is when the jaw is lifted without tilting the head)”
o Check if patient is breathing → look at chest, listen/feel breaths of the patient
o If still breathless for 10 seconds, then you have to “BREATHE” for the patient

• Breathing
o “I will deliver 2 rescue breaths, each breath over a full second and ensure it is sufficient to
produce visible chest rise”
o “I will adhere to a compression to ventilation ratio of 30 chest compressions to 2 ventilations
for 5 cycles”
o “If the patient has an advanced airway (Endotracheal tube, LMA), I will give 1 breath every 6 to
8 seconds and there should be no pause in compressions or ventilations”

JMFV D2017, UST-FMS
III. Rapid defibrillation
• Attach the AED, turn it on, follow the prompts, resume chest compressions after shock
• Shockable rhythms
o VF (ventricular fibrillation – completely erratic rhythm w/ no identifiable waves) OR
o Pulseless VT (ventricular tachycardia - also known as VF) – rhythm >100 or 120 beats/min with ≥
3 irregular beats in a row, arising distal to the bundle of His
IV. Effective advanced life support
V. Integrated post-cardiac arrest care

During Cardiopulmonary resuscitation check for:

1. Hypovolemia
2. Hypoxia
3. Hydrogen ion (Acidosis)
4. Hypo/hyperkalemia
5. Hypoglycemia
6. Hypothermia
7. Toxins
8. Tamponade (Cardiac)
9. Tension pneumothorax
10. Thrombosis (Coronary or Pulmonary)
11. Trauma

JMFV D2017, UST-FMS

#2#UPPER#AIRWAY#OBSTRUCTION#p.100%
%
DEFINITION# ETIOPATHOGENESIS#
• Something%blocking%or%obstructing%the%airway%or%windpipe%(from%upper%nares%to%distant% • Common:%children%with%infectious%or%anatomic%abnormalities%(children%=%smaller%airways)%
end%of%trachea)% o Smaller%airways%have%a%great%narrowing%in%inflammation%
• Leads%to%change%in%normal%breathing.%%You%would%see%this%in%patients%who%have%stridor,% o Obstruction%of%airflow:%inspiration%>%expiration%
where%in%it’ll%cause%a%harsh,%vibratory%sound%due%to%the%obstruction%of%the%airway%causing% • In%forced#inspiration:%large%negative%intrathoracic%pressures%generated%below%obstruction%
a%turbulent%flow.% →%extrathoracic%tracheal%narrowing%
o Causes%an%↑%turbulence%&%velocity%of%airflow%→%vocal%cords%&%
aryepligottic%folds%vibrate%→%inspiratory#strider%
• In%exhalation%–%extrathoracic%trachea%→%balloon%shape%during%expiration%
• Causes:%infectious,%nonKinfectious,%chronic%cases%
***INFECTIOUS***#
1.#CROUP%% 2.#EPIGLOTTITIS% 3.#BACTERIAL#TRACHEITIS% 4.#&#5.#RETROPHARYNGEAL#ABSCESS#%
(aka%laryngotracheobronchitis)% or%PERITONSILAR#ABSCESS%
DEFINITION% DEFINITION% DEFINITION% ETIOLOGY%
• Syndrome%of%air%swelling%in%glottis%% • Infection%of%the%epiglottis% • Bacteria%can%adhere%and%cause% • Group%A%streptococci%and%
ETIOLOGY% ETIOLOGY% local%mucosal%damage%→% anaerobes%
• Most%cases:%Parainfluenza%virus%types%1%and%3% • Less%common%now%since%there’s%now% impairment%of%mucociliary% • Staph.1Aureus:1higher%
• Others:%respiratory%syncytia,%influenza%or%adenovirus,%usually%<%5yr% immunization%against%Haemophilus1 clearance%of%trachea.%%% incidence%in1retropharyngeal%
CLINICAL%MANIFESTATIONS% influenza1Type%B%(cause%of%epiglottitis)1 ETIOLOGY% CLINICAL%MANIFESTATIONS%
• Coryza% • Others:%%βKhemolytic%streptococci,% • Leading%cause:%Staphylococcus1 • Fever%
• Brassy%cough%(sounds%like%seal%bark)% Staphylococcus1aureus,1and%streptococcus1 aureus% • Sore%throat%
• Hoarseness% pneumoniae1 • Next:%Hemophilia1influenza%Type% • Difficulty%swallowing%(hard%
• Inspiratory%stridor% • Age:%all,%especially%in%2K7%year%old% B% time%eating)%
• Severe:%retractions%and%cyanosis% CLINICAL%MANIFESTATIONS% CLINICAL%MANIFESTATIONS% • Retropharyngeal%may%also%
DIAGNOSIS% • %High%fever% • Brassy%cough%ff.%by%% have%noisy%breathing%
• Neck%radiograph:%steeple%sign%(narrowing%of%subglottic%area)% • Sore%throat% • High%fever%and%toxicity% DIAGNOSIS%
TREATMENT% • Dyspnea,%% • Respiratory%distress% • Retropharyngeal#abscess%
• No%treatment% • Rapidly%progressive%respiratory%distress% DIAGNOSIS% o Lateral%XKRay:%thickened%
• Goal:%prevent%↑%airway%obstruction% • Child%prefers%upright%“sniffing”%position% • Lateral%neck%x%ray:%ragged% retropharyngeal%space%of%
• Oxygen%therapy%for%moderate%to%severe%croup% DIAGNOSIS% irregular%tracheal%border% nasopharynx%
Medications% • %CBC%and%blood%culture%(infectious%cause)% • CBC:%moderate%leukocytosis% • Peritonsilar#abscess#%
• Mist%vaporizer:%moisten%&%↓%viscosity%of%airway%secretions%and% • Radiograph:%“thumb%sign”%K%swollen% with%bands% o CBC:%leukocytosis%w/%shift%
exudates%→%coughing%=%removes%them% epiglottis%in%lateral%neck%area% TREATMENT% to%the%left%%
• Racemic%epinephrine:%topical%αKadrenergic%stimulant% TREATMENT% • Parenteral%antibiotics:% o Endoscop:%tonsilar%
o Causes%mucosal%vasoconstriction%→%↓%edema%in%inflamed% • Humidified%oxygenKenriched%gas%face%mask% cefotaxime,%ceftriaxone%or% abscess%
subglottic%region:%0.5K2.0%mL%of%2.25%%solution% • Pulse%oximeter%to%check%the%O2%sat% ampicillin%with%sulbactam% #
o Corticosteroids%(dexamethasone):%0.6mL/kg%up%to%10mg/dose% • Parenteral%antibiotics:%cefotaxime,% Severe:%artificial%airway%and%
ceftriaxone%or%ampicillin%with%sulbactam% supplemental%oxygen#
!
#2#UPPER#AIRWAY#OBSTRUCTION#p.100%
%
***NONPINFECTIOUS***#causes%of%acute%UAO%include%1)%foreign%body%aspiration,%2)%spasmodic%coup%and%3)%Angioedema%
1.#FOREIGN#BODY#ASPIRATION% 2.#SPASMODIC#CROUP% 3.#ANGIOEDEMA%
DEFINITION/ETIOLOGY% DEFINITION% DEFINITION%
• Foreign%body%lodged%into%larynx,%trachea%or%bronchus% • Basically%like%croup,%except%its%“spasmodic”% ETIOLOGY%
CLINICAL%MANIFESTATIONS% • “Spasmotic”%only%happens%briefly,%and%sporadically% • Due%to%allergy%
• Cough% ETIOLOGY% CLINICAL%MANIFESTATIONS%
• Choking% • Mostly%in%children%1K3%years%old% • Anaphylactic%shock:%
• Gagging% • Due%to%a%viral%or%allergic%cause% o Difficulty%of%breathing%
• Stridor%and%or%wheezing% CLINICAL%MANIFESTATIONS% o Anxiety%
• If%passed%in%smaller%airway:%“silent%phase”%→%recurrent%pneumonia,%wheezing,%abscess% • Mostly%during%night%time,%with%same%symptoms%as%croup% o Itchy%skin%
and%bronchiectasis% • Hoarseness% o Vomiting%
DIAGNOSIS% • Barking%cough% o Sneezing%
• Radiograph:%air%trapping% • Noisy%inspiration% o Coughing%
• Bronchoscopy%(diagnostic%and%therapeutic):%help%guide%in%removing%the%foreign%body% • Respiratory%distress.% DIAGNOSIS%
TREATMENT% DIAGNOSIS% • %XKRay:%narrowing%of%the%subglottis%
• If%patient%is%breathing:%wait%to%see%if%patient%can%clear%foreign%body%by%him/herself% • XKray:%subglottic%narrowing%and%steeple%sign% TREATMENT%
• If%can’t%breath:%Heimlich%maneuver% TREATMENT% • Epinephrine%(allergic%type%of%obstruction)%
• Direct%laryngoscopy:%removal%with%forceps% • %Cool%mist%to%relieve%the%symptoms% • IVF%
• EDUCATE!%PREVENT/avoid%their%children%from%playing%with%small%objects%that%they% % • Corticosteroids%
might%put%in%their%mouths%or%nose% %
%
***CHRONIC#CAUSES***#
CHOANAL#ATRESIA% LARYNGOMALACIA/TRACHEOMALACIA% VASCULAR#ANOMALIES%
DEFINITION% DEFINITION% DEFINITION%
• Persistence%of%buconasal%membrane%in%posterior%margin%of% • Delay%or%defect%in%maturation%of%the%structures%in%the%larynx% CLINICAL%MANIFESTATIONS%
the%hard%palate%=%really%rare.% CLINICAL%MANIFESTATIONS% • Child%prefers%keeping%their%neck%
CLINICAL%MANIFESTATIONS% • Obstruction%during%inspiration%due%to%prolapse%of%structures%that%support%the% hyperextended%
• Doesn’t%cause%any%clinical%problems%unless%w/%obstruction% larynx%and%trachea% • Stridor:%from%tracheal%compression%due%to%
• Obstruction:%apnea,%cyanosis%or%respiratory%distress% • Breathing%problems%problems%breathing% things%like%mediastinal%cysts,%teratomas,%
DIAGNOSIS% DIAGNOSIS% lymphomas%or%lymphadenopathies%
• %%CT%scan,%MRI%or%fluoroscopy% • Endoscopy:%structures%obstructing%the%airways% TREATMENT%
TREATMENT% TREATMENT% • Surgery%
• Surgically%remove%the%membrane%causing%the%obstruction% • Reassurance%and%respiratory%support%if%needed,%and%sometimes%epiglottoplasty%
%
!

3. Bronchial Asthma in Acute Exacerbation p42

Definition
• Asthma is a chronic inflammatory condition of the airways resulting in episodic airflow obstruction
secondary to hyper- responsiveness to provocative exposures or triggers.
• Acute asthma exacerbation is an acute or subacute episode of decompensated asthma characterized
by progressively worsening shortness of breath, cough, wheeze, and chest tightness, or a combination
of all these symptoms

Etiology:
• This can be triggered by EXTRINSIC IgE-mediated factors
o Such as dust mites, pollens, and animal dander
o Think: E! EExtrinsic mEE-diated = EENvironment
• Or INTRINSIC non-IgE- mediated factors
o Such as irritants, cold air, noxious fumes (environmental or tobacco smoke, wet paint), viral
infections, physical exertion; and gastroesophageal reflux
o GERD: acid reflux → irritate airway & lungs → affect breathing → ↑ sensitive to environment →
harder to breathe → acute exacerbation
o Think iii! IIntrinsic NON-miidiiated = IIritants
• Underassessment or under-treatment of asthma could also lead to exacerbation

Pathophysiology (sequence)
• Exposure or the presence of mediators/triggers leads to an immunologic hyper-responsiveness. In the
early phase, within 15 to 30 minutes of exposure, bronchoconstriction is the predominating factor
leading to airway obstruction. In the late phase, 4 to 12 hours after exposure, tissue inflammation,
immune cellular infiltration into the airways, airway edema, and excess mucus production exacerbate
the airway obstruction.
• The airway obstruction would cause a non-uniform ventilation such that a VQ mismatch occurs causing
Alveolar hypoventilation.
o Arterial Carbon Dioxide Partial Pressure (PCO2) will increase & PO2 will decrease leading to
Respiratory Acidosis which would cause Pulmonary vasoconstriction. Pulmonary
vasoconstriction would impair surfactant synthesis & predispose the patient to atelectasis
o Airway obstruction also predisposes the patient Hyperinflation (air to get trapped into the
lungs). There would then be decreased compliance (lung’s ability to stretch/expand) &
Increased work of breathing which would further exacerbate the hypoxemia (decrease PO2)
• Decrease in PO2 would again lead to respiratory Acidosis, pulmonary vasoconstriction & the vicious
cycle repeats

Clinical Manifestations
• Tight & non-productive cough w/ or w/o wheezing
• PEFR (Peak Expiratory Flow Rate) & FEV1 (Forced Expiratory Volume at 1s) worsening – decreases in
lung function are better indicators of severity of airway obstruction compared to signs & symptoms
• Tachypnea
• Dyspnea – expiration will be more difficult due to premature closure of the airways, but some children
may have inspiratory difficulty as well
• Use of accessory muscles of respiration à particularly in younger children, prolonged use of the
diaphragm & abdominal muscles can cause abdominal pain
• Cyanosis
• Hyperinflation of the chest
• Tachycardia
• Pulsus paradoxus - abnormally large decrease in systolic blood pressure (>10mmHg) and pulse wave
amplitude during inspiration, reliable indicator of airway obstruction but is extremely difficult to
perform correctly in children in distress

JMFV D2017, UST-FMS
Diagnosis
• Pulse oximetry – to know the oxygen saturation hence the severity of exacerbation
• Salbutamol Challenge test can be performed, specially in cases not known to have asthma, in order to
demonstrate whether the airway obstruction is responsive to a bronchodilator, which is suggestive of
asthma
• Pulmonary Function (Spirometry or Peak Flow): assess degree of airway obstruction
o Measures response to therapeutic agents
o Determines long-term course of illness
o Forced Expiratory Volume at 1 second (FEV1) or Peak Expiratory Flow Rate (PEFR)
• ABG (PCO2, PO2, pH) – predicts potential for subsequent ventilatory failure
o Hypoxemia – 1st abnormality to be observed in acute asthmatic episodes
• Chest X-Ray – not routinely done but is performed if potential complications like pneumothorax,
pneumomediastinum & aspiration are suspected

Clinical manifestations (Signs & Symptoms) would vary depending on the severity of the exacerbation. We
classify the attack as mild, moderate or severe which will eventually guide us to the appropriate
management of the patient

Management
• Goal: Rapid reversal of airway obstruction & correction of hypoxemia
• Initial management
o Oxygen supplementation for O2 sat <90%
o 3 doses x Inhaled SABA (Salbutamol) q20min (3 doses in 1h at 20min intervals) via nebulizations
or metered-dose inhaler (MID) with spacer
• Moderate:
o Continue SABA
o Add oral systemic corticosteroid such as Prednisone
o Add inhaled anti-cholinergic
• Severe
o High dose inhaled short acting beta 2 agonist with an anti-cholinergic such as Ipratropium
should be given every 20 minutes for 1 hour
o Oral systemic corticosteroid
o IV corticosteroid
§ Methylprednisolone (60-80mg)
§ Hydrocortisone (200mg)

JMFV D2017, UST-FMS
• Management at home: Asthma Control Plan (Philippine Consensus for Childhood Asthma)

GREEN ZONE YELLOW ZONE RED ZONE
Doing Well Acute Attack Emergency
Level Well-controlled Mild-moderate Attack Severe Attack
Symptoms Asymptomatic At least 1: Cough, Impending Respiratory
wheezing, chest Arrest. Trouble
tightness, shortness of walking/talking,
breath. cyanosis, unresponsive
Waking at night d/t to quick relief
asthma medications
ADL Can do usual Can do some but not all Can not do usual
activities activities activities
PEFR >80% 60-79% <60%
MANAGMENT
SABA Continue Inhaled SABA ie Salbutamol/Terbutaline (3 doses in
current 1h at 20min intervals) via nebulizations or metered-
medications dose inhaler (MID) with spacer
Response to Good Good à stay at home, Poor à Proceed to the
SABAà Action then continue ER, while in transit,
maintenance meds continue SABA q20min!

Incomplete à ER!
At the ER/Hospital Perform initial assessment: Hx, PE (auscultation, use
of accessory muscles, HR, RR, PEF or FEV1, O2 Sat,
ABG & other tests as indicated)
O2 Yes to achieve O2 sat >90% (>95% in children)
Supplementation
Repeat SABA Salbutamol/Terbutaline 1 dose q20 x 1h
Oral Prednisone/Prednisolone 20mkday if no initial
Glucocorticosteroid response to SABA. Sedation is CONTRAINDICATED!
Action after 1h Re-assess: PE, PEF, O2 Sat, other tests as needed
Response PEF 60-80% PEF <60%

PE: Moderate symptoms, PE: Severe symptoms at
accessory muscle use rest, chest retractions,
no improvement after
initial treatment,
Inhaled B2 Agonist Ipratropium. Ipratropium +
+ Inhaled Anti- Continue treatment for
cholinergic 1-3h provided there is
improvement.
IV Glucocorticoids Methylprednisolone (60-
80mg)
Hydrocortisone
(200mg)
Response à Action Good, sustained 1h after Incomplete w/in 1-2h.
last dose of treatment PE: Mild-moderate
(4h total), PE normal, symptoms, PEF <70%,
PEF>70%, no distress, O2 O2 Sat not improving à
Sat >95% à DISCHARGE Admit to regular ward
HOME.
Poor w/in 1h. Severe
Continue SABA symptoms, drowsiness,
Consider oral confusion, PEF <30%,
glucocorticoid PCO2 > 45mmHg, PO2 <
Patient education: take 60mmHg à Admit to
meds correctly, review ICU
action plan, close follow-
up, avoidance of triggers
JMFV D2017, UST-FMS

Actions in the Regular Ward:
hospital while Oxygen
admitted Inhaled B2 agonist +
Anti-cholinergic
Systemic Glucocorticoid
IV Methylxanthines
Monitor PEF, O2 Sat,
pulse

ICU:
Oxygen
Inhaled B2 agonist +
Anti-cholinergic
Systemic Glucocorticoid
IV Methylxanthines
SC/IM/IV B2 Agonist
Possible intubation &
mechanical ventilation
Response à Action Improvement à
Discharge if PEF > 60% &
sustained on
oral/inhaled medications
for at least 4h

No improvement w/in 6-
12h à remain at ICU/ if
from ward, transfer to
ICU

17. Status Asthmaticus p54/208
AKA: Severe asthma, near-fatal Asthma
Definition
• Asthma exacerbation that is poorly responsive to adrenergic agents associated with signs/symptoms of
potential respiratory failure
• Absence of meaningful response to
o 2 aerosol treatments with B2-agonists or
o 2-3 SC injections of epinephrine at 15min intervals or
o 2-3 IM injections of epinephrine

Etiology/Ethiopathogenesis
• Anatomic/physiologic peculiarities of the airway in early life that predispose infants/children to SA
o Decreased smooth muscles in the peripheral airways à less support
o Mucous gland hyperplasia in the major bronchiàincreased intraluminal mucous production
o Narrow peripheral airways up to 5y/o à vulnerable to obstructive diseases
o Decreased elastic recoil of the young lung à early airway closure
o Highly compliant chest
• Pathologic Changes causing airway narrowing
o Bronchial wall thickening from edema & inflammatory cell infiltration
o Hypertrophy & hyperplasia of bronchial smooth muscle & submucosal glands
o Deposition of collagen beneath the epithelial basement membrane
o Fatal if >50% of the luminal diameter of the small airways are occluded
• Causes/triggers
o Respiratory tract infections
o Underassessment/undertreatment of asthma exacerbations
o Exposure to allergens
o Exposure to intrinsic factors
o Withdrawal/too sudden reduction of systemic steroids
o Overuse of antiasthmatic medications – sympathomimetics, theophylline

JMFV D2017, UST-FMS

• History of prior intubation/mechanical ventilation for asthma – may point to a life-threatening episode
• Symptoms: Cough, dyspnea & wheezing
• PE: Altered sensorium, upright posture, use of accessory muscles of respiration, tachypnea,
tachycardia, pulsus paradoxus, hyperinflation of the chest with diffuse wheezing, PEFR <120L/min or
FEV1 <1L
• DDx: Asthma Mimics like Epiglottitis, angioedema or vocal cord dysfunction

Labs/Ancillaries
• Spirometry – FEV1 indicates severity of exacerbation
o ↓ FEV1/FVC
o ↑ RV and total lung capacity (TLC)
• ABG: assesses impact of airway obstruction on ventilation → Mild hypoxia, Respiratory alkalosis
• CXR: non-specific signs of hyperinflation; r/o pneumothorax

Management
• Non-pharmacologic: First assess with peak flow or FEV1 in combination with medications on arrival to
ER, focused HxPE
• Pharmacologic
o Inhaled short acting β-2 agonists: relaxes bronchial smooth
muscle (β2-adrenoceptors): Albuterol
o Prophylaxis: long acting β-2 agonists: Salmeterol
o Systemic corticosteroids: inhibit synthesis of cytokines; inactive NF-kB, the transcription factor
that induces production of TNF-α and other inflammatory agents:
§ Betamethasone, Prednisone
o Oxygen supplementation
o Poor response → progressive deterioration → intubation/mechanical ventilation
• Discharge
o Clear, sustained improvement of symptoms
o Peak flow or FEV1 >70% predicted
o Clear/sustained improvement of symptoms
o Teach patient self-management
o Continue use of inhaled B2-agonist and oral steroid
• Avoidance of triggers, inhaler technique

JMFV D2017, UST-FMS
4. Respiratory Distress Syndrome p77

Definition
• First described as Hyaline Membrane Disease in 1903
• Currently, it is known as a respiratory disorder usually developing in the 1st few hours of life in
premature infants <36w AOG
• It is a structural lung immaturity secondary to a qualitative/quantitative deficiency of pulmonary
surfactant

Incidence
• Generally, incidence increases with decreasing AOG at birth & is usually worse in male infants
• A higher risk is also associated with the following even if infants are term
o Infants of diabetic mothers with poor metabolic control
o Infants born after perinatal asphyxia
• 50% of infants born 26-28w
• 20-30% of infants born 30-31w

Etiology/Pathogenesis
• The distal respiratory epithelium responsible for gas exchange has 2 distinct cell types
o Type 1 Pneumocytes – cover most of the alveolus
o Type 2 Pneumocytes – actively metabolizing cells containing cytoplasmic lamellar bodies which
are the source of pulmonary surfactant. Seen as early as 22w AOG & become prominent 34-
36w AOG
• Surfactant
o Complex lipoprotein made up of Lecithin (Dipalmitoyl phosphatidylcholine) which is the
principal phospholipid & Phosphatidylglycerol
o Functions to lower alveolar surface tension
• Common causes
Pulmonary Non-pulmonary
Group B streptococcal pneumonia Hypothermia
Transient tachypnea of newborn Congenital heart disease
Pulmonary hypoplasia Perinatal asphyxia
Congenital lung malformation Anemia
Meconium aspiration CNS injury Hypoglycemia
HTN / Persistent pulmonary HTN Metabolic diseases
Pneumothorax/pleural effusion Metabolic acidosis

• Pathophysiology
o Prematurity imparts structural lung immaturity & decreased/impaired surfactant synthesis &
secretion
o Deficiency in Pulmonary surfactant à abnormally high lung surface tension àAlveoli can not
remain open during respiration à Atelectasis à V/Q Mismatch à Hypoxemia, hypercarbia
§ Respiratory & metabolic acidosis à Vasoconstriction of pulmonary vessels à impaired
endothelial and epithelial integrity à leakage of proteinaceous exudate formation of
Hyaline Membranes (hence the name)
§ High inspired O2 & Barotrauma à inflammatory cell cytokine influx
o Both changes à Lung injury à RDS

Occur immediately after birth upto 3h after birth
• Difficulty initiating normal respiration
• Tachypnea
o Due to inadequate oxygenation/ventilation, >60cpm for babies, >30cpm for adults
• Expiratory grunting/whining
o Sound produced by forceful closure of the glottis to maintain a normal FRC.
o A decrease in grunting may be the 1st sign of improvement
• Retractions
o Reduction in lung compliance & an attempt by the infant to increase negative intrapleural
pressure
• Nasal flaring
JMFV D2017, UST-FMS
o Attempt by the infant to decrease airway resistance
• Apnea
o Sign of hypoxia/respiratory fatigue in severe RDS
• Cyanosis
o Reflects an increase in desaturated hemoglobin >3-5mg/dl
• Decreased activity
o Secondary to hypoxia or may be an attempt by the infant to conserve energy

Diagnosis
• Prenatal
o AF Lecithin:Spingomyelin (L:S) Ratio
§ >2:1 à Lung maturity
o Foam Stability Test
§ Amniotic fluid is mixed with different volumes of 95% ethanol à shaken with air à
foam develops which is stable for several hours = presence of surfactant = lung maturity
• Postnatal
o Clinical signs & symptoms
o CXR: Reticulogranular, ground-glass appearance with airbronchogram
o ABG: Progressive hypoxemia, hypercabia, metabolic acidosis
o CBC, Blood GS/CS: To r/o infectious causes of RDS
o 2D-Echo: To r/o pulmonary HTN & PDA as causes of RDS
o Hyperoxia Test: Administer 80-100% O2 to differentiate pulmonary & cardiac causes of RDS

Management
• Ensure adequate ventilation and oxygenation to avoid pulmonary vasoconstriction, ventilation
perfusion abnormalities, atelectasis
• Mild to moderate RDS: continuous positive airway pressure (CPAP) via mask, nasal canula or
endotrachial tubes (4-6cm H2O pressure to maintain arterial oxygen tension between 60-80mmHg)
• Mechanical ventilator
o PO2 not maintained at >50mmHg despite 100% O2
o Blood pH <7.20
o pCO2 > 60mmHg
o Persistent apneaa
• Surfactant replacement therapy
o Exosurf – synthetic surfactant
o Survanta – rescue therapy made from minced bovine lung, initiated during the 1st 24h via ET at
4ml/kg q12 x 4doses
• Nitric oxide
o Given if surfactant doesn’t work
o Inhaled with high frequency ventilation
• Correct Acid-base disturbances
o Metabolic acidosis: sodium bicarbonate/IV 1-2meq/kg over 15min
o Respiratory acidosis: assisted ventilation
• Limit fluids to reduce risk of PDA, NEC & bilopancreatic diversion
• Antibiotics
o Penicillin or ampicillin + Aminoglycoside
o Hard to differentiate b/w Group B Strep pneumonia & RDS
• Blood transfusion
o Maintain venous hematocrit of 40% for better organ perfusion and oxygenation
• Dopamines/dobutamines à support cardiac function
• Thermoregulation – keep infant warm: incubator/droplight
• Urinary output, BUN, Crea à evaluate renal function and blood flow to the kidney

JMFV D2017, UST-FMS
5. Anaphylaxis/Anaphylactoid Reactions p.65, Tintinalli’s Emergency Medicine 8E, World Allergy Organization
Definition
• Anaphylaxis is an IgE-mediated, antigen-induced reaction which causes massive release of biochemical
mediators from previously sensitized mast cells and basophils, leading to a clinical syndrome consisting
of 2 or more of the following organ involvement
o Cutaneous: Urticaria, angioedema, pruritus
o Respiratory: Asthma, laryngeal edema, bronchospasm, wheezing
o Cardiovascular: Hypotension, tachycardia, CV collapse, MI, arrhythmias
o GI: nausea, vomiting, crampy abdominal pain, diarrhea
• Anaphylactoid reaction is a non-IgE mediated reaction which do not require previous sensitization
involving 1 more of the following mechanisms
o Complement activation
o Direct mast cell activation by pharmacologic agents
o Alteration in arachidonic acid metabolism by acetyl-salicylic acid (ASA) and NSAIDS

Etiology
• Food: milk, egg, peanuts, shellfish
• Drugs: β-lactam antibiotics, NSAIDS, ASA, anesthetic agents
• Allergen extracts
• Venoms from insect stings and snake bites

Pathogenesis
• The classical mechanism associated with human-allergic disease is initiated by an antigen (allergen)
interacting with allergen-specific IgE bound to mast cells and/or basophils
• It begins with allergic sensitization; this is when an allergen is first encountered. They are internalized
by APCs and expressed on their cell surface
o The allergens are then presented to other cells involved in the immune response, particularly T-
cells
o Through a series of specific cell interactions B-lymphocytes are transformed into plasma cells
which are able to synthesize IgE
o The IgE then binds, via its Fc portion, to cell surface receptors on mast cells & basophils leaving
its Fab portion available for future interaction with the specific allergen
• Once an allergen is re-encountered, it binds to the Fab portion of the IgE bound to mast cells. This will
initiate a more aggressive and rapid memory response
o Cross-linking of a sufficient number of mast cell/basophil-bound IgE antibodies by allergen
initiates a process of intra-cellular signaling, which leads to degranulation of cells, with the
release of mediators of inflammation
• The immune system's response to allergen exposure can be divided into 2 phases
o Early phase reaction
§ Occurs within 15min from the exposure
§ Chemical mediators released by mast cells including histamine, prostaglandins,
leukotrienes and thromboxane produce local tissue responses characteristic of an
allergic reaction
§ Sneezing, edema and mucus secretion with vasodilatation in the nose, leading to nasal
blockage, and bronchoconstriction in the lung, leading to wheezing
o Late phase reaction
§ Occurs 4-6 hours after the disappearance of the first phase symptoms and can last for
days or even weeks
§ Cellular mediators, fibrin deposition and tissue destruction resulting from the sustained
allergic response
§ Increased bronchial reactivity, edema and further inflammatory cell recruitment

• Symptoms begin within seconds to minutes, occasionally within 1h after exposure to causative agents
• Early stages
o Sense of impending doom
o Laryngeal edema may manifest as hoarseness, dysphonia or lump in the throat
o Loss of consciousness
• Others include
o Nasal, ocular, palatal pruritus, sneezing diaphoresis, disorientation, fecal or urinary
incontinence or urgency
JMFV D2017, UST-FMS

o Biphasic reactions: Early anaphylaxis resolves only to be followed by a recurrence of
anaphylaxis hours later
• Primary endangering manifestations (Major symptoms)
o Upper airway obstruction (laryngeal edema)
o Severe bronchial dysfunction, obstruction
o Cardiac dysfunction
o Hypotension

Diagnosis
• Immediate hypersensitivity skin tests to identify specific causes
• Diagnosis relies on prompt recognition of the syndrome
• No definite laboratory work-up locally available, in the US: Assay of mast cell derived preformed
mediator “tryptase” – documents massive activation of mast cells
Differential Diagnosis
• Vasovagal collapse – pallor, nausea, diaphoresis, slow pulse but maintained blood pressure
• Hereditary angioedema – strong FHx, laryngeal edema, abdominal pain, abdominal pain without
pruritus, urticarial & hypotension
• Arrhythmias, MI
• Aspiration
• Pulmonary embolism
• Seizure disorders
• Scombroid poisoning – eating fish products that are not fresh/contaminated by bacteria causing
formation of histamine
• Other causes of shock – cardiogenic shock etc

Management
• Monitor vital signs closely & WOF signs of cardiorespiratory failure
• Address early phase reaction: target chemical mediators (block histamine action on peripheral tissues)
o Epinephrine
§ Aqueous dilution 1:1000 at 0.01ml/kg per IM on the the lateral thigh (vastus lateralis
muscle) q 5-15min
§ First and most important treatment for anaphylaxis, and it should be administered ASAP
§ Decreases mediator release from mast cells, prevents or reverses obstruction to airflow
in the upper and lower respiratory tracts, and prevents or reverses cardiovascular
collapse
o Diphenhydramine
§ H1 Receptor antagonist
§ 1mg/kg per IM q4-6h thereafter as long as symptoms persist
o Ranitidine
§ H2 Receptor antagonist
§ 1-2mg/kg/day divided q6-8h per IV
• Address late phase reaction: target cellular mediators
o IV Hydrocortisone 4mg/kg bolus then q6h
• Supportive: supplemental oxygen, rapid IV NSS Infusion for fluid resuscitation, endotracheal intubation
for severe upper airway obstruction, Inhaled SABA for bronchospasm not responsive to epinephrine
• Positioning
o If without upper airway swelling: supine position with the lower extremities elevated to
maximize perfusion of vital organs
o If with upper airway swelling: remain upright (and often leaning forward)
o Pregnant: Left lateral decubitus to minimize compression of the inferior vena cava by the gravid
uterus
• For patients maintained on beta blockers
o Patients receiving beta-blockers may be resistant to treatment with epinephrine and can
develop refractory hypotension. In this situation, glucagon should be administered because it
has inotropic and chronotropic effects that are not mediated through beta-receptors
o Shift to Calcium channel blockers instead
Prevention
• Avoidance of known allergens
• Instruct patient how to use an Epinephrine pen should s/he have another attack
• Administer drugs PO if feasible
• Advise patient to wear & carry warning identification
JMFV D2017, UST-FMS

6. Pediatric Intestinal Obstruction p.97
Definition
• Intestinal obstruction is the partial or complete cessation of anterograde flow of intestinal contents
due to abnormalities in function and/or organic lesions along the wall or in the vicinity of the intestinal
tract

Etiology
• Functional
o Paralytic ileus secondary to hypokalemia and other electrolyte abnormalities
o Drug-induced from opioid analgesics, anti-depressants, anti-muscarinics
• Mechanical (Newborn)
o Upper GIT
§ Congenitally hypertrophic pyloric stenosis: pylorus of the stomach is hypertrophic not
allowing anything to pass
§ Malrotation
§ Duodenal atresia: 1st part of small bowel (duodenum) hasn’t developed properly →
can’t let anything pass → obstruction
o Lower GIT
§ Small bowel atresia
§ Hirschsprung’s Disease: Aganglionic megacolon
• Mechanical (Infant)
o Intussusception: a portion of the bowel telescopes within itself
o Incarcerated inguinal hernia

• Vomiting: Persistent, projectile with bile-stained or bloody vomitus
• Abdominal pain characterized by incessant crying
• Progressive abdominal distention
• Empty rectal vault on DRE
• Abnormal stools
o Hirschsprung’s disease: non-passage of meconium 24h after birth
o Intussusception: bloody mucoid/currant jelly stools
• Dehydration à hemodynamic instability
o From persistent vomiting, intraluminal fluid accumulation, extraperitoneal extravasation
• Vomiting à Hypokalemia à Metabolic alkalosis

Laboratory tests
• CBC, urinalysis (urine SG), serum glucose & electrolyte studies
• Scout Film of the Abdomen
o Observe the intestinal gas pattern: look for air in the sacrum (paucity is suggestive)
o Pneumoperitoneum, step-ladder appearance
• Barium Enema

Management
• Aggressive fluid resuscitation to restore adequate circulation
o PNSS or LRS at 10ml/kg fast drip for 1-2 doses
• KCl
o Given if with adequate UO
• Monitor VS & degree of dehydration
• Prophylactic antibiotic covering G+ & G- organisms
• Surgery if necessary

JMFV D2017, UST-FMS
7. Diarrheal diseases & Dehydration p.52, IMCI
Definition
• Diarrhea is the passage of 3 or more liquid stools in a 24 hours, with the more important feature being
loose/watery consistency rather than the number of bowel movement.
• Best described as excessive loss of fluid and electrolyte in the stool.
• Maybe acute or chronic
o Acute – lasting for a few hours or days
o Chronic (persistent) – lasting for >2 weeks
• Dysentery – diarrhea may also be bloody, in which case it is called dysentery. It is small-volume,
frequent bloody stools with mucus, tenesmus, and urgency

• Dehydration is defined as the fluid loss without loss of supporting tissues or the contraction of
extracellular volume in relation to cell mass.
• It can result from
o External loss of water and salt
o External loss of salt alone
o External loss of water alone

Etiopathogenesis
Mechanism Pathophysiology Stool Etiologic agents Effect of fasting
Exam/Presentation or infection
Secretory Secretagogue (e.g. Cholera Watery, large-volume Cholera, Toxigenic Persist with
toxin) binds to receptor on fecal outputs that are E. coli, carcinoid fasting
the surface of the typically painless syndrome, VIP,
epithelium of the bowel to neuroblastoma,
stimulate intracellular Normal osmolarity congenital chloride
accumulation of cAMP or diarrhea,
cGMP leading to excessive Clostridium difficile
secretion of Cl or HCO3 cryptosporidiosis
with decreased absorption (AIDS)
of Na or H2O
Osmotic Ingestion of osmotically Watery, acidic stools Laxatives, lactose- Resolves with
active or poorly absorbed with reducing intolerance, fasting
solute which draw enough substances lactulose
fluid into the lumen to
exceed the reabsorptive Increased osmolality
capacity of the colon
Increased Decreased intestinal Loose to normal- Irritable bowel Infection may
intestinal transit time appearing stool, syndrome, contribute to
motility stimulated by thyrotoxicosis, increased
gastrocolic reflex postvagotomy motility
dumping syndrome
Inflammatory Inflammatory mediators Frequent, small- Infectious:
can destroy the mucosal volume, bloody stools Salmonella,
lining, decreasing the (+ WBC, RBC or shigella, amebiasis,
absorptive surface leading proteins) Yersinia etc
to osmotic diarrhea &
allow passage of RBCs and Pain, fever, bleeding, Non-infectious:
WBCs. or other IBD, autoimmune,
Mediators can also trigger manifestations of Crohn’s disease,
a secretory type of inflammation Ulcerative colitis
diarrhea by increasing net
secretion

JMFV D2017, UST-FMS
Common Etiologic Agents for Infectious Diarrhea
Bacterial Viral Parasitic
Rotavirus Norwalk agent Escherichia coli Entamoeba histolytica
Adenovirus Calicovirus (Enterotoxigenic, Enteropathogenic, Giardia lamblia
Coronavirus Astrovirus Enteroinvasive, Enterohemorrhagic, Strongyloides
Enteroadherent) Trichuris trichuria
Vibriocholerae Cryptosporidia
Shigella
Campylobacter jejuni
Staphyloccocus aureus
Clostridium difficile
Clostridium perfringens
Yersinia enterocolitica
Vibrio parahaemolytica
Aeromonas hydrophila
Bacillus cereus

Differential Diagnosis

Assess Hydration Status: IMCI Guidelines

JMFV D2017, UST-FMS
Plan A: Treat Diarrhea at Home
• Indications
o Children with no dehydration
o Improved status after Plan B or C
o Children that cannot be returned to the health worker if diarrhea gets worse
• Goals
o Treat child’s current episode of diarrhea at home
o Give early treatment for future episodes of diarrhea
• 4 rules for treating diarrhea at home
1. Give the child more fluids than usual to prevent dehydration
§ Give ORS, if not possible – water. Give as much as the child will take, continue until
diarrhea stops (replace volume per volume)
§ Instructions: Dissolve 1 packet of ORS solution in 200 ml of water and give as follows:

2. Give Zinc supplementation
§ <6 months – 10 mg QD x 14 days
§ >6 months – 5 years old – 20 mg QD x 14 days
3. Give the child plenty of food to prevent under nutrition
§ Continue to breastfeed frequently, if not breastfed, give usual milk
§ If < 6 months old and not yet taking solid food, dilute milk formula with equal amount of
water for 2 days
§ If > 6 months or already taking solid food,
• Give cereal or other starchy food mixed with vegetables, meat, or fish. Add 1 to 2
teaspoonfuls of vegetable oil to each serving
• Give fresh fruit juice or mashed bananas to provide Potassium
• Give freshly prepared food. Cook and mash or grind food well
• Encourage child to eat, offer at least 6 times daily
• Give same foods after diarrhea stops, give extra meal each day for 2 weeks
4. Take child to health worker if child does not get better in 3 days or develops any of the
following:
§ Many watery stools
§ Repeated vomiting
§ Marked thirst
§ Eating or drinking poorly
§ Fever
§ Blood in stool
Plan B: Treat Some Dehydration with ORS
• Approximate the amount of ORS to be given over a 4-hour period
o Weight unknown:

o Weight known:
§ Weight in kg x 75 = ORS in ml
o If the child wants more ORS, give more. Encourage mother to continue breastfeeding
o For infants < 6 months who are not breast fed, also give 100 – 200 ml clean water during this
period
• Observe the child carefully and help the mother give ORS
o For under 2 years, give teaspoonful every 1 to 2 minutesFor older, give frequent sips from a cup
o If child vomits, wait for 10 minutes then give solution more slowly thereafter
o If the child’s eyelids become puffy, stop ORS and give plain water or breast milk then give ORS
according to plan A when puffiness is gone
• Reassess after 4hours of initial hydration
o No signs of dehydration à (+) Urine output, child falls asleep à Plan A
o Signs of dehydration à Repeat Plan B but offer food, milk, juice as in Plan A
o Signs of severe dehydration à Plan C
• If mother must leave before completing Plan B
o Instruct how much ORS to finish in 4-hour treatment. Give ORS packets enough for rehydration
and 2 days

JMFV D2017, UST-FMS
Plan C: Treat Severe Dehydration Quickly

•If possible, observe the patient at least 6 hours after rehydration to be sure mother can maintain
hydration giving ORS by mouth
• If patient is > 2 years old and there is cholera in your area, give appropriate oral antibiotic when patient
is alert
Management of Associated Problems
• Dysentery – blood in the stool
o Treat for 5 days with an oral antibiotic recommended for Shigella in your area: Trimethoprim
(TMP) + Sulfamethoxazole (SMX)
§ Children: TMP 5 mg/kg + SMX 25 mg/kg BID for 5 days
§ Adults: TMP 160 mg + SMX 800 mg BID for 5 days
o Teach the mother to treat the child as described in Plan A
o See the child again after 2 days if:
§ < 1 years old, initially dehydrated, there is still blood in the stool, no improvement
o If the stools is still bloody after 2 days change oral antibiotic to alternative recommended for
Shigella in your area
§ Nalidixic Acid
• Children: 15 mg/kg QID for 5 days
• Adults: 1
g TID for
5 days
§ Ampicillin:
Children: 25
mg/kg QID
• Persistent Diarrhea (>14 days)
o Refer to a hospital
• Severe under nutrition
o Do not attempt
rehydration
o Refer to hospital for
management
o Give ORS 5 mL/kg/hr
• Fever
o Give Paracetamol q4 for Temperature 39.0°C or greater
o If there is Falciparum malaria in the area, and child has fever of 38.0°C and above OR history of
fever in the past 5 days: Give antimalarial
JMFV D2017, UST-FMS
#9#CIRCULATORY#SHOCK#&#FAILURE#
8 p.21%%
DEFINITION% STAGES#OF#SHOCK#
• Significant%↓%in%systemic%tissue%perfusion%→%↓%tissue%oxygen%delivery% %
• Prolonged%↓%oxygen%→%generalized%cellular%hypoxia%→%disruption%of%critical% • PRETSHOCK%
biochemical%processes%which%can%cause%the%following:% o Aka%compensated%shock%
o Cell%membrane%ion%pump%disruption% o Body’s%homeostatic%mechanisms%rapidly%compensate%for%↓%perfusion%
o Intracellular%edema% o Clinical%signs:%tachycardia%and%vasoconstriction%
Inadequate%regulation%of%pH%
%
o
• SHOCK%
o Cell%death%
o During%this%state,%regulatory%mechanisms%are%overwhelmed%
o If%there%is%end%organ%damage%it%will%eventually%lead%to%death%
o Signs%and%symptoms%
% ! Tachycardia% ! Metabolic%acidosis%
1)#HYPOVOLEMIC#SHOCK% ! Tachypnea% ! Oliguria%
• Most%common%type%of%shock% ! Hypotension% ! Cold%clammy%skin%
%
• ↓%in%preload%→%↓%in%cardiac%output%
• ENDTORGAN%DYSFUNCTION%
o Caused%by%fluid%loss%(diarrhea,%vomiting,%osmotic%diureses,%
o Irreversible%organ%damage%and%eventually%death%
burns)%and%hemorrhage%(major%trauma,%GI%bleeding)%
o Signs%and%symptoms%
%
! ↓%urine%output%leading%to%anuria%→%coma%→%acidosis%due%to%
2)#DISTRIBUTIVE#SHOCK%
↓CO%→%multiple%organ%failure%→%death%
• ↓%systemic%vascular%resistance%
%
• Abnormal%distribution%of%blood%flow%within%the%microcirculation% MANAGEMENT%
• Inadequate%tissue%perfusion%→%functional%hypovolemia%(↓preload%but%↑CO)%
• Immobilization:%assume%cervical%spine%instability%
CAUSES%
• Primary%Survey%
• Sepsis#(most%common)% o Rapidly%identify%if%there%is%airway%compromise%or%altered%sensorium%
o Systemic%inflammation%and%widespread%tissue%injury%
• Airway%
o Severe:%organ%dysfunction,%hypoperfusion%or%hypotension%
o Make%sure%it%is%clear%
o Hypoperfusion:%lactic%acidosis,%oliguria,%and%alteration%in%mental%status.%
• Breathing%
o Septic%shock:%hypotension%occurs%despite%having%adequate%fluid%
o Look%for%chest%rise%and/or%listen%for%breath%sounds%
• Anaphylactic#Shock%
• Circulation%
o Massive%release%of%mediators%from%mast%cells%&%basophils%%
o Evaluate%for%tachycardia,%mental%status,%urine%output%
! d/t%exogenous%stimulus%→%↓BP%and%bronchoconstriction%
• Volume%resuscitation%
#
o 1T3%rapid%isotonic%crystalloid%bolus%infusion%20mL/kg%%
3)#CARDIOGENIC#SHOCK# nd
• Vasopressors%(2 %line)%
• Pump%failure%→%↓%in%systolic%function%→%↓%in%CO%
o Hypotensive%despite%adequate%fluid%resuscitation%
4#MECHANISMS#
o ↑%Heart%Rate%–%Epinephrine%
1) Cardiomyopathaties% 3) mechanical%abnormalities%%
o ↑%Contractility%–%Dobutamine,%Amrinone%
2) Arrhythmias%% 4) obstructive%disorders%
o Arterial%constriction%–%norepinephrine,%phenylephrine%
!
9. Acute Abdomen p.111
Definition
• Acute abdomen is a condition where the patient experiences moderate to severe abdominal pain of
less than 24h duration
• Has many causes and only after a thorough history taking and complete PE aided by laboratory and
radiologic examination, can a physician differentiate those conditions needing surgical vs medical
management
Pathogenesis
• Depends on the particular disease entity but abdominal pain is divided into 3 neuroanatomic
categories: visceral, parietal, and referred.
Visceral Pain Somatic Pain Referred Pain
Pain transmission Unmyelinated C fibers Myelinated A-δ fibers Interplay b/w 2 fibers
Character Dull crampy, gnawing, Sharp, sudden, well- Felt in areas remote
midline, difficult to localized pain from the diseased organ
localize
Mechanism Obstruction, ischemia, or Irritation of myelinated Visceral and somatic
inflammation can cause fibers that innervate the afferent neurons from a
stretching of unmy- parietal peritoneum, different anatomic
elinated fibers that usually the portion region converge on 2nd-
innervate the walls or covering the anterior order neurons on the
capsules of organs abdominal wall spinal cord at the same
spinal segment

JMFV D2017, UST-FMS
10. Acute Cholangitis p116
Definition/Pathogenesis
• Bacterial infection superimposed on an obstruction of the biliary tree
• 2 factors are necessary for cholangitis to occur:
o Biliary obstruction
o Bactobilia
• Biliary obstruction causes an increase in intrabiliary pressure, bile stasis, diminished biliary secretion &
cholangiovenous reflux à this leads to increased permeability of bile ductules, permitting
translocation of bacteria and toxins from the portal circulation into the biliary tract
• Bacteria gain access into the biliary tree via
o Ascending route (duodenobilious reflux)
o Descending route (hematogeneous spread)
• Patients usually manifest with the Charcot’s Triad of RUQ Pain, Fever & Jaundice
• In its severe form – Acute suppurative cholangitis, pus is present under pressure in the bile ducts which
can lead to a rapid spread of bacteria via the liver into the blood causing septicemia. Patients usually
manifest with Reynold’s Pentad: Charcot’s Triad + Hypotension + Altered Sensorium

Etiology
• Forms of obstruction
o Gallstones impacted in the CBD – 85% of cases
o Bile duct strictures
o Obstructing Neoplasms – ampullary cancer, pancreatic cancer, cholangiocarcinoma
o Parasitic infections – Ascaris lumbricoides, Chlonorchis sinensis
o Congenital abnormalities of the BD – choledochal cysts, Caroli’s disease
• Bacteria most commonly cultured in these cases include
o Enteric gram negative & positive organisms
§ E. coli
§ Enterococci
§ Klebsiella
§ Pseudomonas
§ Proteus
o Anaerobic organisms
§ Bacteroides fragilis
§ Clostridium perfringens
o Usually polymicrobial

• Charcot’s Triad
o RUQ Pain, Fever, Jaundice
o Full triad is present in only 70% of the cases
• Reynold’s Pentad
o RUQ Pain, Fever, Jaundice + Hypotension, Mental confusion
o Denotes severe cholangitis/Acute Suppurative Cholangitis
o Associated with a high mortality rate & requires urgent biliary drainage

Laboratory/Ancillary Procedures
• Leukocytosis with immature neutrophil forms
• Elevated serum bilirubin & Alkaline phosphatase
• Elevated AST & ALT
• Blood culture often reveals infecting organisms
• PT may be deranged specially in patients with long-standing biliary obstruction
• LGBPS – initial imaging modality that should be done
o Can detect the cause of obstruction
o Has a low sensitivity in detecting a CBD stone itself, it may show evidence of obstruction such as
biliary ductal dilatation
• ERCP
o Endoscopic Retrograde Cholangiopancreatography
o Diagnostic as well as Therapeutic modality
o Can demonstrate bile duct stones, strictures & congenital anomalies
o Tissue sample for biopsy or brush cytology can also be obtained in cases of malignant causes of
biliary obstruction
• MRCP & EUS
JMFV D2017, UST-FMS
o Magnetic Resonance Cholangiopancreatography
o Endoscopic Ultrasonography
o Techniques to evaluate the bile duct & its surrounding structures
o Have a role in the diagnosis but are not necessary in patients with acute cholangitis

Management
• NPO for organ rest
• IV Fluids to cover for 3rd space losses
• IV Antibiotics STAT
o Ampicillin + Aminoglycoside or 3G Cephalosporin
§ Ampicillin + Gentamycin – pregnant patient
§ Cefoxitin 2g/IV q6-8h – initially, usually sufficient
§ Piperacillin- tazobactam 3.375g/IV q6h – more severe cases
§ Meropenem 1g/IV q8h - if resistant organisms are suspected
o Flouroquinolones – high biliary excretion, also a good choice
o Metronidazole – usually added to cover anaerobes
• Biliary decompression via ERCP
o If antibiotics offer no response
o Mainstay of treatment of acute cholangitis
o If adequate, a 3-day regimen of antibiotics will be sufficient
• Sphincterotomy + Stone extraction – done for CBD stones
• Biliary stenting – effective in cases of bile duct strictures
• Nasobiliary drain or Biliary stent – initially placed in severely sick patients & those with coagulation
problems, once stable ERCP or surgery can be performed
• Biliary drainage via Percutaneous Transhepatic Biliary Drainage/Surgery – if ERCP is unsuccessful

JMFV D2017, UST-FMS
11. Gastrointestinal Bleeding p.302, CMDT 2017, IM Platinum 2nd Edition
Definition
• Upper GI Bleeding
o Bleeding proximal to the Ligament of Treitz usually manifesting as hematemesis & melena
o Vomitus with blood clots – reflect massive bleeding
o Coffee Ground Emesis – reflects a slow rate of bleeding with retention of blood in the stomach
& alteration of blood to form hematin
o Melena – usually reflects UGIB, passage of black or tarry stool indicating blood has made transit
for at least 14h in the GIT for hemoglobin to be broken down. Melena without hematemesis
indicates bleeding beyond the pylorus
• Lower GI Bleeding
o Bleeding distal or below the Ligament of Treitz
o Hematochezia is the passage of fresh blood or clots per rectum, usually reflects LGIB but it may
also be a manifestation of a brisk UGIB.

Bleeding Peptic Ulcer Disease
• Most common cause of UGIB
• Etiopathogenesis: Result as a combination of alterations in gastric & duodenal mucosal defense in
response to or as a result of multifactorial predisposing clinical conditions such as increased acidity, H+
pump failure, H. Pylori, ASA, NSAIDs (Anti-inflammatory = inhibition of COX2, GI side effects = inhibition
of the housekeeping enzyme COX1)
• Ulcer – a break in the mucosal surface >5mm
• Clinical Manifestations
o Nocturnal dyspepsia relieved by antacids & meals
o Burning/gnawing epigastric pain
o UGIB
Gastric Ulcer Duodenal Ulcer
st
Location Distal to the junction between 1 portion of the duodenum
antrum & acid secretory mucosa (within 3cm of the pylorus)
Risk of Malignancy Common – should be biopsied Rare
Etiology H. Pylori, NSAIDs
Pathophysiology Normal or decreased gastric acid Increased acid secretion
output Decreased HCO3 secretion
Character of Abdominal pain Burning or gnawing precipitated Burning or gnawing which
by food awakens the patient from sleep
between 12mn to 3am, relieved
by food/antacids
Complications Bleeding: Melena or coffee-ground emesis, most common
complication
Perforation: sudden, severe, generalized abdominal pain. 2nd most
common complication
Gastric outlet obstruction: pain worsening with meals, vomiting of
undigested food

• Diagnosis: establish the presence of an ulcer, then localize
o Barium study – 1st test commonly used to document an ulcer
o Endoscopy – diagnostic study of choice
§ Permits visualization of mucosa: Photographic documentation of a mucosal
defect and tissue biopsy (to R/O malignancy or H pylori)
§ Able to detect lesions too small to be seen by radiographic exam
§ Forrest Classification of Ulcers
• Type 1A – arterial spurting
• Type 1B – arterial oozing
• Type 2A – visible vessel
• Type 2B – adherent clot
• Type 2C – pigmented flat spot
• Type 3 – no stigmata of recent bleed. (+) fibrin-coated clean-based ulcer
o H. Pylori detection
§ Rapid urease – invasive as biopsy is required
§ Urea breath test – non-invasive, simple & rapid. Test of choice for documenting
eradication
§ Fecal H. Pylori antigen test – inexpensive & convenient
JMFV D2017, UST-FMS
• Management
o Initial resuscitation
§ Airway protection
§ Resuscitation of intravascular volume with PNSS or LRS & transfusion of blood/products
when necessary
§ Correction of coagulopathy if present
o High dose PPI: Omeprazole 80mg/IV bolus followed by 8mg/h infusion for 72h
o Therapeutic endoscopy
§ Thermal therapy (heater probe or electrocoagulation)
§ Sclerotherapy with ethanol or epinephrine solution
o Surgery for intractable or recurrent bleeding
§ Excision
§ Vessel ligation, Selective arterial embolization
§ Vagotomy
§ Antrectomy/Gastrectomy
o H. Pylori eradication
§ Omeprazole 20mg BID
§ Clarithromycin 500mg BID
§ Metronidazole 500mg BID
o Stop & avoid using NSAIDs

Esophagogastric Varices
• 2nd most common cause of UGIB
• Result from liver disease, particularly cirrhosis, & portal hypertension when the portal pressure
gradient is >10mmHg
• The variceal rupture is either due to increased variceal pressure or erosion caused by esophagitis.
• Factors that increase the risk of hemorrhage:
o Males > Females
o Child Pugh C
o Red whale markings: Marks the most vulnerable parts of the wall of the esophagus higher
pressures
o Large varices
o Pressure of >12 mmHg: Strongest predictor of variceal hemorrhage
• Treatment
o Pre-primary prevention: To prevent the onset of varices
§ Simvastatin - Reduce pressures in the live à Increase hepatic flow à Reduce hepatic
pressure gradient à prevents formation of varices
o Primary Prevention: To prevent the index bleed
§ Non-selective b-Blocker: Nadolol 80mg/day – prevent small varices to become large
varices. Dose should be adjusted to obtain a 20- 25% decrease in HR or HR < 55bpm
§ Endoscopic variceal ligation: given to patients with contraindications to b-blocker
therapy, no significant advantage over b-blockers
o Definitive Management of Acute Variceal Hemorrhage: To achieve hemostasis for an actively
bleeding vessel
§ Aggressive resuscitation via volume replacement: 2 Large bore IV cannula +
resuscitation with crystalloids
§ Blood transfusion to maintain:
• Hemoglobin at 8g/ day
• Systolic BP of 90-100mmHg
• HR= <100 bpm
§ Prompt identification and control of hemorrhage
• Scope patient once he is stable: Endoscopy is the mainstay of diagnosis
§ Variceal Band Ligation
• Treatment of choice, use upto 6 bands
• Give either Somatostatin, Octreotide, Terliprussin to stop bleeding during
variceal ligation
• Somatostatin 275mcg IV Bolus followed by 3mg/IV infusion over 3h: Constricts
the blood vessels in the splanchnic circulation
• Octreotide 50mcg/h IV Infusion: Analog of somatostatin, effective in decreasing
hepatic gradient only for a short period à mortality percentage is not changed
• Terliprussin: Analog of vasopressin, given every 4 hours à Gradual decrease and
maintains the hepatic gradient = less mortality
JMFV D2017, UST-FMS
§Antibiotic prophylaxis
• 5-7 days with Ceftriaxone 1g/IV OD decreases the rate of bacterial infections &
increase survival in patients with bleeding varices
§ Injection sclerotherapy
• Only done when band ligation is not available or is difficult to do (small vessels
difficult to band)
§ Begin beta-blocker once stable
§ Transjugular Intrahepatic Portosystemic Shunt - shunt blood from very high pressure
portal system to the right side of the heart
• Done if pharmacologic/endoscopic modalities failed
• Early TIPS (within 24h of bleed) is indicated in patients with HVPG>20mmHg
o Secondary Prevention: To prevent re-bleeding
§ Pharmacologic, endoscopic, surgical

Erosive Gastritis & esophagitis
• Common causes of UGIB, defined as endoscopically-visualized subepithelial hemorrhages & erosions
representing inflammatory changes of the mucosal epithelium
• Predisposing factors include alcohol, salicylates, and NSAIDs. Infection, toxic ingestion, radiation, and
stress from severe illness

Mallory Weiss Tear
• A linear mucosal rent near or across the gastroesophageal junction that is often associated with
retching, vomiting, or incessant coughing

Hemorrhoids
• Most common cause of LGIB presenting as hematochezia and protruding rectal mass
STAGE Characteristics Management
I Enlargement with bleeding Fiber supplementation
Cortisone suppository
Sclerotherapy
II Protrusion with spontaneous reduction Fiber supplementation
III Protrusion requiring manual reduction Fiber supplementation
Banding
Operative hemorrhoidectomy
IV Irreducible protrusion Fiber supplementation
Operative hemorrhoidectomy

Diverticular Disease
• Small mucosal herniations protrudingHemorrhage from a colonic diverticulum: most common cause of
hematochezia in patients >60y/o
• Bleeding most commonly from the right colon, usually abrupt & painless
• Localization of diverticular bleeding should include colonoscopy, which may be diagnostic &
therapeutic

Anal Fissure
• Most common cause of rectal bleeding in infancy acquired from trauma to the anal canal following
defecation
• Most common in the posterior wall of the anal canal
• Relative ischemia in the region of the fissure leads to poor healing

JMFV D2017, UST-FMS
12. Porto-systemic Encephalopathy p.703 CMDT 2017

Definition
• Hepatic encephalopathy is a complication of liver cirrhosis which is a state of disordered CNS function
resulting from the inability of the liver to adequately detoxify noxious agents of gut origin, this inability
of the liver to detoxify is secondary to hepatocellular dysfunction and portosystemic shunting caused
by either an underlying chronic hepatic pathology or acute hepatic failure, after exclusion of brain
disease
o Acute liver failure/chronic liver disease à hepatocellular dysfunction or portosystemic shunting
à inability of the liver to adequately detoxify noxious agents of gut origin à disordered CNS
function
• In the setting of acute hepatic failure, it is a syndrome characterized by psychiatric as well as
neurologic abnormalities with jaundice manifesting within 2 to 8 weeks from the onset of symptoms in
the absence of any pre-existing liver disease

Etiology
• Viruses such as Hepatitis
• Chemicals such as Ammonia
• Drugs such as opioids and sedatives
• Gastrointestinal bleeding (Bleeding into the intestinal tract may significantly increase the amount of
protein in the bowelàmore amino acids à more ammonia)
• Surgery, cancer, and radiation
• In the presence of chronic liver disease, precipitating factors include azotemia, hypokalemia, high
protein diet, gastrointestinal bleeding, and hypovolemia
• Other precipitants: Constipation, alkalosis, and potassium deficiency induced by diuretics, opioids,
hypnotics, and sedatives; medications containing ammonium or amino compounds; paracentesis with
consequent hypovolemia; hepatic or systemic infection; and portosystemic shunts (including TIPS)

Pathophysiology
• Normally
o Ammonia is metabolized from dietary amino acids by resident bacterial flora in the colon.
o The ammonia is reabsorbed by the portosystemic circulation.
o 80-90% of the total ammonia produced is shunted to the liver where it is detoxified into urea
and eventually excreted in urine.
o The remaining 10-20% is shunted to the other ammonia metabolizing organs: the brain, heart,
and kidneys
• When more than 60% of hepatic function is lost or when portosystemic shunting towards the brain,
heart, and kidneys is present, there is failure of ammonia detoxification.
• As ammonia levels rise, the brain, heart, and kidneys attempt to compensate but eventually become
overloaded and fail to metabolize the overwhelming amount of ammonia, thus hyperammonemia
occurs
• Ammonia exerts multiple neurotoxic effects resulting to neurologic and psychiatric abnormalities.

Types
• Type A – associated with Acute Liver Failure
• Type B – associated with porto-systemic Bypass & no intrinsic liver disease
• Type C – associated with Cirrhosis and portal hypertension or portal-systemic shunts

• The major clinical features of hepatic encephalopathy include: altered mental status, personality
changes, neuro-ophthalmologic changes, motor abnormalities, and electroencephalographic findings.
• Based on these clinical features, hepatic encephalopathy may be classified to indicate the severity of
the disease.
o Grade 1 - normal EEG finding as well as the motor abnormality being tremors only. Symptoms
include a sleep reversal pattern, emotional lability, irritability, and mild confusion
o Grade 2 - and the succeeding stages are characterized by abnormal EEG findings which reveal
slow, high amplitude, triphasic waves, as well as the presence of asterixis. Symptoms include
lethargy, inappropriate behavior, and disorientation
o Grade 3 – somnolence, aggressive behavior, and severe confusion
o Grade 4 - may reveal a comatose patient with or without response to normal stimuli

JMFV D2017, UST-FMS
Diagnosis
• Diagnosis is based primarily on detection of characteristic symptoms and signs, including asterixis

Management
Since the main pathology in hepatic encephalopathy is the elevation of ammonia levels treatment is geared
towards reducing ammonia formation
• Lactulose
o Mainstay of treatment in hepatic encephalopathy; A non-absorbable synthetic disaccharide
syrup
o Digested by bacteria in the colon to short-chain fatty acids, resulting in acidification of colon
contents
§ This acidification favors the conversion of ammonia (NH3) to ammonium ion (NH4)
§ NH4 is not absorbable & easily excreted in the urine, whereas NH3 is absorbable and
thought to be neurotoxic.
o Also induces catharsis which promotes turnover of gut flora, decreasing the number of
ammonia forming flora
o 30 ml PO TID to QID and is titrated to achieve 3 to 5 soft stools per day
o Continued use of lactulose after an episode of acute encephalopathy reduces the frequency of
recurrences.
• Metronidazole & Neomycin
o Antibiotics traditionally used to increase turnover of gut ammonia-producing intestinal flora
o Neomycin: Aminoglycoside which interferes with bacterial protein synthesis by binding to the
30S ribosomal subunit
o Metronidazole 250mg PO TID: inhibits nucleic acid synthesis by disrupting DNA
o Poor safety profile due to poor safety profile: Neomycin causes ototoxicity and nephrotoxicity
while Metronidazole causes peripheral neuropathy
• Rifamixin
o Derivative of Rifampicin, which binds to the beta subunit of bacterial RNA polymerase to
disrupt DNA formation, has been used for its better safety profile
o Antibiotic given in order to promote turnover of ammonia-producing intestinal flora
o 550mg PO BID
• Dietary protein restriction (60-80 g/day as tolerated)
o No longer advised as a standard of care in hepatic encephalopathy as the ensuing malnutrition
has been found to outweigh any beneficial effects
o Reserved for the small subset of patients who completely are unable to tolerate protein and
often trial of shifting to vegetable sources for protein is attempted before complete restriction
of protein in the diet.
• Diet with Branched Chain Amino Acids
o Leucine, valine and isoleucine
o BCAAs supply the TCA-cycle with carbon skeletons and thereby enhance the procuction of alfa-
ketoglutarate (α-KG)
o α-KG can be reductively aminated to glutamate (Glu) and glutamate may be amidated to
glutamine (Gln)
§ BCAA à aKG à Glutamate
§ Glutamate + Free NH4 à Glutamine (Reaction is catalyzed by Glutamine Synthetase
which present in large amounts in skeletal muscle)
o This way, you contain the ammonia in Glutamine
• Correct the underlying triggers
o Dehydration, GI Bleeding, electrolyte imbalances (Repletion of K) etc

JMFV D2017, UST-FMS
13. Hypertensive Crisis p.144, JNC 7, JNC 8, CMDT 2017
Definition
• Hypertensive crisis is a sudden, acute blood pressure elevation to levels higher than what is normal for
the affected individual
• 2 Types
o Hypertensive Urgency
o Hypertensive Emergency
• Hypertensive Urgency
o JNC 7: Situations associated with severe elevations in BP without progressive target organ
dysfunction.
o CMDT 2017: These include patients with asymptomatic severe hypertension that persists after
a period of observation which requires BP reduction (not necessarily to normal) within a few to
24 hours using Oral medications
• Hypertensive Emergency
o JNC 7: A severe elevation in blood pressure (usually >180/120 mm Hg) complicated by evidence
of impending or progressive target organ dysfunction. Hypertensive emergency is a clinical
diagnosis and the clinical state of the patient is more important than the absolute value of the
BP
o This requires immediate (within 1 hour) BP reduction (not necessarily to normal) to prevent or
limit target organ damage using parenteral agents
o Clinical manifestations of target organ damage usually involve derangements in the neurologic,
cardiac, or renal systems
§ Myocardium – most common target organ with a manifestation of ACS (Unstable angina
or MI)
§ Hypertensive Encephalopathy – headache, irritability, confusion, and altered mental
status due to cerebrovascular spasm
§ Hypertensive Nephropathy – hematuria, proteinuria, and acute kidney injury due to
arteriolar necrosis and intimal hyperplasia of the interlobular arteries
§ Others include, but not limited to: acute hemorrhagic or ischemic stroke, acute
papilledema, acute pulmonary edema, aortic dissection and eclampsia
o Types:
§ Accelerated hypertension - characterized by headaches, blurred vision, and focal
neurologic deficits
§ Malignant hypertension - Accelerated hypertension with papilledema, Encephalopathy
or nephropathy accompanying hypertensive retinopathy has historically been termed
malignant hypertension

JNC 7 Blood Pressure Classification (AV Chrobanian et al: JAMA 289: 2560, 2003)
Classification Systolic Diastolic NB
(mmHg) (mmHg)
Normal <120 and <80 J
Pre-hypertension 120-139 or 80-89 Not a disease category
Stage 1 140-159 or 90-99
Hypertension On 2 or more readings on at least 2
different visits one to several weeks apart
Stage 2 >160 or >100
Hypertension
Hypertensive BP elevation with NO evidence of end
Urgency >180 or >120 organ damage
Hypertensive BP elevation WITH evidence of end organ
Emergency damage

Etiology
• Consequence of uncontrolled longstanding primary or essential hypertension – 90% of cases
• Stimulant intoxication, including cocaine, methamphetamine, and phencyclidine as well as withdrawal
syndromes from the anti-hypertensives such as clonidine and beta blockers
• Uncontrolled causes of secondary hypertension such as renal parenchymal disease, renovascular
disease, pheochromocytoma, Cushing’s syndrome, Primary Hyperaldosteronism, Coarctation of the
aorta, and obstructive sleep apnea, adverse drug interactions with monoamine oxidase inhibitors
(MAO-I)

JMFV D2017, UST-FMS

Pathogenesis
• Normal
o Autoregulation. In normotensive people, there is ordinarily a broad range of pressures through
which arteries and arterioles can dilate and constrict to maintain normal and consistent
perfusion
• Chronic Hypertension
o Chronic hypertension causes arterial walls to accommodate chronically excessive pressures.
This autoregulation setpoint in hypertension limits the vessels’ ability to respond appropriately
to acute decreases or increases in BP
o When BP abruptly increases, regardless of stimulus, larger arteries reflexively vasoconstrict in
an effort to limit pressure reaching the tissues, which would interfere with normal cellular
activity
o In this situation, an acute lowering of BP by a clinician seeking to re-achieve a “normal” BP will
reduce the blood flow to tissue without prompt compensatory vessel dilation, which can lead to
ischemia of end-organ tissue.
o Therefore, it is important when treating hypertensive emergencies, to not decrease BP either
too rapidly or by too great of an amount.

Laboratories/Ancillaries
• Requested with the goal of determining the extent of end organ damage in order to guide treatment
decisions as certain organ dysfunctions can become relative contraindications for starting certain
antihypertensives
• It is imperative to request for a 12 lead electrocardiogram in order to determine whether there is an
ongoing myocardial infarction. Biomarkers for myocardial infarction such as Troponin I should also be
requested if the patient’s clinical findings are suggestive. ECG findings may also suggest the presence of
electrolyte abnormalities and cardiac chamber enlargement
• Urinalysis should be requested to screen for any hematuria or proteinuria indicative of acute kidney
injury, results should be correlated with serum creatinine levels
• Serum electrolytes should also be measured not only to guide correction but also to guide the choice
of antihypertensive agent
• A Chest X-ray should be requested if pulmonary edema is a consideration in a patient with equivocal
chest physical examination findings.
• Women of child-bearing age require a pregnancy test.
• If any focal neurologic signs are present, or a decrease in mental status is noted, a CT scan of the head
is needed to evaluate for hemorrhage or infarct

Management: Management goals are different for urgencies and emergencies
• In the setting of a hypertensive urgency, blood pressure may be lowered over the course of the next 24
hours using oral anti-hypertensive agents
• In comparison, the immediate goal for treating hypertensive emergency is to reduce the SBP by 10-
15%, but by no more than 25% (Reduce MAP by no > 25%; MAP = 2SBP + DBP/3), within the first hour
and if the patient is then stable, to 160/100-110 mm Hg over the ensuing 2-6 hours
• IV Nicardipine
o First line agent as it is the most potent & longest acting of all the parenteral CCBs, it is indicated
in most hypertensive emergencies except in acute heart failure, caution with coronary ischemia
o Acts primarily as an arterial vasodilator
o Onset: 5-10min
o Duration: 15-30min, may exceed 4h
o Adverse effects:
§ Has the potential to precipitate reflex tachycardia, and for that reason it should not be
used without a beta-blocker in patients with coronary artery disease as it may
precipitate MI
§ Hypotension
§ Headache
o Dose: 5mg/h; titrate by increments of 1-2.5 mg/h every 15 minutes to 15 mg/h
o Sample order: Nicardipine drip 10mg in 90cc PNSS to run initially at 10cc/hr, titrate by
increments of 5cc/hr to maintain BP </= 150/90
• IV Labetalol
o Combined beta- and alpha-blocking agent is the most potent adrenergic blocker for rapid blood
pressure reduction. It is indicated in most hypertensive emergencies except acute heart failure
o Dose: 20–80 mg IV bolus every 10 min 0.5–2.0 mg/min IV infusion
o Onset: 5-10min
JMFV D2017, UST-FMS
o Duration: 3-6h
o Adverse effects:
§ Vomiting, scalp tingling, bronchoconstriction, dizziness, nausea, heart block, orthostatic
hypotension
• IV Furosemide
o A Loop diuretic which may be added for patients with features of heart failure or fluid
retention. Also acts as an adjunct to a vasodilator
o Dose: 10-80 mg
o Onset: 15min
o Duration: 4h
o Adverse effects:
§ Hypokalemia, hypotension
• Hypertensive Urgency
MOA Dose Adverse Effects
Oral Clonidine Central 0.1 -0.2mg initially; Sedation
sympatholytic then 0.1mg every Rebound
hour to 0.8mg hypertension
Oral Captopril ACEI 12.5-25 mg Excessive
hypotension
Oral Nifedipine CCB 10mg initially; may Hypotension,
be repeated after tachycardia,
30 minutes headache,
angina, MI, CVA
DO NOT LOWER BP TO NORMAL IMMEDIATELY TO AVOID ORGAN HYPOPEFRUSION

JMFV D2017, UST-FMS

#15$ACUTE$HEART$FAILURE$IN$ADULTS$
14 p.123&
DEFINITION:&Heart&failure&develops&when&the&heart,&via&an&abnormality& MANAGEMENT$
of&cardiac&function&(detectable&or&not),&fails&to&pump&blood&at&a&rate& &
commensurate&with&the&requirements&of&the&metabolizing&tissues&or&is& ACUTE&CARDIOGENIC&PULMONARY&EDEMA&
able&to&do&so&only&with&an&elevated&diastolic&filling&pressure& • Nitrates:&sublinguinal&nitroglycerin&(0.4]0.6mg&every&5]10&minutes&
& as&needed),&if&SBP&≥&95]100&→&IV&
SIGNS/SYMPTOMS$of$Heart$Failure:&The&Framingham&Criteria&for& • Sodium&nitroprusside:&start&at&0.1ug/kg/min&if&unresponsive&to&
diagnosis&of&heart&failure&consists&of&the&concurrent&presence&of&either& nitrate&or&if&cause&is&severe&mitral&or&aortic&regurgitation&or&
2&major&criteria&or&1&major&and&2&minor&criteria& marked&hypertension&
• Major&Criteria:&paroxysmal&nocturnal&dyspnea,&neck&vein& • Furosemide:&20]80mg/IV&
distention,&rales,&acute&pulmonary&edema,&S3&gallop& • Morphine&sulfate:&3]5mg/IV&
• Minor&Criteria:&nocturnal&cough,&dyspnea&on&ordinary& • Intubation&and&mech&vent.&–&if&w/&sever&hypoxia&
exertion,&pleural&effusion,&tachycardia&(>120bpm),&bilateral& &
ankle&edema& CARDIOGENIC&SHOCK&/&NEAR&SHOCK&
& • Oxygen&therapy&
DIAGNOSTIC$TESTS$ • In&absence&of&obvious&intravascular&volume&overload,&brisk&IV&
• 12L&ECG& administration&of&fluid&volume&
• CBC&with&platelet,&Na,&K,&Mg,&iCa,&BUN,&CREA& • In&presence&of&volume&overload:&give&cardiovascular&support&drugs&
• ABG& to&attain&stable&hemodynamic&status&
• CXR& • Urgent&coronary&revascularization&if&available&&
• Transthoracic&Doppler& &
• Coronary&Arteriography&–&for&refractory&cases& ACUTE&DECOMPENSATION&OF&CHRONIC&HEART&FAILURE&
& • Clinical&manifestations&are&secondary&to&volume&overload,&
AHF&can&be&grouped&clinically&into& elevated&ventricular&filling&pressure&and&depressed&cardiac&output&
1) Acute&Cardiogenic&Pulmonary&Edema& • Mild&to&moderate&symptoms&can&be&treated&with&IV&or&oral&
2) Cardiogenic&Shock& diuretics&and&do&not&need&hospitalization&
3) Acute&Decompensation&of&Chronic&Left&Heart&Failure& • Moderate&to&sever&symptoms&require&admission&under&cardiac&
& ICU;&IV&drugs&can&be&withdrawn&in&a&decremental&manner&while&
& orally&administered&drugs&are&optimized&
& &
&
&
!
15. Acute Coronary Syndrome p.221, AHA ACS-NSTEMI 2014, AHA ACS-STEMI 2013

Definition
• Operational term which refers to a spectrum of conditions compatible with acute myocardial
infarction/ischemia due to an abrupt cessation of coronary blood flow
• Spectrum: Unstable Angina à NSTEMI à STEMI
o 2 Categories
§ NSTE-ACS
• Unstable Angina
• NSTEMI
• These 2 are closely related conditions whose pathogenesis and clinical
presentations are similar but vary in severity. The conditions differ primarily by
whether the ischemia is severe enough to cause myocardial damage leading to
detectable quantities of myocardial injury biomarkers
§ STEMI-ACS
• Unstable Angina
o Chest pain that is new onset, accelerating (ie. occurs with less exertion, lasts longer, less
responsive to medication), or occurs at rest
o It signals the presence of possible impending infarction based on plaque instability
• NSTEMI
o Indicates myocardial necrosis marked by elevations in the troponin I and CKF MB without ST
segment elevations seen on ECG
o Partial coronary artery occlusion
• STEMI
o Indicates myocardial necrosis = elevation of cardiac enzymes with ST segment elevation on ECG
o Complete coronary artery occlusion, indication for reperfusion

• The hallmark of ACS is the sudden imbalance between myocardial oxygen consumption and demand,
which is usually the result of coronary artery obstruction
• 2 Types of ACS (AHA, 2014) based on pathogenesis/etiology
o MI Type 1 - caused by a primary coronary artery process such as spontaneous plaque rupture
o MI Type 2 - related to reduced myocardial oxygen supply and/or increased myocardial oxygen
demand (in the absence of a direct coronary artery process)
• ACS almost always are associated with rupture of an atherosclerotic plaque and partial or complete
thrombosis of the infarct-related artery
o ACS is caused primarily by atherosclerosis à formation of non-severe atherosclerotic lesion
that was previously hemodynamically insignificant yet vulnerable to rupture, this vulnerable
plaque is typified by a large lipid pool, numerous inflammatory cells & a thin fibrous cap à
rupture of atherosclerotic plaque à partial/complete thrombosis of the infarct-related artery
• Ischemic triggers include: exercise, assuming upright postion, cigarette smoking, cold exposure
• Possible triggers of MI
o 51.1% no trigger
o 18.4% emotional upset
o 14.1% moderate physical activity
o 8.7% Heavy physical activity

• Symptoms
o Palpitations
o Pain, which is usually described as pressure, squeezing, or a burning sensation across the
precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm,
not relieved by rest/nitroglycerin, >10 minutes in a crescendo pattern
§ Angina equivalents: epigastric pain, exertional dyspnea, syncope
o Exertional dyspnea that resolves with pain or rest
o Diaphoresis from sympathetic discharge
o Nausea from vagal stimulation
o Decreased exercise tolerance
• Physical examination results are frequently normal. If chest pain is ongoing, the patient will usually lie
quietly in bed and may appear anxious, diaphoretic, and pale. Physical findings can vary from normal to
any of the following:
JMFV D2017, UST-FMS

o Hypotension - Indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute
valvular dysfunction
o Hypertension - May precipitate angina or reflect elevated catecholamine levels due to anxiety
or to exogenous sympathomimetic stimulation
o Diaphoresis
o Pulmonary edema and other signs of left heart failure
o Extracardiac vascular disease
o Jugular venous distention
o Cool, clammy skin and diaphoresis in patients with cardiogenic shock
• PE can be normal but we should check for signs of HF since this should be treated immediately: S4,
paradoxical splitting and murmur of an MR (papillary muscle dysfunction

Differentials
• Costochondritis (muskuloskeletal) – coupling pain on palpation, pain worsened by movement
• Abdominal aortic aneurysm – pulsatile abdominal mass
• Aortic dissection - back pain, unequal palpated pulse volume, a difference of ≥15 mm Hg between both
arms in systolic blood pressure (BP), or a murmur of aortic regurgitation
• Acute pericarditis – pericardial friction rub
• Cardiac tamponade – Beck’s triad: muffled heart sounds, hypotension, jugular venous distention
• Pneumothorax - acute dyspnea, pleuritic chest pain, and differential breath sound

Diagnosis
• ACS includes UA, NSTEMI & STEMI. It is important to differentiate the 3 as treatment varies
• Request 12-Lead ECG within 10min of the patient’s arrival at the ER, can be normal which does not r/o
ACS so perform serial ECG monitoring q15-30min, specially if symptoms recur. This will differentiate
NSTEMI/UA vs STEMI
ECG Findings
NSTEMI/Unstable Angina STEMI
ST segment depression Any ST elevation of >1mm in 2 contiguous
T wave inversion leads except V2 & V3
Transient ST segment depression
In V2/V3:
> 1.5mm in women
> 2.0mm in men >40y/o
> 2.5mm in men <40y/o

New-onset LBBB

Before: ST elevation of at least 1mm in two
or more limb leads or at least 2mm in two or
more chest leads.

• To differentiate between NSTEMI & UA, request for cardiac enzymes
o Troponin I – most sensitive/specific. Rises few hours after onset and remain elevated for up to 2
weeks
o NSTEMI – elevated cardiac enzymes
o UA – normal cardiac enzymes
• CXR – useful to identify potential pulmonary causes and may show widened mediastinum (aortic
dissection) à chest pain. This may also show cardiomegaly.

Treatment (NSTEMI)
Goals for NSTEMI/UA
• Stabilize the acute coronary lesion
• Treat the residual ischemia
• Employ long term secondary prevention

Early hospital care
• Oxygen
• Anti-ischemic/Analgesic therapy for Relief of chest pain (Nitrates, Morphine, b-Blockers)
• Anti-thrombotic (Aspirin, heparin, clopidogrel, GPIIbIIIa inhibitors)

JMFV D2017, UST-FMS
Supplemental oxygen
• Provide oxygen only to hypoxemic patients, O2 Sat <90% or with respiratory distress
• Routine supplemental O2 have not demonstrated benefit but instead can have untoward effects in
normoxemic patients, as hyperoxia can cause direct coronary vasoconstriction, inreased coronary
vascular resistance, reduced coronary blood flow and increased risk of mortality

Anti-ischemic Therapy
• Nitrates: Increases coronary blood flow
o Endothelium-dependent vasodilator of coronary & peripheral vasculature by
§ Releasing Nitric Oxide which stimulates guanylyl cyclase and causes and increase in
cGMP à dephosphorylation of myosin light-chain phosphate à smooth muscle
relaxation
o Dilate capacitance vessels to ↓ preload and ventricular wall tension, also reduces afterload by
its effect on arterial circulation
o Give sublingual up to 3 doses (NTG: 0.3-0.4mg/kg) q5mins then assess for need of IV NTG
usually indicated for patients with Persistent Ischemia, HF or hypertension
o Contraindicated with recent use of PDE-inhibitors like Sildenafil à May cause Hypotension
• Beta-blockers: Decreases myocardial oxygen demand
o Reduces the myocardial oxygen demand by inhibiting the increase in HR, Arterial pressure,
myocardial contractility by adrenergic activation
§ Decrease HR, contractility and BP à ↓ MV02
§ Decrease myocardial ischemia, reinfarction and occurrence of complex ventricular
dysrhythmias
o Increases long-term survival
o Oral beta-blockers should be initiated in the 1st 24h given that there are no contraindications
found in the patients such as signs of HF, low-output state, risk of cardiogenic shock (>70 y/o,
HR >110, SBP <120, late presentation), PR interval >0.24 sec, 2nd or 3rd degree heart block
without a pacemaker, active asthma and reactive airway disease
o IV beta blockers are potentially harmful when risk factors for shock are present
o Preferred oral Beta-blockers are those without increased sympathomimetic activity:
Metoprolol, Bisoprolol, Carvedilol
• Calcium Channel Blockers
o Given if b-Blockers are not successful (recurrent ischemia s/p b-blocker), are contraindicated, or
cause unacceptable side effects in the absence of
§ LV Dysfunction
§ Increased risk of cardiogenic shock
§ PR Interval >0.24s
§ 2nd or 3rd degree heart block without a pacemaker
o CCB decreases transmembrane calcium current, which results in reduction in contractility
throughout the heart and decreases in sinus node pacemaker rate and atrioventricular node
conduction velocity
o Dihydropyridine CCBs (Nifedipine & Amlodipine)
§ Most marked peripheral vasodilation but little direct effect on contractility, AV
conduction and HR.
§ Nifedipine can increase mortality in patients with CAD thus not routinely recommended
for ACS patients
§ Immediate-release Nifedipine is contraindicated in the absence of a b- Blocker
o Non-Dihydropiridine CCBs (Verapamil or Diltiazem)
§ Negative inotropic and negative chronotropic and dromotrophic effects; added to those
effects studies have shown that it can decrease reinfarction in some patients
§ Verapamil (80-160 mg q8h) and Diltiazem (30-80mg q6h)

Analgesic Therapy
• Morphine Sulfate
o Potent analgesic and anxiolytic effects as well as hemodynamic actions such as venodilatation
and deceased heart rate and Systolic BP -- so it is reasonable to administer this IV if chest pain
persists despite being given maximally tolerated anti- ischemic meds
o NSAIDs (except Aspirin) should not be administered: Traditional and selective COX-2 inhibitors
markedy block endothelial prostacyclin production that leads to unopposed platelet
aggregation that can interfere in the beneficial action of the aspirin wherein we can attribute
increased risk of MACE (major adverse cardiac events)
o 1-5mg/IV q5-30min
JMFV D2017, UST-FMS

o Hypotension and respiratory depression are the most serious complications of excessive use of
morphine. Naloxone (0.4 mg to 2.0 mg IV) may be administered for morphine overdose with
respiratory or circulatory depression.

Dual Antithrombotic Therapy: Anti-platelet & Anti-coagulant
Antithrombotic therapy to prevent further thrombosis. Long term therapy to prevent progression to complete
• Aspirin (Anti-platelet)
o COX-1 inhibitor: blocks release of thromboxane (platelet activator) thus preventing platelet
aggregation and thrombus formation
o Established first-line therapy in patients (NSTE-ACS)
o ↓ incidence of MI recurrence and death
o Should be non-enteric coated. Enteric-coated aspirin should be avoided because of delayed and
reduced absorption
o Lower dose is favored since it is only associated with increased bleeding with the absence of
improved outcomes
o Initial dose: 162-325mg PO to be chewed, for a more rapid buccal absorption
o Maintenance dose: 81-162mg/day PO
• Clopidogrel (Anti-platelet)
o P2Y12 receptor inhibitor – major role in the inhibiting the amplification of platelet activation
o Administration of clopidogrel with aspirin was superior to administration of aspirin alone in
reducing the incidence of cardiovascular death and nonfatal MI or stroke
o Initial dose: 300mg PO (4 tablets)
o Maintenance dose: 75mg/day PO
• LMWH: Enoxaparin (Anti-coagulant)
o Have a molecular weight approximately 1/3 that of UFH and have balanced anti-Xa and anti-IIa
activity à readily absorbed after subcutaneous administration and have less platelet activation
o No need for monitoring but less effectively reversed by protamine, also more affected by renal
dysfunction
o Enoxaparin seems to be superior to unfractionated heparin in reducing mortality and bleeding
outcomes during percutaneous coronary intervention and particularly in patients undergoing
primary percutaneous coronary intervention for ST elevation myocardial infarction
o Initial dose: 30mg/IV
o Maintenance dose: 1mg/kg/SC q12

Other measures
• Statin therapy
o Reduces the rate of MI recurrence, coronary heart disease mortality, need for revascularization
and stroke
o MOA: HMG-CoA Reductase Inhibitors – plaque stabilizers
o High-intensity statin therapy should be initiated or continued in all patients with NSTE-ACS and
no contraindications to its use
o Obtain a fasting lipid profile within 24h
o Atorvastatin 20mg FC tab initially, 10-20mg OD
o Rosuvastatin 10-40mg OD
• ACE-Inhibitors
o Should be started within 24h of MI
o Should be given to patients with LV dysfunction (LVEF <0.40), hypertension, DM and stable CKD,
unless contraindicated
§ CI: significant renal dysfunction
o Prevent ventricular remodeling with subsequent reduction of CHF & Reduce the morality rate
o Decreases sympathetic activity & improves endothelial function
o Captopril 6.25mg q6-8, max of 50mg TID
o Enalapril 2.5mg/day max of 20mg BID

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Treatment (STEMI)
Goals of treatment
• Relief of ischemic chest pain (Oxygen, Nitrates, b-Blockers, Morphine)
• Assessment of hemodynamic status & correction of abnormalities present
• Initiation of reperfusion with primary percutaneous coronary intervention (PCI) or fibrinolysis
• Anti-thrombotic therapy to prevent recurrent ischemia & life-threatening ventricular arrhythmias
(Aspirin, clopidogrel)
• Prevention of ventricular remodeling (ACEi, Reperfusion)
Supplemental Oxygen
• Only to patients with O2 Sat <90% or with respiratory distress
Reperfusion
Prompt restoration of myocardial blood flow is essential to optimize myocardial salvage & to reduce mortality
• PCI
o Enhanced survival & lower rate of intracranial hemorrhage & recurrent MI vs Fibrinolysis
o Time from the 1st medical contact to PCI (Door to balloon): <90min in a PCI-capable hospital or
<120min in a non-PCI capable hospital
• Fibrinolysis
o Recommended in patients with symptom onset within 12hours who can not receive PCI within
120min of medical contact
o Door to needle is <30min
o Contraindications
§ Known bleeding disorder, prolonged traumatic CPR, Aortic dissection, persistent HTN >
200/120, pregnancy, major trauma/surgery within the last 2 weeks, active internal
bleeding
• Coronary Artery Bypass Graft Surgery – not usually performed in patients with STEMI but is only
indicated when there is PCI or Fibrinolysis failure.
Medications
• Dual anti-thrombotic: Anti-platelet, anti-coagulant
• Morphine Sulfate
• Sublingual NTG
• Statin Therapy
• B-Blockers

JMFV D2017, UST-FMS
16. Venous Thromboembolism p.212, Medicine2 Pulmonology Module Workbook 2016
Definition
• VTE is a one-disease concept wherein part of a thrombus from the deep veins of the legs embolizes in
the pulmonary circulation.
o Thrombus – abnormal clot that forms in a vessel
o Embolus – part of a thrombus which breaks off & lodges elsewhere
• VTE includes
o Deep Vein Thrombosis
o Pulmonary Embolism

Risk Factors
• Basic Risk Factor: Virchow’s Triad of Thrombosis
o Stasis
o Hypercoagulability
o Endothelial injury
• Clinical Risk Factors
o Acute MI, Stoke, Malignancy, Pregnancy
• Molecular Risk Factors
o Deficiencies in protein C, S or AT3

Pathogenesis
• Venous thrombi start to form either in
o The vicinity of a venous valve, where eddy currents arise
o Or at the site of intimal injury
• Platelets start to aggregate with release of mediators that initiate the coagulation cascade, causing the
formation of a red thrombus.
• At any time during the formation of a venous thrombus, a portion or all of the thrombus can detach as
an embolus.
• Once embolism occurs, it can trigger very serious pulmonary and cardiac effects (impaired gas
exchange; increased pulmonary vascular resistance), depending on the extent of the reduction of the
cross sectional area of the pulmonary vascular bed as well as the preexisting status of the
cardiopulmonary system.
• Over 90 percent of cases of acute PE are due to emboli emanating from the proximal veins of the lower
extremities. Thrombus formed above the popliteal vein e.g. iliofemoral, (above-the-knee, thigh or
proximal thrombi) appear to be the source of most clinically recognized pulmonary embolus.
• In contrast, the majority of thrombi that arise below the popliteal vein (below-the-knee, distal or calf
vein thrombi) appear to resolve spontaneously and do not commonly embolize to the lung

• PE
o Dyspnea – most common symptom of PE
o Tachypnea – most common sign of PE
o Massive PE: Dyspnea, syncope, hypotension, central cyanosis
o Small PE located near the pleura: pleuritic pain, cough or hemoptysis
o Classic signs of PE: Tachycardia, low-grade fever, neck vein distention, accentuated pulmonic
component of S2
• DVT
o Unilateral leg swelling – most common sign of DVT
o Homan’s sign – tenderness/pain behind the knee on dorsiflexion of the ipsilateral foot
o Warmth, pain, redness

Diagnosis
• Well’s Criteria – one of the most clinically tested decision rule based on history taking & physical
examination to diagnose VTE

JMFV D2017, UST-FMS
• Well’s Criteria for DVT DVT:
o (Upper table)
o Interpretation (CMAJ, 2006)
§ 1point – DVT is likely
§ <1point – DVT unlikely
• Well’s Criteria for PE
o (Lower table)
o Interpretation
§ >4 – PE is likely
§ <4 – PE is unlikely

PE:
Laboratory Tests
• PE
o CBC – non-specific: may show leukocytosis
o ABG – non-specific: low O2 & CO2, may be
normal
o D-Dimer Assay – a negative test may rule
out PE in patients with a low to moderate
pretest probability and a non-diagnostic
VQ scan
o CXR – non-specific, can be normal
§ Hampton’s Sign: A peripheral wedge
shaped infiltrate which signifies a PE
with infarction
§ Westermark’s Sign: Localized decrease in pulmonary vascular markings (focal oligemia)
§ Palla’s Sign: Increase in pulmonary artery size, can be seen in CXR & Chest CT
o CT Pulmonary angiography – remains the gold standard for diagnosis, shows filling defects or
sharp cutoff on the pulmonary artery or small pulmonary vessels
o VQ Scan of the Lungs – 2nd line diagnostic test: A normal perfusion lung scan virtually excludes
PE. High probability scan for PE is >2 segmental perfusion defect
• DVT
o Contrast Venography – has long been considered the "gold standard" for the diagnosis of DVT.
Uses contrast & X-ray to show blood flow through the veins
o Impedance plethysmography (IPG) – non-invasive test which measures venous outflow from
the lower extremity and can detect proximal vein thrombosis
o Duplex Scan – most widely used modality for evaluating patients with suspected DVT. A positive
test shows a non-compressible vein or no/decreased blood flow

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Management
• Anticoagulants
o Main treatment regimen, administered to avoid further clot formation in the lower extremities
thus preventing further embolic episodes
o Unfractionated heparin (UFH) IV or SQ- initial drug of choice
§ Bolus of 80 IU/kg IV and maintenance infusion at 18 IU/kg.
§ Duration is usually 7-10 days (5 days is just as effective
§ Partial thromboplastin time (aPTT) of the patient maintained between 2-3 times the
upper limit of the laboratory normal
o Oral anticoagulation with warfarin - may be started on the first day of heparin therapy (usual
overlap is 3 – 5 days, as full effect of warfarin requires 5 days.)
§ PT should be monitored with an INR target of
• 2.5, with a range of 2.0- 3.0 (1st 3mo)
• 1.5-1.9 – after 3mo
o Low molecular weight heparin (LMWH) e.g. Enoxaparin.
§ 1 mg/kg/SQ q12 hours for up to 3 months in VTE patients with reversible risk factors.
§ For recurrent emboli and nonreversible risk factors, therapy may have to be given
indefinitely.
§ Less bleeding complications from LMWH than UFH
• Thrombolytic Therapy
o Streptokinase, Urokinase, and recombinant Tissue Plasminogen activator (rTPA). Accelerate the
resolution of the pulmonary artery clot and may be used especially in patients with massive
embolism and systemic hypotension.
• Newly-developed Anti-coagulants/Anti-thrombotics
o Most are monotherapeutic
o Specific factor Xa inhibitors e.g. Fondaparinux) in contrast to the LMWH which is
polytherapeutic
• NOAC
o New oral anti-coagulants
o Dabigatran, Rivaroxaban, Apixaban
• Non-pharmacologic
o IVC filter, intermittent pneumatic compression device (IPC), graduated compression stockings
(GCS), and anti- embolic stockings (AES).

Prophylaxis
• UFH – SQ, every 8 hrs; needs aPTT monitoring
• LMWH
o Fondaparinux is a Factor Xa inhibitor, pentasaccharide, given for prophylaxis in medical patients
at 2.5 mg/ subcutaneous q 24hours.
o Rivaroxaban- Factor Xa inhibitor given for prophylaxis in patient who underwent orthopedic
surgery
• Early ambulation, especially for post-operative patients.
• Graduated elastic compression stockings – provide pressure on the lower extremities, to prevent
venous stasis.
• Intermittent pneumatic compression – is a mechanical device attached to the extremities, which
provides some form of passive leg exercises, therefore stimulating muscle contraction
• Inferior vena caval interruption – a most popular and widely used device is the Greenfield filter

JMFV D2017, UST-FMS
18. Hemoptysis p.169, CMDT 2017
Definition
• Hemoptysis is the expectoration of blood in gross amounts or in streaks from a source below the glottis
(Larynx, trachea, bronchi, lungs)
• Massive hemoptysis
o Occurs in 5% of cases is defined as 200-600ml of blood expectoration in 24h
o Clinically, massive hemoptysis is any bleeding that results in impairment of lung function & gas
exchange
o Originates from a bronchial artery in 90% of cases with a 20% fatality rate

Etiology: It can be caused by several factors
• Infections – PTB, paragonimiasis, aspergilloma, amoebic liver abscess (pleuro-pneumonic
complication), necrotizing pneumonias, lung abscess
• Bronchiectasis
• Acute/chronic bronchitis
• Neoplasms – lung malignancies, endobronchial adenoma, carcinoid tumor, choricarcinoma, osteogenic
carcinoma
• Iatrogenic – lung biopsy, catheter-induced, ETT, bronchoscopy
• Trauma – blunt/crushing injuries, penetrating rib fractures
• Cardiovascular conditions – MS, Acute pulmonary edema, aortic aneurysm rupture in a bronchus,
AVMs
• Others: DIC, Anticoagulation, Thrombocytopenia, Aspiration of foreign bodies/gastric contents, Good
Pasture Syndrome, SLE, Wegener’s granulomatosis
• Cryptogenic hemoptysis – 20% of cases where the cause remains unknown despite extensive
evaluation

Pathogenesis
• The lungs are supplied with a dual circulation.
o The pulmonary arteries arise from the right ventricle to supply the pulmonary parenchyma in a
low-pressure circuit.
o The bronchial arteries arise from the aorta or intercostal arteries and carry blood under
systemic pressure to the airways, blood vessels, hila, and visceral pleura.
• Although the bronchial circulation represents only 1-2% of the total pulmonary blood flow, it can
increase dramatically under conditions of chronic inflammation- eg, chronic bronchiectasis-and is
frequently the source of hemoptysis.

Clinical manifestations depend on the primary disease, site, degree, and rate of hemorrhage.
• Minor hemoptysis may present with just blood streaked sputum, with or without discomfort or
bubbling sensation over the chest.
• Massive hemoptysis, defined as expectoration of 200 to 600 ml of blood over 24 hours may present
with signs and symptoms of asphyxiation and hemodynamic alterations: Tachypnea, dyspnea, ronchi,
Pallor, hypotension, small and rapid pulse

• Work-up includes a complete otorhinolaryngeal examination with rhinoscopy and nasopharyngeal and
laryngeal endoscopy, to rule out any upper airway sources of bleeding.
• A chest X-ray may be requested to determine whether a pulmonary pathology is the most likely cause.
• AFB and gram staining of sputum are also indicated to search for the root cause of hemoptysis.
• ABG: assess oxygenation, ventilation and acid-base status
Management
• The initial goal of management of massive hemoptysis is therapeutic, not diagnostic.
• Priorities
o The airway should be protected with endotracheal intubation if needed
o Ventilation must be ensured
o And effective circulation must be maintained
• Stop the bleeding
• MILD
o Avoid strenuous activities
o Chest percussion and physiotherapy
o Diagnostic bronchoscopy: control bleeding
JMFV D2017, UST-FMS

• MASSIVE
o Admit to ICU
o Position: lie on side affected or head down
o Assess oxygenation, make sure to maintain airway patency
o Intubate, oxygenate and mechanically ventilate for impending respiratory failure
o Hemodynamic status, use crystalloid or colloid infusions
o BRONCHOSCOPY: to localize, isolate and arrest hemorrhage
§ Balloon occlusion
§ Arterial embolization
§ Assess for possible surgery
• Once the source of bleeding has been located suctioning or lavage, endobronchial tamponade may be
attempted.
• Resectional surgery may be performed in severe cases while arterial embolization may be performed if
surgery is contraindicated. If the source still cannot be identified bronchial arteriography or pulmonary
arteriography may be indicated. The airway must be maintained patent at all times as asphyxiation
poses a greater threat than blood loss.

JMFV D2017, UST-FMS
19. Pneumothorax p176, CMDT 2017
Definition
• Pneumothorax is a collection of air/gas in the pleural space that increases intrapleural pressure causing
overexpansion of the hemithorax & varying degrees of lung collapse
• It is classified as either spontaneous (Primary or Secondary) or traumatic
• Spontaneous Pneumothorax is one that occurs without antecedent trauma
o Primary spontaneous pneumothorax
§ Happens when there is no clinically apparent lung disease or underlying conditions
known to promote pneumothorax in a patient with a family history of pulmonary
pathology &/or is smoking
§ Tall, think men 20-40 y/o are usually affected & it is believed to be caused by ruptured
pleural blebs or bullae in response to high negative intrapleural pressures
o Secondary spontaneous pneumothorax
§ Occurs as a complication of an underlying lung disease, the most common of which is
airway obstruction secondary to COPD
§ Other examples include infections such as pulmonary tuberculosis, and necrotizing
pneumonia, neoplasms that may be primary or metastatic, interstitial lung disease,
trauma, or iatrogenic as in during cardiopulmonary resuscitation, mechanical
ventilation, endotracheal intubation, and other diagnostic or therapeutic interventions
• Tension Pneumothorax
o Is one that occurs when the pleural pressure build-up becomes excessive throughout the
breathing cycle forcing the lungs to collapse, this impedes venous return & prevents the heart
from pumping blood effectively
o A check valve mechanism (one-way valve) allows air to enter then pleural space on inspiration
& prevents egress of air during expiration
o This occurs in the setting of penetrating trauma, lung infection, CPR & CPAP mechanical
ventilation
• Bronchopleural Fistula
o A direct communication between the bronchus & the pleura causing persistent pneumothorax

Pathogenesis
• Intrapleural pressure is normally negative (less than atmospheric pressure) because of inward lung and
outward chest wall recoil.
o In pneumothorax, air enters the pleural space from outside the chest or from the lung itself via
mediastinal tissue planes or direct pleural perforation.
o Intrapleural pressure increases, and lung volume decreases.
• In tension pneumothorax, a lung or chest wall injury allows air into the pleural space but not out of it (a
one-way valve). As a result, air accumulates and compresses the lung, eventually shifting the
mediastinum, compressing the contralateral lung, and increasing intrathoracic pressure enough to
decrease venous return to the heart, causing shock. These effects can develop rapidly, particularly in
patients undergoing positive pressure ventilation

Clinical manifestations are dictated largely by the extent of lung collapse, the presence of tension
pneumothorax & the severity of the underlying disease, if present. But over all, there is
• Symptoms – may be apparent even in a minimal pneumothorax (<3cm) which may begin during
sleep/at rest
o Sudden sharp chest pain worsened by a deep breath & often localizes the side of involvement
(pleuritic chest pain)
o Varying degrees of dyspnea/chest tightness
o Anxiety, nasal flaring, easy fatigability
• Signs – some signs depend on the underlying disease, if present
o Inspection: Over-expansion & lagging of the affected hemithorax, contralateral
tracheal/mediastinal shift
o Palpation: Decreased fremitus
o Percussion: Hyper-resonance over the affected side
o Auscultation: Decreased to absent breath sounds on the affected side
o Tension: Distended neck veins, marked tachycardia, hypotension, hemodynamic and cognitive
abnormalities (ominous signs of impending cardiopulmonary failure)

JMFV D2017, UST-FMS
• Diagnosis may be confirmed via Chest X-ray which will reveal a Visceral Pleural Line as well as
atelectasis and mediastinal or tracheal shift to the opposite side. Subcutaneous emphysema or
pneumomediastinum may also be visualized if present.
• Additional ancillaries include Chest CT scans for cases of secondary spontaneous pneumothorax whose
underlying etiology is unknown.
• ABG determination is only indicated in impending or actual respiratory failure to assess oxygenation,
ventilatory & acid-base status

Management
• Goals
o Drain air from the pleural space to re-expand the lung
o Prevent recurrence
o Treat the underlying disease, if any
• Compute for Pneumothorax volume (%) to know if you would pursue a conservative management or
not. On X-ray measure % Pneumothorax = (Remaining Lung/Lung space in cm) x 100
o <15% & the patient is stable; observation may suffice since this is a small pneumothorax & the
lungs can reabsorb the gas
o >15%- aspirate
• Needle aspiration can be performed in the emergency room to resolve this emergency.
• The patient is placed in a semi- recumbent position. The area of the 2nd LICS MCL is sterilized and
infiltrated with 1 to 2% lidocaine up to the parietal pleura. A 14 to 16 gague cannula is inserted through
the parietal pleura and connected to a stopcock at which point air is aspirated gently. The procedure is
stopped once resistance is felt.
JMFV D2017, UST-FMS

#23$ACUTE$RESPIRATORY$FAILURE$
20 p.133%
HYPOXEMIA% ACUTE$RESPIRATORY$DISTRESS$SYNDROME$(ARDS)%
• Definition:%decrease%in%partial%pressure%of%oxygen%%%%%%(N:%75<105)% • Definition:%respiratory%failure%with%refractory%hypoxemia,%↓%lung%compliance,%and%non<
• Causes:%ventilation<perfusion%(V/Q)%mismatch,%right<to<left%shunt,%hypoventilation,%low% cardiogenic%pulmonary%edema%with%a%PaCO2/FiO2%ratio%≤%200.%%%
inspired%O2%content%(important%only%in%altitudes),%and%diffusion%impairment% • Pathogenesis:%dependent%on%endothelial%injury%
% • Causes:%sepsis,%pneumonia,%aspiration,%multiple%blood%transfusions,%inhaled/ingested%toxins,%
HISTORY/PE$ trauma%
• ↓%HbO2%saturation%(hemoglobin%oxygen),%cyanosis,%tachypnea,%shortness%of%breath,%pleuritic% • Overall%mortality:%30<40%%
chest%pain,%altered%mental%status% %
% HISTORY/PE%
DIAGNOSIS$ • Acute%onset%(12<48%hours)%tachypnea,%dyspnea,%tachycardia,%+/<%fever,%cyanosis,%labored%
• Pulse%oximetry:%demonstrates%↓%HbO2%saturation% breathing,%diffuse%high<pitched%rales%and%hypoxemia%in%the%setting%of%one%of%the%systemic%
• CXR:%to%evaluate%for%an%infiltrative%process%(ie.%pneumonia),%atelectasis,%large%pleural%effusion,% inflammatory%causes%or%exposure%%
or%pneumothorax%and%to%assess%for%ARDS% • Phase$1$(acute$injury):%normal%PE;%possible%respiratory%alkalosis%
• ABGs:%calculate%the%alveolar<arterial%(A<a)%oxygen%gradient:% • Phase$2$(6I48$hours):%hyperventilation,%hypocapnia,%widening%A<a%gradient%
o %[Patm%–%47)%x%FiO2%–%(PaCO2/0.8)%–%PaO2% • Phase$3:%acute%respiratory%failure,%tachypnea,%dyspnea,%↓%lung%compliance,%scattered%rales,%
• ↑%A<a%gradient%suggests%shunt,%V/Q%mismatch%or%diffusion%impairment% diffuse%chest%opacity%seen%on%CXR%
% • Phase$4:%severe%hypoxemia%unresponsive%to%therapy,%↑%intrapulmonary%shunting,%metabolic%
TREATMENT% and%respiratory%acidosis%
• Address%the%underlying%etiology%% %
• Administer%O2%before%initiating%evaluation% DIAGNOSIS%
• ↑%oxygenation%parameters%if%the%patient%is%on%mechanical%ventilation% • Criteria%for%ARDS%diagnosis%(according%to%American<European%Consensus%Conference%
• in%hypercapnic%patients:%↑%ventilation%to%↑CO2%exchange% Definition):%
% o Acute%onset%of%respiratory%distress%
Mechanical%Ventilator%Parameters%Affecting%Oxygenation%and%Ventilation% o A%PaCO2/FiO2%ratio%≤%200%
↑%Oxygenation% ↑%Ventilation% o Bilateral%pulmonary%infiltrates%on%CXR%
↑%FiO2% ↑%respiratory%rate% o No$evidence$of$cardiac$origin%(capillary%wedge%pressure%<%18mmHg%or%no%
↑%PEEP% ↑%tidal%volume%% clinical%evidence%of%elevated%left%arterial%pressure)%
% %
TREATMENT%
• Mechanical%ventilation%with%low%tidal%volumes%to%minimize%ventilation%induced%lung%injury%
• Treat%underlying%disease%and%maintain%adequate%perfusion%to%prevent%end<organ%damage%
• Use%PEEP%(positive%end%expiratory%pressure)%to%recruit%collapsed%alveoli,%and%titrate%PEEP%and%
FiO2%to%achieve%adequate%oxygenation%
• Goal%oxygenation%is%PaO2%>%60mmHg%or%SaO2%>%90%%on%FiO2%≤%0.6%
• Slowly%wean%patients%from%ventilation%%
%
!
21. Adrenal Crisis/Acute Adrenal Insufficiency p.155, CMDT 2017
Definition
• Is an extreme decompensated form of adrenal insufficiency characterized by a deficiency in
glucocorticoids (Cortisol) with or w/o mineralcorticoid deficiency causing a decrease in peripheral
vascular resistance leading to vascular collapse & shock
• Adrenal Gland (remember)
o Cortex: Zona Glomerulosa Salt Mineralocorticoid: Aldosterone
o Cortex: Zona Fasiculata Sugar Glucocorticoid: Cortisol
o Cortex: Zona Reticularis Sex Androgens: DHEA, androstendione
o Medulla Stress Catecholamines: Nor/epinephrine

Etiology
Any disorder affecting the hypothalamic-pituitary-adrenal axis resulting to glucocorticoid deficiency can give
rise to adrenal insufficiency. And depending on which level is affected the disorder can be categorized into
primary, secondary, or tertiary adrenal insufficiency.
• Primary – abnormality is in the adrenal gland itself
o Addison’s Disease – autoimmune adrenocortical destruction causing deficiencies of
mineralocorticoids and glucocorticoids. Because of this, an additional dysfunction in the renin-
angiotensin-aldosterone system is present thus crisis secondary to Addison’s disease is often
more common and more severe
o CAH – 21-Hydroxylase deficiency, an enzyme involved in the synthesis of cortisol
o Adrenal hemorrhage
o Infections (HIV, TB) – TB is the most common infectious cause AI worldwide
• Secondary – any pathology affecting the pituitary gland
o Mass lesion
• Tertiary – any pathology affecting the hypothalamus
• Both 2 & 3 result in ↓ ACTH production by pituitary, most often due to cessation of long-term
glucocorticoid treatment
• Other predisposing factors include any stress-inducing event such as a major systemic illness, surgery,
and adrenal hemorrhage

Pathogenesis
• Decreased glucocorticoid (cortisol) leads to a decrease in vascular sensitivity to norepinephrine and
angiotensin II such that peripheral adrenergic tone is reduced leading to vascular collapse and shock.
• Lack of cortisol may also induce hypoglycemia

• A patient with adrenal crisis may present in the ER with hypotension, tachycardia, and shock
disproportionate to the severity of the current illness
• They may also present with a history of nausea and vomiting with a background of weight loss and
anorexia.
• The patient may also complain of abdominal pain, fever especially in those caused by infections, and
hyperpigmentation in those with primary adrenal insufficiency
• A patient presenting with purpura known to have adrenal insufficiency should raise suspicion adrenal
infarction in Waterhouse Friedrichsen Syndrome secondary to meningococcemia
• Hypoglycemia can worsen weakness & mental functioning
• Hypotension may be worsened by vomiting
• Sugar and/or salt cravings
• Hyperpigmentation (due to ↑ACTH secretion à↑Melanocyte Stimulating hormone ) seen in
Addison’s disease in areas of sun exposure or friction

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Diagnosis
• May reveal unexplained hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia, azotemia, and
eosinophilia.
• Because the clinical manifestations of adrenal crisis are nonspecific it is important to request for the
proper laboratories and ancillaries to clinch the diagnosis.
• Since the pathology is basically glucocorticoid deficiency, cortisol levels should be investigated in order
to determine the presence of this condition.
• Normally cortisol levels peak during early morning and during periods of stress.
o <5 ug/dl are suggestive of insufficiency
o 10 ug/dl still make an individual highly suspect
o >20 ug/dl – less likely
• A 250 ug synthetic ACTH stimulation test + Blood cortisol level
o An increase of 10 ug/dl from baseline and an absolute cortisol level >20 ug/dL an hour after
administration rules out primary adrenal insufficiency but cannot completely eliminate the
possibility of secondary adrenal insufficiency especially of recent onset.
o 8am Plasma cortisol level < 3ug/dL in the absence of exogenous glucocorticoid administration
→ DIAGNOSTIC
o Failure of cortisol to rise > 18ug/dL following ACTH administration → CONFIRMS DIAGNOSIS
o Random plasma cortisol level > 18ug/dL → EXCLUDES DIAGNOSIS

Treatment
• Management should not be delayed while waiting for the results of the laboratories requested for
• 1O: Glucocorticoid and mineralcorticoid replacement
• 2/3O: Glucocorticoid replacement ONLY (mineralcorticoid production is not ACTH dependent)
• 4’S of Adrenal Crisis Management
o Salt: IV access must be gained immediately, and IVF should be started with PNSS for
resuscitation & to address hyponatremia
o Steroid: IV Hydrocortisone 100mg q8 or Dexamethasone should then be started immediately
o Support
§ 50% dextrose to correct hypoglycemia
§ Vasopressors and oxygen as well as other supportive measures should be instituted as
indicated
o Search: Once the patient is stable further laboratories can be requested to determine the exact
etiology of the adrenal insufficiency.
• Fludrocortisone may be given in those with concurrent mineralocorticoid deficiency
• Glucocorticoids should be tapered to maintenance dosage over 1-3 days once appropriate.

Prevention
• Educate patient how to inject dexamethasone for emergencies
• Wear medical alert bracelet
• Carry prefilled syringe with dexamethasone sodium phosphate (4mg/mL in 154mmol/L NaCl solution)
• Double steroids during minor illnesses

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22. Diabetic Ketoacidosis p.158, CMDT 2017
Definition/Etiology
• Is an extreme decompensated state of diabetes mellitus characterized by the triad of
o Hyperglycemia of >250 mg/dl
o Ketosis as reflected by positive urine ketones
o High anion gap metabolic acidosis as reflected by a
§ pH of less than 7.3
§ An anion gap of >10 (Methanol Uremia DKA PEG INH Lactic Acidosis Ethanol Salicylates)
• It is often precipitated by sudden discontinuation of insulin or an increased insulin requirement from
infections, trauma, cerebrovascular accident, myocardial infarction, sympathomimetics, and
pancreatitis.
• Occurrence
o Usually in T1DM as the endogenous insulin present in patients with T2DM protects against
lipolysis
o May also occur in T2DM in cases of stress from any of the mentioned causes

Pathophysiology
• A state of decreased net effective action of circulating insulin such that glucose utilization is decreased
creating a state of relative starvation, stimulating the release of counter-regulatory hormones such as
Glucagon, Cortisol, Catecholamines, and Growth Hormone
• This promotes processes that increase blood glucose levels to maintain cellular function such as
Gluconeogenesis and Glycogenolysis.
• Lipolysis is also stimulated such that adipose is converted into free fatty acids which accumulate and
are oxidized into ketones because they are unable to enter the citric acid cycle without insulin à
Ketosis
• The kidneys attempt to filter the excess highly osmotic glucose leading to severe dehydration and in
compendium with ketosis, serum electrolyte derangement.

• Patients usually present with polyuria, polydipsia, nausea/vomiting, abdominal pain, dehydration,
hypotension, Kussmaul’s breathing (rapid & deep), and fruity breath due to exhaled acetone
• Mental status changes may also be evident: psychosis, delirium, drowsiness is common but frank coma
occurs in 10% of cases

Diagnosis
Diagnostic tests are aimed towards evaluating the severity of the disease
• Random plasma glucose would show hyperglycemia
• ABG would show high anion gap metabolic acidosis (low pH, low HCO3).
o Anion gap: (Na – (Cl + HCO3))
• Serum/urine ketones: elevated
• CBC: Leukocytosis
• Na/K/Cl: Hyperkalemia, but depleted intracellular K+ d/t transcellular shift from ↓ insulin (therefore
total body K+ is depleted)

Mild Moderate Severe
Plasma Glucose 250-600mg/dL
Arterial pH 7.25-7.30 7.0-7.24 <7.00
HCO3 15-18 10-15 <10
Urine Ketones POSITIVE
Anion Gap >10 >12 >12
Sensorium Alert Alert/drowsy Stupor/coma

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Treatment
• IV Fluids - Hypovolemia and vascular collapse are the most common cause of death in uncomplicated
ketoacidosis as such correction is an urgent therapeutic priority
o 0.9% PNSS – fluid of choice to re-expand plasma volume. 2-3L over the 1st 1-3h
• Potassium
o Hypokalemia must be ruled out because insulin can exacerbate this. Potassium levels must be
normalized before starting insulin
o Replace if <5.0
• Insulin
o Continuous IV infusion of Insulin aimed towards decreasing glucose at a rate of 50 to 75
mg/dl/hour
o An initial bolus of 0.15 U/kg followed by infusion rate of 0.1 U/kg/hour can be used
o When glucose reaches 250 mg/dl, rate can be decreased to 0.05 to 0.1 U/kg and
o Dextrose may be added until acidosis resolves.
• Treatment goal is
o Glucose of less than 200 mg/dl
o Serum bicarbonate of more than 18 meq/L
o pH of more than 7.3
o Anion gap of less than 12 meq/L.
o Once this is achieved, insulin infusion maybe discontinued and shifted towards maintenance
dosing.

Complications
• Life-threatening mucormycosis (caused by Rhizopus infection)
• Cerebral edema
• Cardiac arrhythmias
• Heart failure

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23. Thyroid Storm p.163, CMDT 2017, Tintinalli’s Emergency Medicine 8E

Definition
• Thyrotoxicosis is a general state of thyroid hormone excess regardless of cause
• Hyperthyroidism is a more specific form of thyrotoxicosis resulting from thyroid gland hyperfunction &
new thyroid hormone production
• Thyroid storm refers to the extreme manifestation of thyrotoxicosis which is an acute severe, life-
threatening hypermetabolic state causing adrenergic hyperactivity or altered peripheral response to
thyroid hormone

Etiology/Pathophysiology
• Usually occurs when an already thyrotoxic patient suffers a serious concurrent illness, event, or injury
such a infection, stress, myocardial infarction, or trauma that frees thyroid hormones from their
binding sites or increases receptor sensitivity such that the effect of thyroid hormones is multiplied

• The mechanism by which such factors worsen thyrotoxicosis may be related to cytokine release &
acute immunologic disturbance caused by the precipitating condition leading to thyroid hyperactivity
• Use of salicylates: increases free thyroid hormone levels

• Clinical manifestations are similar to those of thyrotoxicosis but more exaggerated
• Fever, cardiac findings such as tachycardia out of proportion to fever, mental status changes,
gastrointestinal symptoms such as diarrhea, abdominal pain, generalized weakness, palmar erythema,
tremors, profuse sweating
• Arrythmias accompanied by pulmonary edema or CHF
• Coma & death in 20% of patients

Diagnosis
• The total serum thyroid hormone levels in crisis are not appreciably greater than those in
uncomplicated thyrotoxicosis therefore, Thyroid storm is a clinical diagnosis
o Free hormone is elevated as compared to the bound hormones
• Scoring criteria is confusing & often not very important since treatment is the same once suspected.
Scoring maybe useful in monitoring treatment response
o Grading: Burch & Wartofsky’s Criteria
§ <25 – Storm unlikely
§ 25-44 – Impending storm
§ >45 – Highly Suggestive of storm
o Temperature, CNS effects, GI-hepatic dysfunction, CV dysfunction, heart failure & precipitant
history
• Electrolytes, BUN, blood sugar, liver FTs, plasma cortisol should be monitored
• Diagnosis is incomplete until a search for the trigger has been made

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Treatment
• Inhibition of thyroid hormone synthesis & secretion
o Propylthiouracyl
§ A thionamide which inhibit synthesis of thyroid hormones. Used only in 3 situations: 1st
trimester of pregnancy Methimazole allergy, Thyroid storm
§ Loading: 500mg-1g/IV then: 250mg q4
o SSKI (Lugol’s solution)
§ Inhibits the release of thyroid hormones by inducing the Wolff-Chaikoff Effect (high
amounts of iodine would shut down the hyperfunctioning thyroid gland inducing a state
of transient hyperthyroidism)
§ 5 drops q6 (8-10 drops q8)
§ Give 1-2h after PTU
• Sympathetic blockade
o Propanolol
§ Primarily a b-Blocker used in thyroid storm for its Anti-adrenergic properties.
§ 60-80mg q4-6h
• Prevent peripheral conversion of T4 à T3
o Minimal effect of PTU & Propanolol
o Hydrocortisone
§ Glucocorticoid with anti-inflammatory effects used in Thyroid storm to prevent
peripheral conversion of T4 à T3
§ Loading: 300mg/IV Then: 100mg q4
§ Treatment with glucocorticoids is a standard practice because of the possibility of
relative adrenal insufficiency
• Supportive therapy
o IVF – depending on indication, NSS/LRS for volume expansion
o Temperature control – cooling blankets, paracetamol (Aspirin is contraindicated because it may
increase free thyroid hormone)
o Oxygen if required
o Digitalis for CHF & to slow ventricular response
o Sedation & nutrition
o Manage the precipitating event

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24. Uremic Emergency p.192, Tintinalli’s Emergency Medicine 8E
Definition
• End-stage renal disease, either acute or chronic, is the irreversible loss of renal function, resulting in
the accumulation of toxins and the loss of internal homeostasis
• Uremia, the clinical syndrome resulting from ESRD, is contamination of the blood with urine. It is
universally fatal without some form of renal replacement therapy. Hyperkalemia, pulmonary edema,
severe metabolic acidosis, encephalopathy, pericarditis, and pericardial effusion or tamponade are just
some of the manifestations of this clinical syndrome.

Etiology
• Acute renal failure (AKI)
o Pre-renal: Massive hemorrhage from any organ system, diarrhea, vomiting, sepsis, CHF &
excessive diuretic use
o Renal: ATN, nephrotoxic drug ingestion & vasculitis
o Post-renal: Obstructive uropathy from stones or masses
• CKD
o DM Nephropathy, HTN Nephrosclerosis, Chronic GN, SLE Nephritis, Gouty nephropathy, PKD,
Chronic pyelonephritis, chronic NSAID use, inadequate RRT for CKD 5
• Acute on top of chronic renal insult
o Dehydration, nephrotoxic drugs, disease relapse/acceleration, infection, obstruction,
hyper/hypocalcemia, heart failure

• Ammoniacal breath
• Neurologic manifestations: apathy, drowsiness, insomnia, tremors, cognitive changes, asterixis,
seizure, coma, lethargy
• Pulmonary: edema, pleural effusion, Kussmaul breathing (rapid and deep) secondary to metabolic
acidosis
• CV: Uncontrolled BP, arrhythmia, pericarditis, pleuritic chest pain with pericardial friction rub heard
throughout the cardiac cycle, cardiac tamponade (distended neck veins, hypotension, muffled heart
sounds)
• GI: Persistent anorexia, nausea & vomiting, GI bleeding secondary to uremic gastritis aggravated by
coagulopathy

Laboratory/ancillary Procedures
• BUN, Serum creatinine
• Serum Na, K, Ca
• ABG
• CBC, urinalysis
• CXR
• Ultrasound of the kidneys
• 12L ECG
• 2D Echo – if cardiac tamponade is suspected

Management
• Renal Replacement Therapy
o The ultimate treatment for uremia is dialysis. Initiation of dialysis is indicated when signs or
symptoms of uremia are present and are not treatable by other medical means, regardless of
the Creatinine Clearance
o Indications for hemodialysis (AEIOU)
§ Intractable Metabolic Acidosis
§ Electrolyte abnormalities (hyperkalemia)
§ Ingestion (salicylates, theophylline, methanol, barbiturates, lithium,
§ ethylene glycol)
§ Fluid Overload
§ Uremic symptoms (pericarditis, encephalopathy, bleeding, nausea, pruritis, myoclonus)
• Treat hyperkalemia, metabolic acidosis
• Pulmonary edema
o Sit patient up, protect airway & assure oxygenation, Furosemide 400-600mg/IV, NTG 10-
200micrograms/min, Morphine 5mg/IV, removal of fluid by dialysis

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• Uremic encephalopathy
o Protect airway, dialysis, avoid disequilibrium
• Pericarditis
o Daily dialysis, low or no heparin dialysis
• Tamponade
o Needle drainage before dialysis to avoid hypotension, low or no heparin dialysis

Prevention
• Advocate adherence with hemodialysis schedule
• Increase frequency of dialysis for ESRD on regular dialysis
• Correct as many risk factors as possible
• Avoid: Nephrotoxic drugs, Infection, dehydration, electrolyte & acid-base imbalances
• Nutrition homeostasis: provide enough calories & protein to prevent development of a hypercatabolic
state & maintain optimal nutrition status

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25. Rabies (Animal Bites) p.313, Harrison’s Principles of IM 19th Edition
Definition
• Rabies is a rapidly progressive, acute infectious disease of the CNS in humans and animals that is
caused by infection with rabies virus.
• The infection is normally transmitted from animal vectors. Rabies has encephalitic and paralytic forms
that progress to death.
Etiology
• The rabies virus is a member of the family Rhabdoviridae
• 2 genera in this family causes human infections
o Vesiculovirus – causes a self-limited and mild systemic illness in humans
o Lyssavirus – the genus where the Rabies virus belongs to which infects a broad range of animals
and causes serious neurologic disease when transmitted to humans
• Rabies Virus
o ssRNA from the Lyssavirus genus of the Rhabdoviridae family
Pathogenesis
• After the virus is inoculated via an animal bite (dog, cat, rat), the virus remains in the site of entry
during the incubation period which may last anywhere from 20 to 90 days (interval between exposure
& clinical disease)
• In the muscles, the virus binds to nicotinic ACh receptors on postsynaptic membranes at
neuromuscular junctions where they replicate
• The virus then spreads centripetally via retrograde axonal transport along the peripheral nerves to the
spinal cord or brainstem
• Replication further occurs in motor neurons of the spinal cord and local dorsal root ganglia then rapid
ascent to brain
• Once CNS infection is established, centrifugal spread then occurs along sensory and autonomic nerves
towards the tissues of the salivary glands (acinar glands), heart, adrenals, and skin
• Pathologic changes in the CNS à Neuronal dysfunction—rather than neuronal death—is responsible
for clinical disease in rabies
o Mild inflammatory changes with mononuclear inflammatory infiltration in the leptomeninges,
perivascular regions, and parenchyma
o Babes nodules – microglial nodules
o Degenerative neuronal changes usually are not prominent, and there is little evidence of
neuronal death
o Neurophagia – occasionally
o Negri body – most characteristic pathologic finding eosinophilic cytoplasmic inclusions in brain
neurons that are composed of rabies virus proteins and viral RNA in Purkinje cells of the
cerebellum and in pyramidal neurons of the hippocampus, and are less frequently seen in
cortical and brainstem neurons
• Prodromal features: fever, malaise, headache, nausea, vomiting, anxiety, agitation, paresthesia,
pain/pruritus near the site of exposure
• 2 acute neurologic forms of rabies are seen in humans: encephalitic (80%) and paralytic (20%)
• Encephalitic Rabies: fever, confusion, hallucinations, combativeness, seizures, autonomic dysfunction
(hypersalivation, gooseflesh, arrhythmias), hyperexcitability followed by brief episodes of lucidity
which become shorter as the disease progresses, aerophobia & hydrophobia. “Foaming of the mouth”
results from hypersalivation & pharyngeal dysfunction. Brainstem dysfunction progresses rapidly to
coma then death if no intervention is performed
• Paralytic Rabies: muscle weakness predominates and cardinal features of encephalitic rabies
(hyperexcitability, hydrophobia, and aerophobia) are lacking. Flaccid paralysis of the limbs to
quadriparesis with facial paralysis, until eventually coma or death ensue.
• Coma & Death: (0 à14 days)
Diagnosis
• Currently, there is no diagnostic tool available which is economically-suited for most Filipinos to
confirm rabies, as such treatment must be instituted once clinical suspicion for the disease arises.
• Ideal: Once rabies is suspected, rabies-specific laboratory tests should be performed to confirm the
diagnosis.
• Diagnostically useful specimens include serum, CSF, fresh saliva, skin biopsy samples from the neck
(Because skin biopsy relies on the demonstration of rabies virus antigen in cutaneous nerves at the
base of hair follicles, samples are usually taken from hairy skin at the nape of the neck)
• RT-PCR amplification to detect Rabies RNA
• Direct fluorescent antibody testing

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Treatment
• There is no established treatment for rabies, hence a palliative approach may be appropriate for some
patients
• First, proper wound cleaning must be performed. The wound must be vigorously washed and flushed
with soap or detergent and water for at least 10 minutes.
• Alcohol, povidone iodine, or any other antiseptic may also be used.
• For frankly infected wounds, open wounds, bleeding wounds, antimicrobials in the form of co-
amoxiclav or cefuroxime may be started
• Anti-tetanus immunization should also be given
• The category of the wound should also be established, then category-based treatment be instituted

Category Management
Category 1 Local wound treatment
Having intact skin licked by an infected animal,
sharing eating or drinking utensils with an
infected patient
Category 2 Immediate start of active vaccination. If the
Uncovered skin nibbled or nipped by an infected animal remains alive and well for 14 days,
animal resulting to bruising, minor scratches or vaccination may be discontinued after the Day 7
abrasions without bleeding, licks on broken skin, dose. However if the animal becomes rabid, dies,
and wounds induced to bleed or in unavailable for 14 days or tests positive for
rabies, the complete regimen until Day 30 should
be given
Category 3 Both active + passive immunization products
Transdermal bites or scratches, contamination of
mucuous membranes with saliva, exposure to
rabies patients through bites, mucous
membrane, or open skin lesions, handling
infected carcass or ingestion of raw infected
meat, and all Category II occurring in the head
and neck

Active Immunization Products
• Rabies vaccine to induce production of antibodies against the microorganism
• Types
o Purified Vero Cell Rabies Vaccine (PVRV) [0.5 ml]
o Purified Chick Embryo Cell Vaccine (PCECV) [1.0 ml]
• Intramuscular sites of administration
o Adults: deltoid area of each arm
o Infants: anterolateral aspect of the thigh
o NEVER in the gluteal area because absorption is unpredictable
• Standard Intramuscular Schedule (1-1-1-1-1): D0-D3-D7 +/- D14-D28/30
• Pre-exposure Prophylaxis (D0-D7-D21/28) is recommended for individuals at high risk of exposure:
laboratory workers, veterinarians, animal-control personnel, health workers handling rabies cases

Passive Immunization
• Given to provide immediate neutralizing antibodies to cover the gap until the appearance of vaccine
detectable antibodies
• Total computed RIG should be infiltrated around and into the wound as much as anatomically feasible
even if the lesion has healed
• Remaining RIG should be administered deep IM at a site distant from the site of vaccine injection
• Types:
o Human Rabies Immune Globuline (HRIG) – from plasma of human donors; Dose = 20 IU/kg
o Highly Purified Antibody Antigen Binding Fragments (F(ab’)2) – from equine rabies immune
globuline (ERIG); Dose = 40 IU/kg
o Equine Rabies Immune Globulin – from horse serum; Dose = 40 IU/kg

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26. Tetanus Harrison’s Principles of IM 19th Edition
Definition
• Tetanus is an acute disease manifested by skeletal muscle spasm and autonomic nervous system
disturbance. It is caused by a powerful neurotoxin produced by the bacterium Clostridium tetani
Etiology
• Clostridium tetani, a motile non- encapsulated anaerobic gram positive rod
• Clostridium tetani exists in either a vegetative or spore forming state. The spores are ubiquitous in soil
and animal feces and are extremely resistant to destruction, surviving on environmental surfaces for
many years.

Pathogenesis
• The spores or bacteria enter the body through abrasions or wounds
• Once in a suitable anaerobic environment (like that in devitalized tissue), the organisms grow, multiply,
and release of 2 tetanus exotoxins
o Tetanolysin which favors expansion of the bacterial population
o Tetanospasmin, a powerful neurotoxin that reaches the central nervous system via
hematogenous spread to the peripheral nerves and retrograde transport.
• Tetanospasmin acts on the motor end plates of the skeletal muscles, in the spinal cord, brain, and
sympathetic nervous system
• It prevents the release of inhibitory neurotransmitters glycine and gama aminobutyric acid from
presynaptic nerve terminals thus releasing the nervous system from its normal inhibitory control.
• This leads to the clinical manifestations of tetanus

• Generalized muscular rigidity, violent muscular contractions, and autonomic instability
• 3 Forms of Tetanus exist: Generalized, Cephalic & Localized
• Generalized tetanus, is the most common. Patients present with pain and stiffness of the masseters or
lock jaw, later becoming rigidity hence development of trismus and risus sardonicus. Dysphagia,
opisthotonus, clenching of the fists, extension of lower extremities results as a consequence of reflex
convulsive spasms and tonic muscle contractions. Mental status is normal.
• Cephalic tetanus results to dysfunction in the cranial nerves most commonly the 7th Cranial Nerve.
Pharyngeal or laryngeal muscles may spasm, with consequent aspiration or airway obstruction
• Lastly local tetanus is manifested by rigidity of muscles in proximity to the site of inoculation

Diagnosis
• Diagnosis is achieved clinically
• Culture of C. tetani from a wound provides supportive evidence
• Serum anti-tetanus IgG may also be measured in a sample taken before the administration of antitoxin
or immunoglobulin

Treatment
• Entry wound should be identified, cleaned & debrided of necrotic material in order to remove
anaerobic foci of infection and prevent further toxin production
• Metronidazole 500mg/IV q6 x 7 days – preferred antibiotic
• Antitoxin should be given early in an attempt to deactivate any circulating tetanus toxin and prevent its
uptake into the nervous system: human tetanus immune globulin (TIG) 3000-5000 IU/IM Single dose, a
portion of which should be injected around the wound
• Tetanus toxoid (DTaP or Td/Tdap depending on age), 0.5 mL IM at presentation, and 6 wk and 6 mo
after presentation, site must be at the opposite site of the body where TIG was administered (Tetanus
toxoid should be given after recovery because tetanus toxin is weakly immunogenic which does not
confer natural immunity)
• Spasm control: Tetanospasmin prevents neurotransmitter release at inhibitory interneurons, and
therapy of tetanus is aimed at restoring normal inhibition. Midazolam is preferred
• Management of autonomic dysfunction: Magnesium sulfate, 40 milligrams/kg IV loading, then 2
grams/h (1.5 grams/h if ≤45 kg) continuous infusion to maintain blood level of 2.0–4.0 mmol/L

Clean, minor wounds All other wounds
Vaccination history Tdap or Td TIG Tdap or Td TIG
Unknown or fewer than 3 doses YES NO YES YES
3 or more doses NO NO NO NO

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27. Increased Intracranial Pressure p.237
Definition
• ICP is the pressure exerted by the cranium on the brain tissue, CSF, and the brain’s circulating blood
volume. Components:
o Blood volume ~150cc (10%)
o CSF volume ~150 cc (10%)
o Brain volume ~1500 cc (80%)
• The Monroe-Kellie Doctrine or Hypothesis states that the skull is non-distensible and the brain is non-
compressible
o Simply: the sum of volumes of brain, CSF and intracranial blood is constant
o And any increase in any one of the said compartments must be compensated for by a decrease
in the other compartments and will likewise raise the ICP
• Normal ICP: 5-15mmHg or 100-200mmH2O
• Increased ICP is defined as ICP >20 mmHg lasting for 5 minutes or longer
Etiology
• Intracranial mass lesion: Tumor, hematoma, abscess
• Increased CSF volume or resistance to outflow: Obstructive hydrocephalus, benign intracranial HTN
• Increased brain volume producing cytotoxic cerebral edema: Cerebral infarction
• Increased brain and blood volume producing vasogenic cerebral edema: Head trauma, meningitis,
eclampsia
• Severe Headache, Decreasing level of consciousness
• Nausea & Vomiting, Lethargy
• Diplopia from 6th CN palsy – abducens nerve has the longest intracranial route, so when you have
increased ICP, it is vulnerable to compression
• Papilledema – disk hyperemia, venous distention, optic cup swelling with elevation of vessels, blurred
disk margins, loss of central retinal pulse
• Cushing’s Reflex (bradycardia, hypertension, hypopnea)
Diagnosis
• Evaluate patient’s level of consciousness
• Assess: focal abnormalities & papilledema
• Cranial CT Scan or MRI: Identify any structural pathology
Treatment
• Mechanical
o Elevate head at 30 degrees to optimize venous drainage
o Keep neck neutral and prevent kinking of the internal jugular vein for drainage
o Controlled Hyperventilation via mechanical ventilation – maneuver done to rapidly decrease
ICP through vasoconstriction
• Medical
o Control hyperglecmia & give antipyretics for fever (since both fever & hyperglycemia can
increase metabolic demand & blood flow hence increase ICP) and anticonvulsants to prevents
seizure, sedate the patient if restless
o Give the patient oxygen, fluids (PNSS) and maintain a normal blood pressure
o Mannitol
§ A hyperosmotic agent which draws water from the brain & induces diuresis
§ Decreases pressure over 10-20min
§ Initial dose: 1-2g/kg
§ Maintenance: 50-300mg/kg q6
o Dexamethasone
§ Effective against inceased ICP brought about by vasogenic edema from brain tumor,
surgery & radiation
§ Initial dose: 5-25mg/IV
§ Maintenance: 2-8mg/IV q6
• Surgical
o Craniotomy for ventriculostomy – treat acute hydrocephalus due to subarachinoid
hemorrhage, posterior fossa tumor/mass and meningitis
o Craniotomy for evacuation of the cause
o Depcompression
• Intensive Care – done only if
o Hypothermia, Coma
o ICP monitoring
• Remember to treat primary disorders ASAP
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28. Acute Stoke p.240, Tintinalli’s Emergency Medicine 8E
Definition
• Stroke is a cerebrovascular disorder resulting from impairment of cerebral blood supply by occlusion
(eg, by thrombi or emboli) or hemorrhage characterized by acute-onset signs and symptoms of focal
neurologic deficits lasting for >24 hours* or leading to death, with no apparent cause other than that
of vascular origin (WHO)
• Transient Ischemic Attack (TIA) on the other hand, is the sudden-onset FND lasting for less than 24
hours, this is not included in the definition of stroke, although they have a common cause

Risk Factors
• Non-Modifiable: Age (risk increases with age), Gender (M > F), Race/Ethnicity, Hereditary
• Modifiable: HTN, cardiac diseases (ie. atrial fibrillation, coronary heart disease, MI), Diabetes,
Dyslipidemia, Smoking, Alcohol, illicit drug use, lifestyle factors such as physical activity and diet, oral
contraceptive use

Pathogenesis
• Stroke is classified as resulting from two major mechanisms: ischemia and hemorrhage
• Ischemic strokes, which account for 87% of all strokes, are categorized by causes as thrombotic,
embolic, or hypoperfusion related.
• Hemorrhagic strokes are subdivided into intracerebral (accounting for 10% of all strokes) and
nontraumatic subarachnoid hemorrhage (accounting for 3% of all strokes)
• The final common pathway for all these mechanisms is altered neuronal perfusion.
• Neurons are exquisitely sensitive to changes in cerebral blood flow and die within minutes of complete
cessation of perfusion. This fact underlies the current treatment emphasis on rapid reperfusion
strategies.
• Transient ischemic attack (TIA) – the standard definition of TIA requires that all neurologic signs and
symptoms resolve within 24 hours regardless of whether there is imaging evidence of new permanent
brain injury; stroke has occurred if the neurologic signs and symptoms last for >24 hours.

• Sudden weakness or numbness of the face, arm, or leg especially on one side of the body
• Sudden confusion, trouble speaking or understanding
• Sudden trouble walking, dizziness, loss of balance, incoordination
• Blurring of vision, diplopia, dysphagia
• Sudden severe headache
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Diagnosis
• Cranial CT Scan
o Differentiates between hemorrhage from ischemic stroke
o Demonstrates size and location of hemorrhage
o May reveal structural abnormalities (ie. brain tumors, AV malformations, herniations,
hydrocephalus)
• Cranial MRI
o More sensitive than CT Scan for detecting cerebral infarction during the acute stage
• 4-Vessel Angiography: Intracerebral/subarachnoid hemorrhage secondary to aneurysm or AVM
• Cardiac Work Up: ECG, 2D Echo with Doppler, Cardiac duplex
• Blood chemistry – for the assessment of the above mentioned risk factors

Management
Cerebral Infarction
• Acute Phase
o Assess airway, breathing, circulation
o Admission to stroke unit
o IV rtPA 0.9mg/kg infused IV over 1 hr w/ 10% IV bolus
o Avoid dehydration. Start IV fluids (isotonic saline)
o If with fever, treat with antipyretics
o Avoid hypo/hyperglycemia
o Treat hypertension with nicardipine drip
• Secondary Prevention
o Assess for risk factors for stroke (ie. dyslipidemia, HTN)
o Antithrombotic meds ie. aspirin 80B325mg/day
o Anticoagulants
Intracerebral Hemorrhage
• Assess airway, breathing, circulation
• Start IV fluids (isotonic saline)
• Treat increased ICP
o Head elevation, controlled hyperventilation to maintain PCO2 25-30mmHg, Mannitol,
Hypertonic saline, corticosteroid (no role in ICP management among stroke patients)
• Surgery
o If cerebellar hemorrhage >3cm
o ICH w/ structural lesions (ie. aneurysm, AVM)
o Young patients with large lobar hemorrhage
• Non-surgical
o Small hemorrhages <10cm3 or minimal neurologic deficits
• NOTE: Anti-thrombotic & anticoagulant medications are contraindicated
Subarachnoid Hemorrhage
• Assess Airway, breathing, circulation
• Start IV fluids (isotonic solution)
• Treat increased ICP
• Investigate underlying cause of subarachnoid hemorrhage; treat accordingly
• Surgery for clipping aneurysm or excision of AVM
• Prevent vasospasm à Nimodipine 30 mg/tab

JMFV D2017, UST-FMS
29. Status Epilepticus p.245
Definition
• Seizure is an episode of abnormal neurologic function caused by inappropriate electrical discharge of
brain neurons.
• Epilepsy is a clinical condition in which an individual is subject to recurrent seizures
• SE is defined as continuous or repetitive seizure activity persisting for at least 30 minutes without
complete recovery of consciousness in between attacks
o However, when seizure duration is >5min, treatment for SE should be instituted, no need to
wait for 30min to consider it SE
• There are several types of SE depending on the seizure type
o Grand mal or Tonic Clonic SE
§ Most common & most life threatening
§ AKA Generalized Convulsive SE (GCSE)
o Simple Partial
o Complex Partial
o Absence
o Myoclonic

Etiology
• Brain tumors, meningitis, encephalitis, head trauma, hyoxia, hypoglycemia & eclampsia
• Sudden withdrawal of anti-convulsants: barbiturates, benzodiazepine
• Gradual lowering of anti-epileptic drugs to subtherapeutic levels in patients with chronic epilepsy

• Profound or continuous tonic and/or clonic activity
• Symmetric or asymmetric
• Overt or subtle with marked impairment of consciousness
• Ictal discharges on EEC

Management
• First line drugs: these stop SE as fast as possible within a few minutes: lorazepam, diazepam
• Second line drugs: these prevent recurrence of seizures or SE: phenytoin, phenobarbital, valproic acid

JMFV D2017, UST-FMS
30. Spinal Cord Compression p.248
Definition
• Acute emergency as the spinal cord has very little reserve as it is structurally small & its compression
may lead to irreversible damage compromising its function

Causes
• Infections: Pott’s disease, epidural abscess
• Tumors: Extramedullary (primary and metastatic), Intramedullary
• Trauma: Stab wound, fracture of the spine may cause bone fragments to impinge on the cord and/or
cause hematoma
• Epidural Hematoma

Clinical Syndrome of Spinal Cord Compression
• Brown-Sequard Syndrome – hemisection of the SC due to stab wounds
o Ipsilateral motor weakness
o Ipsilateral proprioceptive loss
o Contralateral pain & temperature sensation loss
• Transection of the SC
o Quadriplegia/paraplegia
o Sensory level
o Bladder & bowel symptoms – pain at the level of compression
• Consider spinal cord compression if any of the following are present
o Back pain with or without radiation in the territory of a nerve root (including a change in the
severity and quality of existing pain)
o Leg weakness, sensory changes / sensory level, Bowel or bladder disturbance

Diagnostic tools
• Plain spine X-rays
• Myelography
• CT Scan
• MRI

Treatment
• Decompression of the spinal cord & surgery must be immediately done before irreversible changes
exact their toll

JMFV D2017, UST-FMS
31. Vaginal Bleeding in Pregnancy p.269
Vaginal bleeding is a common event at all stages of pregnancy and different clinical entities would cause it
depending on which particular age of gestation the bleeding has occurred. To narrow down the possible
differentials of vaginal bleeding, we divide the duration of pregnancy into the 1st and 2nd half and discuss the
etiologies based on that division.

Bleeding in the 1st half of Pregnancy
• Is one which occurs in the first 20w of gestation
• If a gravida comes to us in the ED with bleeding, we institute general measures first prior to our
diagnostic search
o If in shock, we start IV Infusion using a large-bore (16-G) cannula or needle and collect blood for
CBC, blood typing and bedside clotting test then we rapidly infuse NSS/LRS per IV.
o Catheterize the bladder to monitor I & O
o Supplemental oxygen at 6-8LPM
o Perform a thorough PE including speculum examination to determine the source & severity of
the bleeding
o Internal Examination will also aid in the diagnosis, establish whether the cervix is open or
closed, if there is tissue at the cervical os or if there is cervical wiggling tenderness
o Obtain a rapid pregnancy test, should it be positive, carry out a TVS and quantitative Serum
HCG to establish the viability of the pregnancy and to provide us details we need in our
diagnosis
• Bleeding in the 1st half can be caused by
o Abortion
o Ectopic pregnancy
o Hydatidiform mole
o Others: Local gynecologic lesions, systemic coagulopathies
• Abortion
o Spontaneous or induced termination of pregnancy
o Pathogenesis: Bleeding into the decidua basalis à necrosis of the adjacent tissues à uterine
contractions à expulsion of conceptus
o Manifestations: Bleeding with crampy pains, partial expulsion of the products of conception,
uterus is small for AOG, cervix may be dilated or closed, there is retained placental fragments
on ultrasound

• Ectopic Pregnancy
o Pregnancy that implants outside the uterine cavity with the fallopian tubes being the most
common site of ectopic implantation
o Manifestations: Bleeding with unilateral abdominal pain, history of PID, anemia, cervical
wiggling tenderness & a palpable adnexal mass, US visualization of an adnexal gestational sac
o Management
§ Cross-match blood and arrange for immediate laparotomy
§ Inspect both ovaries & fallopian tubes intraoperatively
• Extensive damage to the tube à salpingectomy (surgical removal of the
fallopian tube)
• Little damage to the tube which rarely happens à salpingostomy (surgical
unblocking of a blocked fallopian tube)

JMFV D2017, UST-FMS

• Hydatidiform Mole
o Characterized by an abnormal proliferation of chorionic villi
o Manifestations: Painless bleeding, early elevation in BP, passage of grape-like cystic structures
per vagina, boggy uterus which is large of AOG, US visualization of multiple cystic structures
within the uterine cavity, abnormally high b-HCG titer
o Management: Evacuate the uterus
§ Vacuum aspiration/suction curettage: lesser risk of uterine rupture, less blood loss,
lower chance of embolizing the abnormal chorionic villi into the systemic circulation
§ Infuse 20u Oxytocin in 1L of fluids to prevent post-evacuation hemorrhage
§ Follow-up with serial HCG measurements q8weeks for 1 year to evaluate the risk for
development of choriocarcinoma

Bleeding in the 2nd half of pregnancy
• Is one which occurs after the 20th week of gestation
• Again, when a gravida in the 2nd half of pregnancy presents at the ED, institute general measures to
stabilize the patient before diagnostic search
o Perform a rapid evaluation of the general condition, do NOT perform vaginal examination at
this stage as placenta previa is a possibility and IE may cause severe hemorrhage
o If in shock, manage appropriately
o If not and vital signs are stable, bleeding is not alarming an Ultrasound should be performed
• Bleeding in this stage may be caused by
o Placenta Previa
o Abruptio Placenta
o Ruptured Uterus
• Placenta Previa
o Implantation of the placenta in the lower uterine segment, which is incapable of generating
active uterine contractions
o Risk factors include previous CS & Multiparity
o Classically presents as PAINLESS bleeding, usually near the end of the 2nd trimester or later
which may be precipitated by intercourse, relaxed uterus, fetal condition may be normal if the
bleeding is not massive
o Management includes volume resuscitation via IV Infusion of NSS/LRS
§ Immediate delivery regardless of AOG if bleeding is profuse & continuous
§ Expectant management if bleeding is light & fetus is still immature
• Keep the patient in the hospital until delivery
• Correct the anemia with FeSO4
• Ensure blood is available for transfusion
§ Indications for delivery
• Mature fetus, dead fetus, fetus with anomaly incompatible with life, mother’s
life is at risk because of excessive blood loss
o Ultrasound – localizes the placenta & confirms the diagnosis
o If unavailable, perform IE under double set-up – be prepared for either vaginal or CS delivery
• Abruptio Placenta
o Premature separation of the normally implanted placenta
o Risk factors: HTN, cigarette smoking, trauma
o Classically presents as PAINFUL uterine bleeding associated with tetanic uterine contractions
and increased baseline uterine pressure, fetal distress (Abnormal FHR pattern)
o Management
§ Rule out coagulopathy by bedside clotting test: failure to clot in 7min = coagulopathy
then treat accordingly
§ Transfuse as necessary, preferably with fresh blood
§ If bleeding is heavy, delivery immediately
§ If bleeding is light to moderate, the course of action depends on the FHT
• Normal FHT, poor contractions à augment labor
• Abnormal FHT à rapid vaginal delivery or timely CS delivery
• Ruptured Uterus
o Shock, tender abdominal distention, easily palpable fetal parts, abnormal uterine contour
o Risk factors: labor induction/augmentation, previous CS
o Bleeding may occur vaginally unless the fetal head is blocking the pelvis
o Management
§ Fluid resuscitation or blood transfusion as necessary prior to surgery
JMFV D2017, UST-FMS
§ Immediate CS delivery
§ Repair the uterus if surgically possible, if not à hysterectomy

Post-partum Hemorrhage
• Any blood loss that results in signs and symptoms of hemodynamic instability in the post-partum
period
o PRIMARY PPH: occurs within 24 hours after delivery
o SECONDARY PPH: occurs after 24 hours to 6 weeks after delivery
o > 500mL for NSD
o > 1L for cesarean section
• Etiology: 4T’s
o Again, general measures should be instituted first prior to diagnostic search, manage shock
appropriately then asses the 4Ts of PPH
• Tone (Uterine tone)
o Uterine atony from Rapid or prolonged labor, overdistended uterus
§ Immediate-onset bleeding of dark blood
§ Relaxed uterus
o Massage the uterus to allow adequate contraction
o Give uterotonic drugs: Oxytocin, Methylergonovine
o If bleeding persists,
§ Perform bimanual compression of the uterus
§ Compress the abdominal aorta
§ Surgery if necessary: vessel ligation, laparotomy or hysterectomy
• Trauma (Lacerations & Uterine rupture)
o Tears/lacerations of the cervix, vagina, or perineum
§ May be due to precipitate delivery, macrosomia, assisted vaginal delivery
§ Uterus is well-contracted & there is passage of fresh blood
o Examine vagina, vulva, perineum & cervix for tears and lacerations
o 1st & 2nd degree lacerations à apply pressure, if bleeding persists à suture
o 3rd & 4th degree lacerations à suture
• Tissue (Retained placental fragments, abnormal placentation)
o Inspect placenta for completeness, explore uterus & evacuate. Give uterotonics
• Thrombin (Coagulation defects)
o Treat according to particular defect

JMFV D2017, UST-FMS

32. Hypertension in Pregnancy p.277, William’s Obstetrics 24e, ACOG Guidelines
Definition
• Systolic BP of 140 mmHg or higher or a diastolic BP of 90 or higher on 2 occasions, at least 4 hours
apart
• Gestational Hypertension
o SBP ≥ 140 or DBP ≥ 90 for the FIRST time during pregnancy, on 2 occasions at least 4 hours
apart
o Diagnosed after 20 weeks AOG
o NO proteinuria
o BP will return to normal after 12 weeks postpartum
• Chronic Hypertension
o SBP ≥ 140 or DBP ≥ 90, on 2 occasions at least 4 hours apart
o Diagnosed before 20 weeks AOG
o No proteinuria
o Persists beyond 12 weeks post partum
• Pre-eclampsia
o SBP ≥ 140 or DBP ≥ 90, on 2 occasions at least 4 hours apart
o Diagnosed after 20 weeks AOG
o (+) Proteinuria 0.3g or 300 mg or more in a 24-hr urine specimen OR in the absence of
proteinuria, any of the severe features to be discussed later
• Eclampsia
o Complication of pre-eclampsia with severe features which is defined as a new-onset grand mal
seizures or unexplained coma during pregnancy or in the post-partum period

Risk Factors

Pathogenesis
• Normally: Trophoblastic invasion is characterized by extensive remodeling of the spiral arterioles
within the decidua basalis. Endovascular trophoblasts replace the vascular endothelial and muscular
linings to enlarge the vessel diameter
• In preeclampsia, there is incomplete trophoblastic invasion. With this, decidual vessels, but not
myometrial vessels, become lined with endovascular trophoblasts. The deeper myometrial arterioles
do not lose their endothelial lining and musculoelastic tissue, giving rise to narrow-caliber vessels. This
leads to impairment in placental blood flow & placental necrosis
• Diminished perfusion and a hypoxic environment eventually lead to release of placental debris or
microparticles that incite a systemic inflammatory response
• This equates to maternal endothelial dysfunction & activation leading to
o Systemic vasospasm
§ Hypertension
§ Seizures
§ Oliguria
§ Liver ischemia
o Capillary leak
§ Edema
§ Proteinura
§ Hemoconcentration
o Activation of Coagulation
§ Thrombocytopenia

JMFV D2017, UST-FMS

Preeclampsia without severe features Preeclampsia with severe features
SBP ≥ 140 or DBP ≥ 90, on 2 occasions at least 4 SBP >160 or DBP >110 on 2 occasions at least 4 hours
hours apart apart while the patient is on bed rest

Diagnosed after 20 weeks AOG Thrombocytopenia (platelet count <100,000/microliter)

(+) Proteinuria 0.3g or 300 mg or more in a 24-hr AST or ALT elevated to >2x the upper limit of normal
urine specimen Oliguria <400cc/day
Proteinuria > 2g/24hrs or +2 on urine dipstick

Serum creatinine > 1.2 mg/dL or a doubling of the
serum creatinine concentration in the absence of other
renal disease

Pulmonary edema

New-onset persistent headache or visual disturbances

Management
• Goals of treatment
o Prevention of convulsions
o Control hypertension
o Delivery at an optimum time and mode
• Magnesium sulfate
o Anticonvulsant of choice: prevents eclampsia by reducing cerebral vasoconstriction and
ischemia
o Loading dose: 4 g/SIVP over 20 minutes then 5 g/deep IM on each buttocks
o Maintenance dose: 5 g/deep IM on each buttocks q6 hours
o Serum therapeutic level: 4-7mEq/L (narrow therapeutic index) so monitor:
§ DTRs must be ++
§ RR must be >12cpm
§ UO of at least 25-30cc/h
o Toxicity
§ 10 mEq/L: loss of patellar rellex
§ 12 mEq/L: respiratory depression
§ 15 mEq/L: altered atrioventricular conduction and (further) complete heart block
§ >25 mEq/L: cardiac arrest
§ Treat with calcium gluconate 1g IV
• Nicardipine
o Calcium channel blocker which is safe to control hypertension in pregnant patients
o 10 mg in 90cc D5W to run at 10ugtts/min, titrate at increments/decrements of 5ugtts/min to
maintain BP of MAP – 20% MAP (140-150/90)
o DO NOT decrease BP abruptly AND not below 130/90 mmHg
o WOF: palpitations, tachycardia, headache
• Optimum time & mode of delivery – definitive treatment for preeclampsia is delivery of the fetus &
placenta, this depends on fetal & maternal factors
o AOG > 37 weeks, if far from term but HTN is severe, give Glucocorticoids for fetal lung
maturation
o Severity of disease
o Fetal status
o Maternal condition
o Nursery capabilities
Complications
• IUGR (intrauterine growth restriction)
• Fetal death
• Abruptio placenta
• Maternal cerebral hemorrhage
• Pulmonary edema

JMFV D2017, UST-FMS
33. Gynecologic Emergencies p.281, Katz Comprehensive Gynecology 6e

Pelvic Inflammatory Disease
Definition
• Comprises a spectrum of infections of the female upper reproductive tract including
o Endometritis – inflammation of the endometrium
o Salpingitis – inflammation of the fallopian tubes
o Oophoritis – inflammation of the ovaries
• The main risk factor for pelvic inflammatory disease is having unprotected intercourse with multiple
sexual partners

Etiolopathogenesis
• PID is usually initiated by ascending infections from the lower genital tract (vagina and cervix)
• Neisseria gonorrhoeae and Chlamydia trachomatis are often implicated, although most cases are
polymicrobial in nature involving the vaginal flora (G. vaginalis, Haemophilus influenzae, enteric Gram-
negative rods, and Streptococcus agalactiae)
• Any sexually active female individual is at risk for PID, but those with multiple sexual partners are at
the highest risk.
• PID represents a spectrum of clinical disease, from mild, vague pelvic symptoms to tubo-ovarian
abscess and, rarely, fatal intra-abdominal sepsis. In some women, the inflammatory process can extend
to the liver capsule to cause perihepatitis (the Fitz-Hugh Curtis syndrome)

• Classic triad:
o Bilateral, dull, vague lower abdominal pain
o Cervical motion tenderness
o Adnexal tenderness
• AUB – presents in 1/3 of women: Post-coital bleeding, Intermenstrual bleeding & menorrhagia
• Fever, Purulent discharge

Diagnosis – mainly clinical but ancillaries may aid in the diagnosis
• CBC: Leukocytosis, ESR & CRP: Elevated, Urinalysis
• TVS to rule out tubo-ovarian abscess
• Laparoscopy – gold standard in the diagnosis of PID
o May determine severity of disease, detects Fitz-Hugh Curtis syndrome & offer opportunity to
perform operative procedures
o Mild: erythema, edema, no spontaneous purulent exudates, tubes freely movable
o Moderate: gross purulent material evident, more marked erythema & edema, tubes may not be
freely movable, fimbria stroma may not be patent
o Severe: pyosalpinx
• The presumptive clinical diagnosis of PID is made in sexually active young women, especially women at
high risk for sexually transmitted infections (STIs), who present with pelvic or lower abdominal pain
and have evidence of cervical motion, uterine, or adnexal tenderness on exam.

Management
• Treatment is indicated for patients with this presumptive clinical diagnosis of PID, even if findings are
subtle or minimal, since complications (tubal infertility, ectopic pregnancy, chronic pelvic, septic shock)
are more common if treatment is withheld or delayed
• 2 types: Out-patient or In-hospital
• Out-patient Regimen
o Given to patients with mild or moderate PID without indications for admission
o First line:
§ Ceftriaxone 250mg/IM single dose + Doxycycline 100mg PO BID for 14 days
§ + Metronidazole 500mg PO BID for 14 days if with Bacterial Vaginosis
• In-hospital Regimen
o Indications for admission
§ Pregnancy, Lack of response or tolerance to oral medications, Nonadherence to therapy
§ Inability to take oral medications due to nausea and vomiting
§ Severe clinical illness (high fever, nausea, vomiting, severe abdominal pain)
§ Complicated PID with pelvic abscess (including tuboovarian abscess)
§ Possible need for surgical intervention or diagnostic exploration for alternative etiology
(eg, appendicitis)
JMFV D2017, UST-FMS
o Regimen A: Cefoxitin 2g/IV q6 or Cefotetan 2g/IV q12 and Doxycycline 100mg PO q12
§ First line
o Regimen B: Clindamycin 900mg/IV q8 and Gentamycin 2mg/kg loading dose then 1.5mg/kg q8
§ Given to patients with TOA, surgery is needed if TOA is documented for drainage

Profuse Vaginal Bleeding
• Determine the vital signs
• Note for the presence of pallor or impending shock (hypotension, weak pulses, diminishing UO)
• Institute fluid resuscitation
o 2 venous access lines
o Give crystalloids: D5LRS, NSS
• CBC & blood typing: Prepare for blood transfusion if necessary
• Determine the amount of bleeding and localize the source
o Vulva, vagina, cervix, uterus

Management
• Vulvar bleeding
o Traumatic in origin
o Apply pressure dressing to reduce the amount of blood loss
• Bleeding from the vagina coming from the cervical os
o Tumor or neoplastic
o Insert a packing to lessen bleeding
• Uterine bleeding
o IV Estrogen 25mg q2-4h or Oral Estrogen 2.5mg q6 until bleeding stops then taper or shift to an
oral regimen for 30-40days
§ On the last 10 days, add 10nmg OD or 10 days à medical curettage
o OCP 1 tablet QID until bleeding is controlled, taper or shift to oral regimen for 30-40days
o Impending shock: D&C is considered the fastest way to control the bleeding

JMFV D2017, UST-FMS
#39$HEAD$TRAUMA$
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(raccoon&eyes),&CSF&rhinorrhea,&headache,&brief&amnesic&episode,&nausea,& &
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!
35. Maxillofacial Injuries p.336, UpToDate Article on Maxillofacial Trauma 2017

Definition/Etiology
• Injuries to the facial region involving soft tissue & facial skeleton resulting from accidental or deliberate
trauma to the face
• The nose, zygoma, and mandible are the most commonly fractured among the facial bones
• Injuries to the mid-face usually results from vehicular accidents with passengers and pedestrians being
more or less equally involved, followed by interpersonal violence
• May be closed or open fractures with incidence being almost equal for both

Pathogenesis
• Injuries occur when energy (most often kinetic) transferred to the body exceeds tolerance of the tissue
• The likelihood of injury is related to the amount of energy transferred & the condition of the
underlying tissue
• Traditionally, trauma has been classified as blunt or penetrating, but in many cases the effect is a
combination

Types of Fractures
• Le Fort I – horizontal fracture, above the apices of the teeth; usually have minimal mobility & stable
occlusion
• Le Fort II – pyramidal fractures in the maxilla involving the nasal, lacrimal & ethmoidal bones & the
zygomatico-maxillary sutures
• Le Fort III – high transverse fractures of the maxilla at the base of the nose & ethmoid region,
extending across the orbits to the lateral rim & separating the zygomatico-frontal suture area

• Periorbital ecchymosis
• Malocclusion & mobility of the mid-face
• Fractures as mentioned above

Diagnosis
• CT Scan or computerized 3D Examination will confirm the diagnosis & help in the planning of
reconstructive surgey
• X-rays of the affected parts may also be helpful

Mandibular Fracture Zygomatic Fracture Facial Soft tissue injuries
In the elderly, the bones become 2nd most common injury to facial Results from either deliberate or
fragile due to atrophy and skeleton: malar bones; two types accidental trauma
resorption of the alveolus. of disruptions:
Condyle is most often fracture 1) Low Velocity Impact: swelling Bleeding is excessive: out of
Treatment: align the mandible in not excessive comminution proportion to the size of
proper occlusion with the (breaking) of bone is rare ie. external injury
opposing maxilla Punch/fall
2) High Velocity Impact: swelling is
marked, comminution (breaking)
common ie. MVA

Management
• The immediate priority is the establishment & preservation of airway, control of bleeding
• Remove any obstruction to the airway like blood clots, displaced tongue, loose teeth, bone fragments,
broken dentures, and foreign bodies
• Do not allow the patient to lie flat on their back to avoid aspiration & to prevent their tongue from
falling back on their airway
• Intubation – may be indicated to maintain the airway
• Analgesics (Morphine, strong narcotics are contraindicated because it decreases respiration which
masks signs of head injury)
• Le Fort II or III: CSF rhinorrhea → antibiotic therapy
• Internal skeleton fixation by external rod and cheek wires → immobilize the maxilla

JMFV D2017, UST-FMS

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Crampy&abdominal&pain& Constipation&(late&finding&–&absence&of&flatus&
Classification:& Abrupt&onset&of&symptoms&(suggestive&of&an& or&bowel&movement)&
• Extraluminal&(including&adhesions&and&neoplastic&disease)& acute&event)& Fever&&
• Intraluminal&(such&as&gallstone&ileus&or&stricture)& Chronic&constipation&& Tachypnea&
• Intramural&(such&as&Crohn’s&disease&process)& Straining&stool&& Previous&abdominal&or&pelvic&surgery&
Recurrent&LLQ&abd.&pain&over&several&yrs& History&of&malignancy&
&
Two&types&of&patients&who&present&w/&mechanical&intestinal&obstruction:& &
1. Previous&abdominal&surgery,&and&ones&who&have&not& DIAGNOSIS&
2. Obstruction&secondary&to&postop&adhesions&(most&common),&hernias,&and& • Lab&tests:&serum&chemistries,&blood&urea&nitrogen&(BUN)&levels,&creatnine,&
malignant&tumors& CBC&,&lactate&dehydrogenase&tests,&urinalysis&
& o WBC&15,000\25,000/mm3&↑&PMN&→&strangulated&
PHYSIOLOGY/PATHOLOGY& o WBC&40,000\60,000/mm3&→&mesenteric&vascular&occlusion&
o Hemoconcentration&
• Small&bowel&obstruction:&
o Urine&specific&gravity&1.025\1.030,&proteinuria,&mild&acetonuria&
o Leads&to&proximal&dilatation&of&intestine&d/t&accumulation&of&GI& o ↑&BUN,&creatinine&
secretions&and&swallowed&air& o Dehydration,&starvation,&ketosis&→&metabolic&acidosis&
o This&bowel&dilatation&stimulates&cell&secretory&activity,&resulting&to& o Loss&of&highly&acid&gastric&juice&→&↓&acid&in&stomach&→&pancreas&↓&
more&fluid&accumulation& bicarbonate&→&metabolic&alkalosis&
o This&will&lead&to&↑&peristalsis&above&and&below&the&obstruction,&with& o Distention&of&diaphragm&→&respiratory&acidosis&
frequent&loose&stools&and&flatus&early&in&its&occurs& o Regurgitation&of&amylase&to&the&blood&→&↑&serum&amylase&
• Large&bowel&obstruction:& • Imaging&tests&
o Causes&bowel&dilatation&above&the&obstruction&→&causes&mucosal& o X&ray&–&large&quantities&of&gas&in&bowel,&no&colonic&gas,&gas\fluid&
edema&&&impaired&venous&and&arterial&blood&flow&to&the&bowel.& levels,&distended&bowel&
o Bowel&edema&and&ischemia&↑&mucosal&permeability&of&bowel,&which& o CT&Scan&–&location&and&cause&of&obstruction&
can&lead&to&bacterial&translocation,&systemic&toxicity,&dehydration&and& o Ultrasound&–&diagnose&obstruction&of&the&small&bowel&
electrolyte&abnormalities& &
& TREATMENT&
& • Intravenous&fluids&and&electrolytes&(ie.&Lactate&ringers&solution,&5%&dextrose&
& in&water)&for&fluid&replacement&and&maintenance&
& • Antibiotics&may&be&administered&
& • Lysis&of&adhesions&
& • Surgery&&
&
!
37. Spine Trauma p. 312
Definition
• Traumatic insult to the spine & spinal cord resulting to the partial or complete compromise of the main
functions of the cord particularly motor, sensory, autonomic & reflex functions
• Acute injuries of the spine & spinal cord are the most common causes of severe disability & death after
trauma, a vast majority of which involve the cervical spine

• Motor vehicular accident
• Falls
• Sports-related injuries
• Traumatic spinal cord injury is a disease that is quite unique in that it occurs instantaneously as a result
of a variety of mechanisms
• Mechanical insult causes persistent compression of the neural tissue
• Cervical spine – most commonly injured level of the vertebral column
• Fractures & subluxations are the common types of spine injury

• SCI can be classified as complete or incomplete injuries
• Complete injuries are those without preservation of motor or sensory function below the zone of the
injury
• Incomplete injuries on the other hand are those with preservation of function below the level of the
injury
• Cervical spine injuries are classified according to different syndromes that provide a greater amount of
predictive accuracy
• Brown Sequard Syndrome
o Results from a penetrating wound producing injury to one side of the SC
o Patients present with
§ Ipsilateral loss of the dorsal column and motor function
§ Contralateral pain & temperature loss below the level of the lesion
• Central Cord Syndrome
o Results from an acute hypextension injury in patients with pre-existing cervical spine disease
o Weakness of both UE & LE but more prominent weakness in UE > LE
o May be associated with bladder-bowel & sexual dysfunction
• Anterior Cord Syndrome
o Results from flexion or axial loading mechanism
o Total loss of motor, pain & temperature sensation below the level of the injury
o Intact dorsal column function
• Conus Medullaris
o Associated with thoracolumbar injuries
o Combination of spinal & nerve root level involvement
• Cauda Equina
o Seen in injuries from L1 down to the sacral levels
o Pure lower motor neuron injuries & flaccid areflexia

Management
• Spinal cord injury should be highly considered in patients with head trauma & multiple injuries
• Attention should also be placed to the first priorities of trauma: Airway, breathing, circulation
• Goals: Early diagnosis of injury, preservation of spinal cord function & restoration of spinal stability
• Immediate immobilization of the head & neck
o Maintenance of the normal axial alignment should be done at all times
o Cervical collar must be placed and any diagnostic study to be done must be carried out with the
patient secured in the initial immobilization device
• Oxygen
o Supplemental oxygen must be given to all patients because relative hypoxia can further damage
the injured cord
• Methyprednisolone
o Once an SCI is documented, give within 8h of the injury
o Initial bolus dose: 30mg/kg over 15min
o Maintenance dose: 5.4mg/kg/h continuous infusion over the next 23hours

JMFV D2017, UST-FMS

• Skeletal traction
o Accomplished for spinal alignment of cervical fractures
o Aims to reduce fracture dislocation to prevent immediate prevention of further neurological
damage
• Referral to Neurosurgery for Surgical Intervention
o Reduction of mal-alignment, decompression of neural elements by removing bone
fragments/foreign bodies, restoration of spinal stability

• X-Ray (Spine series)
o Indicated in all trauma patients with localized pain, deformity, crepitus, edema, altered
sensorium, neurological dysfunction or head injury
o Patients should receive spinal radiography while still immobilized on the original stretcher or
spine board
• CT Scan
o Diagnostic modality of choice for evaluation of acute spine trauma
o Also indicated if plain film id inconsistent with the patient’s clinical condition
• MRI
o Being used increasingly as the spinal cord & its surrounding structures can be visualized directly
and non-invasively

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38. Thermal Burn/Injury p.370, 339, American Burn Association Guidelines 2016
Definition
• Injuries sustained as a result of the transfer of heat down a temperature gradient with body tissues
being the receiving end. When the heat transferred is higher than what the tissues can equilibrate,
thermal burns/injuries occur
• Burn size
o Refers to the total body surface area affected estimated by the “Rule of Nines” or the Lund &
Browden Chart
• Depth of burn
o Refers to the thickness of burn involvement classified as 1st, 2nd, 3rd or 4th degree burns
• Critical/primary areas
o Refers to the face, neck, hands, feet, major joints & perineum. These areas need special
attention because they may cause special problems

• Types of burns
o Scald burn – hot liquids, hot water, soup, sauces, porridges (most common: hot liquids)
o Flame burn – house fires, careless smoking, vehicular accidents (most common: open flame)
o Flash burn – explosions of gas or flammable liquids releasing heat for a brief period of time
o Contact burn – contact with hot metals, plastic, glass or hot coals
o Chemical burn – caused by strong alkali or acids
o Electrical burn – caused by electrical current passing through tissues
• The amount of tissue destruction depends on the temperature & the time of exposure to the agent.
• There are 3 zones of injury within a major burn according to Jackson’s Burn Model
o Zone of coagulation: cells are irreversibly damaged or necrotic
o Zone of stasis: cells are injured & if not treated, will die within 24-48h
o Zone of hyperemia: cells are minimally injured & will recover within 7-10d


Burn depth Involved structures Symptoms/Signs Heals in
st
1 degree Involves only the Dry lesion with redness, pain. Not 5-7days, desquamates
epidermis typical of included in the estimation of BSA
sunburns
Partial Entire epidermis + upper Pink, red in color that blanch with 2-3 weeks by
thickness, dermis pressure, painful and wet (+/-) epithelialization,
superficial blisters or weeping lesions minimal scarring
Partial Entire epidermis + most of Red/white, diminished sensation but 3-5 weeks,
thickness, dermis present. Blanching is sluggish/absent hypertrophic scar with
deep possible contracture
Full thickness All skin layers + Black/white, leathery in texture, no Requires immediate
subcutaneous tissue blanching, little or no pain coverage
4th degree Up to muscle/bone White, brown, gray, black waxy in Requires immediate
texture, anesthetic skin. debridement of
Pathognomonic: thrombosed vessel necrotic tissue and
coverage

Diagnosis/Assesment
• Estimate the burn size by the Rule of Nines or the
Lund & Browden Chart
o Expressed in % BSA
o Rule of Nines – refer to the image, rough
estimate
o Lund & Browden Chart – 1 fist/palm size =
1% BSA, most accurate, accounts for
variation in body size/shape
• CBC, blood typing, serum electrolytes (Na, K, Cl),
BUN, RBS, Creatinine, ABG, CXR, ECG

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Management

At the scene of the accident
• Perform primary survey & secure the airway, breathing & circulation
• Halt the burning process by removing the patient from the scene of the fire, remove burning clothes
• Apply cold compress: Tap water > cold water
• Irrigate chemical burns with liberal amounts of water, do not neutralize the chemical agent as this may
release more heat worsen the injury
• Cover the patient with clean sheets to protect the wound
• Transfer to the ER
At the ER
• Make a quick estimate of the extent of the injury, fill-out burn chart & record
• Elicit history of the incident. Note the possibility of smoke inhalation, associated injuries, pertinent
medical history
• Determine if the patient needs hospitalization or treat in the OPD
• Indications for admission
o Partial thickness burns >10% BSA
o Involvement of face, neck, both hands, both feet, perineum
o 3rd degree burns in all age groups
o Electrical (contact) and chemical burns
o Associated injuries: soft tissue trauma, fractures, smoke inhalation, head injury
o Complicating medical problems: diabetes mellitus, pulmonary disease, peptic ulcer
o Suspected child abuse or neglect / self inflicted / psychological problems
• Out-patient Care
o Burns & Injury: cold compress; clean wound with soap and water; debride dead tissue (blisters
2-3cm may be left intact); local antibiotics can be used with wound dressings and systemic
antibiotics are not required.
o Thermal Burns: topical antimicrobials can be given (silver sulfadiazine (silvadene), calcium
nitrate – silver sulfadiazine, povidione-iodine, nitrofurazone, chlorhexidine gluconate,
gentamicin); overtreatment is the most common cause of complications → so petroleum jelly
or non-adherent porous dressings are sufficient except when the burn is grossly contaminated
o Thermal Injury: Tetanus prophylaxis should be administered; if a patient has no tetanus
immunization history give 250units of tetanus human globulin or 3,000 units of anti-tetanus
serum (ATS). Booster dose of tetanus toxoid should be given if the patient had not been
boostered for the last 5 years.
o Oral analgesics can be given for pain relief
In the hospital (admitted patients)
• Volume replacement via Parkland’s Formula
o PLRS is used
o 4cc PLRS x kg Body Weight x %TBSA
o 1⁄2 administered over the 1st 8 hours post-injury
o 1⁄2 administered over the next 16 hours post injury
o Titrate fluid to urine output
§ Adults: 30cc/hour
§ 100 cc/hour for electrical burns
§ Children: 1 cc/kg/hour
• Wound management
o Exposure Therapy (Open Dressing): superficial burn wounds involving the face and
perineum → light and cool environments without topical antibiotics after debridement
o Occlusive Dressing (Close method): for circumferential burns and those requiring transport
w/ or w/o topical antibiotics
o Excisional Therapy: most demanding procedure where all non-viable tissues are removed
followed by immediate wound coverage (either temporary or permanent – done between
the 2nd and 5th post burn days)
o Laser Doppler Velocrimetry (LDV): most promising in detecting burn depth; measures the
degree of blood flow within and surrounding burned tissues
o Escharotomy / Fasciotomy: circumferential and constricting burns
o Escharotomy: only if skin and subcutaneous tissue are constricting
o Fasciotomy: deep compartment hypertension
o Skin Grafting: remains unhealed by the end of the 4th week

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39. Fractures 5th Edition p.299, Tintinalli’s Emergency Medicine 8E
Definition/Etiology
• Are disruptions of bone tissue or simply a break in bone continuity which occurs when the modulus of
elasticity is exceeded in events such as
o (1) an application of force exceeding the strength of the bone: sudden traumatic injury,
violence, MVA, fall
o (2) repetitive stress: fatigue fractures occurring in the lower extremities
o (3) an invasive process that undermines the bone’s integrity: pathologic fractures from
malignancies or infections

Closed Fracture
• Is one where the fracture surface does not communicate with skin or mucous membrane
• Diagnosis
o MOI: Obtain a detailed history concerning the nature of the accident
o Physical signs
§ Local swelling
§ Visible/palpable deformity
§ Marked localized ecchymosis
§ Marked localized tenderness
§ PRETERNATURAL MOBILITY (Bone is mobile in continuity/ abnormality in direction or
extent of joint mobility): Definitive sign of a fracture
§ Crepitus
o X-Ray AP & Lateral views
§ Film should include the entire length of the injured bone & joints above & below it
• Treatment
o Treat first any life-threatening conditions first as in the ABCs of trauma
o Apply external immobilization through the use of cast or splint
o Determine optimal treatment either closed or open reduction techniques

Open Fracture
• An open fracture is a fracture associated with overlying soft tissue injury, creating communication
between the fracture site and the skin
• Classification (Gustilo & Anderson)
o Type I: Clean wound <1cm ling
o Type II: Laceration >1cm but without extensive tissue damage
o Type IIIA: Extensive soft tissue lacerations or flaps but maintain adequate tissue coverage of
bone
o Type IIIB: Extensive soft tissue loss with periosteal stripping & bony exposure: usually massively
contaminated
o Type IIIC: Open fracture with an arterial injury that requires repair regardless of size of the soft
tissue wound
• Diagnosis: same as closed
• Treatment
o Cover the wounds immediately with a sterile dressing and splint the involved extremity
o Do not push protruded soft tissue or bone back into the wound unless there is vascular
compromise
o Anti-tetanus prophylaxis
o IV broad-spectrum antibiotics as osteomyelitis is a complication of open fractures
o Immediate debridement INSIDE THE OPERATING ROOM
o Reduce & stabilize the fracture
o Leave the wound open & do secondary closure later

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40. Acute Urinary Retention p.298, Tintinalli’s Emergency Medicine 8E
Definition
• Acute urinary retention is a painful urologic emergency characterized by a sudden inability to empty
the urinary bladder
• Though it can occur at all ages and gender, it usually occurs in elderly males with benign prostatic
hyperplasia

Pathogenesis
• Normally (you can choose not to say this)
o The voiding process or micturition involves the complex integration and coordination of high
cortical neurologic functions (Sympathetic, parasympathetic, somatic) and Muscular functions
(detrusor and sphincter smooth muscle)
o As the sensory impulse of bladder distention transmits to cortical centers, these areas of the
brain smoothly coordinate voluntary urination
o Continent urine storage in the bladder requires both relaxation of the detrusor muscle (through
β-adrenergic stimulation and parasympathetic inhibition) and contraction of the bladder neck
and internal sphincter (through α-adrenergic stimulation)
o The contraction of bladder detrusor muscle (by cholinergic muscarinic receptors) and relaxation
of both the internal sphincter of bladder neck and the urethral sphincter (through α-adrenergic
inhibition) contribute to smooth urination
• Anything that causes interference with the neurologic & muscular control of the voiding process can
result in voiding dysfunction, hence urinary retention

Etiology: The causes generally fall under 2 categories: Obstructive: Bladder outlet obstruction & Myogenic:
Bladder muscle failure
• Obstructive causes
o Penis: Phimosis (foreskin can not be retracted), meatal stenosis, foreign body constriction (rings
& rubber bands)
o Urethra: tumors, foreign bodies, calculi, hematoma
o Prostate gland: BPH, carcinoma, severe prostatitis, bladder neck contracture, prostatic
infarction
• Myogenic causes
o Neurologic: Motor paralysis, spinal shock, spinal cord syndrome, tabes dorsalis, diabetes,
multiple sclerosis, syringomyelia, herpes zoster
o Drugs: Antihistamines, anticholinergics (ie. Atropine, phenothiazines, diazepam, NSAIDs),
antispasmodics, tricyclic antidepressants, α-adrenergic stimulators /β-agonists (ie.
Isoproterenol, terbutaline)
o Psychogenic: Acute anxiety
o Traumatic: Urethral/bladder injury

• History
o Elderly patients with progressive decrease in the force & caliber of the urinary stream
o Nocturia, dribbling, prior history of retention, prior catheterization, dilatation or prostatectomy
o Bone pain & weight loss could be manifestations of malignancy
o Incontinence is a paradoxical manifestation: overflow of a markedly distended bladder
• PE
o Distended bladder: prominent hypogastrium
o Slight pressure will cause tremendous discomfort
o In fat individuals, percussion will reveal a dull sound of distended bladder
• AUR may be an ominous sign of a more serious underlying condition such as a Cerebrovascular
accident, TIA, malignancy & DKA

Diagnosis
• Diagnosis can be established clinically by history & physical exam
• But Bedside Ultrasound can easily identify urinary retention
• CBC, Urinalysis/urine culture to identify infection (once urine is obtained)
• Prolonged obstruction may result in impaired renal function and electrolyte imbalance, so obtain renal
function studies (BUN/sCr) and serum electrolytes

JMFV D2017, UST-FMS
Management
They Immediate goal is to empty & decompress the urinary bladder
• Initially, perform Urethral catheterization
o French 16 or 18 foley catheter + xylocaine jelly
§ To lubricate thus preventing involuntary contraction of the pelvic muscles
§ To ease the pain of catheterization
o If this fails,
• Decompress the bladder via suprapubic catheterization
o Identify the symphysis pubis à then mark the point about 1cm above the SP
o Inject xylocaine jelly
o Nick with a stab knife & puncture straight posteriorly
o A sudden give indicates you are in the bladder
• Keep the catheter in place as indwelling
• Immediate referral is the rule (urology, neurology)

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41. Ocular Trauma p.402
• Orbital Hemorrhage
• Blow-out Fracture
• Hyphema
• Lens Dislocation
• Perforating Globe Injuries

I. Orbital Hemorrhage
• Hemorrhage in the orbit can result from accidental or surgical trauma. AKA Traumatic Retrobulbar
Hemorhhage
• Etiology: Blunt trauma to the eye, surgery
o Symptoms: Pain, decreased vision
o Signs
§ Proptosis with resistance to retropulsion
§ Diffuse conjunctival hemorrhage extending posteriorly
§ Eyelid ecchymosis
§ Congested conjunctival vessels
§ Increased IOP
§ Limited extraocular motility
• Management
o Non-pharmacologic
§ Hospitalization if IOP is not reduced or if vision is threatened
§ Emergency orbital decompression surgery may be required (Ophthalmologist)
o Pharmacologic
§ Relieve IOP: Oral CAI + Beta blockers or hyperosmotic agents like Mannitol
§ Oral analgesics
• Laboratories/Ancillaries
o CT scan of the orbits (axial & coronal view) can be delayed until treatment has been instituted

II. Blow-out Fracture
• Orbital fractures commonly with facial trauma, may be associated with injuries to the orbital contents,
intracranial structures & paranasal sinuses. Decreased visual acuity, intraocular injuries, strabismus,
and ptosis
• Etiology: blunt trauma
o Symptoms
§ Pain especially on vertical eye movement
§ Local tenderness
§ Binocular double vision
§ Eyelid swelling
§ Crepitus after nose blowing
o Signs
§ Restricted eye movement and double vision worse on upward gaze
§ Subcutaneous or conjunctival emphysema
§ Hypesthesia in the distribution of the infraorbital nerve
§ Palpable step-off along the orbital rim
§ Point tenderness
§ Enophthalmos which may be initially masked by orbital edema
§ Ptosis
• Management
o Non-pharmacologic
§ Bilateral eye patch
§ Ice packs within the orbit
§ Instruct the patient not to blow his nose
§ Refer to Ophthalmology for surgical repair
o Pharmacologic
§ Nasal decongestants
§ Broad spectrum antibiotics
• Labs/Ancillaries
o CT Scan of the orbit/head
o Head radiographs
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III. Hyphema
• Presence of blood in the anterior chamber
• Usually caused by blunt trauma to the head and/or eye
• Clinical manifestations
o Symptoms: Pain, blurred vision
o Signs: Blood in the AC, layering or clot or both. Total hyphema may be black or red
§ 8-Ball hyphema – blood fills the whole AC
• Management
o Non-pharmacologic
§ Evacuation of the hyphema specially with the 8-ball type as corneal staining is
unavoidable
o Pharmacologic
§ Atropine, TID
§ No Aspirin-containing products or NSAIDs
§ Mild analgesics only
§ Topical steroids if the eye becomes photophobic & to prevent fibrinous AC reactions
§ Decrease IOP via anti-glaucoma medications

IV. Lens Dislocation
• Ectopia lentis
• Dislocation of the lens out of the pupillary aperture which may be traumatic or hereditary
• Dislocation – there is complete disruption of the zonular fibers. 2 types
o Anterior dislocation – the lens is dislocated towards the anterior chamber
o Posterior dislocation – the lens is pushed backwards toward the vitreal cavity
• Sublaxation – partial disruption of the zonular fibers leaving the lens decentered but remains partially
in the pupillary aperture
• Etiology: Trauma, Marfan’s syndrome, high myopia, homocystinuria
o Symptoms
§ Decreased vision
§ Monocular diplopia – double vision that persists when covering one eye
o Signs
§ Decentered or displaced lens
§ Iridodonesis – quivering of the iris
§ Phacodenesis – quivering of the lena
• Management
o Referral to other specialties
§ Marfan’s Syndrome – refer to cardiology
§ Homocystinuria – refer to IM
o Surgery by an Ophthalmologist

V. Perforating Globe Injuries
• Penetrating injuries to the globe with an entrance & exit wounds causing escape of aqueous, lens,
vitreous or uveal tissue at the site of injury
• Etiology: Sharp objects, high velocity pellet or fragments of metal
o Symptoms
§ Decreased vision, Pain, Eye redness
o Signs
§ Hemorrhage around the area of injury
§ Non-red orange reflex
§ Serous fluid oozing out may point to escape of vitreous
§ Extrusion of lens/uvea
§ Flat anterior chamber – due to the release of aqueous humor
• Management
o Non-pharmacologic
§ Do not touch the eye, remove grossly visible debris
§ Apply eye shield without patching the eye, no pressure must be applied
§ Refer to an Ophthalmologist for surgery
o Pharmacologic: Oral analgesics, tetanus immunization, oral antibiotics

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42. Foreign Bodies in the Upper Aerodigestive Tract p.441
Definition
• Inhalation or ingestion of foreign bodies
• Usually occurs in:
o Toddlers
o Mentally retarded
o Alcohol=intoxicated adults
• In the airway – foreign body may log in larynx, trachea or bronchus
• In the digestive tract, there are 3 areas of constriction in the esophagus where foreign bodies may
become impacted
o Cricopharyngeal area: narrowest area in esophagus
o As the esophagus crosses the aortic arch & left main bronchus
o As the esophagus pierces the diaphragm
• 3rd leading cause of accidental death in children <1 year of age
• 4th leading cause of death in children 1-6 years

Etiopathogenesis
• Airway foreign body is common among toddlers because
o Lack of molars necessary for the proper mastication of food
o Have less controlled coordination in swallowing and immaturity
• Esophageal foreign body is common in adults
o Dentures
o White part of balut
o Fishbone

• Airway Foreign Body
o Clinical Phases:
§ 1st phase: choking, gagging, cough, airway obstruction during aspiration, which occurs
at the moment of aspiration
§ 2nd phase: asymptomatic as reflexes fatigue lasting for hours or weeks
§ 3rd phase: complications ie. Infection, erosion, obstruction causes pneumonia,
atelectasis, abscess or fever
o Laryngeal & Tracheal Foreign body
§ Biphasic stridor
§ Jackson=Jackson triad:
• 1. Asthmatoid wheeze
• 2. Audible slap
• 3. Palpable thud on trachea
o Bronchial Foreign body
§ Prolonged wheeze in the expiratory phase
§ Unequal breath sounds, unilateral wheezing, hypersonority or dullness, hemoptysis
• Esophageal Foreign Body
o Parental suspicion that the child has swallowed a foreign body
o Poor appetite, Emesis, Dysphagia, odynophagia
o Drooling & stasis of saliva
o Esophageal perforation: fever with tachypnea, tachycardia & pain

Diagnosis
• Airway: CXR & Neck X-Ray with PA view taken at end-inspiration and expiration
o Obliterated bronchial air column
o Inspiratory hypoinflation or atelectasis
o Expiratory hyperinflation or emphysema
o Lobar or segmental pneumonia
• Esophageal Findings: Chest, neck, abdominal X-ray (PA Lat)

Management
• Airway Foreign Body: Endoscopy to remove the foreign body
• Esophageal Foreign Body
o Observation first
o If w/ respiratory distress or total obstruction or if foreign body is sharp: Immediate
esophagoscopy
JMFV D2017, UST-FMS
43. Acute Appendicitis p.293, Schwartz’s Principles of Surgery 10e
Definition
• Appendicitis is the inflammation of the vermiform appendix which can range from a simple or
congestive form to a more complicated transmural involmvement to a perforated appendix

• Appendicitis is caused by luminal obstruction of the vermiform appendix, typically by a fecalith. Other
less frequent causes include obstruction by
o Lymphoid hyperplasia (2o to IBD or Infections)
o Parasites
o Or rarely neoplasms & foreign bodies
• This proximal obstruction presents as a closed-loop obstruction which causes intraluminal pressure to
increase, add to that the continued normal secretions of the appendiceal mucosa, this would rapidly
lead to the distention of the appendix.
• This distention stimulates nerve endings of visceral afferent stretch fibers à Vague, dull, diffuse pain in
the midabdomen or lower epigastrium
o Pain is non-localizable as the appendix has the same covering as the organs covered with
peritoneum à same sensory innervation
• Further distention from continued mucosal secretion & rapid multiplication of the resident bacteria of
the appendix à Reflex nausea & vomiting & visceral pain increases
• Stages
o Uncomplicated
§ Congestion
§ Suppurative
o Complicated – 25% of cases
§ Gangrenous
§ Perforative – most common in <5 (45%) and >65y/o (51%)
• Congestion (4-6h)
o Congestion occurs when the intraluminal pressure continues to increase such that it overcomes
the venous & lymphatic pressure
o This would occlude the draining capillaries & venules but arterial inflow continues resulting in
engorgement & vascular congestion
• Suppurative
o The congested appendix is a good medium for bacterial proliferation à this would incite an
inflammatory reaction
§ More anaerobes vs normal appendix: E. coli, Bacteroides, Fusobacterim nucleatum,
Peptostreptococcus
o The inflammatory process soon involves the serosa, as the parietal peritoneum is irritated à
classic shift of the pain to the RLQ
o The whole appendix becomes swollen, turgid & is coated with a fibrous exudate
• Gangrenous
o Occurs when intraluminal pressure exceeds arterial pressure à impairment of blood supply
with vessel thrombosis and full thickness necrosis
o Area of poorest blood supply suffers most
§ Ellipsoidal infarcts develop in the antimesenteric border
• Perforative
o As distension, bacterial invasion, compromise of the vascular supply, and infarction progress,
perforation occurs, usually on the antimesenteric border just beyond the point of obstruction
leading to
§ Outpouring of the inflammatory cells & mediators, this will be walled off from spreading
by the formation of a appendiceal phlegmon: palpable mass in 2-6% of cases, represents
a matted loop of bowel adherent to an inflamed appendix or a periappendiceal abscess
§ Failure of phlegmon formation will allow the contents to the peritoneal cavity leading to
localized or generalized peritonitis

• The inflammatory process in the appendix presents as pain, which initially is of a diffuse, non-
localizable visceral type (periumbilical, central abdominal) and later becomes more localized as the
peritoneal lining gets irritated
• Symptoms include (PANT: Pain, anorexia, nausea & vomiting, elevated temperature)
o RLQ pain
o Anorexia
JMFV D2017, UST-FMS
o Nausea & vomiting
o Fever
• Signs
o Direct Tenderness at the McBurney’s Point (RLQ)
§ b/w ASIS & Umbilicus
o Rebound tenderness
§ Sign of peritoneal irritation, differentiates medical vs surgical abdomen
o Muscle guarding at the Right Iliac Fossa
o Rovsing’s Sign
§ Indirect tenderness
§ Press LLQ à air travels à right distends à RLQ Pain
§ Indicator of peritoneal irritation
o Psoas Sign
§ Pain with extension of the right leg which indicates a focus of irritation in the proximity
of the right psoas muscle
o Obturator Sign
§ Stretching of the obtuzrator internus through internal rotation of a flexed thigh suggests
inflammation near the muscle
o Iliopsoas Sign
§ Pain upon extension of right hip. Suggests retrocecal appendix
o Dumphy’s Sign
§ Increased abdominal pain with coughing
o Anatomic variations in appendiceal location
§ Retrocecal appendix – less-striking abdominal findings; more flank tenderness
§ Appendix hangs in cervix – no abdominal findings, R-sided rectal tenderness
§ Gravid uterus – RUQ pain

Diagnosis
• Mainly clinical: Alvarado scoring

• CBC:
Leukocytosis
• Urinalysis: to r/o ureteral stone & UTI as causes of lower abdominal pain. Presence of UTI does not r/o
appendicitis if history & PE point to AP
• HCG – for possibly pregnant women
• Imaging may be performed but not necessary in most cases
o Graded-compression Ultrasound. Suggestive of AP: Thickening of the appendiceal wall,
presence of periappendiceal fluid. Demonstration of an easily compressible appendix
measuring <5 mm in diameter excludes the diagnosis of appendicitis
o HR CT Scan: Dilated appendix >5mm, Wall is thickened, Periappendiceal fat stranding –
inflammation, Thickened mesoappendix, Periappendiceal phlegmon, Free fluid, Fecaliths – not
pathognomonic

JMFV D2017, UST-FMS
Differential Diagnosis: Acute Abdomen
• Acute Mesenteric Adenitis
o Most often confused with appendicitis in children
o Almost invariably, a URTI has subsided or is present
o Pain is diffuse and tenderness is not as sharply as sharply localized as that of appendicitis
o Voluntary guarding is sometimes present but true rigidity is rare
o Generalized lymphadenopathy
o Relative Lymphocytosis
o Self-limiting
• Diverticulitis: Elderly
• Perforating Carcinoma of the cecum/sigmoid
o Elderly
o CT Scan needed
• Female
o PID – right tube, pain is lower in the pelvic area and (+) Cervical wiggling tenderness on PE. (+)
Intracellular diplococcic on urethral smear/vaginal discharge
o Mittelsmerchz pain – mid menstrual cycle pain
o Right sided ovarian cyst rupture or R ovarian torsion. TVS or CT Scan
• Acute Gastroenteritis – would not present with an acute abdomen in most cases
• Intestinal Obstruction – obstipation

Management
• Preoperative requirements – fluid and electrolyte resuscitation, pain management (only when the
diagnosis has been obtained to avoid masking of symptoms), antibiotics
• Antibiotics
o Uncomplicated – second generation cephalosporins (Cefoxitin, Cefotetan, Cefuroxime)
§ Prophylactic against post-op site infection: Give just before or at the time of surgery, up
to 24h post-op
o Complicated – broad spectrum with aerobic and anaerobic
§ Therapeutic: Given up to 7-10 days post-op or until fever/WBC normalize
§ Give IV antibiotics until WBC count is normal and patient is afebrile for 24 hours
• Open Appendectomy
o Standard of care in our institution
o Emergent Appendectomy: Time from presentation to OR = <12h
o Urgent Appendectomy: Time from presentation to OR = 12h-24h
Prognosis
• Early postoperative problems – ileus, surgical site infection, intraabdominal abscess
• Delayed complication – intestinal obstruction secondary to postoperative adhesions

JMFV D2017, UST-FMS

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ORAL

During Cardiopulmonary resuscitation check for:

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

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vomiting,&dizziness& SUBSCALE& STIMULUS/RESPONSE& PTS& &

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

JMFV D2017, UST-FMS

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