BLOCK Q REVIEWER

NACIONGAYO, NAIG, NG, NICOLAS, NIDOY, NUNEZ, OBMERGA, ONA, ORTIZ, PACANA, PADLAN,
PANIS, SILOR, TAN

TABLE OF CONTENTS

BRONCHIAL ASTHMA ………………………………………………………….. 2

ACUTE CORONARY SYNDROME ……………………………………………..7
LEPTOSPIROSIS ………………………………………………………………...16
CHRONIC LIVER DISEASE …………………………………………………….25
THYROTOXICOSIS………………………………………………………………35
COPD ………………………………………………………………………………43
PULMONARY TB …………………………………………………………………52
COMMUNITY-ACQUIRED PNEUMONIA & PLEURALE EFFUSION ……... 61
CHRONIC KIDNEY DISEASE …………………………………………………..68
SHOCK …………………………………………………………………………….75
ACUTE PANCREATITIS …………………………………………………………82
UPPER GI BLEEDING …………………………………………………………...90
HEART FAILURE …………………………………………………………………98
ACUTE PYELONEPHRITIS …………………………………………………….105
 BRONCHIAL ASTHMA

Gerdie Obmerga

Must-Knows

● Definition:
○ Syndrome characterized by chronic airflow obstruction.
○ Airway is often reversible; resolve spontaneously or with treatment
○ Episodic or intermittent Symptoms

● Risk Factors and Triggers:

○ Atopy is the major risk factor for asthma. Allergic rhinitis, which may be found in over 80% of asthmatic patients, and
atopic dermatitis (eczema).
○ ALLERGENS: Most common allergens > (House dust mites) Dermatophagoides species
○ INFECTIONS: VIRAL URTI such as rhinovirus, respiratory syncytial virus, and coronavirus are the most common
triggers of acute severe exacerbations
○ OBESE: Asthma occurs more frequently in obese people (body mass index >30 kg/m2)
○ DRUGS: Beta adrenergic blockers- increased cholinergic bronchoconstriction; Angiotensin-converting enzyme
inhibitors- inhibit breakdown of kinins, which are bronchoconstrictors > Rarely worsen asthma
○ AIR POLLUTION: sulphur dioxide, ozone, and diesel particulate > asthma symptoms
○ EXERCISE: Attacks follow exertion> Higher ventilation> Lower heat content of air > asthma symptoms
○ OCCUPATIONAL FACTORS: Always ask for the past and present occupation

● Pathophysiology:
○ AIRWAY HYPERRESPONSIVENESS: characteristic physiologic abnormality of asthma
○ Limitation of airflow is due mainly to bronchoconstriction > airway edema, vascular congestion, and luminal occlusion with
exudate may contribute
○ Eosinophil infiltration: characteristic feature of asthmatic airways

● Epidemiology:
○ Peak age of 3 years
○ Twice as many males as females are asthmatic, but by adulthood the sex ratio has equalized.

● Complications
○ Exacerbations in Asthma: Acute or subacute worsening of symptoms

Subjective

● Presentation (Symptoms)
○ Symptoms: (reversible and variable)
■ wheezing, dyspnea, Chest tightness, and coughing
■ Worse at night, awake in the early morning hours
■ Increased mucus production > tenacious mucus that is difficult to expectorate
■ Prodromal symptoms may precede an attack: Itching under the chin, discomfort between the scapulae, or
inexplicable fear (impending doom)

● Usual past medical / family / social history

○ FAMILY HISTORY: risk factor for eczema, allergic rhinitis, and bronchial asthma
○ History of Atopy (Atopic dermatitis, eczema, or other allergic skin conditions)

Objective
● Signs:
○ Inspiratory, and to a greater extent expiratory, rhonchi/wheeze throughout the chest
○ Hyper expansion of the thorax\
○ Nonproductive cough (cough-variant asthma)

2
 Assessment

Differentials Rule In Rule Out

Upper airway obstruction: by a tumor or (+) Acute onset

laryngeal edema (+) wheezes
(+) stridor
(+) hoarseness of voice

Endobronchial disease: Tumor, (+) if with localized wheezing (+) Generalized wheezing, less likely
pulmonary mass, foreign
body, mucus plug

Acute left ventricular dysfunction Cause: (+) “cardiac wheeze”

heart failure
Hallmarks of heart failure:
(+) cardiomegaly
(+) engorged neck veins

Chronic obstructive pulmonary disease (+) less variability, .

(+) never completely remit
(+) show much less (or no) reversibility
to bronchodilators

Eosinophilic pneumonias and systemic (+) wheezes

vasculitis, including Churg Strauss (+) fever
syndrome and polyarteritis nodosa (+) cough
(+) difficulty breathing
(+) chest pain

***WRITING DIAGNOSIS: Bronichial Asthma (not in/in) Acute Exacerbation, asthma severity (Mild, Moderate, Severe), asthma
symptoms control (well-controlled, partly controlled, uncontrolled)

ASTHMA SYMPTOMS CONTROL

In the past 4 WEEKS, has patient had INTERPRETATION

● Daytime asthma symptoms >2x/week? Well controlled: none present

● Any night waking due to asthma? Partly controlled: 1-2 present
● Reliever needed for symptoms >2x/week? Uncontrolled: 3-4 present
● Any activity limitation due to asthma?

Plan

DIAGNOSTIC CRITERIA: History of variable respiratory symptoms AND confirmed variable expiratory airflow limitation

Diagnostic Features Criteria for making the diagnosis

History of variable respiratory symptoms

● Cough ● More than one (combination) respiratory symptoms

● Dyspnea ● Occurs variably over time and intensity
● Wheezing ● Worse at night or early morning
● Chest Tightness ● Triggered by exerise, allergens, viral infections,
laughter

3
Confirmed variable expiratory airflow limitation

● Documented airflow limitation ● FEV1/FVC is reduced (Normal: 0.75-0.80 in adults)

● Documented execessive variability in lung function ● The greater the variation > more likely the diagnosis
(see test below)

Diagnostics Rationale Expected Findings

Complete Blood Count ● To evaluate blood cells and ● Leukocytosis and there can be
provide information on infection eosinophilia
and inflammation

Chest X-ray ● Integral part of the diagnostic ● Severe patients may show
evaluation involving the hyperinflated lungs
parenchyma, pleural, airways, and ● In exacerbations, there may be
mediastinum evidence of a pneumothorax

Spirometry: Positive Bronchodilator ● Most common lung function test. ● In asthma: increase FEV1 >12%
Reversivility Test To confirm airflow limitation and >200 ml from baseline 10-15
min. After albuterol/ salbutamol
200-400 mcg

Bronchoprovocation test ● To test for airway responsiveness ● In asthma: decrease FEV1 >20%
with methacholine or histamine or
>15% with hyperventilation, saline,
mannitol

Peak flow monitoring ● To confirm variable expiratory ● Average daily diurnal PEF
airflow limitation variability >10%

ASTHMA SEVERITY

SEVERITY DESCRIPTION

● Mild Asthma ● Well controlled with step 1 or step 2

● Moderate Asthma ● Well controlled with step 3
● Severe Asthma ● Requires step 4 or 5 or uncontrolled despite
treatment

● Treatment
○ GOALS:
■ Minimal (ideally no) chronic symptoms, including nocturnal
■ Minimal (infrequent) exacerbations
■ No emergency visits
■ Minimal (ideally no) use of a required β -agonist
■ No limitations on activities, including exercise
■ Peak expiratory flow circadian variation <20%
■ (Near) normal peak expiratory flow
■ Minimal (or no) adverse effects from medicine

● ASTHMA TREATMENT: ASSESS > ADJUST > REVIEW (CYCLE)

● Review response after 2-3 months, or according to urgency
○ Consider stepping-up if: uncontrolled symptoms, exacerbations or risks
○ Consider steppind-down: symptoms controlled for 3 months, low risk of exacerbations

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 PRESENTING SYMPTOMS PREFERRED INITIAL CONTROLLER

● Symptoms or SABA <2x/month No controller (Step 1)

● NO waking, risk factor for exacerbation,
exacerbation in the last year

● Infrequent Symptoms or SABA >2x/week Low dose ICS (Step 2)

● Waking >1x/month, >1 risk factor for exacerbation

● Troublesome symptoms most of the days Moderate-High Dose ICS or Low Dose ICS/LABA (Step 3)
● Waking >1x/week

● Initial presentation is with severely uncontrolled Short-course Oral corticosteroids and regular controller (High
asthma dose ICS or moderate-dose ICS/LABA)
● Initial presentation with an acute exacerbation

STEP PREFERRED ALTERNATE CONTROLLER RELIEVER

CONTROLLER

Step 1 None Consider Low-dose ICS As needed SABA

(eg. Budesonide 200-400mcg DPI 1 puff (eg. Salbutamol neb every 8
OD, Fluticosone proprionate 100-250 mcg hours prn for DOB)
DPI 1 puff BID)

Step 2 Low-dose ICS Leukotriene receptor antagonist As needed SABA

(eg. Budesonide 200-
400mcg DPI 1 puff OD,
Fluticosone proprionate
100-250 mcg DPI 1 puff
BID)
Low-dose theophylline (eg. Salbutamol neb every 8
(eg. Montelukast 10mg/tab 1 tab ODHS, hours prn for DOB)
Theophylline 100mg/cap 1 cap BID)

Step 3 Low-dose ICS/LABA Mod-High dose ICS As needed SABA or Low

(eg. Salmeterol + Low-dose ICS + LRTA dose ICS/Formeterol
Fluticasone 25/125 mcg May add theophylline
MDI 1 puff BID) (eg. Fluticasone 250-500 mcg MDI- mod-
High dose ICS)

Step 4 Mod-High dose ICS/LABA Add tiotropium (as third controller) As needed SABA or Low
High dose ICS + LRTA dose ICS/Formeterol
May add theophylline
(eg. Tiotropium (spiriva) 2.5 mcg MDI 1 puff
OD)

Step 5 Refer to specialist Add low-dose OCS As needed SABA or Low

Add-on treatment (e.g. (eg. Prednisolone 1mg/kg PO OD) dose ICS/Formeterol
Tiotropium, Anti-IgE, Anti-
IL5)

*Only Asthma in acute exacerbation that are severe or Life threatening requires hospital admissions

Assessment for Severity of Exacerbation

Mild or moderate Severe Life-Threatening

Clinical Manifestation Talks in phrases Talks in words Drowsy/confused

Prefers sitting to lying Sits hunched forward Sillent Chest
Not Agitated

Respiratory rate Increased >30/min

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 Use of accesory muscles No Yes

Pulse rate 100-120 bpm >120 bpm

O2 saturation 90-95% <90%

PEF >50% predicted or best < 50% predicted best

Admitting Orders
● Admit to ward (Severe) to ICU (LIfe-threatening)
● Diet: Diet as tolerated with SAP; Increase OFI (if not dyspneic) NPO temporarily (if dyspneic)
● Monitor VS q1hour.
● IVF: D5NR 1L x 12 hours or D5NM 1L x 12 hours
● Diagnostics:
○ Chest X-ray PA/L (rule-out pneumothorax and detect other structural lung problems)
○ CBC, K, RBS, crea (Baseline measurement for initiation of therapy)
○ 12 L ECG
○ Pulmonary Function Test (to establish diagnosis)
○ Sputum GS/CS (if with pneumonia)
○ ABG (if toxic-looking)
○ Peak Expiratory rate pre and post bronchodilator treatment BID-TID
● Therapeutics (NASA: Nebulization, Antibiotics, Steroids, Aminophylline)
○ Nebulization 3x every 15minutes then reassess: Salbutamol neb 1 vial every 4-6 hours or Salbutamol + Ipratropium neb
1 vial every 4-6 hours or if tachycardic patients Ipratropium neb 1 vial Tevery 8 hours-QID
○ Antibiotics if with probable bacterial infection: (See CAP management)
○ Acute Attacks:
■ Hydrocortisone 250mg/vial 1 vial IV stat then 100mg/vial 1 vial IV q4-6 hours
■ If still not controlled: Aminophylline bolus at 5-6mg/kg BW now
○ More Stable:
■ Prednisone 20mg/tab 1 tab BID for 3 days then taper
■ Doxyfylline 400mg/tab BID
○ Anti-Ulcer drugs: Omeprazole 40mg/vial 1 vial IV OD
● If not controlled: Standby intubation
● Oxygen support at 2-4 LPM via NC for desaturation
● Connect to pulse oximeter
● Input and output q shift and record
● Moderate high back rest
● WOF: HR: >120 RR: >30 O2sat: <90%
● Refer to Pulmonology service
● Refer Accordingly

References
● Harrison’s Principles of Internal Medicine, 19th ed.
● Harrison’s Principles of Internal Medicine, 20th ed.
● IM Platinum 3rd edition
● Expanded Medicine Blue Book
● Global Initiative for Asthma 2015

6
 ACUTE CORONARY SYNDROME

Alyssa Willis Ng

Must-Knows
● Definition: Acute MI - there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia.
Under theses conditions, any of the following criteria meet the diagnosis for MI:

Detection of a rise and/or fall in cardiac biomarkers (preferably cardiac troponins/cTn), with at least one value above the
99th percentile with at least on of the following:
● Symptoms of ischemia
● New or presumed new signifcant ST-segment and/or T wave changes or new LBBB
● Development of pathologic Q waves on the ECG
● Imaging evidence of new loss of viable myocardium or new wall motion abnormality
● Identification of an intracoronary thrombus by angiography or autopsy

Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new
LBBB (Type 3)

PCI-related MI (Type 4a)

Stent thrombosis associated with MI (Type 4b)

CABG-related MI (Type 5)

NSTEMI-ACS
○ UA
■ Angina or equivalent ischemic discomfort with at least on of the following:
● Occurs at rest (or with minimal exertion), usually lasting >10 minutes
● Severe and of new onset (e.g. within the prior 4-6 weeks) of at least CCS III severely
● Occurs with a crescendo
○ NSTEMI
■ Clinical features of UA plus evidence of myocardial necrosis (elevated cardiac biomarkers
○ Prinzmetal Variant Angina
■ Ischemic pain that occurs at rest but not usually with exertion, associated with transient ST-segment elevation
■ Due to transient, focal spasms of an epicardial coronary artery (MC: right coronary artery)
■ Diagnostic hallmark: coronary angiography (demonstrates transient coronary spasm)
■ Treatment: Nitrates and CCBs
■ Avoid Aspirin - may increase severity of ischemic episodes
■ Statin - reduces risk of major adverse events
STEMI

● Pathophysiology
○ NSTEMI
■ “NSTE-ACS is most commonly caused by an imbalance between oxygen supply and oxygen demand resulting
from a partially occluding thrombus forming on a disrupted atherothrombotic coronary plaque” - Harrison’s, 19th
ed.
■ 4 basic pathologic mechanisms:
● MC: plaque rupture, erosion or calcified protruding nodule that leads to an intracoronary thrombus formation
and inflammatory response
● Dynamic obstruction (e.g. vasospasm in Prinzmetal)
● Severe mechanical obstruction due to progressive coronary atherosclerosis
● Increased myocardial oxygen demand (e.g. tachycardia, fever, thryotoxicosis in presence of fixed epicardial
coronary obstruction) and/or decreased supply (e.g. anemia)
○ STEMI
■ “STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary
artery previously affected by atherosclerosis”
■ coronary artery thrombus develops rapidly at a site of vascular injury - cigarette smoking, hypertension, and lipid
accumulation

7
● Epidemiology

Type of Myocardial Infarction (MI) Description

Type 1 Spontaneous MI Atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with
resulting intraluminal thrombus in >1 of the coronary arteries that leads to decreased
myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis

Type 2 MI Secondary to A condition other than CAD contributes to an imbalance between myocardial oxygen
Ischemic Imbalance supply and/or demand
(e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism,
tachyarrhythmias/bradyarrhythmias, anemia, respiratory failure, hypotension,
hypertension with or without LVH)

Type 3 MI Resulting in Death Cardiac death with symptoms suggestive of ischemia and presumed new ischemic
when Biomarkers are changes (or new LBBB), but death occurring before blood samples can be obtained
Unavailable

Type 4a MI Related to PCI MI associated with PCI defined by:

● Elevation of cTn values to >5x the 99th percentile of the upper reference
limit in those with normal baseline values
● Rise in cTn values >20% if baseline values are elevated and are stable or
failing
● AND either
○ Symptoms suggestive of MI
○ New ischemic changes on the ECG or new LBBB
○ Angiographic loss of patency of a major coronary artery or a side
branch or persistent slow flow or no flow or embolization
○ Imaging demonstration of new loss of viable myocardium or new
regional wall motion abnormality

Type 4b MI related to Stent MI associated with stent thrombosis is detected by coronary angiography or autopsy in
Thrombosis the setting of myocardial ischemia and with a rise and/or fall in cardiac biomarkers with
at least one value >99th percentile of the upper reference limit

Type 5 MI related to CABG MI associated with CABG - defined by elevation of cardiac biomarker values >10x the
99th percentile of upper reference limit in patients with normal baseline values; AND
either:
● New pathologic Q waves or new LBBB, or
● New graft or new native coronary artery occlusion on angiogram, or
● Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality

TIMI scoring for NSTE-ACS

Points

Age > 65 1

> 3 CAD risk factors 1

· HTN
· DM
· Obesity
· Increased cholesterol
· family history
· active smoker

Known CAD (Stenosis >50) 1

ASA use in the past 7 days 1

Recent (<24h) severe angina 1

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Increased cardiac markers 1

ST deviation >0.5 mm 1

Total score: 7
Score 3: 5% chance of death/MI, 13% chance of death/MI, urgent revascularization in the next 14 days
Score 6/7: 19% chance of death/MI, 41% chance of death/MI, urgent revascularization in the next 14 days

TIMI scoring for STEMI

Points

Age 65-74 2

Age >75 3

DM, HPN, Angina 1

SBP <100 3

Weight <67kg 1

Anterior STE, LBBB 1

Time to hospital >4 hrs 1

Total score: 14
Score = 5 à 12% mortality within 30 days
Score > 8 à 36% mortality within 30 days

Killip Scoring for STEMI

Class Description Mortality

I No rales/signs of pulmonary/venous congestion 0-5%

Normal BP

II Bibasal rales, moderate heart failure 10-20%

Normal BP
S3 gallop
Tachypnea, right sided CHF (venous/hepatic congestion)

III Severe heart failure 35-45%

Mid-basal rales with pulmonary edema
S3 and S4
Normal BP

IV Shock (SBP <90 + evidence of peripheral vasoconstriction) 85-95%

Peripheral cyanosis
Mental confusion, oliguria

Subjective

NSTEMI STEMI

Chest discomfort Precipitating Factor

● Substernal region or epigastrium ● Vigorous physical exercise, emotional stress, or
● Radiates to the left arm, shoulder and/or neck or jaw medical or surgical illness
● Anginal equivalents (e.g. dyspnea, epigastric
Pain

9
 discomfort, nausea, weakness) - more frequent in
women, elderly, patients with DM
At least one of three features
1. Occurs at rest (or with minimal exertion)
2. Lasts for >10 mins
3. Relatively recent onset (i.e. within prior 2 weeks)
4. Occurs with crescendo pattern (i.e. distinctly more
severe, prolonged, or frequent than previous
episodes)
● Deep and visceral
● Heavy, squeezing, crushing, stabbing or burning
● Central portion of the chest (beneath the xiphoid)
and/or the epigastrium, may radiate to the arms
● Less common sites of radiation:
○ Abdomen, back, lower jaw, neck
● Occurs at rest
● May begin during a period of exertion, does not
usually subside with cessation of activity
● Accompanied by weakness, sweating, nausea,
vomiting, anxiety, sense of impending doom

Painless STEMI
PLUS ● With DM
● Elderly
Evidence of myocardial necrosis ● Female

May present as sudden-onset DOB → pulmonary edema

Sudden LOC
Confusional state
Profound weakness
Arrythmia
Unexplained drop in arterial pressure

Objective

NSTEMI STEMI

Hypotension See Killip scoring

Tachycardia Substernal chest pain >30 mins
Basilar rales Diaphoresis
3rd or 4th heart sounds Anxious and restlessness
Diaphoresis Pallor
Pale, cool skin Cool extremities

Levine’s sign - clenched fist over chest

BP: normal and/or hypertension (¼ with anterior infarction)

PR: normal and/or tachycardia (¼ with anterior infarction)

Anterior infarct
Tachycardia and/or hypertension due to sympathetic nervous system
hyperactivity
abnormal systolic pulsation caused by dyskinetic bulging of infarcted
myocardium in the periapical area within the first days

Inferior infarct
Bradycardia and/or hypotension due to parasympathetic hyperactivity

Quiet precordium
Apical impulse difficult to palpate
Signs of ventricular dysfunction
● 3rd and 4th heart sounds
● Decreased intensity of first heart sound
● Paradoxical splitting of second heart sound
Transient midsystolic or late systolic apical systolic murmur - dysfunction of
mitral valve
Pericardial friction rub - transmural STEMI

Decreased carotid pulse

10
Assessment

Differentials (at least 5) Rule In

Chronic Stable Angina Sudden onset chest pain

Relieved by rest, 2-5 mins duration, crescendo-decrescendo pattern

Unstable Angina Sudden onset chest pain

No elevation of cardiac biomarkers

Pericarditis Sharp pain,radiates to the trapezius, relieved by sitting up, exacerbated by supine

Acute Aortic Syndrome/Aortic Dissection Sudden onset; severe tearing chest pain; differential pulse pressure

Pulmonary Embolism Pleuritic chest pain; cough; hemoptysis; DOB; hypotension

Pneumothorax Sudden onset; DOB; Tachypneic; Decreased O2 sat; Decreased breath sounds

Pneumonia Pleuritic chest pain; Fever; Cough, colds; Signs of infection

GERD Epigastric pain; Burning pain; Exacerbated in postprandial state; Relieved by antacids

Peptic Ulcer Epigastric pain; Burning; Relieved by antacids

Gallbladder Disease Epigastric pain; RUQ pain; radiates to the back; fever; jaundice

Acute Pancreatitis Epigastric pain; radiates to the back; stabbing pain

Costochondritis Point tenderness; sharp pain; localized by one finger; relieved by painkillers

Muscle strain Sharp pain on movement; localized by one finger

Panic Attacks DOB; Anxiety; Incongruent presentation

Illness Anxiety Disorder (Hypochondriac) Incongruent signs and symptoms

Malingering intentional production of false or grossly exaggerated physical or psychological problems

● Diagnostics (Labs, Imaging)

CSAP NSTEMI STEMI

12 L ECG May be normal if May be normal ST segment elevation +/- Q waves

asymptomatic
New ST-segment depression (⅓
New ST elevation at the J point in two
May find ST segment patients); may be transient but
contiguous leads of >0.1 mV in all leads
and T wave changes, LV may persist for several days
other than leads V2-V3 – For leads V2-V3
hypertrophy, following NSTEMI.
the following cut points apply: ≥0.2 mV in
intraventricular
T-wave changes are more men ≥40 years, ≥0.25 mV in men <40
conduction disturbances
common but are less specific years, or ≥0.15 mV in women
signs of ischemia, unless they are
new and deep T-wave inversions New or presumed new LBBB
(≥0.3 mV) Isolated posterior MI

11
Serum Cardiac No increase in trend Increasing levels Trop I and trop T: increases after STEMI
Biomarkers many times higher than upper limit
Serial cardiac troponin I or T levels
at different times: CK: rises within 4-8 hours and returns to
normal by 48-72 hrs
● At presentation
● 4-6 hrs after
● Beyond 6 hrs in those
with normal levels
Cut-off troponin value: 99th
percentile of upper reference level

2D echo with Doppler Assess LV function Transthoracic echocardiography: Abnormalities of wall motion
assess LV
Assess wall motion
abnormalities, EF, Used to ID pericardial effusion,
presence of thrombus concomittant valve abnormalities

Chest x-ray No specific info Identify other differentials of chest

pain
Used in ruling out other
non-cardiac causes of
chest pain

CBC Anemia may trigger ischemia

PT/PTT Baseline; patient will be started on anticoagulants

Electrolytes Baseline kidney function and liver function prior to starting meds

FBS, LP, HbA1c Identify risk factors: dyslipidemia and diabetes

Stress testing ECG exercise testing: most widely used to diagnose IHD and estimating prognosis
Stress imaging, preferred when ECG is abnormal

Others Thyroid function tests, CT angio: rule out ACS if with normal findings

Cardiac Troponins CK-MB

Time to Detection 3-12 hours 4-8 hours

Peak levels 24 hours 24 hours

Duration in blood 5-14 days 2-3 days

Advantages Great spec and sens. Than CK Rapid, cost efficient

Detection of recent MI up to 2 weeks after onset Able to detect early evidence of injury/reinfarction

Disadvantages Low sensitivity in very early phase of MI (<6 Less sensitive

hours) requires repeat after 8-12 hours if egative Loss of specificity in setting of keletal muscle injury
Minor elevations: azotemia/CKD, CHF, (surgery, minor IM injections)
myocarditis, pulmonary embolism

12
● Treatment

ACRUBANGS PPP

Medication Dosage Mechanism Contraindications

ASA 80mg/tab 4 tabs chewed and Antiplatelet; platelet cyclooxgenase inhibitor Active bleeding or intolerance
swallowed aspirin
80mg/tab 1 tab OD thereafter (Maintain indefinetely)

Clopidogrel 75mg/tab 4 tabs chewed and platelet P2Y12 receptor blocker

swallowed
75mg/tab 1 tab OD thereafter
thienopyridine - an
inactive prodrug that is converted into an active
metabolite that causes irreversible blockade of
the platelet P2Y12 receptor
(May be stopped after 1 year if stable)

Reperfusion Non Invasive → Streptokinase Invasive → Coronary

therapy Tissue Plasminogen Activator Angiography + PCI or CABG
Within 3 hrs of symptom onset

Unfractionated Enoxaparin 0.6 cc SQ q12 x 5 LMWH; inhibits factor Xa by increasing inhibition Active bleeding
heparin days rate of clotting proteases that are activated by
antithrombin III

Fondaparinux 0.5 cc SQ OD Inhibits Factor Xa by binding to antithrombi

Beta Blockers* Carvedilol 6.25mg/tab ½ tab BID Occupy β receptors and competitively reduce presence of acute or severe
(target HR 50- Metoprolol 50mg/tab 1 tab BID receptor occupancy by catecholamines and heart failure, low cardiac
60 bpm) Bisoprolol (most selective B1) 5 other β agonists. output, hypotension, or
mg OD contraindications to beta-
Reduces heart rate → decreased 02 demand, blocker therapy
increased coronary perfusion (e.g., high-degree
atrioventricular block, active
bronchospasm).

ACE- Captopril 6.25 mg/tab 1 tab TID inhibit the converting enzyme peptidyl
inhibitors/ARBs Enalapril 5 mg/tab 1 tab OD dipeptidase that hydrolyzes angiotensin I to
angiotensin II and (under the name plasma
kininase) inactivates bradykinin, a potent
vasodilator, which works at least in part by
stimulating release of nitric oxide and
prostacyclin.

Nitrates ISDN 5 mg/tab 1 tab SL PRN q5
min x 3 doses for chest pain (7am-
4pm-11pm)
ISMN 30mg/tab 1 tab OD
direct relaxant effect on vascular smooth
muscles, and the dilation of coronary vessels
improves oxygen supply to the myocardium. The
dilation of peripheral veins, and in higher doses
peripheral arteries, reduces preload and
afterload, and thereby lowers myocardial oxygen
consumption
low systolic arterial pressure
(<90 mmHg) or in whom there
is clinical suspicion of RV
infarction (inferior infarction on
ECG, jugular venous pressure,
clear lungs, and hypotension).
Contraindicated if patient is
taking phosphodiesterase-5
inhibitor for erectile
dysfunction within the
preceding 24 h, because it
may potentiate the
hypotensive effects of nitrates

Glycoprotein Abciximab Inhibit platelet aggregation

2b/3a receptor Eptifibatide
inhibitors Tirofiban
(for patients
undergoing PCI)

Statins Atorvastatin 80mg/tab ODHS Plaque stabilization, reduces mortality

13
Pain control Morphine sulfate 2 mg SIVP PRN Reduces sympathetically mediated arteriolar
for chest pain and venous constriction

PPI Omeprazole 40mg/cap 1 cap OD It suppresses stomach acid secretion by specific

+ +
pre-BF inhibition of the H /K -ATPase system found at
the secretory surface of gastric parietal cells

Pampatae Lactulose 30 cc ODHS, defer if BM (Bed rest and the effect of the narcotics used for
> 2x/day the relief of pain often lead to constipation)

Calcium channel blockers are recommended for patients who have persistent symptoms or ECG signs of ischemia after treatment
with full-dose nitrates and beta blockers and in patients with contraindications to either class of these agents.*
● Verapamil 80mg/tab 1 tab TID
● Amlodipine 10mg/tab 1 tab OD

Non-Pharmacologic
1. Activity
a. Bed rest for the first 6–12 h.
b. Upright posture by dangling their feet over the side of the bed and sitting in a chair within the first 24 h.
(psychologically beneficial and reduction in the pulmonary capillary wedge pressure)
c. 2nd/3rd day, ambulation around bedroom
d. 3rd day, goal of 185 m (600 ft) at least three times a day.
2. Diet
a. NPO or clear liquids by mouth for first 4-12 hours
b. ≤30% of total calories as fat and have a cholesterol content of ≤300 mg/d.
c. complex carbohydrates should make up 50–55% of total calories.
d. High in potassium, magnesium, and fiber, but low in sodium.

14
Admitting Orders
● Admit to Coronary Care Unit
● Diet: NPO/clear liquids with SAP during first 4-12 hours
● Monitor VSq1 with temp., I & O qshift and record
● IVF: Heplock
● Diagnostics:
○ 12L ECG stat
○ Troponin I stat
○ CBC, ESR, CRP
○ PT/PTT
○ Crea, Na, K, Ca, Cl, Mg, Alb, Ph, Crea, BUN
○ FBS, LP
○ CXR-PAL
○ 2D echo with DS
● Therapeutics:
○ Aspirin 80mg/tab 4 tab now, chewed and swallowed, then 80 mg OD thereafter
○ Clopidogrel 75mg/tab 4 tabs now, chewed and swallowed, then 75 mg OD thereafter
○ ISDN 5mg/tab 1 tab q5 mins x 3 doses sublingual
○ Enoxaparin 0.6 cc SQ BID
○ Carvedilol 6.25mg/tab ½ tab BID
○ Captopril 6.25mg/tab 1 tab TID
○ Omeprazole 40mg/tab 1 tab PO OD pre-BF
○ Atorvastatin 80mg/tab 1 tab ODHS
○ Morphine sulfate 2mg SIVP PRN for chest pain
○ Lactulose 30 cc PO ODHS, defer if BM >2x/day
● Hook to cardiac monitor
● Complete bed rest with no bathroom privileges for first 12 hours
● May hook to nasal cannula at 4 lpm if O2 <94%
● Refer to CVS for PCI/CABG
● Refer PRN

References
Harrison’s Principles of Internal Medicine, 19th ed.
Harrison’s Principles of Internal Medicine, 20th ed.
IM Platinum 3rd edition.

15
 LEPTOSPIROSIS

Hanna Clementine Tan

Must-Knows
● Definition: zoonotic disease occurring in temperate and tropic climates caused by the spirochetes Leptospira species
belonging to the order Leptospiracaea, and is characterized by a broad spectrum of clinical manifestations varying from
asymptomatic disease to fulminant, fatal disease.
● Etiology: LEPTOSPIRA SPECIES
○ Pathogenic Leptospira species are divided into serovars according to their antigenic composition. More than 250 serovars
make up the 26 serogroups.
○ Traditionally comprised only two species: the pathogenic L. interrogans and the free-living L. biflexa, now designated L.
interrogans sensu lato and L. biflexa sensu lato, respectively.

Characteristics of the organism:

○ Coiled, thin, highly motile organisms
○ Have hooked ends and two periplasmic flagella
○ polar extrusions from the cytoplasmic membrane are responsible for motility
○ Stain POORLY but can be seen through DARK FIELD MICROSCOPY and after silver impregnation staining of tissues
○ Require special culture media for growth (Nice to know: Ellinghausen-Mccullough-Johnson-Harris (EMJH) medium)

Transmission:
○ Contact of abraded skin, cuts, mucous membranes with urine, blood, or tissue from an infected animal or, more
commonly, exposure to environmental contamination
○ Water is an important vehicle of transmission
○ Outbreaks may occur from exposure to flood waters contaminated with infected urine
○ Incubation period: 1-2 weeks but ranges from 1 - 30 days

Risk factors:
○ Direct or indirect contact with animals
○ Exposure to water and soil contaminated with animal urine
○ Recreational exposure: canoeing, windsurfing, swimming, ingestion of contaminated water, waterskiing, whitewater
rafting, jungle trekking, and caving

● Pathophysiology
○ After entry, disseminates hematogenously - known as the Leptospiremic phase, during this incubation phase, organisms
can be isolated from the BLOODSTREAM
○ Evade complement-mediated killing by binding factor H, a strong inhibitor of the complement system, on their surface
○ Resist ingestion and killing by neutrophils, monocytes, and macrophages
○ Immune phase: appearance of antibodies - disappearance of organisms from blood, but persists in various organs: liver,
lung, kidney, heart, and brain. Organisms can be cultured from urine.

16
● Epidemiology
○ Worldwide distribution but occurs most commonly in the TROPICS and SUBTROPICS
○ Climate and occasionally poor hygienic conditions favor the pathogen’s survival and distribution
○ Peak incidence during the rainy season in the tropics
○ RODENTS, especially RATS, are the most important reservoir although other animals may also harbor the organism
○ Some serovars are associated with particular animals:
■ Icterohaemorrhagiae and Copenhageni: rats
■ Grippotyphosa: voles
■ Hardjo:cattle
■ Canicola: dogs
■ Pomona:pigs
● Clinical Manifestations
○ Hallmarks: bleeding and multiorgan failure
○ BIPHASIC
■ Acute leptospiremic phase is characterized by fever of 3–10 days’ duration, during which time the organism can be
cultured from blood.
■ Immune phase, resolution of symptoms may coincide with the appearance of antibodies, and leptospires can be
cultured from the urine.
● Complications
○ SEVERE LEPTOSPIROSIS
○ Higher mortality rates are associated with an age >40, altered mental status, acute renal failure, respiratory insufficiency,
hypotension, and arrhythmias.
○ Triad of hemorrhage, Acute kidney injury, jaundice: WEIL’S SYNDROME
■ Acute kidney injury: may be oliguric or nonoliguric
● Electrolyte abnormalities
○ Hyponatremia
○ Hypokalemia
○ Loss of magnesium in urine: characteristic of leptospiral nephropathy
○ Hypotension: associated with acute tubular necrosis, oliguria, anuria (requires fluid resuscitation and possibly
vasopressor therapy; hemodialysis may be life saving)
■ Necrotizing pancreatitis
■ Cholecystitis
■ Skeletal muscle involvement - rhabdomyolysis (with moderately elevated serum creatine kinase levels)
■ Neurologic manifestations - aseptic meningitis (more common in children)
■ Cardiac involvement: nonspecific ST- and T-wave changes in ECG. Repolarization abnormalities and arrhythmias are
considered poor prognostic factors. Possible myocarditis.
■ Rare hematologic complications: hemolysis, thrombotic thrombocytopenic purpura, and hemolytic-uremic syndrome.
○ Long-term symptoms following severe leptospirosis (may persist for years)

17
 ■ Fatigue
■ Myalgia
■ Malaise
■ Headache
■ Autoimmune-associated uveitis (recognized sequela of leptospirosis)

Subjective: MILD LEPTOSPIROSIS (spontaneously resolves in 7-10days)

● Presentation (signs and symptoms)
○ Flu-like illness of sudden onset
■ Fever
■ Chills
■ Headache - intense, localized to frontal or retroorbital regions, sometimes with photophobia
■ Nausea
■ Vomiting
■ Abdominal pain
■ Conjunctival suffusion (redness without exudate)
■ Myalgia - intense and affects the calves, back, abdomen
○ Usual past medical / family / social history
■ Wading in flood water
■ Recreational activities (mentioned above)
■ Traveling to tropical or temperate climate countries

Objective: MILD LEPTOSPIROSIS

● Physical exam findings
○ Fever
○ Conjunctival suffusion
○ Pharyngeal injection
○ Muscle tenderness
○ Lymphadenopathy
○ Rash - Often transient; may be macular, maculopapular, erythematous, or hemorrhagic (petechial or ecchymotic)
○ Meningismus
○ Hepatomegaly
○ Splenomegaly
○ Mild jaundice
○ Lung auscultation: crackles

Subjective: SEVERE LEPTOSPIROSIS

● Presentation (signs and symptoms)
○ Onset may not be different with mild leptospirosis
○ Triad of HEMORRHAGE, JAUNDICE, ACUTE KIDNEY INJURY: WEIL’S SYNDROME
○ Melena
○ Hemoptysis
○ Hematuria
○ Petechiae
○ Ecchymosis
○ Cough, chest pain, respiratory distress, hemoptysis - pulmonary hemorrhage
○ Oliguria/anuria
Objective: SEVERE LEPTOSPIROSIS
● Physical exam findings
○ May not be different with mild leptospirosis but more pronounced jaundice and
Tender hepatomegaly

Assessment
Sample case:
A 20 yo Male from Paco, Manila, college student, consulted for fever, malaise, retroorbital headache, photophobia, nausea,
abdominal pain, and muscle pain most prominent in bilateral calves, that started 1 week prior to consult. He took paracetamol with
partial relief of the muscle pain, headache, and fever but it was never resolved. 1 day prior to consult, he said he only urinated once
in 24 hrs and his urine was very concentrated, dark yellow in color with streaks of blood, despite drinking lots of water, and he
noticed that his skin started turning yellowish. He also said he waded in dirty flood water 2 weeks ago, when it rained very hard due
to typhoon yolanda.

18
ROS:
(+) anorexia, (-) weight loss) (-) edema, (-) joint pain, (-)rash
(-) DOB, chest pain, cough, hemoptysis
(-) dysuria, (-) constipation, (-) diarrhea, (-) melena, (-) hematochezia

On physical examination,
BP was 80/50, HR 120, RR 24, T 38.7C
Icteric sclerae, PPC, (+) conjunctival suffusion
ECE, (+) crackles bibasal lung fields
AP, DHS, Tachycardic, no murmur
Soft abdomen, tender right upper quadrant, (+) palpable liver edge
FEP, PNB, CRT<2s, (+) jaundice
A tourniquet test was done and after deflating the cuff, 5 petechial rashes in one square inch was noted. (The skin below the cuff is
examined for petechiae one to two minutes after deflating the cuff; presence of 10 or more new petechiae in one square inch area is
considered a positive test)

Differentials (at least 5) Rule In Rule Out

Leptospirosis (+) fever, headache, muscle pain, Cannot rule out at this point
abdominal pain, flu like sympmtoms
(+) hepatomegaly
(+) jaundice
(+) conjunctival suffusion
(+) oliguria
(+) history of wading in flood water

Dengue (+) fever, headache, muscle pain, (+) conjunctival suffusion

abdominal pain, other flu like symptoms (+) history of wading in flood water
(+) hepatomegaly (+) jaundice
(+) crackles - indicative of fluid (-) tourniquet test
accumulation (-) history of mosquito bite

Chikungunya (+) fever, headache, flu like symptoms (-) arthralgia

(+) rash (+) history of wading in flood water
(-) history of mosquito bite

Viral hepatitis (+) jaundice (+) conjunctival suffusion

(+) fever (+) history of wading in flood water
(+) abdominal pain

Malaria (+) fever (-) sweats

(+) nausea (-) history of travel to malarial endemic
(+) muscle pain places
(+) jaundice (+) history of wading in flood water
(+) oliguria

Influenza (+) fever (+) jaundice

(+) nausea (+) oliguria
(+) headache (+) conjunctival suffusion
(+) muscle pain (+) history of wading in flood water

Community acquired pneumonia (+) fever (+) jaundice

(+) crackles (-) history of cough
(+) oliguria
(+)conjunctival suffusion

Acute Cholangitis (+) fever (+) conjunctival suffusion

(+) jaundice (+) oliguria
(+) abdominal pain (+) history of wading in flood water
(+) tender RUQ (+) retroorbital headache with
(Charcot’s triad HAHA medj pilit but u photophobia
know more differentials, more points!
LOL)

19
DIAGNOSIS: LEPTOSPIROSIS, SEVERE (Weil’s syndrome)
Plan
Diagnostics (Labs, Imaging)
Diagnostics
CBC
PT/PTT
Serum Na, K, BUN, Crea,
AST, ALT, TB, DB, IB
*Lepto IgM (rapid test) or
Lepto IgM IgG ELISA
*Lepto MAT
(only available in high testing centers
such as CDC or in our case maybe NIH
or NKTI or whatever but is a STANDARD
serologic procedure)
*Blood culture/urine culture
*Dark field microscopy
Urinalysis
CXR PAL
Rationale Expected Findings
WBC - infection Elevated WBC
Platelet - might have thrombocytopenia PLT may be decreased - might need
transfusion
Hb may be decreased (hematuria)
Px has hematuria, rule out coagulopathy, May be prolonged
might have to intervene if severely
prolonged
Electrolytes, BUN, Crea: Patient already Hyponatremia
oliguric, check how bad the AKI is Hypokalemia
AST, ALT, bilirubins - check for liver hyperphosphatemia
function Elevated BUN, crea
AST/ALT may be normal or elevated
Elevated bilirubins
Confirm diagnosis (+) IgM
Confirm diagnosis Titer of 1:200 to 1:800
Fourfold or greater rise in titer is
detected between acute- and
convalescent-phase serum
used for determination of the antibody
titer and for tentative identification of the
involved leptospiral serogroup—and,
when epidemiologic background
information is available, the putative
serovar
Confirm diagnosis (+) growth of organisms
To check for spirochetes (+) spirochetes
Check for infection, hematuria, mild proteinuria
proteinuria, casts, etc, to see how bad Pyuria
kidney injury is Hematuria
hyaline or granular casts
Rule out pneumonia If hemorrhage:
Check how bad congestion is (since (+) small nodular densities and patchy
crackles) alveolar infiltrates; air-space nodules,
Rule out pulmonary hemorrhage ground grass appearance
20
 * No need to order all of them. Just placed most of the tests available to confirm Lepto

● Treatment

Admitting Orders
● Admit to ICU (bec hypotensive, with hematuria, severe lepto, might hemorrhage anytime)
● Diet: As tolerated with strict aspiration precautions
● Monitor: VS q 1h with temp, I and O q shift

21
● SD1 NE: 8mg in 250cc D5W start at 0.2mkm maintain MAP >/= to 65
● IVF: (assume 50kg) 1L pNSS bolus as fast drip, reassess if still dehydrated, continue hydration with close monitoring, (follow
algorithm above)

● Meds:
○ Penicillin 1.5M units IV q6h for 7 days
○ Paracetamol 500mg PO q4h PRN for fever
○ Furosemide 40mg IV prn for frank congestion/ to increase urine output
Refer to renal for possible HD if no improvement
Refer to TCVS for possible IJ cath insertion
Refer to IDS

Harrison’s:

22
IN CASE MAY PULMONARY COMPLICATIONS YUNG BINIGAY NA CASE:

PROPHYLAXIS (Nice to know in case tanungin)

Pre exposure:
Doxycycline (hydrochloride and hyclate) 200 mg once weekly, to begin 1 to 2 days before exposure and continued throughout the
period of exposure

Post exposure:
● LOW-RISK EXPOSURE is defined as those individuals with a single history of wading in flood or contaminated water without
wounds, cuts or open lesions of the skin.
○ Doxycycline 200 mg single dose within 24 to 72 hours from exposure
● MODERATE-RISK EXPOSURE is defined as those individuals with a single history of wading in flood or contaminated water
and the presence of wounds, cuts, or open lesions of the skin, OR accidental ingestion of contaminated water.
○ Doxycycline 200 mg once daily for 3-5 days to be started immediately within 24 to 72 hours from exposure6 [Grade C]
● HIGH-RISK EXPOSURE is defined as those individuals with continuous exposure (those having more than a single exposure
or several days such as those residing in flooded areas, rescuers and relief workers) of wading in flood or contaminated water
with or without wounds, cuts or open lesions of the skin. Swimming in flooded waters especially in urban areas infested with
domestic/sewer rats and ingestion of contaminated water are also considered high risk exposures.
○ Doxycycline 200 mg once weekly until the end of exposure [Grade B]

23
References
1. Harrison’s
2. Uptodate
3. Medscape
4. https://www.pcp.org.ph/images/For%20Posting/Leptospirosis_GUIDELINES_contents.pdf

Phil. 4:13 :)
Good luck to us!

24
 CHRONIC LIVER DISEASE

June Rose Naig

MUST KNOWS:
Definition:
A condition defined histopathologically characterized by the development of fibrosis to the point that there is architectural distortion
with the formation of regenerative nodules resulting to decrease in hepatocellular mass, function, and an alteration of blood flow.

Etiology:
1. Alcoholism
2. Chronic viral hepatitis
a. Hepatitis B
b. Hepatitis C
3. Autoimmune hepatitis
4. Nonalcoholic steatohepatitis
5. Biliary cirrhosis
a. Primary biliary cholangitis
b. Primary sclerosing cholangitis
c. Autoimmune cholangiopathy
6. Cardiac cirrhosis
7. Inherited metabolic liver disease
a. Hemochromatosis
b. Wilson’s disease
c. Alpha antitrypsin deficiency
d. Cystic fibrosis
8. Cryptogenic cirrhosis

PATHOPHYSIOLOGY:
Alcoholic Cirrhosis
3 enzymes for alcohol metabolism in the liver
1. Cytosolic alcohol dehydrogenase
2. Microsomal ethanol oxidizing systems
3. Peroxisomal catalase
Ethanol oxidation (alcohol dehydrogenase) → Acetaldehyde(aldehyde dehydrogenase) → Acetate
Effects of Ethanol intake
1. increased intracellular accumulation of triglycerides (by increasing fatty acid uptake, reducing fatty acid oxidation and
lipoprotein secretion)
2. impaired protein synthesis, glycosylation and secretion
3. Formation of reactive oxygen species → oxidative damage to hepatocyte membranes (acetaldehyde is a highly reactive
molecule that combines with proteins to form protein-acetaldehyde adducts) -

Protein-acetaldehyde adducts → interfere with specific enzyme activities including microtubular formation and hepatic protein
trafficking → acetaldehyde-mediated hepatocyte damage → ROS result in Kuppfer cell activation → profibrogenic cytokines are
produced initiating excess collagen and extracellular matrix → connective tissue appears in both periportal and pericentral zones and
eventually connects portal triads with central veins forming regenerative nodules → Hepatocyte loss + increased collagen
production and deposition + hepatocyte destruction → liver contracts and shrinks in size

Cirrhosis Due to Chronic Viral Hepatitis B or C

● Liver damage is immune-mediated
● Progression liver disease is characterized by portal-based fibrosis with bridging fibrosis and nodularity developing,
ultimately culminating in the development of cirrhosis
● Liver is small and shrunken with characteristic features of a mixed micro- and macronodular cirrhosis seen on liver biopsy
● Inflammatory infiltrate is found in portal areas with interface hepatitis and occasionally some lobular hepatocellular injury
and inflammation

25
Biliary Cirrhosis
● Result from necroinflammatory lesions, congenital or metabolic processes, or external bile duct compression
● 2 anatomic sites of abnormal bile retention
○ Intrahepatic
○ Extrahepatic
● Major causes of chronic cholestatic syndromes
○ Primary biliary cholangitis
○ Autoimmune cholangitis
○ Primary sclerosing cholangitis
○ Idiopathic adulthood ductopenia
● Histopathologic Features
○ Cholate stasis
○ Copper deposition
○ Xanthomatous transformation of hepatocytes
○ Irregular so-called biliary fibrosis
○ Chronic portal inflammation
○ Chronic lobular inflammation

Epidemiology:
● 80% of hepatitis C virus develop chronic hepatitis C and of those, about 20-30% will develop cirrhosis 20-30 years; many
have concomitant alcohol use
● True incidence of cirrhosis due to hepatitis C alone is unknown
● 20% of hepatitis B virus patient develop cirrhosis
● 300-400 million individuals have hepatitis B → approx 25% develop cirrhosis

Classification (if any):

Historical Classification
1. Micronodular
● Nodules <3mm in diameter
● Caused by alcohol, hemochromatosis, cholestatic causes of cirrhosis, and hepatic venous outflow
2. Macronodular
● Various sized nodules >3mm
● Secondary to chronic viral hepatitis
3. Mixed

Complications:

Portal Hypertension
● Elevation of hepatic venous pressure gradient >5mmHg

26
 ● Usually revealed by the presence of thrombocytopenia, splenomegaly and development of ascites, encephalopathy,
and/or esophageal varices with or without bleeding

Classification

PRE-HEPATIC HEPATIC POST-HEPATIC

Affects the portal venous system before it Most common; can be presinusoidal, Affects the hepatic veins and venous
enters the liver sinusoidal, postsinusoidal drainage to the heart

● Portal vein thrombosis Presinusoidal ● Budd-chiari syndrome

● Splenic vein thrombosis ● Schistosomiasis ● Inferior vena caval webs
● Massive splenomegaly (Banti’s ● Congenital hepatic fibrosis ● Cardiac causes
Syndrome) ● Primary biliary cirrhosis
● Sarcoidosis
Sinusoidal
● Cirrhosis
● Alcoholic hepatitis
Post-Sinusoidal
● Hepatic sinusoidal obstruction
(venoocclusive syndrome)

Complications of Portal Hypertension

1.Gastroesophageal Varices

Mechanism ● Resistance to portal flow leads to increased resistance in portal pressure

● Decreased splanchnic arteriolar resistance leads to increased splanchnic flow (increased portal
blood flow)

Treatment ● Primary prophylaxis: routine screening by endoscopy, nonselective beta blockers, endoscopic
variceal band ligation
● Treatment of acute bleed: vasoconstriction agents (e.g., somatostatin, octreotide), balloon
tamponade, endoscopic intervention (sclerotherapy, variceal band ligation), TIPS, surgery
● Prevention of rebleeding after an initial bleed: repeated variceal band ligation, beta-blockers,
portosystemic shunt surgery

2. Ascites

Mechanism ● Due to portal hypertension, vasodilation of the splanchnic arterial system occurs, resulting in:
○ Increased splanchnic pressure due to increased portal venous flow → ascites
○ Underfilling of arterial system → RAAS activation → hyperaldosteronism → Na+/H2O
retention → ascites
○ Decreased synthetic function of the liver → hypoalbuminemia → decreased oncotic
pressure → ascites

Treatment Small Ascites

● Na restriction (<2 g of Na/day, avoid canned or processed foods)
Moderate Ascites
● Diuretics with isokalemic dose (100 mg spironolactone & 40mg furosemide)
● Maximum diuretic dose (per day):
○ Spironolactone: 100-200 mg/d, increased cautiously to 400-600 mg/d
○ Furosemide: 40-80 mg/d, increased cautiously to 120-160mg/d
● Fluid restriction is not advised (unless with severe hyponatremia <120mmol/L)
Tense Ascites
● Initial therapeutic paracentesis
● Sodium restriction, oral diuretics
Refractory Ascites
● Avoid NSAIDs, ACEI, ARBS, and beta blockers
● May add oral midodrine especially if BP <90/60
● Large-volume paracentesis with albumin infusion every 2 weeks
● Consider TIPS procedure (may precipitate encephalopathy)
● Referral for liver transplantation

3. Hypersplenism

27
Mechanism ● Hypersplenism with the development of thrombocytopenia is a common feature of patients with
cirrhosis and is usually the first indication of portal hypertension

Treatment ● Splenomegaly itself usually requires no specific treatment

● Transfusion with platelet concentrate as necessary during episodes of bleeding

Hepatic Encephalopathy
● Altered mental status and cognitive function occurring in the presence of liver failure
● Encephalopathy is more commonly seen in chronic liver disease
Etiopathogenesis
● Symptoms are due to neurotoxins that are not removed by the liver because of vascular shunting
● Precipitating Events
○ Hypokalemia
○ Infection
○ Increased dietary protein load
○ Electrolyte disturbances
○ GI bleeding
● Diagnosis is clinical
● Correlation between severity of liver disease and serum ammonia levels is often poor
Manifestations
● Symptoms: confused, changes in behavior, violent, difficult to manage, sleepy and difficult to rouse
● Asterixis or liver flap: sudden forward movement of the wrist after it is bent back on an extended arm
● Cerebral herniation is a feared complication of brain edema

Management Remarks

Nutrition ● Protein restriction is discouraged as it has negative impact on overall nutrition

● Replace animal-based protein with vegetable-based protein in the diet because of more
calorie-to-nitrogen ratio

Lactulose ● Mainstay of treatment for encephalopathy

● Goal is to promote 2-3 soft stools per day
● Mechanism of action:
○ Colonic acidification
○ Catharsis
● May be administered per rectum to patients who are at risk of aspiration

Antibiotics ● Adjunctive lactulose

● Poorly absorbed antibiotics: neomycin & metronidazole (given alternately to reduce individual
side effects)
● Rifamixin 550mg BID has been very effective with a better safety profile

Supportive ● Management/correction of the aforementioned precipitating factors

● Zinc supplementation and L-ornithine-L-aspartate may be helpful

Spontaneous Bacterial Peritonitis

● Spontaneous infection of the ascitic fluid without an intra-abdominal source, usually in the setting of liver cirrhosis
○ Low protein ascitic fluid (<1g/dL or 10 g/L) is particularly susceptible to SBP because the endogenous
antimicrobial (opsonic) activity of the ascitic fluid correlates directly with its protein concentration
○ Diuretic-sensitive patients should be preferably treated with sodium restriction and oral diuretics rather than with
serial paracentesis
● Etiopathogenesis
○ Most common organisms are E. coli and other gut bacteria
○ Isolation/growth of >2 organisms should raise suspicion for perforated viscus (secondary bacterial peritonitis)
● Manifestations and Diagnosis
○ Presents as fever, altered mental status, elevated WBC, and abdominal pain/discomfort
○ Fluid sample analysis:
■ ANC >250/uL
■ Positive culture
■ No evidence of an intra-abdominal surgically treatable source of infection
● Management

28
 ○ Antibiotics
■ Cefotaxime 2g IV q8 x 5 days
■ Ofloxacin 400mg PO BID x 8 days
■ Ciprofloxacin 200mg IV q12 x 2days, followed by Ciprofloxacin 500mg PO q12 x 5days
○ Intravenous Albumin
■ If given in combination with cefotaxime, it has been shown to reduce risk of renal failure and improve
survival
■ IV albumin 1.5g/kg/body weight at the time the infection is detected (preferably within 6 hrs) and
1g/kg on day 3

Other Complications:
● Hepatorenal syndrome
○ Development of renal failure in a patient who has advanced liver disease due to cirrhosis, severe alcoholic
hepatitis, acute liver failure, or less often, a metastatic tumor
● Hepatopulmonary syndrome
○ Triad:
■ Liver disease
■ Increased alveolar-arterial gradient while breathing room air
■ Evidence for intrapulmonary vascular abnormalities, referred to as intrapulmonary vascular dilatations
● Hepatic hydrothorax
○ Presence of pleural effusion in a patient with cirrhosis and no evidence of underlying cardiopulmonary disease
○ Results from the movement of ascitic fluid into the pleural space through defects in the diaphragm, and it is
usually right-sided
● Portopulmonary hypertension
○ Presence of pulmonary hypertension in patients with portal hypertension
○ Presents with fatigue, dyspnea, peripheral edema, chest pain, and syncope
● Cirrhotic cardiomyopathy
○ Characterized by normal to increased cardiac output and contractility at rest, but a blunted response to
pharmacologic, physiologic, or pathologic stress
● Portal vein thrombosis
○ Likely related to unbalanced hemostasis and slowing of portal flow
● Portal hypertensive gastropathy
○ Congestive gastropathy
○ Diffuse mucosal oozing with no other lesions, such as varices, to account for the GI bleeding and anemia

SUBJECTIVE:
Presentation (signs and symptoms):

Anorexia** Amenorrhea/oligomenorrhea/metrorrhagi Jaundice*

a (women)

Weight loss** Impotence (men) Dark or “cola-colored” urine*

Weakness** Infertility Pruritus*

Fatigue** Decreased libido (men) Hematemesis/melena/hematochezia*

Easy bruising Lower extremity edema* Confusion or sleep disturbances*

* - suggests advanced disease or the development of a major complication
** - nonspecific

Hypogonadism in men as manifested by impotence, infertility, loss of libido and testicular atrophy are predominantly seen in patients
with alcoholic cirrhosis and hemochromatosis

Past Medical Hx, Fam Hx, Personal, Social Hx

● Comorbidities such as hypertension. Diabetes, blood dyscrasias, surgeries
● History of alcohol intake, smoking, illicit drug use
● Diet, occupation, sexual history

OBJECTIVE:
Physical Examination Findings

29
System Findings Remarks

Vital Signs Decreased blood pressure Contributes to the development of

Hepatorenal syndrome

Skin findings Jaundice*, spider angiomata Jaundice results from increased serum
bilirubin

Spider angiomata results from alterations

in sex hormone metabolism; not specific

Head and Neck Parotid gland enlargement, fetor hepaticus Parotid gland enlargement seen in patients
with alcoholic liver disease, probably due
to alcohol; usually secondary to fatty
infiltration, fibrosis, and edema

Fetor hepaticus is the sweet, pungent

smell to the breath; caused by increased
concentrations of dimethyl sulfide

Chest Findings Gynecomastia Caused by increased production of

androstenedione from the adrenals,
enhanced aromatization of
androstenedione to estrone, and increased
conversion of estrone to estradiol

Abdominal findings Hepatomegaly Firm and nodular consistency

Splenomegaly
Ascites* (abdominal distension, fluid wave,
flank dullness to percussion)
Caput medusae
Cruveilhier-Baumgarten murmur
Normal liver span at MCL: 7-10cm
Splenomegaly is caused by congestion of
the red pulp resulting from portal
hypertension

Caput medusae due to opening of the

umbilical vein

Cruveilhier-Baumgarten murmur results

from collateral connections between the
portal system and the remnant of the
umbilical vein

Genitourinary findings Testicular atrophy Due to development of hypogonadism

Extremity Findings Palmar erythema Palmar erythema is an exaggeration of the

Nail changes (Muehrcke nails, Terry nails)
Clubbing
Hypertrophic osteoarthropathy
Dupuytren’s contracture
normal speckled mottling of the palm
caused by altered sex hormone
metabolism
Muehrcke nails are paired horizontal white
bands separated by normal color; caused
by hypoalbuminemia

Terry nails, proximal ⅔ of the nail plate

appears white while distal ⅓ is red; caused
by hypoalbuminemia

Clubbing is more common in biliary

cirrhosis

Neurologic Asterixis* Bilateral but asynchronous motions,

outstretched, dorsiflexed hands; seen in
patients with hepatic encephalopathy
* - suggests advanced disease or the development of a major complication

30
ASSESSMENT
When to suspect cirrhosis
● Stigmata of CLD discovered on PE
● Evidence of cirrhosis on laboratory or radiologic testing by direct visualization undergoing a surgical procedure
● Evidence of decompensated cirrhosis, which is characterized by the presence of dramatic and life-threatening
complications, such as variceal hemorrhage, ascites, spontaneous bacterial peritonitis, or hepatic encephalopathy

DIFFERENTIAL DIAGNOSIS:

Disease Entity Rule In Rule Out

Systemic Lupus Erythematosus Elevated transaminases Cannot satisfy at least 4 of 17 SLICC criteria
Fatigue (at least 1 of 11 clinical criteria and 1 of 6
Malaise immunologic criteria)
Anorexia (-) antinuclear antibodies or anti-dsDNA
Jaundice antibodies
Hepatomegaly
Ascites
Neurologic symptoms

Schistosomiasis Works as farmer, often wading in rice No exposure in endemic areas

fields with infected snails
Jaundice
Ascites
Hepatosplenomegaly
Encephalopathy (neuroschistosomiasis)

Heart Failure Easy fatigability (-) Encephalopathy

Ascites (-) Variceal hemorrhage
(-) hypoalbuminemia
(-) inc. in jugular venous distention
(-) decrease in cardiac output

Nephrotic Syndrome Ascites (-) azotemia

Edema Hypercholesterolemia
Hypoalbuminemia Periorbital edema upon awakening
Hypercoagulability

Hemolytic Anemia Elevated liver enzyme (-) Ascites

Jaundice (-) Edema
Easy fatigability Rapid onset of symptoms
Splenomegaly

PLANS:

Diagnostics Rationale Expected Findings

Labs

AST/ALT AST is more often elevated than ALT. Moderately elevated (AST:ALT ratio
However, normal aminotransferases do >1)
not preclude a diagnosis of cirrhosis

ALP Higher levels may be seen in patients Elevated 2-3 times the upper limit of
with underlying cholestatic liver disease normal
such as primary sclerosing cholangitis
or primary biliary cirrhosis

31
Gamma-glutamyl transpeptidase Correlate reasonably well with alkaline Elevated
phosphatase in liver disease but are
nonspecific. Levels of GGT are typically
much higher in chronic liver disease
from alcohol than other causes. This
may be the result of alcohol-inducing
hepatic microsomal GGT or alcohol
causing GGT to leak from hepatocytes

CBC Thrombocytopenia is mainly caused by Thrombocytopenia

portal hypertension with attendant Leukopenia/neutropenia
congestive splenomegaly. An enlarged
spleen can result in temporary
sequestration of up to 90 percent of the
circulating platelet mass.

Serum albumin Albumin is synthesized exclusively in Hypoalbuminemia

the liver. Albumin levels fall as the
synthetic function of the liver declines
with worsening cirrhosis.

Prothrombin time
Most of the proteins involved in the Prolonged prothrombin time/ elevated
coagulation process are produced in INR
the liver. Thus, the prothrombin time
reflects the degree of hepatic synthetic
dysfunction. An elevated INR that
corrects with vitamin K administration
suggests impaired intestinal absorption
of fat-soluble vitamins and is compatible
with obstructive jaundice. An elevated
INR that does not correct with vitamin K
suggests moderate to severe
hepatocellular disease with impaired
synthetic function (particularly if
unexplained hypoalbuminemia is also
present).

Bilirubin May be normal in well-compensated Hyperbilirubinemia

cirrhosis. However, they rise as the
cirrhosis progresses. In patients with
primary biliary cirrhosis, a rising serum
bilirubin portends a poor prognosis

Serum sodium Hyponatremia is common in patients Hyponatremia

with cirrhosis and ascites and is related
to an inability to excrete free water. This
results primarily from high levels of anti-
diuretic hormone secretion.

Imaging

Ultrasound Suggest presence of cirrhosis Surface nodularity

Increased echogenecity with irregular
appearing areas
Atrophy of right lobe and hypertrophy of
caudate or left lobes

Findings of portal hypertension:

32
 Increased diameter of the portal vein,
presence of collateral veins, and
decreased flow within the portal
circulation on Doppler imaging

CT Not routinely used Hepatic nodularity

Atrophy of the right lobe and
hypertrophy of the caudate or left
lobes, ascites, or varices
Patency of the portal vein

Liver Biopsy: Gold standard for diagnosis of cirrhosis

TREATMENT
Major Goals of managing patient with Cirrhosis:
● Slowing or reversing the progression of liver disease
● Preventing superimposed insults to the liver
● Identifying medications that require dose adjustments or should be avoided entirely
● Managing symptoms and laboratory abnormalities
● Preventing, identifying, and treating the complications of cirrhosis
● Determining the appropriateness and optimal timing for liver transplantation

Alcoholic Cirrhosis
● ABSTINENCE: cornerstone of therapy
● Glucocorticoids: used in patients without infection
● Oral Pentoxifylline: decreases the production of a TNF and other pro-inflammatory cytokines
● Infliximab or etanercept: inhibitors of a TNF
● Acamprosate calcium: reduces craving for alcohol

Chronic VIral Hepatitis

● Management revolves around specific therapy treatment of whatever complications occur
● Antiviral therapy for Hepatitis B
○ Reduce aminotransferase levels and HBV DNA levels
○ Improve histology by reducing inflammation and fibrosis
○ Lamivudine
○ Adefovir
○ Telbivudine
○ Entecavir
○ Tenofovir

Please see section on complications for other management regimen

ADMITTING ORDERS:
Admit to ICU
Diet: NPO temporarily; Total Cal = 1800 cal/day; 250-500 mg Na/day; Protein intake 0-20 mg/day in 6 divided feedings if with
hepatic encephalopathy, otherwise increase protein intake; fluid restriction to 1-1.5 l/day
Monitor NVS q2 hours; I & O qshift and record
Stool charting qshift; Weigh OD in am, measure abdominal girth OD (at level of umbilicus); insert foley catheter
IVF: D10W x 16 hrs or D5 0.3 NaCl x 24 hrs
Diagnostics:
1. CBC
2. Blood GSCS
3. PT/PTT
4. AST, ALT, ALP
5. Total protein, albumin, globulin, A:G ratio
6. Serum ammonia
7. BUN, Crea, Na, K, Urine Na (dehydration vs. hepatorenal syndrome)
8. FBS, Urinalysis, CXR, ECG
9. Hepatitis profile
10. Ultrasound of liver, hepatobiliary tract and pancreas (whole abdomen utz)

33
 11. Ascitic fluid/Abdominal Paracentesis (for very tense ascites)
12. Endoscopy for UGIB
13. Kato-Katz examination of stool
14. COPT

Tx:
1. Lactulose 30 cc TID to make 4-5 bowel movements per day
2. If with hepatic encephalopathy: Aminoleban (branched chain amino acids) 500cc IV q 12hr (2 bottles/day) or Falkamin 1
sachet in 180ml water BID-TID PO
3. If with pedal edema and/or ascites: Furosemide 40mg OD-BID PO or Furosemide 20mg IV OD-TID or Spironolactone
25mg BID-QID
4. For portal hypertension: Propanolol 10mg TID, ISDN 20 mg/tab 1 tab BID
5. Watch-out for complications
a. Bleeding due to decrease in clotting factors (abnormal protime)
i. Give 4-6 units of FFP + 1-2 doses of Vit. K preparation
ii. Vit. K preparation: Phytomenadione 1 amp IV (10mg/ml amp) OD-BID or Menadione 10mg 1 tab
TID-QID PO
b. Gastrointestinal bleeding due to gastric erosions: prophylactic H2-blockers, antacids or cytoprotective
agents
c. Infections: consider prophylactic antibiotics with Metronidazole, Amoxicillin or Cephalosporin
d. Renal failure: cautious fluid management with CVP insertion and monitoring. Consider albumin infusion and low
dose dopamine and furosemide drip
e. Pulmonary infections and ARDS - intubation and PEEP
f. Hepatic encephalopathy vs. cerebral edema: Do CT scan to differentiate
i. Hepatic encephalopathy: Lactulose + Aminoleban
ii. Cerebral edema: Mannitol and hyperventilate, steroids
g. Hypoglycemia: Hypertonic glucose D50 50 IV
h. Discontinue hepatotoxic drugs (anti-tuberculosis drugs, anticonvulsants etc); Avoid Diazepam or Dilantin for
seizures
Possible Referrals: IDS, Renal, Neuro, Hema, GI
Long term plans: Low salt diet, alcohol cessation, for liver transplant

References:
Harrison’s
Medicine Blue Book
Uptodate
European Association for the Study of Liver CPG for Management of patients with decompensated cirrhosis

34
 THYROTOXICOSIS

Kevin Austin Ona

Must-Knows

Definition
Classification:
→ Thyrotoxicosis: State of thyroid hormone excess; may be endogenous or exogenous
→ Hyperthyroidism: State of excessive thyroid function; endogenous

Causes of Thyrotoxicosis

Primary Hyperthyroidism Thyrotoxicosis without Secondary Hyperthyroidism

Hyperthyroidism

Graves’ Disease Subacute Thyroiditis TSH-secreting pituitary adenoma

Toxic Multinodular Goiter Silent Thyroiditis Thyroid hormone resistance syndrome
Toxic Adenoma Other causes of thyroid destruction: Chronic Gonadotropin-secreting Tumors
Functioning Thyroid Carcinoma amiodarone, radiation, infarction of Gestational Thyrotoxicosis
Metastases adenoma
Activating mutation of the TSH receptor Ingestion of excess thyroid hormone
Activating Mutation of Gsa (McCune- (thyrotoxicosis factitia) or thyroid tissue
Albright Syndrome)
Struma Ovarii
Drugs: iodine excess (Jod-Basedow
phenomenon)

Etiology
Graves Disease
- Autoimmune hyperthyroidism caused by thyroid-stimulating immunoglobulin (TSI) which chronically stimulates TSH
receptor
- 60-80% of thyrotoxicosis
- Risk Factors: high iodine intake
- Typically between 20-50 years of age, also in elderly
- Clinical picture:
- Biochemically-confirmed thyrotoxicosis
- Diffuse Goiter on palpation
- Ophthalmopathy
- Dermopathy

Epidemiology
- Incidence of thyrotoxicosis increases with age
- Graves’ disease is the most common cause of thyrotoxicosis, especially in children
- Thyrotoxicosis is 3-5x more common in females, especially among pubertal children
- Thyroid storm more common in adolescents

Pathophysiology
Review of Thyroid Hormone Synthesis, Metabolism and Action

Thyroid Gland
- Produces thyroxine (T4) and triiodothyronine (T3)
- Autoimmune disorders of the gland can stimulate overproduction of thyroid hormones (thyrotoxicosis) or cause glandular
destruction and hormone deficiency (hypothyroidism)

Thyroid Hormone
- thyroxine (T4) and triiodothyronine (T3)
- Acting through thyroid hormone receptors α and β, these hormones play a critical role in cell differentiation and
organogenesis during development and help maintain thermogenic and metabolic homeostasis in the adult

35
Thyroid Hormone Synthesis

Mechanism
- There is note of increase in circulating thyroid hormones.
- In Graves’ disease, thyroid-stimulating immunoglobulins (TSI) chronically stimulate TSH receptor leading to thyroid gland
production of T4 and T3.
- Combination of environmental and genetic factors, including polymorphisms in HLA-DR, the immunoregulatory
genes CTLA-4, CD25, PTPN22, FCRL3, and CD226, as well as the gene encoding the thyroid-stimulating
hormone receptor (TSH-R), contributes to Graves’ disease susceptibility
- Graves Ophthalmopathy: There is infiltration of the extraocular muscles by activated T cells; the release of
cytokines results in fibroblast activation and increased synthesis of glycosaminoglycans that trap water, thereby
leading to characteristic muscle swelling. Late in the disease, there is irreversible fibrosis of the muscles. It’s
been thought that TSH-R is a shared autoantigen that is expressed in the orbit.

36
Signs and Symptoms of Thyrotoxicosis (Descending Order of Frequency)

Symptoms Signs

Hyperactivity, irritability, dysphoria Tachycardia, Atrial fibrillation in the elderly (sinus tachy often
Heat intolerance and sweating assoc. with palpitations)
Palpitations Tremor (Fine)
Fatigue and weakness Goiter
Weight loss with increased appetite Warm, moist skin
Diarrhea (sec. to decreased GI transit time) Muscle weakness, proximal myopathy without fasciculation
Polyuria Lid retraction or lag
Oligomenorrhea, loss of libido Gynecomastia
*Excludes the signs of ophthalmopathy and dermopathy specific for Graves’ Disease

Thyroid Storm
- Also referred to as thyrotoxic crisis, extreme accentuation of hyperthyroidism, usually with Graves disease or toxic
multinodular goiter
- An acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones in individuals with
thyrotoxicosis

Pathophysiology
- Decompensated state of thyroid hormone-induced, severe hypermetabolism involving multiple systems
- No evidence of critical increase in production of T3 or T4 as compared to uncomplicated thyrotoxicosis
- decreased binding to thyroid-binding globulin leading to increased free T4 or T3 has been proposed
- Shown to be associated with increase in catecholamine receptor and increased responsiveness to catecholamines
- Enhanced cellular responses to thyroid hormones

Precipitating factors
- Partially treated or untreated thyrotoxicosis
- thyroidal/ non-thyroidal surgery (esp. In inappropriately prepared patients)
- Acute or sub-acute non-thyroidal illness: infection, stroke, trauma, DKA
- Parturition
- Conditions associated with rapid rise in hormone levels
- Vigorous thyroid palpation
- Withdrawal or non-compliance to anti-thyroid medications
- Acute iodine load (radioiodine therapy, iodinated contrast dyes)
- Salicylates

Complications
- High output cardiac failure
- Cardiac Arrhythmia
- Cardiogenic Shock
- Mortality from cardiac failure, arrythmia, hyperthermia

Subjective (Thyroid Storm)

- Patients with severe and life-threatening thyrotoxicosis typically have an exaggeration of the usual symptoms.
- Patients with a hyperthyroid or thyrotoxic profile as described above, and those with precipitating factors are of high
suspicion for impending or ongoing thyroid storm when presenting with the signs and symptoms below.

Symptoms and Signs

General - Hyperpyrexia
- Profuse sweating
- Poor feeding
- Fatigue

Cardiac - Cardiac arrythmia (more commonly supraventicular)

- Congestive heart failure/ high output failure signs

37
Respiratory - distress

Abdominal - Severe nausea, vomiting

- Diarrhea
- Abdominal pain
- Hepatic failure with jaundice

Neurologic - Altered mentation: agitation, anxiety, delirium, psychosis, stupor, coma

- Pyramidal signs, hyperreflexia
- Seizures

Objective

Thyroid Exam - May be diffusely enlarged or nodular

- If the lower border is not felt, the goiter may be retrosternal. Large retrosternal goiters can cause
venous distention over the neck and difficulty breathing, especially when the arms are raised
(Pemberton’s sign).
- (+) bruit or thrill - indicates increased vascularity, associated with turbulent flow

HEENT - Ophthalmopathy (in Graves’ disease)

- Lid lag

Cardiac - tachycardia to rates that can exceed 140 bpm disproportionate to fever
- Hypertension with wide pulse pressure
- Hypotension in later stages
- Congestive heart failure/ high output failure signs
- Hyperdynamic precordium

Respiratory - Tachypnea
- Congestion (crackles)

Extremities - Hand tremor

- Warm, moist skin

Neurologic - Altered sensorium

- Hyperreflexia
- Pyramidal signs
- Proximal muscle weakness

Assessment

Differentials Rule In Rule Out

Septic Shock Altered sensorium May present with decreased

Hypotension (on later stage), temperature, Little to no urine output,
Tachycardia, Hyperpyrexia Must have a source of infection

Hypertensive Emergency Altered sensorium, Dizziness, Seizures, History of hypertension, Persistently

Nausea, Hypertension (on early stage) elevated blood pressure

Heart Failure Altered sensorium, Dizziness, Nausea, Long standing heart disease, edema
Shortness of breath
Signs of congestion

Pheochromocytoma Headache, diaphoresis, tremor, Persistently elevated blood pressure,

weakness, anxiety, abdominal pain Postural hypotension
Tachyarrythmia, Fever, Congestion

Panic Disorder Diaphoresis, shortness of breath, psychiatric symptoms: derealization, fear

nausea, abdominal pain, dizziness of dying/ losing control

38
 Accelerated heart rate

Malignant Hyperthermia Hyperpyrexia,Tachycardia Use of medications (anesthetic meds),

muscle rigidity

Burch and Wartofsky’s Criteria

- <25 points: Thyroid Storm is unlikely
- 25-44 points: Impending Storm
- >= 45 points: Highly suggestive of thyroid storm

Plan

Diagnostics

Diagnostics Rationale Expected Findings

Sensitive TSH -Single best screening test for Low in primary thyrotoxicosis
Analysis hyperthyroidism
-should be taken with free T4 and total T3

Free T4 RIA To assess circulating levels of free T4 Elevated

Free T3 RIA To assess circulating levels of free T3 Elevated

Thyroid Stimulating Especially used when Graves’ Disease is of Elevated in Graves’ disease
Antibodies primary consideration, not routinely used

Blood Sugar Catecholamine-induced inhibition of insulin Mild to moderate hyperglycemia

release and increased glycogenolysis

Calcium Hemoconcentration and enhanced bone Mild hypercalcemia

resorption

CBC To evaluate blood parameters critical for Leukocytosis (shift to left if with infection)

39
 management Leukopenia
Signs of infection

Liver function test Thyroid dysfunction noted Elevated

Radioactive Iodine Measures radioactive iodine trapped into Thyrotoxicosis with elevated RAI uptake:
Uptake and Thyroid thyroid tissues - Graves’ disease: increased uptake
Scan distributed homogenously
- Toxic adenoma: focal areas of increased
uptake with suppressed tracer uptake in the
rest of the gland
- Toxic MNG: gland enlarged with distorted
architecture & multiple areas of relatively
increased or decreased tracer uptake

Thyrotoxicosis with low RAI uptake:

- Painless thyroiditis
- Amiodarone induced thyroiditis
- Subacute thyroiditis

Evaluation of Thyrotoxicosis

Interpretation of Data

Result Differentials

TSH FT4

Low High -Primary thyrotoxicosis: Graves’ disease, multinodular goiter, toxic adenoma
-Destructive Thyroiditis, excess iodine intake, excess thyroid hormone

Low Normal -Subclinical hyperthyroidism (if normal FT3)

-T3 toxicosis (if high FT3)

40
 Normal/ High High -Secondary thyrotoxicosis: TSH secreting pituitary adenoma or thyroid hormone
resistance syndrome

Treatment

Mechanism Drug Dose Action

Inhibition of PTU 500-1000 mg LD and 250 mg q4h -inhibits TPO; inhibits peripheral conversion in high
new hormone PO or per rectum/ per NGT doses; decrease circulating TSI; restores normal
production suppressor cell activity

Methimazole 60-80 mg/ day (20 mg q6hrs sa -inhibits TPO

harrison)

Inhibition of SSKI 5 drops q6h 1 hr after PTU (Wolff-

release of pre- chaikoff effect)
released
hormones Lugol’s sol’n 4-8 drops PO q6-8 hrs
Blocks thyroid hormone releas; decreases fractional
Sodium ipodate 1-3 g PO QID turn-over of thyroid iodine and T4 secretion rate

Iopanoic Acid
500 mg PO q12hrs

Control of Propranolol 60-80 mg PO q4hrs or 2mg IV q4hrs -reduces sympathetic overdrive; high doses also
adrenergic decrease peripheral conversion of T4 to T3
symptoms
50-200 mg PO QID
Atenolol Cardioselective (may be used in asthma or COPD
100-200 mg patients)
Metoprolol
50-100 mcg/kg/min To decrease heart rate
Esmolol

Supportive Acetaminophen 325 - 650 mg PO q4-6hrs PRN -for fever and pain
management
Hydrocortisone
300 mg IV bolus load, then 100 mg -also decreases peripheral conversion; addresses
Glucose IV q8hrs relative adrenal insufficiency

5-10% solution

alternatives Lithium 300 mg POq8h -mimics iodine; inhibits coupling of iodotyrosinases

and peripheral conversion
Potassium 1 g PO QID
perchlorate

Cholestyramine 4 g PO QID -hastens removal of T4 and T3 from serum

Antibiotics To address infection

Admitting Orders
● Admit to ICU
● Secure IV line. Insert foley catheter.
● Diet: as tolerated, no added salt, SAP
● Monitor NVSQ1, strict InO qshift
● IVF: D5NM x 8-12 hours
● Diagnostics: CBG, Sensitive TSH analysis, FT4, CBC, Na, K, Crea, AST, ALT, Chest Xray, ECG, Urinalysis, ABG when
indicated
● Therapeutics:
○ PTU 500-1000 mg LD and 250 mg q4h PO or per rectum/ per NGT
○ SSKI 5 drops q6h 1 hr after 1st dose of PTU
○ Propranolol 60-80 mg PO q4hrs or 2mg IV q4hrs
○ Hydrocortisone 300 mg IV bolus load, then 100 mg IV q8hrs

41
 ○ Cholestyramine 4 g PO q6hrs
○ Paracetamol 600 mg IV q4-6hrs PRN for fever
○ If with frank seizure, Diazepam 5 mg IV PRN
○ If with atrial fibrillation, Digoxin 0.5 mg IV then PO PRN
● When indicated, hook to O2 via NC @ 2 lpm PRN.
● Hook to cardiac monitor at all times.
● Refer to Endocrinology, ORL (if with enlarged mass and obstructive symptoms), CVS (if with profound cardiovascular
problem), MSS (for financial aid).

Long term Plan

- Discontinue iodine therapy, taper glucocorticoids when with clinical improvement (defervescence, resolution of central
nervous system and CVS manifestations)
- Withdraw beta-blockers when thyroid function tests return to normal
- Switch PTU to Methimazole
- Titrate thionamides to maintain euthyroidism
- Definitive therapy for Graves’ disease: radioactive iodine, or thyroidectomy

References
DEM Curriculum, DEM, University of Illinois College of Medicine
Expanded Medicine Blue Book
Harrison’s Principles of Internal Medicine 20th Ed.
IM Platinum
Medscape
UptoDate
WebMD

42
 CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Ria Mikhaella Panis

Must-Knows
● Definition: disease state characterized by persistent respiratory symptoms and airflow limitation that is not fully reversible;
requires the presence of chronic airflow obstruction, determined by spirometry, that usually occurs in the setting of noxious
environmental exposures
● Encompasses the following conditions:
○ Emphysema - anatomically-defined condition characterized by destruction of the lung alveoli with air space enlargement
enlargement
○ Chronic bronchitis - clinically-defined condition with chronic cough and phlegm
○ Small airway disease - small bronchioles are narrowed and reduced in number
● Acute exacerbation: worsening of respiratory symptoms beyond normal day-to-day variations, leading to change in
medication (frequent exacerbation of at least 2x/year) or change in mental status (most important sign in very severe
exacerbations)
○ Associated with increased airway inflammation, increased mucus production, and marked gas trapping
○ Mainly triggered by respiratory infections (viral, bacterial) or environmental factors
● Etiopathogenesis
○ Characterized by: expiratory airflow limitation that IS NOT FULLY REVERSIBLE
○ Hallmark: Airflow obstruction
○ Essentially: peripheral airway obstruction and loss of alveolar attachments to small airways cause chronic airflow limitation
leading to progressive air trapping during expiration leading to hyperinflation
○ Unusual in the absence of smoking or prior history of smoking, except for patients with alpha-1 antitrypsin deficiency
○ Elastase-Antielastase Hypothesis: remains a prevailing mechanism for its pathophysiology
○ Pathologic Changes:
■ Chronic inflammation and structural changes resulting from repeated injury and repair
■ Increased number of specific inflammatory cell types in different parts of the lung
● Risk Factors
○ Tobacco smoke - cigarette, pipe, cigar, water-pipe, environmental tobacco smoke
○ Indoor air pollution - biomass fuel used in cooking and heating
○ Occupational exposures - organic and inorganic dusts, chemical agents, fumes
○ Outdoor air pollution - contributes to lungs’ total burden of inhaled particles
○ Genetic factors - severe hereditary deficiency of alpha-1 antitrypsin
○ Age and sex - aging and femal sex
○ Lung growth and development - any factor that affects lung growth during gestation and childhood (low birth weight,
respiratory infections)
○ Low socioeconomic status - may reflect exposure to indoor/outdoor pollutants, crowding, poor nutrition
○ Asthma and airway hyperreactivity - airway limitation
○ Chronic bronchitis - increase frequency of total and severe exacerbations
○ Infections - severe childhood respiratory infections are associated with reduced lung function and increased respiratory
symptoms in adulthood

Subjective
● A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and
a history of exposure to risk factors
○ Exertional dyspnea - described as increased effort to breathe, heaviness, air hunger, or gasping; progressive over time,
worse with exercise, persistent
○ Chronic cough - may be intermittent, may be nonproductive, and recurrent wheeze
○ Chronic sputum production - any pattern
● Manifestations of COPD exacerbations
○ Key symptoms: increased dyspnea
○ Others: increased sputum purulence and volume, increased cough, wheezing
○ Symptoms usually last 7-10 days during exacerbations, but 20% of patients do not recover at 8 weeks
● Usual past medical / family / social history
○ PMH: recurrent lower respiratory tract infections, A1-antitrypsin deficiency, asthma, low birth weight, childhood respiratory
infections
○ FMH: COPD
○ PSH: smoking, pollution, occupational exposures, low socioeconomic status, other risk factors

43
Objective
● Physical exam findings may vary with severity of COPD
● Early in disease
○ May be normal
○ Prolonged expiration, wheezes on forced exhalation
● Increased severity
○ Pink puffers (predominantly emphysema): thin, non-cyanotic, prominent use of accessory muscles
○ Blue bloaters (predominantly chronic bronchitis): heavy and cyanotic
○ Signs of hyperinflation: barrel chest, hyperresonance on percussion
○ Decreased breath sounds
○ Wheezes, crackles
○ Distant heart sounds
○ Depressed diaphragm with limited movement based on chest percussion
● End-stage COPD
○ Tripod position: leaning forward with arms outstretched and weight supported on the palms or elbows; facilitates use of
accessory muscles (of the neck and shoulder girdle)
○ Expiration through pursed lips
○ Hoover’s sign - paradoxical retraction of the lower interspaces during inspiration
○ Cyanosis
○ Asterixis due to severe hypercapnia
○ Neck vein distention especially during expiration - due to increased intrathoracic pressure
○ Signs of cor pulmonale - enlarged, tender liver, bipedal edema, ascites
● Others:
○ Yellow stains on fingers due to nicotine and tar from burning tobacco/ clue of ongoing and heavy smoking
○ Clubbing - not typical in COPD, even with associated hypoxemia; suggests comorbids such as lung cancer, interstitial
lung disease, bronchiectasis

Assessment

Differential Diagnoses

Differentials Likely Less Likely

Asthma Cough Onset early in life (childhood usually)

Exertional dyspnea Symptoms vary widely day to day (vs COPD
(+) wheezes that is persistent and progressive)
Relieved by bronchodilator Symptoms worse at night/early morning
Allergy, rhinitis, eczema also present
Family hx of asthma
Obesity coexist

Bronchiectasis Sputum production (large volumes of purulent Commonly ass. With bacterial infection
sputum) CXT/CT - bronchial dilation, bronchial wall
thickening

Pneumonia Cough Fever, chills

Respiratory distress: tachypnea, use of Crackles
accessory muscles, central cyanosis, altered Pleural friction rub
mental status
Decreased breath sounds

Congestive heart failure Chronic cough CXR - dilated heart, pulmonary edema
Exertional dyspnea Pulmonary function tests: volume restriction, not
Anorexia airflow

TB Cough, anorexia, respiratory distress Fever, chills

Onset: all ages CXR: lung infiltrate
High local prevalence

Chronic bronchitis with Chronic productive cough Normal spirometry (no airflow limitation)
normal spirometry

44
Diagnostics

Diagnostics Rationale Expected Findings/ Comments

Spirometry Required to make the diagnosis of COPD Post-bronchodilator FEV1/FVC ratio <0.70 confirms
persistent airflow limitation
FEV1, FEV1/FVC and other measures of expiratory
airflow are reduced

CXR PAL Not required to diagnose COPD.
To exclude alternative diagnoses, evaluate for
comorbidities, or to look for complications of
COPD.
Frontal: Rapidly tapering vascular shadows,
increased radiolucency of the lung, flat diaphragm,
long, narrow heart shadow.
Lateral: flat diaphragmatic contour and increased
retrosternal airspace due to hyperinflation.

Bullae - radiolucent areas larger than 1cm and

surrounded by arcuate hairline shadows; due to
locally severe disease, may or may not be
accompanied by widespread emphysema

Severe: pulmonary hypertension and cor

pulmonale;prominent hilar vascular shadows and
encroachment of the heart shadow in retrosternal
space, cardiac enlargement

Comorbids: lung cancer with airway obstruction,

bronchiectasis, pleural disease, interstitial lung
disease, heart failure

Complications: pneumonia, pneumothorax

Pulse oximetry To evaluate O2 sats and need for supplemental

oxygen

ABG Considered when there is low FEV1 (<50%
predicted), low oxygen saturation by pulse ox,
depressed level of consciousness, acute
exacerbation of COPD, and assessment of
hypercapnia in at risk patients 30-60 mins after
initiation of supplemental oxygen
Mild-mod: mild or moderate hypoxemia without
hypercapnia
As the disease progresses, hypoxemia becomes
more severe and hypercapnia may develop

CBC Rule out anemia and infection as cause of DOB Essentially normal
Dec hgb - possible anemia
Inc WBC - possible ongoing infectious

Serum bicarbonate Among stable COPD patients with normal Increased bicarbonate in chronic hypercapnia
kidney function, an elevated HCO3 may
indirectly identify chronic hypercapnia as it
compensates with metabolic acidosis

Chest CT Not routinely requested

May identify individuals with predominantly
upper lobe disease who may be candidates for
lung volume reduction surgery

COPD Assessment
● The goals of COPD assessment in order to guide therapy are:
○ Determine the severity of airflow limitation
○ Impact on patient’s health status
○ Risk of future events (exacerbations, hospital admissions, death)
● To achieve this goals, assessment must consider the following aspects of the disease separately:
○ Presence and severity of spirometric abnormality
○ Current nature and magnitude of the patient’s symptoms
○ History of moderate and severe exacerbations and future risk
○ Presence of comorbidities

45
Classification of Severity of Airflow Obstruction

Assessment of Symptoms
● Note: there is only a weak correlation between FEV1, symptoms, and impairment of patient’s health status, hence the need for
symptomatic assessment
● mMRC (Modified Medical Research Council Dyspnea Scale) - provides a single number for degree of breathlessness
● CAT (COPD Assessment Test - health status measure

CAT Assessment

46
Combined COPD Assessment

Classification of exacerbated COPD among hospitalized patients

No Respiratory Failure Acute Respiratory Failure ARF (life threatening)

(non-life-threatening)

RR 20-30 >30

Use of accessory muscles No Yes

Change in mental status No Yes (acute)

Hypoxemia Improved with 28-35% FiO2 Improved with 35-40% FiO2 Not improved with O2 via
venturi mask or requiring
>40% FiO2

PaCO2 Not increased Hypercarbia (increased from Hypercarbia (increased from

baseline or elevated at 50-60 baseline or elevated
mmHg) >60mmHg or without acidosis
(pH 7.25 or less))

Plan
● Only 3 interventions have been demonstrated to improve survival of patients with COPD
○ Smoking cessation
○ Oxygen therapy in chronically hypoxemic patients
○ Lung volume reduction surgery (LVRS) in select patients with emphysema
● Suggestive, but not definitive, evidence in reducing mortality rates
○ ICS (inhaled corticosteroids)
○ Muscarinic antagonists

Goals of Therapy
1. Symptomatic relief - reduce respiratory symptoms, improve exercise tolerance, improve health status
2. Reduce future risk - prevent disease progression, prevent and treat exacerbations, reduce mortality

47
Pharmacologic Therapy

Medication Comments Examples

Beta-Agonists ● Alters airway smooth muscle tone → improved Short-Acting

emptying of lungs ● Salbutamol
● Short-acting: 4-6h ● Terbutaline
● Long-acting: >12h
● LABA is more effective than SABA Long-Acting
● Provides subjective benefit in acute episodes, ● Formoterol
but not necessarily helpful in stable disease ● Salmeterol
● Vilanterol
● Adverse effects: tachycardia, arrhythmia, ● Olodaterol
tremors, hypokalemia ● Indaceterol

Anticholinergics / ● Blocks acetylcholine’s effect on muscarinic Short-Acting

Antimuscarinic receptors ● Ipratropium bromide
● Bronchodilating effect lasts longer than beta- ● Oxitropium bromide
agonists
● Improves symptoms and health status and Long-Acting
effectiveness of pulmonary rehabilitation and ● Tiotropium
reduces exacerbations ● Umeclidinium
● Adverse effects: dry mouth, bitter metallic ● Glycopyrronium
taste, arrhythmias

Methylxanthines ● Non-selective phosphodiesterase inhibitor ● Theophylline

● Improves FEV1 and breathlessness when ● Aminophylline
added to salmeterol ● Doxofylline
● Adverse effects: tachycardia, arrhythmias,
headache, insomnia

Inhaled Corticosteroids ● Added for: symptomatic patients with ● Beclomethasone

FEV1<50%, or repeated exacerbations ● Budesonide
● Avoid chronic treatment with ICS ● Mometasone
● ICS + LABA in moderate to very severe ● Fluticasone
COPD is more effective than each alone
● Adverse effects: hoarseness, candidiasis

PDE-4 Inhibitors ● Improves lung function ● Roflumilast

● Reduces moderate to severe exacerbations in
those with chronic bronchitis or are in
LABA/ICS tx
● Adverse effects: anorexia, weight loss,
diarrhea, headache

Antibiotics ● Long-term azithromycin and erythromycin use ● Azithromycin 250mg/day or

reduces exacerbations over 1 year 500mg 3x/week
● Erythromycin 500mg BID
● For 1 year

Mucolytics/ ● Reduce risk of exacerbations in select ● N-acetylcysteine

Antioxidants populations ● Carbocysteine

Vaccinations
● Influenza Vaccine - can reduce serious illness and death
● Pneumococcal Vaccine (PCV13 and PPSV23) - recommended for all patients at least 65 y.o., and for younger COPD
patients with significant comorbids (ex. Chronic heart or lung disease)
○ PPSV23 - shown to reduce incidence of CAP in patients <65 with FEV1 <40%, or with comorbids (especially
cardiac)

48
Smoking Cessation

Management of Stable COPD

Non-Pharmacologic

GOLD Group Essential Recommended Depending on Local

Guidelines

A Smoking cessation Physical Activity Flu vaccine

Pneumococcal vaccine

B-D Smoking cessation

Pulmonary rehabilitation

Pharmacologic

Patient Group Preferred Treatment Next Step Other Possible Treatment

A Any bronchodilator (can be Continue, stop, or try Antioxidant mucolytics

short- or long-acting) alternative class of
bronchidilator

B Start with LAMA or LABA LAMA + LABA Add SAMA, SABA

C Start with LAMA LAMA + LABA if with further Add SAMA, SABA
exacerbations, OR
LABA + ICS

D LAMA + LABA LAMA + LABA + ICS Add SAMA, SABA

Or Consider PDE-4 inhibitor
LABA + ICS trial before tripple (roflumilast) if FEV1<50%
therapy predicted and presence of
chronic bronchitis
Consider macrolide in former
smokers

Supplemental Oxygen
● Titrate to keep SaO2 of at least 90% in patients with arterial hypoxemia
○ PaO2 <55 mmHg or SaO2 <88%, or
○ PaO2 55-59 mmHg with right heart failure or erythrocytosis
● Recheck and reassess in 60-90 days

49
Management of Acute Exacerbations

Classification Overview of Management

Mild SABA

Moderate SABA + antibiotics +/- oral corticosteroids

Severe Requires hospitalization or ER visit

Change in mental status: most important sign
Some managed as ARF

Management Remarks

Bronchodilators Initial: SABA +/- SAMA

Frequency depends on severity of exacerbation
Maintainance LABA initiated before discharge

Antibiotics Evidence for patients with exacerbations and increased sputum purulence
Common bacteria implicated: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella
catarrhalis
Duration: 5-7 days
Procalcitonin-guided treatment may reduce antibiotic exposure and side effects with same clinical
efficacy

Glucocorticoids Reduces hospital stay, hastens delivery, reduces chances of subsequent exacerbations, improves
oxygenation
Most common acute complication: hyperglycemia

Oxygen Maintain O2 sats 88-92%

Does not reduce minute ventilation

Indications for Ventilatory Support

Non-Invasive Ventilation Invasive Mechanical Ventilation

Selection Criteria Indications

● Severe dyspnea with use of accessory muscles and ● Unable to tolerate NIV or NIV failure
paradoxical abdominal motion ● Respiratory or cardiac arrest
● Respiratory acidosis (pH 7.35 and less) and/or ● Somnolence, impaired mental status
hypercapnia (PaCO2 >45) ● Massive aspiration or persistent vomiting
● Progressive hypoxemia despite supplemental ● Persistent inability to remove respiratory secretions
oxygen ● Severe hemodynamic instability without response to
fluids and vasoactive drugs
Exclusion Criteria (presence of any of the following) ● Severe ventricular or supraventricular arrhythmias
● Respiratory arrest ● Life-threatening hypoxemia in those unable to
● Cardiovascular instability tolerate NIV
● Change in mental status; uncooperative
● High aspiration risk
● Viscous or copious secretions
● Recent facial or gastroesophageal surgery
● Craniofacial trauma
● Fixed nasopharyngeal abnormalities
● Burns
● Extreme obesity

Admitting Orders
● Admit to:
○ Ward
○ ICU, if:
■ Severe dyspnea not responding to meds
■ Change in sensorium
■ Persistent worsening hypoxemia (PaO2 <40; normal is 60-100)
■ Severe or worsening respiratory acidosis (pH < 7.25)

50
 ■ Need for mechanical ventilation
■ Hymodynamic instability (requiring pressors)
● Diet:
○ DAT with SAP
○ NPO if dyspneic or with decreased sensorium
● IVF: 1L PNSS x 16h
● O2: Face mask/ nasal cannula/ invasive or non-invasive mechanical ventilation, maintain sats of 90% +
● Monitor
○ VSQ1 with temp
○ I/O q-shift and record
○ CBG q-shift (glucocorticoids can cause hyperglycemia)
● Dx:
○ CBC
○ ABG
○ CXR
○ Sputum GSCS
○ Sputum AFB x 2
○ Spirometry once stable
○ Procalcitonin
● Tx:
○ Salbutamol + ipratropium neb Q6 RTC
○ Prednisone 40mg/tab OD x 5-7 days
○ Ceftriaxone + Azithromycin
○ Paracetamol 500mg/tab 1 tab Q4 PRN for fever
○ N-acetylcysteine 600mg/tab ½ tab in 1 glass H2O BID
● Referrals: Pulmo

Discharge Criteria
● Inhaled beta-agonist use no more frequent than every 4 hours
● Patient is able to walk across room
● Patient is able to eat and sleep without frequent awakening by dyspnea
● Patient has been clinically stable for 12-24 hours
● ABG has been stable for 12-24 hours
● Patient (or home caregiver) fully understands the use of medications
● Follow-up plans and home care arrangements have been completed, follow up <30 days after discharge

References
● GOLD 2018
● Harrison’s 20th ed
● IM Platinum 2018

51
 PULMONARY TUBERCULOSIS

Ysabel Regina Ortiz

MUST-KNOWS

● Etiology: Mycobacterium tuberculosis

○ Rod-shaped bacilli, highly aerobic, non-spore-forming, non-motile
○ Resistant to desiccation due to cell wall being rich in lipids and mycolic acid
○ Visualized in:
■ acid-fast stains i.e. Ziehl-Neelsen stain (bright red)
■ fluorescence stains i.e. auramine-rhodamine stain (reddish-yellow)
○ Forms caseating granulomas in tissue, which contain Langhans giant cells (horseshoe-shaped nuclei)

● Pathophysiology:
○ Most common site for development is the lungs
○ Sputum-smear positive cases, especially those with cavitary lesions or laryngeal TB, are the most likely to transmit
infection
○ Infectious droplet nuclei are aerosolized by coughing, sneezing, or speaking (~ 3000 infectious nuclei / cough) → droplets
remain suspended in air for several hours
○ On inhalation, 90% of bacilli are trapped in upper airways and expelled by ciliated mucosal cells while 10% reach the
alveoli
○ Naive unactivated alveolar macrophages phagocytose the bacilli, which multiply within the macrophages
○ 2-4 weeks after infection, 2 host responses develop:
1. Macrophage-activating response: T cell-mediated; macrophages kill and digest bacilli
2. Tissue-damaging response: delayed-type hypersensitivity reaction; unactivated macrophages that contain
multiplying bacilli are destroyed; causes caseous necrosis

● Definition of Terms:
○ Presumptive TB:
■ Any person who presents with sx or signs (radiologic findings) suggestive of TB
■ > 15 y/o and has any of the ff:
Cough of at least 2-weeks duration
Unexplained cough of any duration in a close contact of a known active TB case
CXR findings suggestive of PTB +/- sx
Any of the following sx: significant & unintentional weight loss, fever, hemoptysis, chest pain,
easy fatigability, malaise, night sweats, shortness of breath, DOB (weak recommendation)
○ TB exposure:
■ Individual in close contact with active adult TB case, but (-) s/sx, (-) TST, (-) lab findings suggestive of TB
○ Latent TB infection:
■ (+) TST, (-) s/sx, (-) radiographic findings, (-) lab findings suggestive of TB
○ Bacteriologically confirmed case of TB:
■ Specimen is (+) by smear microscopy, culture, or WHO-approved rapid diagnostic test (Xpert MTB / Rif)
○ Clinically diagnosed case of TB:
■ Does not fulfill criteria for bacteriologically confirmed TB but has been diagnosed with active TB by a clinician who
has decided to give the patient a full course of TB treatment (based on imaging, histology, extrapulmonary cases
w/o lab confirmation)
○ Pulmonary TB:
■ Bacteriologically or clinically confirmed TB case involving lung parenchyma or tracheobronchial tree
○ Extra-pulmonary TB:
■ Bacteriologically or clinically confirmed TB case involving organs other than the lungs, e.g. abdomen, genitourinary
tract, joints and bones, lymph nodes, meninges, pleura, skin
○ Primary TB:
■ Occurs soon after initial infection with tubercle bacilli
■ Often seen in children due to immature cell-mediated immunity
■ Associated with formation of a Ghon focus
○ Postprimary / Adult-Type TB
■ May result from endogenous reactivation of distant LTBI or recent infection

52
 ■ Localized to apical and posterior segments of upper lobes, where higher mean oxygen tension favors mycobacterial
growth

● Classifications

I. Based on Anatomical Site and Bacteriologic Status

Anatomical Site Bacteriological Status Definition

Pulmonary TB Bacteriologically confirmed Smear-positive At least 1 of 2 sputum specimens (+)

for AFB +/- radiographic abnormalities

Culture-positive (+) sputum culture +/- radiographic

abnormalities

Rapid (+) sputum for MTB using Xpert MTB /

Diagnostic Test- Rif +/- radiographic abnormalities
positive

Clinically diagnosed > 2 sputum specimens AFB (-) but w/ radiologic evidence
consistent with active TB, no response to empiric
antibiotics and symptomatic meds, and physician has
decided to treat as TB
> Px w/ strong evidence for HIV/AIDS w/ 2 AFB (-) sputum
specimens, and physician has decided to treat as TB

Extrapulmonary Bacteriologically confirmed Smear / culture / rapid diagnostic test from extrapulmonary
TB site is AFB (+)

Clinically diagnosed Px w/ histological, clinical, or radiologic evidence

consistent w/ active EPTB, and physician has decided to
treat as TB

II. Based on History of Previous Treatment

Classification Definition

New Case Never had tx for TB or has taken anti-TB meds for < 1 month

Retreatment Case Previously treated w/ anti-TB meds for at least 1 month

Relapse Declared cured or has completed treatment and is now bacteriologically /

clinically diagnosed TB

Treatment After Failure Failed tx at the end of the most recent course:
> sputum smear / culture (+) at 5 months or later during tx
> clinically diagnosed without any clinical improvement throughout

Treatment After Lost to Follow-up Lost to ff/up for at least 2 months; now bacteriologically / clinically
(TALF) diagnosed TB

Previous Treatment Outcome Outcome not known / documented

Unknown (PTOU)

Other

III. Based on Drug-Susceptibility Testing

53
 Classification Remarks

Monoresistant Resistance to only 1 first line anti-TB drug

Polydrug-resistant Resistance to more than 1 first-line anti-TB drug (other than both isoniazid and
rifampicin)

Multi-drug resistant (MDR-TB) Resistance to at least both isoniazid and rifampicin

Extensively drug-resistant TB Resistance to any fluoroquinolone and to at least one of 3 2nd line injectable
(XDR-TB) drugs (capreomycin, kanamycin, amikacin) in addition to multidrug resistance

Rifampicin-resistant TB (RR- Resistance to rifampicin +/- resistance to other anti-TB drugs

TB)

● Complications
○ Can cause persistent pulmonary damage even after being considered “cured”
○ Chronic impairment of lung function
○ Bronchiectasis
○ Aspergilloma
○ Chronic pulmonary aspergillosis
■ Large residual cavities from TB can be colonized by Aspergillus fumigatus
○ Responsible for 20-25% of all HIV-related mortality

SUBJECTIVE
● Presentation
○ Cough of at least 2 weeks duration
■ Often initially nonproductive and limited to the morning
■ Subsequently with purulent sputum
■ Hemoptysis in 20-30% of cases (usually secondary to erosion of BV in cavity wall)
○ Diurnal fever
○ Night sweats due to defervescence
○ Weight loss
○ Anorexia
○ General malaise
○ Weakness
○ Pleuritic chest pain
● Pertinent History
○ Close contact with adults that have PTB → family, friends, co-workers
○ Previous TB infection, duration of treatment, and if patient was declared cured

OBJECTIVE
● Physical findings of limited use in PTB
● May have rhonchi due to partial bronchial obstruction
● Low-grade, intermittent fever (absence does not exclude TB)
● Wasting
● Pallor and finger clubbing

Note:
In EPTB, history and physical examination depend on which organs are affected. In descending order of frequency, the
extrapulmonary sites most commonly involved in TB are the lymph nodes, pleura, genitourinary tract, bones and joints, meninges,
peritoneum, and pericardium. For this reviewer, we will still discuss them but not in depth because they can be used as differentials
for other disease entities.

54
Extrapulmonary TB

TB lymphadenitis Painless swelling of the lymph nodes, most commonly at posterior cervical and
supraclavicular sites

Pleural TB May be small and asymptomatic or large enough to cause fever, pleuritic chest pain, and
dyspnea
Pleural effusion on PE: dullness to percussion and absence of breath sounds

Genitourinary TB Urinary frequency, dysuria, nocturia, hematuria, and flank or abdominal pain

Skeletal TB Pain and swelling in weight-bearing joints (spine: 40%, hips: 13%, knees: 10%)
Gibbus: collapse of vertebral bodies resulting in kyphosis

TB Meningitis and Tuberculoma Headache, altered mental status, low-grade fever, malaise, anorexia, neck rigidity, paresis
of cranial nerves

Gastrointestinal TB Abdominal pain, swelling, obstruction, hematochezia, palpable mass in abdomen

Pericardial TB Dyspnea, fever, dull, retrosternal pain, pericardial friction rub

Miliary TB From hematogenous spread of tubercle bacilli; yellowish granulomas 1 - 2 mm that

resemble millet seeds; fever, night sweats, anorexia, weakness, weight loss,
hepatomegaly, splenomegaly, lymphadenopathy

ASSESSMENT
Differentials for prolonged cough

Differentials Rule In Rule Out

Pulmonary tuberculosis Cough of at least 2 weeks duration,

unintentional weight loss, night sweats,
intermittent fever, easy fatigability, DOB,
hemoptysis, adventitious breath sounds
in apical lung fields

Community-acquired pneumonia Cough, fever, DOB Adventitious breath sounds (e.g.

crackles) usually in lower lung fields,
tachypnea, tachycardia

Cough-variant asthma Non-productive Associated with a trigger, does not

usually present with weight loss / night
sweats / fever, (+) expiratory wheeze,
usually with family history of atopy

COPD Chronic productive cough, DOB Smoking history, exertional dyspnea, +/-
wheezing, central cyanosis

Lung cancer Chronic cough, unintentional weight loss, Chest pain, persistent / recurrent
hemoptysis, easy fatigability infection

Heart failure Productive cough, DOB, easy fatigability Orthopnea, PND, bilateral crackles in
lower lung fields, +/- murmurs, +/-
displaced apex beat, edema

GERD Cough Retrosternal burning sensation,

regurgitation, dysphagia, chest pain,
globus sensation, odynophagia

Interstitial lung disease Non-productive cough Progressive breathlessness, history

occupational exposure to asbestos /
silicon, with concomitant connective
tissue disease

55
PLAN
Diagnostics
Direct Sputum Smear Microscopy
(DSSM)
Rapid Molecular Diagnostic Tests (Xpert
MTB / Rif Assay)
TB Culture and Drug Susceptibility Test
Tuberculin Skin Test (TST)
Chest Radiography
ALT
Serum creatinine
HIV Testing
Rationale Expected Findings
Primary diagnostic method for a At least 1 sputum smear positive =
definitive diagnosis of active TB bacteriologically confirmed
Can be used to monitor progress of
patients during treatment and confirm
cure at the end
Gene Xpert testing for the presence of
Mycobacterium tuberculosis and
rifampicin resistance
Recommended for:
> smear-negative adults w/ CXR findings
suggestive of TB
> presumptive drug-resistant TB
> HIV (+) patients with TB manifestations
Gold standard for TB diagnosis
Not routinely performed among new
cases of PTB
Recommended for:
> all smear-negative TB symptomatic
pxs at risk for drug resistance
> all cases of retreatment, treatment
failure, MDR suspects, known contacts
of MDR-TB
Screening tool for TB infection in children Size of reaction measured by width of
and LTBI induration, not erythema
< 5 mm: (+) if with HIV infection + close
contact of active contagious case
≥ 5 mm: (+) if with HIV infection, close
contact of active contagious case,
abnormal CXR with fibrotic changes,
immunosuppressed
≥ 10 mm: (+) in pxs with clinical
conditions that inc. risk of reactivation
(silicosis, chronic renal failure, DM,
malignancies, underweight, injection
drug users), < 4 y/o, foreign born,
residents and employees in high-risk
settings (prison, jail, healthcare facilities)
≥ 15 mm: (+) healthy individuals ≥ 4 y/o
Recommended for all smear-negative No radiographic findings considered
presumptive PTB patients specific for active TB
To determine baseline liver function; H,R
and Z are hepatotoxic; drug-induced
hepatitis is the most serious and
common adverse effect of first line anti-
TB meds
To determine baseline kidney function;
AKI is a rare and severe complication
Key intervention for reducing burden of
HIV-associated TB; HIV status also
alters TB treatment
56
 FBS DM increases the risk of TB 3x; poor
glycemic control increases risk of poorer
outcomes in pxs with TB

Major & Minor Side Effects of Anti-TB Drugs

Drug Minor Side Effects Management Major Side Effects Management

Isoniazid (H) > Peripheral neuropathy > Pyridoxine (Vit. B6) > Psychosis and convulsion
> Drowsiness > Reassure and give > Jaundice due to hepatitis
drug at bedtime
> Anorexia, nausea, abd. > Give drug with small
pain meals / at bedtime Discontinue
taking the
Rifampicin (R) > Red-orange urine > Reassure > Thrombocytopenia, medications and
> Flu-like sx > Paracetamol anemia, shock refer
> Anorexia, nausea, abd. > Give drug with small > Decreased urine output
pain meals / at bedtime > Jaundice due to hepatitis

Pyrazinamide (Z) > Joint pains from > Aspirin / NSAID > Jaundice due to hepatitis
hyperuricemia > Give drug with small
> Anorexia, nausea, abd. meals / at bedtime
pain

Ethambutol (E) > Visual impairment (optic

neuritis)

Streptomycin (S) > Deafness, tinnitus, and

dizziness
> Decreased urine output
> Severe skin rash

57
Treatment Regimen for Tuberculosis

Treatment Regimen
Category Classification
Initial Phase Continuation Phase

I New PTB 2 HRZE 4 HR

New EPTB, except CNS and bones or joints

Ia New EPTB (CNS / bones or joints) 2 HRZE 10 HR

II Previously-treated drug-susceptible PTB or 2 HRZES and 1 HRZE 5 HRE

EPTB, except CNS / bones or joints

IIa Previously-treated drug-susceptible EPTB in 2 HRZES and1 HRZE 9 HRE

CNS / bones or joints

Drug- Individualized based on previous treatment courses and drug

resistant TB sensitivity testing

Note:
● Intensive phase: majority of tubercle bacilli are killed, symptoms resolve, and usually the patient becomes noninfectious
● Continuation phase: for elimination of persisting bacteria and prevention of relapse

Treatment Outcomes

Outcome Definition

Cured Bacteriologically-confirmed TB patient (sputum-positive at the beginning of treatment) and

is smear- or culture- negative in the last month of treatment and on at least 1 previous
occasion in the continuation phase

Treatment Completed Px completes tx, but does not meet the criteria of “cured” or “failure”; includes:
> bacteriologically confirmed, completed tx, but no DSSM follow-up in last month of tx and
on at least 1 previous occasion
> clinically diagnosed who has completed tx

Treatment Failed Bacteriologically-confirmed, sputum smear (+) at 5 months or later during the tx OR
Clinically-diagnosed, sputum examination cannot be done, does not show clinical
improvement during tx

Treatment Success “Cured” and “treatment completed”

Died Px who dies for any reason during course of tx

Lost to Follow-Up Px whose tx was interrupted for ≥ 2 consecutive months

Not Evaluated No treatment outcome assigned; includes pxs transferred to another tx facility w/ outcome
unknown

Treatment Goals:
1) Prevent morbidity and death by curing TB while preventing the emergence of drug resistance
2) Interrupt transmission by rendering patients non-infectious to others

ADMITTING ORDERS
*Pulmonary tuberculosis patients generally do not require admission, unless with unstable vital signs or unstable co-morbidities

● Diagnostics:
Sputum AFB x 2
- Spot-spot strategy: collect 1st specimen at time of 1st consultation, then collect 2nd specimen after 1 hour or
the following morning
- Ideally collected through spontaneous expectoration

58
 - Sputum induction should be done for individuals who are unable to expectorate (15-20 mins nebulization with 5
ml 2.5-5% hypertonic saline)
CXR-PAL, apicolordotic
ALT, serum creatinine
ICC Elisa
FBS
*TB culture and sensitivity - for retreatment cases, treatment failure, and contacts of known drug-resistant TB cases
*Xpert MTB/Rif - for smear-negative presumptive TB cases with radiologic findings suggestive of PTB; for presumptive
drug-resistant TB

● Therapeutics:
*Single-drug formulations are useful for 1) those at risk for adverse reactions (elderly, liver disease) 2) those with co-morbid
conditions requiring dose adjustments (liver or kidney disease) or expected to have significant drug interactions (HIV, DM)
*Daily regimen is recommended for TB tx especially if fixed dose combination (FDC) drugs are used

59
● Refer to TB-DOTS (directly observed therapy, short course)
● Screen household contacts of active TB Cases for disease activity
● Patient education
- Covering one’s mouth when coughing to minimize spread of potentially infectious aerosols
- Use of surgical face masks until deemed non-infectious
- Lifestyle modifications (smokers, alcoholics, and underweight individuals have slightly inc. risk of contracting TB)
● Monitoring
- See table below: “Monitoring Response to Treatment Using Follow-Up DSSM”
- All PTB and EPTB patients should also be monitored clinically using body weight

Monitoring Response to Treatment Using Follow-Up DSSM

Category Follow-up Schedule for DSSM Remarks

I 2-HRZE Get 1st DSSM at end of intensive phase (2nd > If sputum (+) after 2nd month, proceed with
4-HR month) continuation phase and repeat DSSM at end of
3rd month.
> If still sputum (+) after 3rd month, refer to
PMDT or Xpert MTB/RIF site for testing

Get 2nd DSSM at end of 5th month > If sputum (+) after 5th month, classify px as
“treatment failed” and refer to PMDT or Xpert
MTB/RIF site for testing

Get 3rd DSSM at end of treatment (6th month) > If sputum (+) at end of treatment, classify px as
“treatment failed” and refer to PMDT or Xpert
MTB/RIF site for testing

II 2-HRZES Get 1st DSSM at end of intensive phase (3rd If sputum (+) at end of intensive phase, refer to
1 HRZE month) PMDT
5 HRE
Get 2nd DSSM at end of 5th month If sputum (+) after 5th month, classify as
“treatment failed” and refer to PMDT or Xpert
MTB/RIF site for testing

Get 3rd DSSM at end of treatment (8th month) If sputum (+) after treatment, classify as
“treatment failed” and refer to PMDT or Xpert
MTB/RIF site for testing

● Isolation is recommended for:

1) Bacteriologically confirmed PTB cases who have not started or are in the early stages of anti-TB treatment (including
EPTB cases with potential for aerosol generation)
2) Presumptive DR-TB or known MDR / XDR-TB cases

References
Clinical Practice Guidelines for the Diagnosis, Treatment, Prevention and Control of TUberculosis in Adult Filipinos 2016 Update
Harrisons Principles of Internal Medicine 20th Ed
IM Platinum

60
 COMMUNITY ACQUIRED PNEUMONIA with PLEURAL EFFUSION

Jeffrey Paolo M. Nuñez

Must-Knows

● Definition
○ Lower respiratory tract infection (pulmonary parenchyma) acquired in the community within 24 hours to less than 2 weeks
● Etiology
○ Results from the proliferation of microbial pathogens at the alveolar level and the host’s response to those pathogens
○ Most common access of microorganisms to the lower respiratory tract is through aspiration from the oropharynx
○ CAP-LR potential pathogens
■ Streptococus pneumoniae
■ Haemophilus influenzae
■ Chlamydophila pneumoniae
■ Mycoplasma pneumoniae
■ Moraxella catarrhalis
■ Enteric Gram-negative bacilli (among those with co-morbid illness)
○ CAP-MR potential pathogens
■ Streptococcus pneumoniae
■ Haemophilus influenzae
■ Chlamydophila pneumoniae
■ Mycoplasma pneumoniae
■ Moraxella catarrhalis
■ Enteric Gram-negative bacilli
■ Legionella pneumophila
■ Anaerobes (among those with risk of aspiration)
○ CAP-HR potential pathogens
■ Streptococcus pneumoniae
■ Haempophilus influenzae
■ Chlamydophila pneumoniae
■ Mycoplasma pneumoniae
■ Moraxella catarrhalis
■ Enteric Gram-negative bacilli
■ Legionalla pneuomophila
■ Anaerobes (among those with risk of aspiration)
■ Staphylococcus aureus
■ Pseudomonas aeruginosa
● Pathophysiology
○ Classic pneumonia (lobar pneumococcal pneumonia) evolves through a series of changes

PHASE DESCRIPTION

Edema Initial phase with the presence of a proteinaceous exudate, and often of
bacteria in the alveoli

Red hepatization Presence of erythrocytes in the cellular intraalveolar exudate

Neutrophil influx is more important from the standpoint of host defense
Bacteria are occasionally seen in pathologic specimens

Gray hepatization No new erythrocytes are extravasating and those already present have
been lysed and degraded
The neutrophil is the predominant cell, fibrin deposition in abundant, and
bacteria have disappeared
Corresponds with successful containment of the infection and
improvement in gas exchange

Resolution (final phase) Macrophage reappears as the dominant cell type in the alveolar space,
and the debris of neutrophils, bacteria, and fibrin has been cleared, as
has the inflammatory response

61
● Classification

Low-Risk CAP Moderate-Risk CAP High-Risk CAP

Vital Signs Stable Unstable

● RR <30 cpm
● PR <125 bpm
● Temp 36-40C
● BP ≥ 90/60
Features ● No altered mental state ●
of acute onset
● No suspected aspiration ●
● No or stable comorbids ●
Chest X-ray ● Localized infiltrates
● No pleural effusion
● No abscess
● RR ≥ 30 cpm
● PR ≥ 125 bpm
● Temp ≥ 40C or ≤ 36C
● BP < 90/60
Any of the criteria under CAP-
MR, PLUS any of the
Altered mental state of acute following:
onset ● Severe sepsis and
Suspected aspiration septic shock
Decompensated comorbids ● Need for
mechanical
● Multilobar infiltrates ventilation
● Pleural effusion
● Abscess

Disposition ● Outpatient ● Ward admission ● ICU admission

*Decompensated comorbidities: Uncontrolled diabetes mellitus, active malignancies, neurologic disease in
evolution, congestive heart failure (CHF FC II-IV), unstable coronary artery disease, renal failure on dialysis,
uncompensated COPD, decompensated liver disease

● Complications

Pleural Effusion
❖ Etiopathogenesis
Collection of fluid abnormally present in the pleural space due to either excess fluid production and or decreased lymphatic
absorption
Most common cause of pleural effusion is left ventricular failure
General classification
■ Transudative effusion: occurs when systematic factors that influence and absorption of pleural fluid are altered
■ Exudative effusion: occurs when local factors that influence the formation and absorption of pleural fluid are altered
❖ Clinical manifestations
Patients may present with pleuritic pain, cough, dyspnea
PE findings include decreased breath sounds with decreased or absent tactile fremitus dullness on percussion
Tracheal deviation and pleural rub may also be noted
❖ Diagnosis
First step: determine if effusion is exudative or transudative by using Light’s criteria:
■ Exudative pleural effusions meet at least one of the following criteria:
● Pleural fluid protein/ serum protein >0.5
● Pleural fluid LDH/ serum LDH >0.6
● Pleural fluid LDH more than ⅔ normal upper limit for serum
Other diagnostics for exudative pleural effusions
■ Description of the appearance of the fluid
■ Glucose and protein level
■ Differential cell count
■ Microbiologic studies and cytology
■ Work up for PTB

Etiology Remarks

Transudative pleural effusions

Effusion due to heart failure ● Most common cause of pleural effusion

● Diagnostic thoracentesis should be performed to
verify if the patient has transudative effusion if:
○ Effusions are not bilateral

62
 ○ Patient is febrile
○ Patient has pleuritic chest pain
● Pleural fluid NT-proBNP >1500 pg/mL is virtually
diagnostic of heart failure

Cirrhosis ● Usually on the right side (passage of fluid from

abdomen through diaphragm)

Other transudative Effusions ● Nephrotic syndrome due to hypoalbuminemia

● Myxedema
● Atelectasis
● Urinothorax
● Pulmonary embolism

Exudative Pleural effusions

Parapneumonic effusion ● Most common cause of exudative pleural effusion in

the US
● Presents with acute febrile illness. Sputum
production and leukocytosis
● If free fluid separates lung from chest wall by
>10mm, a therapeutic thoracentesis should be
performed
● More invasive procedure is indicated if:
○ Loculated pleural fluid
○ Pleural fluid pH <7.2
○ Peural fluid glucose <3.3 mmol/L
○ Positive gram stain or culture of pleural
fluid
○ Gross pus in pleural space

Effusion secondary to malignancy ● Lung Ca, breast Ca, lymphoma

● Glucose levels may be low if tumor burden is high

Effusion secondary to pulmonary embolism ● Most commonly overlooked in the differential

diagnosis of a patient with undiagnosed pleural
effusion

Tuberculous pleuritis ● Most common cause of exudative pleural effusion in

the other parts of the world
● Associated with primary TB
● Predominantly small lymphocytes
● Diagnosed by high levels of adenosine deaminase
(>40 IU/L) or interferon gamma (>140 pg/mL)

Hemothorax ● Hematocrit should be obtained on the pleural fluid if

initial tap reveals bloody pleural fluid
● Hct > ½ of peripheral blood, consider hemothorax
and CTT must be done
● If pleural hemorrhage >200mL/h, consider
thoracoscopy or thoracotomy

Subjective
● Presentation (signs and symptoms)
○ Commonly presents with acute cough, abnormal vital signs of tachypnea, tachycardia, & fever with at least one abnormal
chest finding of diminished breath sounds, ronchi, crackles or wheeze
● Predisposing Factors (usual past medical / family / social history)
○ Comorbid conditions: Asthma, COPD, smoking, and compromised immune system) are risk factors for H. influenzae
infection
○ Previous surgeries, especially if symptoms are of new-onset presenting during admission at a hospital
○ Exposure to family members or community members with CAP

Objective

63
● Signs and Symptoms (General)
○ Signs: Cough, fever, tachycardia, tachypnea, fever
○ Rales heard over the involved lobe or segment
○ Increased tactile fremitus, bronchial breath sounds, and egophony may be present if consolidation has occurred.
○ Decreased tactile fremitus and dullness on chest percussion may result from parapneumonic effusion or empyema.
● For stratification of CAP: Refer to Classification

Assessment

Differentials Rule In Rule Out

HAP

Tuberculosis

COPD

Asthma

Malignancy

Plan

Diagnostics Rationale Expected Findings

CXR ● Essential in the diagnosis of CAP, Chest radiography findings may be

assessing severity, differentiating
pneumonia from other conditions and in
prognostication
● Best radiologic evaluation consists of
standing PA and lateral views of the chest
● Does not predict the likely etiologic agent
negative in patients who present very
early with CAP. In these patients, repeat
chest radiography within 24 hours is
recommended
Viral pneumonias tend to display few or
no infiltrates on chest radiography, but,
when infiltrates are present, they are
almost always bilateral, perihilar,
symmetric, and interstitial.

Bacterial pneumonias have a

predominantly focal segmental or lobar
distribution, with or without pleural
effusions. Atypical bacterial pathogens
have variable radiographic findings,
ranging from focal segmental to bilateral
interstitial disease.

CBC ● Determination of infection Expect neutrophilic predominance with

increased WBC in the background of
CAP

Sputum GSCS ● Optional in low risk CAP, necessary for

moderate and high risk CAP
● Strongly influenced by the quality of
collection, transport, and processing
● Main purpose of gram stain is to ensure
that a sample is suitable for culture
○ >25 neutrophils/lpf
○ <10 squamous epithelial cells/lpf

Blood CS ● Optional in low risk CAP, necessary for S pneumoniae and H influenzae, are
moderate and high risk CAP frequently associated with positive blood
cultures

Sputum AFB ● Important to rule out PTB, especially in a No AFB seen

64
 country like ours where there’s high
prevalence rate.

● Treatment

65
Admitting Orders
● Admit to Ward (if CAP-MR), ICU (if CAP-HR)
● Diet: DAT with SAP
● IVF: HL
● Laboratories
○ Chest X-ray
○ CBC
○ Creatinine
○ Blood CS
○ Sputum GSCS
○ Sputum AFB
● Medications
○ Refer to table above
● Others
○ CURB-65 (predicts mortality of CAP)
■ confusion, urea, respiratory rate, blood pressure, 65 years of age or older; one point for each feature present: 0-1 low
severity (risk of death <3%), 2 moderate severity (risk of death 9%), and 3-5 high severity (risk of death 15-40%)
○ Response to therapy is expected within 24-72 hours of initiating treatment
■ Monitor temperature, RR, HR, BP, sensorium oxygen saturation, and inspired oxygen concentration
■ Responded if:
● Fever decreases within 72 hours
● Temperature normalizes within 5 days
● Respiratory signs (tachypnea) return to normal
○ De-escalation of antibiotic therapy once patient is improving, stable, and has a functioning GI tract:
■ Resolution of fever for more than 24 hours
■ Less cough and resolution of respiratory distress (normalization of respiratory rate)
■ Improving white blood cell count, no bacteremia
■ Etiologic agent is not a high-risk (virulent/resistant pathogen) (e.g., Legionella, S. aureus, or Gram-negative enteric
bacilli)
■ No unstable comorbid condition or life-threatening complication such as myocardial infarction, congestive heart failure,
complete heart block, new atrial fibrillation, supraventricular tachycardia, etc.

66
 ■ No sign of organ dysfunction such as hypotension, acute mental changes, BUN to creatinine ratio of >10:1, hypoxemia,
and metabolic acidosis
■ Patient is clinically hydrated, taking oral fluids and is able to take medications
○ Duration of Treatment
■ Most bacterial pneumonias: 5-7 days
■ Enteric Gram-negative pathogens, S. aureus, and P. aeruginosa: 14 days
■ Mycoplasma and Chlamydophila: 10-14 days
■ Legionella: 14-21 days
○ Failure to improve after 72 hours of treatment is an indication for reassessment
■ Incorrect diagnosis or presence of a complicating noninfectious condition (pulmonary embolism, congestive heart
failure, vasculitis, myocardial infarction)
■ Resistant microorganism or an unexpected pathogen that is not covered by the antibiotic of choice
■ Antibiotic is ineffective or causing an allergic reaction
■ Impaired local or systemic host defenses (aspiration, endobronchial obstruction, bronchiectasis)
■ Local or distant complications of pneumonia (parapneumonic effusion, empyema, lung abscess, ARDS, metastatic
infection, endocarditis)
■ Overwhelming infection
■ Slow response in the elderly patient (S. pneumoniae and L. pneumophila)
■ Exacerbation of a comorbid illness
■ Nosocomial superinfection
○ Hospital discharge
■ In the absence of any unstable comorbid condition or complication, the patient may be discharged once clinical stability
occurs and oral therapy is initiated
■ During 24 hours before discharge, patient should have:
● T 36-37.5 degrees Celsius
● Pulse < 100/min
● RR 16-24/min
● SBP > 90mmHg
● O2 sat > 90%
● Functioning GI tract
■ Repeat chest X-ray is not necessary in patients who are clinically improving, but
■ are recommended during a follow-up visit 4-6 weeks after discharge

References
● Harrison’s 20th edition
● IM Platinum
● Expanded medicine bluebook
● PCCP CAP CPG

67
 CHRONIC KIDNEY DISEASE

Jan Nidoy

ETIOLOGY
Encompasses a spectrum of different pathophysiologic processes associated with abnormal kidney function and progressive decline
in glomerular filtration rate (GFR).

In recently updated classification, stages of CKD are stratified by both estimated GFR and degree of albuminuria in order to predict
risk of progression of CKD

The term “end stage renal disease” represents a stage of CKD where the accumulation of toxins, fluid, electrolytes, normally
excreted by the kidneys results in uremic syndrome, which can lead to death if not removed by renal replacement therapy using
dialysis or kidney transplant. There is marked disturbance in the activities of daily loving, well-being, nutritional status, and water and
electrolyte homeostasis.

KDIGO (Kidney Disease Improving Global Outcome) Definition of CKD

- Abnormalities of kidney structure/function, present for more than 3 months with implications for health.

68
LEADING ETIOLOGIES: Diabetic Nephropathy, Glomerulonephritis, Hypertension associated CKD ( vascular and ischemic)

Criteria for CKD( either of the following present for more than 3 months)

> Albuminuria
Urinary albumin excretion rate (AER) >/= 30 mg/24H
Urinary albumin to creatinine ratio (ACR) >/= 30 mg/g ( or
Markers of Kidney damage 3 mg/mmol)

> Urine sediment and abnormalities

> Electrolyte and other abnormalities due to tubular disorders
> Abnormalities detected by histology
>Structural abnormalities detected by imaging
> History of kidney transplantation

Decreased GFR GFR <60 mL/min/1.73 m2 ( G3A-G5)

OLD STAGING OF CKD (KDOQI)

PATHOPHYSIOLOGY

2 MECHANISMS:
1. Initiated by underlying etiology
2. Progressive mechanisms involving hypofiltration and hypertrophy of remaining viable nephrons.

69
RISK FACTORS

1. Small for gestational age birth weight

2. Childhood obesity
3. Hypertension
4. DM
5. Auto-immune disease
6. Advanced age
7. African ancestry
8. Family history of kidney disease
9. Previous episode of AKI
10. Presence of proteinuria, urinary sediments, or structural abnormalities of urinary tract
11. Inherited forms of CKD- Polycystic Kidney disease

CKD Progression

Regardless of etiology, CKD will eventually progress to ESRD. CKD progression is usually defined as progressively declining eGFR
and progressively increasing albuminuria.

> Decline in GFR category ( ex G1 to G2), accompanied by >/= 25% drop in eGFR from baseline

> Rapid progression: sustained decline >5 mL/min/1.73m2

● The normal peak of GFR is 120 mL/min/1.73 m2 at third decade of life

● Factors affecting the likelihood and rate of CKD progression:
○ Baseline eGFR and degree of albuminuria
○ Primary renal disease
○ Ongoing exposure to nephrotoxic agents
○ Others: obesity, hypertension, age, ethnicity, and laboratory parameters

70
ANNUAL DECLINE IN GFR (ml/min/1.73m2)

SEX Normal Annual Decline in Annual decline in GFR in Annual decline in GFR when
GFR after peak GFR Diabetics Baseline eGFR <30

MALE 0.8 per yr 2.1 per yr 1.8 per yr

FEMALE 1.4 per yr 2.7 per yr 2.0 per yr

CLINICAL MANIFESTATIONS

SYSTEMIC FINDINGS

1. Hypertension and peripheral edema- due to modest increase in total body content of sodium and water.
2. Hyperkalemia- due to decline in urinary K excretion, leading to K retention. Precipitated by increased dietary K intake,,
protein catabolism, hemolysis, hemorrhage, transfusion of RBC, metabolic acidosis, medications ( RAAS inhibitors,
spironolactone, NSAIDS). HYPOKALEMIA is uncommon
3. Metabolic acidosis- common in CKD due to disturbance in ammoniagenesis, leading to impaired excretion of protons.
NAGMA in early stages, HAGMA in late stages.
4. Osteitis fibrosa cystica- classic lesion of secondary hyperPTH. High bone turnover with increased PTH levels.
5. Osteomalacia and adynamic bone disease- low bone turnover with normal or low PTH levels. FGF-23- phosphatonin
produced by osteocytes which promotes phosphate excretion
6. Calciphylaxis- Almost exclusive to advanced CKD. Calcific Uremic Arteriolopathy. LIVEDO RETICULARIS- patches of
ischemic necrosis especially on legs, thighs, abdomen, and breasts (warfarin treatment is a risk factor for its
development)
7. Cardiovascular abnormalities- leading cause of morbidity and mortality in CKD patients
● Ischemic vascular dse
● Heart failure
● LVH and dilated cardiomyopathy
● Chest pain, friction rub- pericarditis seen in advanced uremia
● UREMIC PERICARDITIS- absolute indication for urgent dialysis (heparin free)
8. Anemia- Normocytic, normochromic observed as early as CKD 3 and universal in CKD 4. Caused by EPO deficiency,
diminished RBC survival, bleeding diathesis, iron deficiency, hyperPTH, chronic inflammation, folate or vit b 12 deficiency,
hemoglobinopathy
9. Prolonged bleeding time- due to decreased factor 3 activity, abnormal platelet aggregation, and adhesion, impaired
prothrombin consumption. Greater susceptibility to thromboembolism especially if with nephrotic range proteinuria
10. Uremic fetor- urine like breath odor with dysguesia
11. Anorexia- due to retention of uremic toxins
12. Mild disturbance in memory, concentration, and sleep (early CKD). Hiccups, cramps, twitching, restless leg syndrome
(late)
13. Abnormal glucose metabolism
14. Sexual dysfunction
15. Pruritus, hyperpigmentation (due to urochromes)
16. Nephrogenic fibrosing dermopathy- progressive subcutaneous induration esp on the arms and legs with exposure to
gadolinium

AKI VS CKD

AKI CKD

Functional Criteria GFR <60 ml/min/1.73m2 for <3mos, or GFR <60 ml/min/1.73m2 for >3 mos
Decrease in GFR by >35% or inc in SCr
by >50% for <3mos

Kidney Damage Present < 3 mos Present > 3 mos

Kidney size Normal or large small , except in DM nephropathy, HIV

associated nephropathy, infiltrative

71
 disease
● Size discrepancy may be
present
● Loss of renal cortex (cortical
thinning)

DIFFERENTIAL DIAGNOSIS

DISEASE RULE IN RULE OUT

1. Ischemic nephropathy Usual history of uncontrolled HTN, UTZ-Asymmetric kidney size,

atherosclerotic disease. suggestive of renovascular dse causing
hypoperfusion or prob obstruction. (vs
Symptoms of Uremia, DOB bilateral small kidneys in CKD)
Signs: Oliguria, increasing Crea

2. Obstructive Uropathy Decreased UO may progress to increase Kidney UTZ shows hydronephrosis
Crea levels eventually to uremic and obstruction which is uncommon in
symptoms if left untreated. CKD

3. Nephrotic syndrome Presence of hypoalbuminemia, HTN HTN is sudden in onset. Kidney biopsy
and edema. Increase serum crea, and is needed to make a diagnosis.
proteinuria.

4. Glomerulonephritis Presence of HTN, edema, Increase Sudden onset HTN. UA showing

serum crea, and proteinuria. presence of casts is highly suggestive of
glomerulonephritis.

5. Heart Failure Dyspnea, SOB, fatigue, weakness, Cannot be totally ruled out. Can co-
edema.orthopnea, cough, HTN exist as Cardio-renal syndrome.

DIAGNOSTICS:
1. CBC- check for anemia, infection, thrombocytopenia
2. BUN/Crea- estimate eGFR
3. Electrolytes- to determine abnormalities from deranged renal function
4. 24 hr urine collection- standard for measuring albuminuria
5. Protein to crea ratio in spot first morning urine- more practical and correlates well with 24 hr urine collection
6. Microscopic hematuria with abnormal RBC morphology (anisocytosis)- GBM disorders
7. Renal UTZ- verifies 2 kidneys, determines symmetry, estimates size and rule out masses/obstruction. Finding of bilateral
small kidneys supports CKD except in early DM nephropathy, amyloidosis, HIV nephropathy, polycystic kidney disease
8. Renal biopsy- not advised for bilaterally small kidneys. Other contraindications; uncontrolled HTN, active UTI, bleeding
diathesis including ongoing anticoagulation, severe obesity

MANAGEMENT

Intervention and Goals in CKD

1. ACE inhibitors/ARBS- reduce intraglomerular HTN and proteinuria. Slows the progression of CKD
● Renoprotective doses
○ Losartan 100 mg OD
○ Candesartan 16 mg OD
○ Irbesartan 900 mg OD
○ Valsartan 320-640 mg OD
○ Lisinopril 40 mg OD
>CAUTION!!- may cause reversible hyperkalemia and AKI especialy in advanced CKD and renovascular HTP
2. Aim for weight loss of 5% if obese
3. Dietary salt restriction- <5 g/day (equivalent to 90 mEq Na/day)
4. Dietary protein restriction- avoid high protein intake >1.3 g/kg/day
5. Glycemic control- A1C <7.0%, FBS 90-130 mg/dL
6. Smoking cessation

72
 7. Lipid lowering therapy- total cholesterol < 200 mg/dl, LDL choles <100 mg/dl
8. Avoid and prevent AKI

Management of Uremic Symptoms

1. Loop diuretics +/- metolazone to maintain euvolemia. Intractable edema, HTN, hyperkalemia in advanced CKD are
indications for initiating dialysis
● GFR 20-50 mL/min- Furosemide 80-160 mg IVmor 160 mg PO, Bumetanide 6 mg IV or PO
● GFR <20 mL/min- Furo 200 mg IV or PO, bumetanide 10 mg IV or PO
2. hyperK- dietary K restriction. Use Kaliuretic diuretics, potassium binding resins to promote k loss through th GI tract
3. HypoCal- if asymptomatic- may give oral Ca. Otherwise, give IV calcium to target Ca 2.1-2.5 mmol/L. CALCIMIMETICS- ex
cinacalcet 30 mg OD, used in CKD 5 with heperparathyroidism. Calcitriol 0.25 mg BID and vit D analogs are not routinely
given.
4. HyperPhos- Low phosphate diet. Phosphate binding agents (ex Sevelamar)
5. NaHCO3 supplementation for met acidosis, may slow down CKD progression. Start when serum level is < 22 mmol/L
● Oral NaHCO3 0.5-1 meq/kg/day. Oral NaHCO3 650 mg contains 7.7 meqs
○ Ex. 60 kg M can have 1 tab TID-QID depending on baseline HCO3
6. Recombinant human EPO- for anemia, initiated once there are adequate bone marrow iron stores
7. Ketoanalogues of Amino acids Supplement- given as a supplement to very low protein diet (0.3 g/kg/day). Shown to delay
onset of uremia and initiation of dialysis. KAA tab 600 mg/tab given 1 tab per 5-10 kg BW. Ex. A 60 kg M on low protein diet
will need 12 tabs/day given as 4 tabs TID. MONITOR! Calcium levels bec it contains different calcium salts.
8. Vit B12, folate
9. iron supplementation
a. FeSo4 325 mg/tab TID to provide elemental iron of 200 mg/day in nondialytic CKD pts
b. Iron sucrose 1000 mg IV in 10 doses (100 mg/dose) is equivalent to iron content in one bag pRBC
c. ESA (Erythropoiesis Stimulating Agent)- used when hgb is less than 100 g/L despite correction. EPO alpha/beta 20-
50 IU/kbw 3x/week SC/IV

RENAL REPLACEMENT THERAPY

Can be in the form of kidney transplant (KT), hemodialysis (HD), or peritoneal dialysis (PD).
● KT is the best option for complete rehab bec HD/PD only replaces fraction of kidney’s filtration function and no effect on
endocrine and anti-inflammatory functions.

ABSOLUTE INDICATIONS RELATIVE INDICATIONS

● Pericarditis/ Pleuritis ● Anorexia and nausea

● Progressive uremic enceph or neuropathy, with ● Impaired nutritional status
signs such as confusion, asterixis, myoclonus, wrist ● Increased sleepiness
or foot drop, or seizures (URGENT INDICATION) ● Decreased energy level, attentiveness, and cognitive
● Clinically significant bleeding diathesis attributable to taking.
Uremia (URGENT INDICATION)
● Persistent metabolic disturbances that are refractory
to medical therapy. EX. hyperK, met acid,
hyper/hypoCal, hyperPhos
● Fluid overload refractory to diuretics
● HTN poorly responsive to antiHTN meds
● Persistent nausea and vomiting
● Evident of malnutrition

ADMITTING ORDERS

Admit to Ward 1 under service 4 ℅ Dr chiu/chuabio

Secure consent for admission.
Diet: 35 kcal/kg/day, low salt (2-4 gm Na/day), low potassium (2-4 gm/day), low phosphate (600-800 mg/day).
IVF: Limit OFI to < 1 liter/day
VS q 2 with NVS, strict I&O q shift and record.
Weigh patient daily
Diagnostics:
1. Kidney UTZ
2. CBC

73
 3. Na, K, Mg, Cal, Phos, Albumin, BUN, Crea, lipid profile, TPAG
4. 24 hour urine collection
5. Urine protein- creatinine ratio
6. Urinalysis
7. Urine GSCS

Therapeutics:

1. Amlodipine 10 mg/tab 1 tab OD

2. Losartan 100 mg/tab 1 tab OD
3. Carvedilol 25 mg/tab 1 tab BID
4. EPO Alpha, 4000 Units SC 3x a week post HD
5. Ferrous SO4 325 mg/tab, 1 tab TID
6. Folic acid 5 mg/tab, 1 tab OD
7. Vit B complex, 1 tab OD
8. Sevelamer 800 mg/tab, 1 tab TID
9. Atorvastatin 20 mg/tab 1 tab ODHS
10. Febuxostat 40 mg/tab, 1 tab ODHS
11. Paracetamol 300 mg/tab IV q6 PRN for fever
12. Diphenhydramine 50 mg/tab 1 tab OD prior to BT

Transfuse PRBC if needed depending on hgb level.

74
 SHOCK

Alyssa Felsophie Silor

● Organ dysfunction from an imbalance between cellular oxygen supply and demand; in relation to impaired oxygen delivery
(circulatory failure) and subsequent cellular hypoxia

Important formulas:

Four types of shock:

1. Distributive
○ HEART PUMPS WELL BUT THERE IS
PERIPHERAL VASODILATION
○ Reduced oxygen delivery (reduction in SVR) with
compensatory increase in CO
○ Slow movement of RBCs to tissues:
i. Dilated vessels are unable to move fluid as
effectively to the cells
ii. Leaky vessels may lead fluid out of the
vascular system → pulmonary edema, pedal
edema
○ Most common cause: SEPSIS - dysregulated host
response to infection → life-threatening organ
dysfunction
○ Septic shock - persistent hypotension requiring

75
 vasopressor support

2. Cardiogenic
○ HEART FAILS TO PUMP BLOOD OUT
○ Reduced oxygen delivery (reduction in CO) due to a
primary cardiac problem with compensatory
increase in SVR
○ Since heart cannot pump effectively, blood may
backup into the lungs → pulmonary edema →
impaired ventilation
○ Systemic hypoperfusion due to severe depression of
cardiac index (<2.2 L/min/m2) and sustained systolic
arterial hypotension (<90 mmHg) despite an elevated
filling pressure (PCWP >18 mmHg)
○ Most common cause: severe LV dysfunction

3. Obstructive
○ HEART PUMPS WELL BUT THE OUTFLOW IS
OBSTRUCTED
○ Reduced oxygen delivery (reduction in CO) due to
extracardiac processes impairing blood flow with
compensatory increase in SVR
○ Physical obstruction of blood flow or ventilation

4. Hypovolemic
○ HEART PUMPS WELL BUT NOT ENOUGH BLOOD
VOLUME TO PUMP
○ Reduced oxygen delivery (reduction in CO) with
compensatory increase in SVR then low CVP and
PCWP due to decreased intravascular volume
○ Most common cause: HEMORRHAGE (external or
internal)
○ Loss of plasma/fluid/RBC

Stages of shock:

1. Compensated shock (preshock) No overt signs of organ dysfunction

2. Decompensated shock (shock) Evidence of organ dysfunction

3. Irreversible shock Permanent leading to MSOF

S>

Distributive Cardiogenic Obstructive Hypovolemic

Altered mental status

Sepsis: MI: Tension pneumothorax: Hemorrhage:

Fever Exertional chest discomfort s/p thoracensis, CVP Dizziness, syncope

Possible focus of infection Dyspnea/SOB insertion, CT-guided biopsy, Dyspnea/SOB
Palpitations transthoracic needle Internal/external blood loss
Syncope aspiration (more on iatrogenic from trauma or surgery
Orthopnea causes) Hematemesis
Hematochezia
(refer to ACS module made Dyspnea/SOB Melena
by Willis)

76
Anaphylactic: Cardiac tamponade: GI losses:

*after exposure to common Dyspnea Dizziness, syncope

allergens Orthopnea Vomiting
Pruritus, urticaria, Fatigue Diarrhea
angioedema, flushing Dehydration
Hoarseness, dyspnea
N/v, crampy abdominal pain,
diarrhea
Palpitations

Pulmonary embolism:

Pleuritic chest pain

Dyspnea/SOB
Cough, hemoptysis

O>
“Windows” to identify organ dysfunction:

CNS Confusion; Encephalopathy - decompensated shock

Kidney Oliguria (UO <0.5ml/kg/hr) - may place IFC to monitor UO hourly

Skin Weak/thready pulses; CRT >2s; Cold, clammy skin

Distributive Cardiogenic Obstructive Hypovolemic

Hypotension (MAP <60mmHg) - not always present

Tachycardia (compensatory: to increase CO)
Tachypnea (compensatory for the developing metabolic acidosis)

High-output: Low-output:

Warm, peripheral extremities Cool extremities

CRT <2s CRT >2s
Bounding pulses Weak pulses

Sepsis: Increased vascular filling Tension pneumothorax: Hemorrhage:

Hypotension, fever,
tachycardia, tachypnea
qSOFA:
RR >= 22cpm
Altered mental status
SBP <= 100mmHg
(score of >=2, investigate for
organ dysfunction)
pressure:
Distended neck veins Pallor
Elevated JVP Hypotension Hypotension, tachycardia,
S3 gallop Chest lag narrow pulse pressure
Decreased/absent BS Orthostatic changes in VS
Hyperresonance Weak/thready pulses
Site of active bleeding
DRE: blood per examining
finger
(see image below for classes
of hemorrhage and possible
sites of bleeding)

Anaphylaxis: Arrhythmias: Cardiac tamponade: GI losses:

Hives (raised edematous Bradycardia Beck’s triad (hypotension, Pallor

patches of skin/mucous
membrane asso with pruritus)
Swelling of conjunctiva, lips,
tongue, throat
Stridor, wheezing
Abdominal tenderness
Hypotension, tachycardia
Excessive tachycardia
Dysrhythmia
neck vein engorgement,
muffled heart sounds)
Pulsus paradoxus
Hypotension, tachycardia,
narrow pulse pressure
Orthostatic changes in VS
Weak/thready pulses
Signs of dehydration:
Restless, irritable → Lethargic

77
 or unconscious
Sunken eyeballs
Drinks eagerly, thirsty →
unable to drink

Pulmonary embolism:

Tachypnea, tachycardia
Hypotension (if large
embolus)
Cyanosis

A>
Shock, _______ , secondary to ________

P>
Please admit under the service of SVC _ / ______ / ______ to W _ B _
Please secure consent for admission and management
Diet: NPO for now
IVF: see table below
SD1: see table below
Monitor NVS Q1; I/O qshift and record
Diagnostics: see table below

Diagnostics: Rationale: Expected findings:

CBC-PC Hgb: to check for anemia Hypovolemic shock: anemia

WBC: to check for infection Distributive (septic) shock: leukocytosis
Distributive (anaphylaxis) shock:
eosinophilia

PT/PTT Bleeding parameters esp in those w/

pulmonary embolism or those for OR

ABG Identify and manage acid-base disorders Hypoxemia, Metabolic acidosis for those
in shock

Renal function tests (BUN, Crea) Assess extent of end-organ dysfunction Elevated for those with EOD

Liver function tests (AST, ALT) Assess extent of end-organ dysfunction Elevated for those with EOD

Therapeutics: see table below

Transfuse __ units of pRBC properly typed and crossmatched to run for 4-6 hours (see table below); PC in bulk; for post-BT CBC
Referrals: depends on the case eh… IDS if sepsis, Allergy if anaphylaxis, CVS if cardiogenic, TCVS if pneumothorax or cardiac
tamponade, SOD if trauma, etc.
Refer PRN. Thank you!

78
 Distributive Cardiogenic Obstructive Hypovolemic

High-flow O2 SD: High-flow O2 High-flow O2

Secure and maintain patent 1st line: Dobutamine Secure and maintain patent Secure and maintain patent
airway (synthetic cathecholamine airway airway
with beta-mediated effects
and minimal alpha adrenergic
effects)

Sepsis: Bradycardia (<=50bpm): Pulmonary embolism: Hemorrhage:

IV fluid resuscitation (30cc/kg Oxygen support Dx: Control site of bleeding (direct
crystalloid within the 1st 3 Plasma D-dimer ELISA (high pressure or dressing, surgical
hours), maintain MAP >=65 Hook to cardiac monitor sensitivity) intervention, investigate
● Elevated source of bleeding)
mmHg
IV fluid resuscitation (if no
signs of pulmonary edema) 12-L ECG IV fluid resuscitation (2L
Vasopressors: ● T-wave inversion in PNSS or PLR over 20-30
1. 1st line: If the ff are present: V1-4 mins)
Norepinephrine ● Hypotension ● S1, Q3, T3
● Altered mental (inverted) Inotropes if still hypotensive
(potent alpha-1 → status
vasoconstriction ● Signs of shock 2D-echo BT if hgb <7.0g/dL
and beta-1 → ● Ischemic chest ● Small-moderate →
discomfort Normal RV
positive inotropic ● Acute HF
● Submassive-
and chronotropic → ATROPINE 0.5mg IV
massive → RV
effects) q5mins (max: 6 doses)
hypokinesis/
2. 2nd line: → if still not effective,
dysfunction
Epinephrine (a/e: DOPAMINE
(McConnell’s sign)
tachyarrhythmia, → if still not effective,
myocardial EPINEPHRINE CTPA (CT-pulmonary
ischemia, → if still not effective, angiography) - 1st line
decreased TRANSCUTANEOUS ● Segmental or more
splanchnic blood PACING proximal thrombus
flow, pulmonary → if still not effective,
Lung scintigraphy - 2nd line
hypertension, and PACEMAKER ● 2 or more
acidosis) segmental
3. Vasopressin Find REVERSIBLE causes: perfusion defects
Hypoxia w/ normal
(reverse
Acidosis ventilation
vasodilation and Hyperkalemia
redistribute flow to Hypothermia Tx:
splanchnic Heart block Small-moderate:
circulation) Toxins
→ Anti-coagulation
4. Dopamine - low risk Trauma
1. Unfractionated
of tachyarrhythmias heparin 80u/kg IV
5. Dobutamine - if still LD then 18u/kg/hr
hypoperfused MD (INR 1.5-2.5x)
OR Enoxaparin
1mg/kg q12 SC,
Septic work-up (CBC, blood
AND warfarin
CS, urine CS, sputum/ETA 5mg/tab 1 tab OD
GSCS, wound GSCS, (INR 2-3)
procalcitonin, CXR) 2. Rivaroxaban 15mg
BID x 3 weeks then
IV antimicrobials within the 20mg OD thereafter
1st hour (see image below)
Submassive-massive:
→ IV anticoagulation
Source control (surgery,
→ Advanced therapy
resection, or drainage of site
1. Systemic
of infection) thrombolysis

79
 2. Percutaneous
BT: catheter-directed
pRBC if <7.0 g/dL therapy
3. Pulmonary
PC if <10,000/mm3 (no
embolectomy
bleeding) 4. Pulmonary
PC if <20,000/mm3 (risk for thromboendarterect
bleeding) omy
PC if >50,000/mm3 (active 5. IVC filters
bleeding or for surgery)

Anaphylaxis: Tachycardia (>=150bpm) Cardiac tamponade: GI losses:

Remove inciting allergen Oxygen support Dx: Fluid resuscitation (oral or IV

(IDEALLY FOREVER) 12-L ECG depending on level of
Hook to cardiac monitor ● Low ECG voltage dehydration)
● Electrical alternans
IV fluid resuscitation
IV fluid resuscitation (if no 2D-echo
1-2 L or 5-10ml/kg of PNSS in signs of pulmonary edema) ● Pericardial effusion
1st 5-10 mins ● Small RV size
If the ff are present: ● Exaggerated
Administer epinephrine ● Hypotension respiratory variation
0.01mg/kg 1:1000 (1mg/ml) ● Altered mental
IM at the mid-anterolateral status Tx:
● Signs of shock 1. Emergency
aspect of the thigh q5-15
● Ischemic chest pericardiocentesis -
mins (max 0.5mg) discomfort definitive tx
● Acute HF 2. Tube
Ancillary agents: → CARDIOVERSION pericardiostomy
1. Diphenhydramine with creation of
25-100 mg IM/IV for If not, pericardial window
urticaria/ → VASOVAGAL maneuvers (for recurrent,
infectious,
angioedema → ADENOSINE 6-12-12 at L
malignant, and
2. Ranitidine 50mg IV antecubital fossa (6mg bolus other chronic
3. Salbutamol neb then after 1-2 mins, may give causes
4. Hydrocortisone 2nd dose which is 12mg)
200mg IV → if still not effective,
AMIODARONE or
Place patient on supine PROCAINAMIDE
position and elevate lower
extremities

Dx: Tension pneumothorax:

12-L ECG
● ST wave changes Dx:
CXR:
● Dysrhythmia
● Contralateral
Cardiac biomarkers tracheal deviation
● Elevated due to ● Ipsilateral
myocyte damage subcutaneous
related to ischemia, emphysema
myocarditis
2D echo Tx:
1. Large-bore needle
(these are done to identify (gauge 16) into the
primary cardiac problem) pleural space (5cm)
through the 2nd
ICS MCL → only
temporizing
procedure
2. Tube thoracostomy
→ definitive tx

80
Fig. Possible sources of hemorrhage

81
 ACUTE PANCREATITIS

Desiree Pacana

Must-Knows
● Definition: Activation of enzymes within the pancreas —> Inflammation of the pancreas
○ proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen, proelastase, and lipolytic enzymes such as phospholipase
A2) are activated in the pancreas acinar cell rather than in the intestinal lumen

● Etiology: REMEMBER G-A-T-E-D-s

1. Gallstones: most common cause
2. Alcohol
3. HyperTriglyceridemia/Trauma
4. ERCP
5. Drugs
6. Sphincter of Oddi dysfunction

● Pathophysiology
○ AUTODIGESTION: Pancreatic enzymes are activated → destroy own tissue → inflammation

initial phase characterized by intrapancreatic digestive enzyme activation and acinar cell injury

second phase activation, chemoattraction, and sequestration of leukocytes and macrophages in the pancreas →
enhanced intrapancreatic inflammatory reaction

third phase digest pancreatic and peripancreatic tissues but also activate other enzymes such as elastase and
phospholipase A2 → digest cellular membranes → proteolysis, edema, interstitial hemorrhage,
vascular damage, coagulation necrosis, fat necrosis, and parenchymal cell necrosis

● Epidemiology
○ The annual incidence: 13 to 45 cases per 100,000 persons
○ Acute pancreatitis results in >250,000 hospitalizations per year
○ Median length of hospital stay: 4 days with mortality of 1%
○ Hospitalization rates increase with age, higher among blacks, higher among males than females

● Classifications

82
Phases of acute pancreatitis

Early (<2 weeks) Severity defined by clinical parameters

Exhibit SIRS and organ failure (involving the respiratory, cardiovascular, renal systems)
Persistent organ failure (>48hours): MOST IMPORTANT CLINICAL FINDING with regard to
SEVERITY

Late (>2weeks) Protracted course and may need imaging to evaluate local complications
PARAMETER OF SEVERITY: persistent organ failure
May require dialysis, ventilator support, etc

Severity of acute pancreatitis

Mild WITHOUT local complications or organ failure

Sef limited
Subsides within 3-7 days after treatment started
ORAL INTAKE RESUMED once
● Hungry
● Normal bowel function
● No nausea and vomiting

Moderate TRANSIENT ORGAN FAILURE (resolves <48hours) OR

Local or systemic complications IN THE ABSENCE of persistent organ failure

Severe PERSISTENT ORGAN FAILURE (>48hrs)

CT scan and MRI → assess necrosis and/or complications

Morphologic Features of Acute Pancreatitis

NORMAL

Interstitial pancreatitis Acute inflammation but without tissue necrosis

Acute pancreatic fluid Peripancreatic fluid with interstitial edematous

collection pancreas
No necrosis
Seen within first 4 weeks since onset of interstitial
edematous pancreatitis

83
Pancreatic pseudocyst Encapsulated collection of fluid with well defined
wall, usually outside pancreas
Minimal or no necrosis
Occurs > 4weeks after onset of interstitial
edematous pancreatitis

Necrotizing pancreatitis Inflammation and tissue necrosis

Acute necrotic Collection of both fluid and necrosis associated

collection (ANC) with necrotizing pancreatitis

Walled off necrosis Mature encapsulated collection of necrosis with

well defined inflammatory wall
Occurs > 4 weeks after onset of necrotizing
pancreatitis

● Defining Severity of Acute Pancreatitis

RISK FACTORS FOR SEVERITY

Age > 60
Obesity, BMI > 30
Comorbid disease

MARKERS OF SEVERITY WITHIN 24 hours

84
 SIRS
APACHE II
Hemoconcentration (Hm > 44%)
Admission BUN (>22 mg/dL)
BISAP (at least 3 or more: increased risk of in hosp mortality)
● B ( BUN > 25 mg/dL)
● I (Impaired mental status)
● S (SIRS at least 2 of 4)
● A (Age > 60)
● P (Pleural effusion)
Organ failure (Modified Marshall Score): score of ≥2 in any system defines the presence of organ failure (see table
below)
Cardiovascular: SBP < 90, HR > 130
Pulmonary: PaO2 < 60
Renal: serum Crea > 2mg/dL

MARKERS OF SEVERITY DURING HOSPITALIZATION

Persistent organ failure (>48hours)

Pancreatic necrosis

● Complications

LOCAL COMPLICATIONS SYSTEMIC COMPLICATIONS

Necrosis (sterile/infected) PULMONARY: ARDS, effusion, pneumonitis

Pancreatic fluid collection (pseudocyst, abscess) CARDIOVASCULAR: Hypotension, sudden death
Pancreatic ascites HEMATOLOGIC: DIC
Obstructive jaundice GI: ulcer formation, gastritis, Mallory-Weiss, rupture of splenic
Bowel compression or fistulization artery/vein or portal vein, thrombosis of splenic vein → gastric
varices, hemosuccus pancreaticus (pseudoaneurysm → bleeding
into pancreatic duct)
RENAL: oliguria, azotemia, ATN
METABOLIC: hyperglycemia, hypocalcemia
OTHERS: Pancreatic encephalopathy, Purtscher’s retinopathy

CLINICAL MANIFESTATIONS
Subjective
1. Abdominal pain (major symptom) described as steady, boring pain located at the epigastrium and periumbilical
region, radiating to the back, chest, flanks, lower abdomen, aggravated by lying supine and relieved by sitting with
trunk flexed and knees drawn up
2. Nausea
3. Vomiting
4. Abdominal distention
5. Dyspnea due to diaphragmatic inflammation from pancreatitis or complications of pancreatitis such as pleural effusions, or
ARDS

85
Objective

GENERAL Distressed and anxious

Disorientation
Hypotension secondary to hypovolemia secondary to exudation of blood and plasma proteins into
retroperitoneum
Tachypnea, tachycardia, low grade fever
Hypoxemia

HEENT Icteric sclerae (if with jaundice secondary to choledocholithiasis or edema of head of pancreas)

CHEST (+) basilar rales

(+) decreased/absent BS, decreased vocal and tactile fremitus if with atelectasis
(+) decreased BS, decreased vocal fremitus, decreased tactile fremitus pleural effusion

HEART USUALLY NORMAL

ABDOMEN (+) Cullen’s sign ( blue discoloration around the umbilicus)

(+) Turner’s sign (blue-red-purple or green-brown discoloration of flanks)
Abdominal tenderness, guarding more marked in the upper abdomen
Increase in abdominal girth with decreased or absent bowel sounds due to ileus secondary to inflammation

EXTREMITIES (+) jaundice (infrequent) due to edema of the pancreatic head with compression of the intrapancreatic
portion of CBD or gallstone pancreatitis
(+) 0.5-2 cm tender red nodules

Assessment
Acute pancreatitis, early/late, mild/moderately severe/severe

Any severe acute pain in the abdomen or back should suggest the possibility of acute pancreatitis. The diagnosis is established by
two of the following three criteria:
(1) typical abdominal pain in the epigastrium that may radiate to the back
(2) threefold or greater elevation in serum lipase and/or amylase
(3) confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging

Differentials Rule In Rule Out

peptic ulcer disease (+) abdominal pain, epigastric, but usually burning
kind of pain
(+) may also present with vomiting, nausea
(+) may present with abdominal distention,
abdominal tenderness on the epigastrium
(+) hypotension, tachycardia if with massive blood
loss
-The pain usually does not radiate to the back,
either be relieved or precipitated by food
depending on location
-(+) history of longstanding NSAID use or prior H.
pylori infection
-may present with hematemesis, melena
-LABS: normal lipase and amylase

Perforated viscus (+) abdominal pain, nausea, vomiting -EXTREME guarding

(+) guarding -Rigidity and rebound tenderness
(+) hemodynamic instability

acute CHOLEDOCHOLITHIASIS: may have pancreatitis
choledocholithiasis and cholangitis as complications; nausea,
and cholangitis vomiting, jaundice, biliary cirrhosis, tenderness
CHOLANGITIS: fever, abdominal pain, jaundice
(Charcot’s triad) → if severe, may present with
altered mental status and hypotension (Reynolds
pentad)
-Pain of biliary tract origin is more right sided or
epigastric than periumbilical or left upper quadrant
and can be
more severe
-(+) history of gallstones or manipulation such as
ERCP
-LABS: elevated AST,ALT,ALP, bilirubins, normal
amylase and lipase (elevated amylase lipase if
biliary pancreatitis)
-Confirmed by UTZ

cholecystitis (+) abdominal pain, typically at epigastrium or -(+) Murphy’s sign

RUQ radiating to shoulder or back
(+) jaundice -LABS: elevated AST, ALT, bilirubins, but the

86
 amylase and lipase usually not elevated greater
than 3x

acute intestinal (+) abdominal pain with anorexia -(+) obstipation and constipation
obstruction; (+) vomiting -(+) history of prior abdominal surgery or Crohn's
(+) abdominal distention disease
(+) may present with tachycardia, hypotension
(orthostatic) if with dehydration

mesenteric vascular (+) abdominal pain -RISK FACTORS: elderly debilitated patients with
occlusion; (+) abdominal distention brisk leukocytosis, abdominal distention, and
bloody diarrhea, intraabdominal malignancies,
recent MI, severe valvular disease, cardiac
arrythmias

-confirmed by CT or magnetic resonance

angiography

If a female of the (+) abdominal pain, nausea, vomiting (+) amenorrhea

reproductive age: (+) increased abdominal girth and abdominal (+) sexually active
Pregnancy tenderness
PREGNANCY TEST!!!!

renal colics (+) severe abdominal pain (+) waxing waning pain
(+) nausea and vomiting (+) hematuria
(+) dysuria, urgency

inferior myocardial (+) atypical presentation of MI → epigastric pain (+) history of previous MI, anginal symptoms,
infarction (+) sudden onset DOB, hypotension, desaturation history of coronary disease, comorbids
(+) diaphoresis
(+) crackles all over
(+) NVE

dissecting aortic (+) abdominal pain radiating to the back -(+) very severe pulsating pain
aneurysm (+) hemodynamic instability -(+) HF symptoms, syncope, stroke
-(+) weak pulses
-(+) heart murmur

pneumonia (+) tachypnea, fever - (+) usually does not present with abdominal pain
(+) parapneumonic pleural effusion -(+) cough
(+) end organ damage if septic
(+) hemodynamic instability if with septic shock

diabetic ketoacidosis (+) abdominal pain -(+) known Type I diabetic patient
(+) nausea and vomiting -polyuria, polydipsia, weight loss
(+) hypotension, tachycardia, tachypnea -(+) neurologic deterioration: altered mental
status, coma, seizures
-(+) signs of dehydration

-serum lipase level is not elevated

Admitting Orders
It is important to note that 85–90% of cases of acute pancreatitis are self-limited and subside spontaneously, usually within 3–7
days after initiation of treatment, and do not exhibit organ failure or local complications.

Admit to ward.
● CRITERIA FOR ICU ADMISSION:
○ Patients who do not respond to aggressive fluid resuscitation in the emergency ward for further aggressive fluid
resuscitation, hemodynamic monitoring, and management of necrosis or organ failure

Secure consent for admission.

Diet: NPO for now. Resume diet after 3rd-6th day if without vomiting. If with ileus, insert NGT and open to drain.
Monitor VSQ2. Insert foley catheter and record input and output of fluids.
IVF: Insert large bore needle. Very important intervention is safe, aggressive fluid hydration. Hook to LR or PNSS at 15-20cc/kg
bolus, followed by 3mg/kg/hr infusion for 8 to 12 hours to maintain urine output > 0.5cc/kg/hr.

87
Supplemental O2 through nasal cannula 2 lpm.
Diagnostics
○ Measure hematocrit and BUN every 8-12 hours and serum electrolytes daily to ensure adequacy of fluid resuscitation

Diagnostics Rationale Expected Findings

Lab CBC For the diagnosis and severity of the Leukocytosis (15-20)
disease, hematocrit used in assessing Hemoconcentration with hematocrit values
adequacy of fluid resuscitation > 44%

Amylase Elevated in pancreatitis Increased level (more than 3-fold)

Returns to normal after 3-7 days

Lipase More specific than amylase Increased level (more than 3-fold)
instrumental in differentiating a pancreatic Elevated for 7-14 days
or nonpancreatic
cause for hyperamylasemia

Renal Function Assessment of severity of pancreatitis, Azotemia with BUN >22 mg/dL
tests systemic complications

Liver function Etiology of pancreatitis Hyperbilirubinemia, serum AST ALT

tests transiently elevated (esp in gallstone
pancreatitis)

RBS May present with hyperglycemia Hyperglycemia

Electrolytes May present with electrolyte imbalance, Hypocalcemia

should have a baseline and will be
monitored during aggressive hydration

Lipid profile Presents with hypertriglyceridemia Hypertriglyceridemia

ABG To check if patient is having metabolic Hypoxemia (arterial PO2 < 60 (may herald
acidosis and hypoxemia, esp if there is onset of ARDS)
desaturation at initial presentation

ECG May show signs of ischemia ST wave elevations

Chest Xray (+) chest findings suggestive of

Imaging atelectasis, pleural effusion, ARDS

Abdominal UTZ Useful to evaluate the gallbladder if

gallstone disease is suspected

ABdominal CT -best evaluated 3–5 days into (1) interstitial pancreatitis

scan hospitalization when patients are not
responding to supportive care to look for
local complications such as necrosis
-Helpful in indicating the severity of acute
pancreatitis and the risk of mortality and
morbidity
(2) necrotizing pancreatitis
(3) acute pancreatic fluid collection
(4) pancreatic pseudocyst
(5)acute necrotic collection (ANC)
(6) walled-off necrosis (WON)

Therapeutics
○ Intravenous narcotic analgesics to control abdominal pain (Meperidine HCL 25-50mh IV Q6-8hrs, defer for SBP <100)
○ Omeprazole 40mg IV OD (since NPO)
○ 10% Calcium gluconate 10mL SIVP in 10mins if with symptomatic hypocalcemia

88
SPECIAL CONSIDERATIONS

GALLSTONE PANCREATITIS evidence of ascending cholangitis (rising white blood cell count, increasing liver enzymes)
→ undergo ERCP within 24–48 h of admission

HIgh risk of recurrence → performing a cholecystectomy during the same

admission or within 4–6 weeks of discharge

HYPERTRIGLYCERIDEMIA Initial therapy may include insulin, heparin, or plasmapheresis.

MANAGEMENT OF COMPLICATIONS

NECROSIS Dx:
● Repeated fine-needle aspiration and Gram stain with culture of pancreatic
necrosis may be done every 5–7 days in the presence of persistent fever
● Repeated CT or MRI imaging should also be considered with any change in
clinical course to monitor for complications (e.g., thromboses, hemorrhage,
abdominal compartment syndrome)

Tx:
1. ANTIBIOTICS: no role for prophylactic antibiotics in necrotizing pancreatitis, start
broad-spectrum antibiotics in a patient who appears septic while awaiting the results of
Gram stain and cultures (Carbapenem, quinolone, Ceftazidime, Cefepime +
Metronidazole)
step-up approach (percutaneous or endoscopic transgastric drainage
followed, if necessary, by open necrosectomy)

PSEUDOCYST Only symptomatic collections should be drained with surgery or endoscopy or by

percutaneous route.

PANCREATIC DUCT DISRUPTION increasing abdominal pain or shortness of breath inn the setting of an enlarging fluid
collection
Placement of a bridging pancreatic stent for at least 6 weeks is >90%
effective at resolving the leak.

PERIVASCULAR diagnosed and treated with mesenteric angiography and embolization.

COMPLICATIONS

EXTRAPANCREATIC Appropriate antibiotics

INFECTIONS (Hospital-acquired
infections)

Long term plans:

● Alcohol cessation
● Assess for development of diabetes, exocrine insufficiency, recurrent cholangitis, or development of infected fluid
collections
● Cholecystectomy should be performed during hospitalization or within 4–6 weeks of discharge if possible for patients with
uncomplicated gallstone pancreatitis

References Harrison’s, IM platinum, uptodate, random internet sites HAHAHA

89
 UPPER GASTROINTESTINAL BLEEDING

Tricia Marie M. Naciongayo

Must-Knows
● Definition: Upper gastrointestinal bleeding is defined as bleeding derived from a source proximal to the ligament of Treitz.
● Etiology
○ Peptic Ulcer Disease
■ Disruption of the mucosal integrity (>5 mm in size, with depth to the submucosa) of the stomach and/or duodenum
leading to a local defect or excavation due to active inflammation
■ H. pylori is able to facilitate gastric residence, induce mucosal injury, and avoid host defense
■ NSAIDs inhibit prostaglandin synthesis
● Endothelial effect: causes stasis, resulting to ischemia
● Direct toxicity to mucosa from ion trapping
● Epithelial effects: increased HCl secretion, decreased mucin and bicarbonate secretion, decreased surface
active phospholipid secretion, decreased epithelial cell proliferation
■ Other causes: infection (CMV, HSV, H. heilmannii), drug/toxin (bisphosphonates, chemotherapy, clopidogrel,
glucocorticoids, mycophenolate mofetil, KCl), and miscellaneous (basophilia in myeloproliferative disease, duodenal
obstruction, infiltrating disease, ischemia, radiation therapy, eosinophilic infiltration, Crohn’s disease, sarcoidosis,
idiopathic hypersecretory disease)
■ Duodenal ulcer: basal and nocturnal gastric acid secretion appears to be increased and bicarbonate secretion is
significantly decreased in the duodenal bulb
■ Gastric ulcer: impairment of mucosal defense factors
● Types:
a. Type I occur in the gastric body and tend to be associated with low gastric acid production
b. Type II occur in the antrum and gastric acid can vary from low to normal
c. Type III occur within 3 cm of the pylorus, are commonly accompanied by DUs, and normal or high
gastric acid production
d. Type IV are found in the cardia and are associated with low gastric acid production
■ Subjective
● Dyspepsia — Upper abdominal pain or discomfort
● Epigastric pain — characterized by a gnawing or burning sensation and occurs after meals; classically, shortly
after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer
● Food or antacids relieve the pain of duodenal ulcers but provide minimal relief of gastric ulcer pain
● Duodenal ulcer pain often awakens the patient at night
● Pain with radiation to the back is suggestive of a posterior penetrating gastric ulcer complicated by
pancreatitis
● Asymptomatic — Approximately 70 percent; Older adults and individuals on NSAIDs are more likely to be
asymptomatic and later present with ulcer complications
● Bleeding — may present with nausea, hematemesis (fresh blood or coffee-ground emesis), or melena. In rare
cases, patients have massive bleeding and present with hematochezia and orthostatic hypotension
● Gastric outlet obstruction — sysmptoms of gastric retention include early satiety, bloating, indigestion,
anorexia, nausea, vomiting, epigastric pain shortly after eating, and weight loss
● Frequently associated with gastroesophageal reflux
● Nausea and weight loss occur more commonly in GU patients
■ Objective
● Epigastric tenderness (usually mild)
● Right upper quadrant tenderness may suggest a biliary etiology or, less frequently, PUD
● Melena from acute or subacute bleeding on DRE
● Succussion splash, resulting from partial or complete gastric outlet obstruction, indicates retained fluid in the
stomach
○ Esophageal Varices
■ Develop because of systemic or segmental portal hypertension (causing obstruction of portal venous outflow) to
decompress the hypertensive portal vein and return blood to the systemic circulation
■ Sites: distal esophagus, stomach and rectum
■ Most common bleeding site: gastroesophageal junction due to thin mucosa
■ Subjective
● History of jaundice, blood tranafusions, risky behaviors (hepatitis infection)
● Symptoms of liver disease

90
 ■ Objective
● Spider angiomata
● Caput medusae
● Rectal hemorrhoids
● Splenomegaly
● Hepatomegaly
● (+) fluid wave test or shifting dullness
● Palmar erythema and leukonychia
○ Stress-related Mucosal Damage: development if stress-related ulcers
■ Risk of stress ulcer bleeding is increased in patients with respiratory failure and those with a coagulopathy or anti-
coagulant use
■ Stress ulceration after head trauma (Cushing’s ulcer) and severe burns (Curling’s ulcer), mucosal ischemia,
breakdown of the normal protective barriers of the stomach, systemic release of cytokines, poor GI motility, and
oxidative stress
■ Subjective
● History of severe illness, major surgery, massive burn injury, head injury associated with increased ICP,
sepsis with positive BCS, severe polytrauma and multiple organ system failure
● Coffee-ground vomitus, melena, hematemesis (extreme cases)
■ Objective
● Epigastric tenderness
○ Mallory-Weiss tear
■ Longitudinal mucosal lacerations (intramural dissections) in the distal esophagus and proximal stomach that are
usually associated with forceful retching, leading to bleeding from submucosal arteries
■ From sudden increase in intra-abdominal pressure, includes vomiting, straining at stool or lifting, coughing, seizures,
hiccups under anesthesia, closed-chest massage, blunt abdominal injury, colonoscopic preparation with
polyethylene glycol electrolyte lavage solution, and gastroscopy
■ Subjective
● Hematemesis following a bout of coughing, retching or vomiting
● History of melena, hematochezia syncope, abdominal pain and excessive alcohol use
● History of hiatal hernia
■ Objective
● Signs of blood loss: tachycardia, hypotension, pallor, orthostatic changes or over shock
○ Neoplasm: benign or malignant tumors that outgrow the blood supply, causing diffuse mucosal ulceration, or erosion into
underlying vessel
■ Kaposi sarcoma is particularly vascular in nature and should be considered in patients with HIV infection or in those
who are immunosuppressed
■ Subjective
● History of dysphagia, involuntary weight loss and cachexia
● Zollinger-Ellison Syndrome — severe peptic ulcer diathesis secondary to gastric acid hypersecretion due to
unregulated gastrin release from a non-β cell often well-differentiated neuroendocrine tumor (gastrinoma)
● Esophageal cancer: smoking, alcohol consumption, caustic injury, and human papilloma virus infection;
usually presents with dysphagia
● Gastric cancer: insidious upper abdominal discomfort varying in intensity from a vague, postprandial fullness
to a severe, steady pain
○ Dieulafoy lesion: dilated (1-3mm), aberrant, submucosal artery that erodes the overlying epithelium in the absence of
an underlying ulcer, aneurysm or intrinsic mural abnormality
■ Bleeding usually occurs in men with comorbid medical conditions (e.g. hypertension, CKD, CVD, diabetes or
alcoholism)
■ Subjective: severe, active GI bleeding without prior symptoms
○ Angiodysplasia: ectatic, dilated, thin-walled vessels that are lined by endothelium alone or endothelium along with small
amounts of smooth muscle
■ Intermittent, recurrent low-grade obstruction of submucosal veins at the level of the muscularis propria. Over
years, the obstruction results in dilatation and tortuosity of the draining areas (i.e. submucosal vessels, venules, and
superficial capillaries)
■ Subjective
● Multiple recurrent episodes of overt bleeding, usually low-grade and painless
● Predisposition: CKD, aortic stenosis (Heyde syndrome if with bleeding angiodysplasia), hereditary
hemorrhagic telangiectasia (a.k.a. Osler-Weber-Rendu disease)
○ Cameron lesion: erosions or ulcers occurring in the sac of a hiatal hernia
■ Hiatal hernia — herniation of viscera, most commonly the stomach, into the mediastinum through the esophageal
hiatus of the diaphragm

91
 ■ Subjective
● Often present with GERD symptoms and anemia
● Incidental finding of large structure in the posterior mediastinum on CXR
○ Aortoenteric fistula: erosion of the aortic graft into the bowel lumen, usually at the 3rd or 4th portion of the duodenum
■ Should be considered in patients with massive or repetitive UGIB and a history of a thoracic or abdominal aortic
aneurysm or a prosthetic vascular graft
■ Subjective
● Hematemesis
● Melena
● Sepsis
● Acute abdominal pain and vomiting of fresh blood
■ Objective
● Signs of blood loss and sepsis
● Mild epigastric tenderness
○ Hemobilia: bleeding from hepatobiliary tree
■ Subjective
● Acute UGIB and a recent history of hepatic parenchymal or biliary tract instrumentation and/or injury, including
percutaneous or transjugular liver biopsy, percutaneous transhepatic cholangiogram, cholecystectomy,
endoscopic biliary biopsies or stenting, TIPS placement, angioembolization, or blunt or penetrating abdominal
trauma
● Other causes include gallstones, cholecystitis, hepatic or bile duct tumors, intrahepatic stents, hepatic artery
aneurysms, and hepatic abscesses
● Classic triad: biliary colic, obstructive jaundice and GI bleeding
● Vasovagal episodes, resulting in bradycardia and hypotension
○ Hemosuccus pancreaticus: bleeding from pancreatic duct
■ Usually in patients with chronic pancreatitis, pancreatic pseudocysts, or pancreatic tumors
■ Bleeding occurs when a pseudocyst or tumor erodes into a vessel
■ Usually involves splenic artery pseudoaneurysm
■ Could be iatrogenic from therapeutic endoscopy of the pancreas or pancreatic duct, including pancreatic stone
removal, pancreatic duct sphincterotomy, pseudocyst drainage, or pancreatic duct stenting
■ Subjective
● History of chronic alcoholism
● Melena (most common)
● Hematemesis (less frequent)
● Bleeding is usually intermittent, repetitive, and often not severe enough to cause a hemodynamic instability
● Characteristic colic pain is a result of the increased intraductal pressure, which is caused by obstruction of the
Wirsung duct due to clot formation
○ Esophagitis: chronic inflammation of the esophagus causing submucosal tears
■ Subjective
● Often have a history of GERD
● Other risk factors include medication use (e.g. NSAIDS, oral bisphosphonates, tetracycline) and infections
(e.g. Candida, herpes simplex virus)
● Intermittent heartburn, most commonly experienced after eating, during exercise, and while lying recumbent
● History of dysphagia, odynophagia and globus sensation in the throat
● Classification: Can be categorized as either variceal or non-variceal UGIB
○ Peptic Ulcer Disease (Forrest Classification)
■ Type IA: arterial spurting
■ Type IB: arterial oozing
■ Type IIA: non-bleeding visible vessel
■ Type IIB: adherent clot
■ Type IIC: pigmented flat spot
■ Type III: no stigmata of recent bleed; fibrin-coated clean ulcer base
● Complications:

Assessment

Differentials Rule In Rule Out

Bleeding PUD History of H. pylori infection

History of chronic NSAID use

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 Gnawing or burning epigastric pain
Nausea and hematemesis/melena

Bleeding esophageal varices Liver cirrhosis Absence of liver disease

Signs and symptoms of CLD

Stress-related mucosal damage Critical illness Absence of stressor

Absence of prophylactic PPI

Mallory-Weiss tear Hematemesis following a bout of Absence of event/activity causing

coughing, retching or vomiting sudden increase in intra-abdominal
Excessive alcohol intake pressure

Neoplasm Progressive dysphagia, involuntary Acute bleeding without history of mass

weight loss, abdominal discomfort effect (i.e. dysphagia, early satiety,
Smoking or alcohol consumption weight loss)

Dieulafoy lesion History of hypertension, CKD, CVD,

diabetes or alcoholism
Severe, painless, active GI bleeding
without prior symptoms

Angiodysplasia Recurrent episodes of painless, low- Bleeding associated with abdominal pain
grade bleeding Absence of predisposing factors
Predisposition: CKD, aortic stenosis,
hereditary hemorrhagic telangiectasia

Cameron lesion History of hiatal hernia Absence of hiatal hernia

Aortoenteric fistula History of a thoracic/abdominal aortic Absence of predisposing factors

aneurysm or a prosthetic vascular graft

Hemobilia History of biliary tract surgery or Absence of predisposing factors

injury,abdominal trauma, biliary tract
pathology
Triad of biliary colic, obstructive jaundice
and GI bleeding

Hemosuccus pancreaticus History of chronic pancreatitis, Absence of predisposing factors

pancreatic pseudocysts, or pancreatic
tumors
Chronic alcoholism
Pancreatic duct manipulation
Melena (most common) and
hematemesis (less frequent)

Esophagitis History of GERD (heartburn, indigestion Absence of GERD or GERD-like

or dysphagia) symptoms

Plan
● Diagnostics

Diagnostics Rationale Expected Findings

CBC Assess level of blood loss and presence Decreased Hgb and Hct
of infection or thrombocytopenia Normal or increased WBC count
Normal or decreased PC

PBS Assess chronicity of blood loss Chronic: microcytic, hypochromic RBC

Acute: normocytic, normochromic RBC

PT/PTT R/O coagulopathies Prolonged PT/PTT or decreased PT

In patients using anticoagulants activity if with coagulopathies

93
 Increased INR with anticoagulant use

BUN, creatinine Assess renal function Elevated in CKD patients or if with AKI

AST, ALT Assess liver function Elevated in liver diseases

Bloodtyping For blood transfusion if necessary

Serum electrolytes Electrolyte imbalance in severe vomiting

Hypercalcemia causes increased gastric
acid production

Serum amylase and lipase If pancreatitis is suspected Elevated

ECG R/O arrhythmia or ACS due to Tachycardia, sinus rhythm, normal axis
hypotension

Gastrin If Zollinger-Ellison syndrome is Elevated

suspected

Endoscopy Confirms the diagnosis and allows for Bleeding ulcer, vessel or mass
targeted endoscopic treatment (e.g. Identify location of bleeding
epinephrine injection, thermocoagulation,
application of clips, and banding)
Biopsy of ulcer/mass to determine
etiology

Angiography Can detect slow (0.5cc/min) bleeding

vessels and do embolization

CXR-PA or Abdominal x-ray, supine & R/O pneumoperitoneum from perforated Presence of air beneath the diaphragm
upright PUD

● Treatment
○ SRMD: PPIs are the treatment of choice for stress prophylaxis
○ Erosive esophagitis from GERD
■ Empiric trial of acid suppression: 8-week course of PPI (e.g. omeprazole 40-80mg/day)
■ Lifestyle modification: avoid fatty food, alcohol, tomato-based food, coffee, tea and other acidic foods; weight
reduction
■ Surgical: Laparoscopic Nissen fundoplication
○ Peptic Ulcer Disease:
■ Acid-neutralizing/Inhibitory Drugs
● Antacids
a. Aluminum hydroxide 5-30mL between meals and HS
b. Magnesium hydroxide 400mg PO q4 (max of 4 doses per day)
● H2 receptor antagonists
a. Cimetidine 400mg BID
b. Ranitidine 300mg ODHS
c. Famotidine 40mg ODHS
● Proton pump inhibitors
a. Omeprazole 20mg BID
b. Esomeprazole 40mg BID
c. Rabeprazole 20mg BID
d. Pantoprazole 40mg BID
e. Lansoprazole 30mg BID
■ Cytoprotective Agents
● Sucralfate 1g QID
● Bismuth subsalicylate (BSS) 300mg QID
● Misoprostol 200mcg QID (prostaglandin analogue; enhance mucosal repair and defense)
● Rebamipide 100mg TID
■ H. pylori eradication

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 ● Triple therapy for 14 days: PPI + Clarithromycin 500mg BID + Amoxicillin 1g BID OR Metronidazole 500mg
TID
● Bismuth-based therapy for 10-14 days (Quadruple therapy): PPI + BSS + Metronidazole 250mg/500mg
QID/TID + Tetracycline 500mg QID
● Non-bismuth quadruple therapy for 10-14 days (clarithromycin resistance)
a. Sequential: PPI + Amoxicillin 1g BID for 5-7 days, then PPI + Clarithromycin 500mg BID +
Nitroimidazole 500mg BID for the next 5-7 days
b. Concomitant: PPI + Clarithromycin 500mg BID + Amoxicillin 1g BID + Nitroimidazole 500mg BID
c. Hybrid: PPI + Amoxicillin 1g BID for 7 days, then PPI + Amoxicillin 1g BID + Clarithromycin 500mg BID
+ Nitroimidazole 500mg BID for 7 days
○ Variceal bleeding:
■ Vasoactive agents
● Somatostatin 250mcg IV bolus followed by 3mg infusion over 12 hours
● Ocreotide 50mcg IV bolus followed by 50mcg/hour infusion
● Vasopressin IV infusion: 0.2-0.4 U/min, up to 0.8 U/min PLUS IV nitroglycerin at 40mcg/min titrated to
maintain SBP of 90
● Terlipressin (initial 48H) 2mg IV q4 until control of bleeding
■ Non-selective beta blockers (e.g. propranolol, nadolol) in patients with varices to reduce portal pressure and
decrease the risk of future hemorrhage
● Propranolol 20-40mg PO BID
● Nadolol 20-40mg PO OD
● Carvedilol 6.25mg PO BID
■ Rubber band ligation or endoloop ligation for esophageal varices via endoscopy
■ Sclerotherapy or cyanoacrylate injection for fundal varices via endoscopy
■ Blakemore-Sengstaken tube insertion for variceal bleeding if unable to do endoscopy
○ Endoscopic hemostasis: Mallory-Weiss tears, Dieulafoy’s lesion and other bleeding vessels
○ Upper GI malignancy: endoscopic hemostasis, surgical resection of tumor, angiography with embolization (can also be
done for bleeding in the biliary tract and pancreatic duct) or external beam radiation

95
Admitting Orders
● Admit to ward (ICU if active bleeding of PUD or bleeding esophageal varices)
● Diet: NPO
● Monitor VS Q1, I&O Qshift (insert FC for more accurate UO), record stool character and amount
● IVF: PNSS or D5LR 1L x 12H
● Diagnostics
○ CBC with PC and PBS
○ BT
○ PT/PTT
○ Serum electrolytes
○ BUN, creatinine
○ AST/ALT
○ 12-L ECG
○ CXR-PA or Abdominal x-ray, supine & upright
○ Endoscopy
● Therapeutics
1. HOLD NSAIDs, steroids and anti-platelets

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 2. Omeprazole 40mg IV OD
3. Consider Tranexamic acid 500mg IV q8
4. For abnormal PT: Vitamin K 1amp OD-BID
5. [vasoactive agent for bleeding varices]
6. Endoscopic hemostasis if able to do endoscopy
● Oxygen support: 2-3 LPM via NC
● Insert NGT to gravity drain
● Transfuse FWB or PRBC if needed

References
1. Harrison’s Principles of Internal Medicine 20th Ed.
2. PSAP-VII Gastroenterology and Nutrition: Management and Prevention of Upper GI Bleeding
3. Annals of Medicine and Surgery 28 (2018) 45–48
4. Case Rep Gastroenterol 2017;11:554–558
5. Digestion 2008;77:214–217
6. Int Surg 2011;96:266–273
7. IM Platinum 3rd Ed.
8. Expanded Medicine Blue Book 7th Ed.
9. UpToDate articles
10. Medscape articles

97
 HEART FAILURE

Marijuzca Nicolas

Definition:

“complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn
leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales” (Harrison’s)

Etiology (Harrison’s, IM platinum – 2016 ESC guidelines)

Type Ejection Fraction (EF) Description Examples

Heart failure Depressed EF <40% · Systolic dysfunction Common:

with reduced · Progressive disorder
EF (HFrEF) initiated by an index event
(eg MI, volume overload)
that leads to a decline in
the pumping capacity of
the heart
· CAD (myocardial infarction, myocardial
ischemia)
· Non-ischemic dilated cardiomyopathy
(familial/genetic, infiltrative disorders)
Other examples:
· Chronic pressure overload
o hypertension
o obstructive valvular disease
· Chronic volume overload
o regurgitant valvular disease
o intracardiac (L→R) shunting, extracardiac
shunting)
· Chronic lung disease
o Cor pulmonale
o Pulmonary vascular disorders
· Toxic/drug induced damage
o Metabolic, viral
· Chagas’ disease
· Disorders of rate and rhythm
o Chronic brady/tachyarrhythmias

HF with Mid- Grey area EF 40-49% Mild systolic dysfunction with For further research
Range EF features of diastolic dysfunction
(HFmrEF)

HF with Preserved EF ≥50% Diastolic dysfunction and Common:

preserved EF increased vascular stiffness · Pathologic hypertrophy (HOCM, HTN)
(HFpEF) · Aging
· Fibrosis
· Restrictive cardiomyopathy
o Infiltrative disorders (amyloidosis,
sarcoidosis)
o Storage diseases
(hemochromatosis)

Other examples:
· Endomyocardial disorders

High-output HF Normal at first then may
decrease over time
Body’s requirements for ixygen Common:
and nutrients are increased · Thyrotoxicosis
and the demand outstrips what · Beriberi
the heart can provide · Chronic anemia
· Systemic arteriovenous shunting

98
Pathophysiology

Epidemiology
· Follows exponential pattern, rising with age, and affects 6-10% of people aged >65
· Coronary artery disease (CAD): most common cause of HF in industrialized countries (60-75%)
· Hypertension contributes to the development of HF in 75% of patients, including most patients with CAD
· 20-30% HFrEF – unknown etiology so referred as having non-ischemic, dilated, or idiopathic cardiomyopathy
· RHD – major cause of HF in Africa and Asia, esp. in the young
· Hypertension – important cause of HF in African and African-American
· Anemia – concomitant factor in HF in developing countries

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Framingham Diagnostic Criteria for HF

Major Criteria Minor Criteria

PND or orthopnea Ankle edema

Neck vein distention Night cough
Rales Dyspnea on exertion
Cardiomegaly Hepatomegaly
Acute pulmonary edema Pleural effusion
S3 gallop Vital capacity decreased by 1/3 from maximal capacity
Increased venous pressure >16 cmH2O Tachycardia >120bpm
Hepatojugular reflux

Major or minor criteria: weight loss >4.5kg in 5 dys in response to treatment

The diagnosis of HF requires simultaneous presence of at least:

2 Major criteria, or
1 Major criterion + 2 minor criteria*

*use of minor criteria acceptable only if they cannot be attributed to another medical condition, such as pulmonary HTN, chronic
lung disease, cirrhosis, ascites, nephritic syndrome

Subjective

Symptoms Remarks

Fatigue and shortness of · Cardinal symptoms of HF

breath (dyspnea) · Fatigue-low cardiac output in HF
· Dyspnea-most important mechanism: pulmonary congestion
· Accumulation of interstitial or intra-alveolar fluid → activates juxtacapillary J receptors →
stimulate rapid, shallow breathing (cardiac dyspnea)

Orthopnea · Redistribution of fluid from the splanchnic circulation and lower extremities into the central
circulation during recumbency → increase in pulmonary capillary pressure
· Nocturnal cough – common manifestation
· RELIEVED BY SITTING UPRIGHT

Paroxysmal Nocturnal · Severe shortness of breath and coughing at night and awaken the patient from sleep,
Dyspnea usually 1-3hrs after patient retires
· Increased pressure in the bronchial arteries → airway compression
· Interstitial pulmonary edema → increased airway resistance
· Cardiac asthma – related to PND, wheezing sec. to bronchospasm
· NOT RELIEVED BY SITTING UPRIGHT

Cheyne-stokes · Low cardiac output

respiration/periodic · Increased sensitivity to arterial PCO2 and lengthy circulatory time
respiration/cyclic · Apneic phase – arterial PO2 falls, arterial PCO2 rises → stimulate respiratory center →
respiration hyperventilation and hypocapnia followed by recurrence of apnea

Acute pulmonary edema

GI symptoms · Anorexia, nausea, vomiting, early satiety assoc. with abdominal pain and fullness – edema
of the bowel wall, congested liver
· RUQ pain – liver congestion and stretching of capsule

Cerebral symptoms · Confusion, disorientation, sleep/mood disturbances – elderly w/ cerebral arteriosclerosis

and reduced cerebral perfusion
· Nocturia – common and contribute to insomnia

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Objective

Sign Remarks

General · Uncomfortable when lying flat

appearance and · Labored breathing, can’t speak in sentences
vital signs · Cardiac cachexia – weight loss and cachexia (poor prognosis)

Jugular veins · Estimation of right atrial pressure

· Jugular venous pressure – elevated with sustained pressure on abdomen (positive
abdominojugular reflex)

Pulmonary · Pulmonary crackles (rales or crepitations) – transudation of fluid from intravascular space into
alveoli
· Absent in chronic HF – increased lymphatic drainage of alveolar fluid
· Pulmonary edema – over both lung fields and may have expiratory wheezing (cardiac asthma)
· Pulmonary effusions – elevated of pleural capillary pressure → transudation of fluid into pleural
cavities
o Usually bilateral, if unilateral frequently in R pleural space

Cardiac · Reduced SBP in advanced HF (severe LV dysfunction)

· Diminished pulse pressure – reduction in stroke volume
· Sinus tachycardia – nonspecific, increased adrenergic activity
th
· Cardiomegaly – point of maximal impulse displaced below the 5 intercostals space and/or lateral
to the midclavicular line and palpable over 2 interspaces
rd
· 3 heart sound (S3, protodiastolic gallop) audible and palpable at the apex – volume overload
with tachycardia and tachypnea; severe hemodynamic studies
th
· 4 heart sound – diastolic dysfunction
· Murmurs of mitral and tricuspid regurgitation
· RVH – sustained and prolonged L parasternal impulse extending throughout systole

Abdomen · Hepatomegaly – when present, enlarged liver is tender and pulsate during systole if tricuspid
regurgitation is present
· Ascites – late sign; increased pressure in hepatic veins and veins draining the peritoneum
· Jaundice – late sign; impairment of hepatic function sec. to hepatic congestion and hepatocellular
hypoxemia, increased both DB and IB

Extremities · Cool peripheral extremities and cyanosis – excessive adrenergic activity → peripheral
vasoconstriction
· Peripheral edema – cardinal manifestation; symmetric, dependent; predominantly in ankles and
pretibial region
· Bedridden: presacral edema, scrotum
· Longstanding: indurated, pigmented skin

Acute Decompensated Heart Failure (ADHF)

· Rapid onsent or worsening of symptoms/signs of HF
· Life threatening and requires urgent treatment

Clinical Classification Typical Triggers Signs and Symptoms Clinical Assessment

Acute Decompensation Patient with chronic compensated
of Chronic HF HF who gradually decompesates
due to non-compliance to meds,
ischemia, or infections
Peripheral edema
Orthopnea
Dyspnea on exertion
Usually no/minimal volume
overload
SBP: generally in the normal range
CXR: often clear despite elevated
filling pressures
Echo: preserved or reduced EF

101
Acute Hypertensive HF Patient with no HF suddenly Dyspnea (severe) SBP >140mmHg in most
decompensates Tachypnea CXR: pulmonary edeme
Possible causes: HTN emergency, Tachycardia Echo: preserved EF in most patients
arrhythmias, or ACS Frank pulmonary edema Hypoxemia common

Cardiogenic shock Progression of advanced HF or End-organ hypoperfusion SBP: low or low normal
develops major myocardial insult Oliguria Echo: severely depressed EF
(large AMI, acute myocarditis) Confusion Evidence of end-organ dysfunction
Cool extremities (renal, hepatic)

Differential Diagnosis

Cc: dyspnea How to differentiate?

Lung parenchymal disease: interstitial lung Exposure history

disease (malignancy), TB, pneumonia Past medical history
Character of productive cough, fever
More unilateral pleural effusion
May have normal cardiac findings

Airway disease BA Past medical/Family history of BA (or atopy/AR)

Possible history of triggers of asthma
Cardiac asthma – more on inspiratory wheeze
BA – expiratory wheeze
BA: episodic/variable, partially reversible

COPD personal history of smoking/exposure to smoking

chronic bronchitis: may have signs of R heart failure (edema, cyanosis)
may be difficult to distinguish from congestive heart failure: use peak expiratory flow:
blow of 150-200ml or less for COPD
emphysema: pursed lips breathing, tripod sitting position, PE: hyperresonant with
wheezing, very distant heart sounds

Chest wall disease (kyphoscoliosis, Decreased diaphragm excursion, inability to get a deep breath (chest wall movement)
neuromuscular weakness) Normal other lung/cardiac findings

ACS Characteristic chest pain

Pericardial disease: restrictive pericarditis, History of possible etiology

cardiac tamponade (infection, heart surgery, trauma)
Chest pain – sharp, center of chest, radiating to trapezius, relived by sitting forward
Pulsus paradoxus, pericardial friction rub
Cardiac tamponade: Beck triad – increased jugular venous pressure, hypotension,
diminished heart sounds

Anemia History of possible etiology (nutritional, blood loss, malignancy, etc.)

Pallor, generalized weakness, hypotension, tachycardia, poor perfusion to other organs
(renal failure, confusion/altered mental status)

Psychological (anxiety) May have normal physical findings

May have identified psychological triggers

Deconditioning History of poor fitness

102
Admitting Orders

Admit to Intensive Care Unit

Secure consent for admission and management

Diet: NPO if dyspneic, tachypneic, or with decreased sensorium

High caloric, high protein diet if with cardiac cachexia
Sodium restriction:2-3 g/day for all patients with HF
Sodium restriction: <2g/day in patients with moderate to severe HF

IVF: heplock
Fluid restriction: unnecessary unless with hyponatremia (<130mEq/L and volume overload)
D5W 500ml x KVO or 10cc/hr

Diagnostics

2D echocardiography Most useful test for evaluation of ejection fraction or LV function

with Doppler Semi-quantitative assessment of LV size, function, wall motion abnormalities, valvular defects

Cardiac MRI Gold standard for measurements of volumes, mass, and EF of both RV and LV
High-quality imaging of the heart obtained in tomographic planes
Can characterize myocardial tissue/structurel anse assess myocardial viability

12-L ECG Cardiac rhythm, LV hypertrophy, prior MI

Normal ECG virtually excludes LV systolic dysfunction
Abnormal ECG increases likelihood of HF, but has low specificity

Chest Xray Cardiac size, shape, and pulmonary vasculature

Kerley B-lines: thin, horizontal linear opacities extending to the pleural surface due to fluid in the
interstitial space
Other findings: peribronchial cuffing, prominent upper lobe vasculature (cephalization)

Cardiac biomarkers B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)
· Upper limits in chronic HF: BNP 35 and NT-proBNP 125
· Upper limits in acute HF: BNP 100 and NT-proBNP 300
Increase with age and renal impairment
Falsely low in obese

ABG Assess lung function, oxygenation status esp. in dyspneic patients

CBC Anemia, signs of infection, bleeding – contribute to HF

Electrolytes, BUN, Electrolyte disturbances or beginning cardiorenal syndrome, ischemic hepatitis or chronic passive
Crea, AST, ALT congestion of liver

FBS, OGTT Diabetes

Lipid profile Dyslipidemia

FT4, TSH Thyroid hormone abnormalities

Blood culture Search for focus of infection

Urine culture, Search for focus of infection

urinalysis

Troponin I Index event – suspicious MI

Blood typing Streamline transfusion if needed in high output states (anemia)

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Therapeutics

Acute Decompensated Heart Failure Heart Failure with Reduced Heart Failure with Preserved Ejection Fraction
(ADHF) Ejection Fraction (HFrEF) (HFpEF)

Furosemide 20-240 mg/day
First line therapy in volume overload
Nitroglycerine 10-20 mcg/min
Isosorbide dinitrate 1mg/hr
Initial therapy for hypertensive AHF
Used for patients with pulmonary
congestion for rapid relief of dyspnea
Dobutamine 2-20 mcg/kg/min
Dopamine 5-20 mcg/kg/min
If hypotensive however DO NOT GIVE
IF
SBP IS ≤ 70 mmHg, start with NE first
Norepinephrine 0.2-1.0 mcg/kg/min
DO NOT GIVE BETA BLOCKERS TO
ADHF
Captopril 6.25-50 mg TID Evidence is lacking for the management
Cornerstone of HF treatment No treatment has been shown to reduce
morbidity or mortality
Losartan 25-100mg OD Approach:
If ACE inhibitor intolerant · Manage individual risk factors
· Reduce symptoms
Carvedilol 3.125-25mg BID o Diuretics for FO
Cornerstone of HF treatment · Prevent acute decompensation
· Improve exercise tolerance
Spironolactone 25-50mg OD
Digoxin 0.125-0.375mg OD
Ivabradine 5.0-7.5 mg BID
Sacubitril/Valsartan 49/51 –
97/103 mg BID
If with fluid retention:
Furosemide 40-240 mg
Hydrochlorothiazide 12.5-100 mg
Tolvaptan 15mg OD
Satavaptan 25mg OD

Monitor VS every 1 hour, along with temperature

IO strictly every 8 hours
Hook to cardiac monitor – if presenting with electrolyte abnormalities that predispose the patient to cardiac dysrhythmia
May give oxygen supplementation via nasal cannula for desaturations ≤ 94%; initially at 2 LPM
Referrals
CVS
1. Cardiac Resynchronization Therapy or Biventricular Pacing
a. if patient has ECG findings of sinus rhythm and a widened QRS complex (most helpful if with
LBBB) [normal QRS ≤ 110 to 120 msec (≤ 3 small squares) NOTE: Bazetts Formula is for abnormal heart rates
hence no need to compute for possible CRT patients as they need to be in sinus rhythm]
2. Implantable Cardioverter-Defibrillator (ICD)
a. to threat tachyarrhythmias (VF or VT) for primary/secondary prophylaxis against sudden cardiac death (SCD)

Long Term Plan

· Manage contributing and associated conditions
· Exercise (exercise testing first)
· Cessation of smoking
· Restriction or abstinence from alcohol consumption
· Avoid illicit drug use
· Sodium restriction to 3g/day
· Fluid restriction (1.5 to 2L per day) in patients with refractory HF or symptomatic or severe hyponatremia (serum sodium
<120meq/L)
· Avoidance of obesity
· Daily weight monitoring is recommended to detect fluid accumulation before it becomes symptomatic
· Daily check for edema and symptom severity (exercise tolerance, breathing at night, dizziness/lightheadedness)
· Adherence to medications
· Prevent infections
o Pneumococcal vaccination
o Annual influenza vaccination

References
Harrison’s, IM platinum, UptoDate, Medscape

104
 UTI – ACUTE PYELONEPHRITIS

Marylaine Padlan

Must Knows:

Definition Urinary Tract Infection – encompasses asymptomatic bacteriuria, cystitis, prostatitis and
pyelonephritis – SYMPTOMATIC DISEASES
Asymptomatic bacteriuria – presence of bacteria, accompanied by WBC and inflammatory of
cytokines in urine, ABSENCE OF SYMPTOMS attributable to the bacteria in the urinary tract,
DOES NOT USUALLY REQUIRE TREATMENT
Cystitis – symptomatic infection of the bladder
Pyelonephritis – symptomatic infection of the kidneys
Uncomplicated UTI - acute cystitis or pyelonephritis in nonpregnant outpatient women w/o
anatomic abnormalities or instrumentation in the urinary tract
Complicated UTI – all other types of UTI
Recurrent UT – not necessarily complicated
Catheter associated bacteriuria –can by symptomatic (CAUTI) or asymptomatic

Etiology - Enteric gram negative rods that have migrated to the urinary tract: E. coli, Staphylococcus
saprophyticus, Klebsiella, Proteus, Enterococcus, Citrobacter
- Complicated UTI: E. coli, Pseudomas aeruginosa, Klebsiella, Proteus, Citrobacter,
Acinetobacter, Morganella, Staphylococcus Aerus, Enterococci
- Candida – either genital contamination or via widespread visceral dissemination IF patient is
immunocompetent

Pathophysiology - Ascending infection from urethra to bladder to the ureter to the kidney
- Host, pathogen, environmental factors determine invasion and symptomatic infection
- Anything that increases the likelihood of bacteria entering the bladder, increases
urinary stasis and obstruction increases risk of UTI
- Hematogenous spread : <2% (S. aureus, Salmonella) - may produce focal areas or
abscess in the kidney
- Foreign bodies: inert surface for bacterial colonization/formation of biofilms

Epidemiology Age: More common in infants and elderly

Sex: Infant:Male> Female; 1-50s: Female>Male; >50s: Female = Males
Risk Factors: use of diaphragm with spermicide, frequent sexual contact, history of UTI, diabetes
mellitus, incontinence, UTI in previous 12 months, ASB during pregnancy , urinary obstruction (i.e.
prostatic hypertrophy), urinary tract anatomical abnormality

Complications renal or perinephric abscess formation, sepsis, renal vein thrombosis, papillary necrosis, or acute
renal failure, with one of the more serious complications being emphysematous pyelonephritis
(EPN).
- Emphysematous pyelonephritis is a necrotizing infection of the kidney usually caused by
E. coli or Klebsiella pneumoniae and is a severe complication of acute pyelonephritis. EPN is
usually seen in the setting of diabetes and occurs more frequently in women

105
Subjective

Signs and Symptoms Cystitis Symptoms - Dysuria, frequency, urgency (Cystitis, Prostatis, CAUTI)
Cystitis Symptoms + Back/flank pain, Nausea, vomiting, fever – pyelonephritis
Cystitis Symptoms + fever, altered mental status, leukocytosis - t/c CAUTI
No urinary symptoms - ASB

Family History History of UTI

Personal Social History Frequent sexual intercourse, use of diaphragms with spermicides, change of sexual partners

Past Medical History/OB Use of foreign bodies such as catheter, UTI during pregnanc
History

Objective

Pertinent: Flank pain, fever, CVA tenderness, abdominal pain, suprapubic tenderness

Assessment

Urinary Tract Related

Pyelonephritis Mild: low grade fever, lower back/ CVA tenderness

Severe: fever (high spiking “picket fence” pattern resolves over
72H therapy), rise in creatinine

Cystitis Dysuria, urinary frequency, urgency, nocturia, hesitancy, (-) fever

suprapubic discomfort, gross hematuria

Prostatits Dysuria,frequency, pain in prostatic pelvic/perineal area, fever,

chills, symptoms of bladder outlet obstruction, recurrent episodes
of cystitis

Complicated UTI Anatomic predisposition; foreign body in the urinary tract

Others

Gynecologic Pathology Dysuria, fever Vaginal discharge

(PID, ectopic pregnancy)

Nephrolithiasis Dysura, hematuria, flank pain Stone passage (actual or history)

Abdominal abscess Fever,flank pain Urinary tract symptoms

Plan

Diagnostics

Urine Dipstick Detects nitrite produced by enterobacters; can detect Pyuria – cystitis, hematuria
leukocyte esterase

Urinalysis Detects infection Check for positive nitrite, leukocyte, blood

(≥5 wbc/hpf of centrifuged urine)

Urine culture GOLD STANDARD; guidance for antibiotics use Threshold:

2
Women: Sensitive - >10 bacteria/mL, Specific
5
-> 10
3
Men: 10

106
CBC Determine infection; signs of sepsis leukopenia (WBC < 4,000) or leukocytosis
(WBC >12,000),

Metabolic Panel Bun Crea Assess kidney function

KUB UTX Determine anatomic anomalies, assess kidney and

urinary tract

Treatment

First line: Fluoroquinolones Ciprofloxacin LD IV 400 mg OPD basis

Ciprofloxacin 500 mg/tab BID PO x 7
days

TMP- SMX x 14 days IF susceptible

Ceftriaxone 1g If unknown susceptibility

TMP – SMX x 14 days

Second line: extended spectrum B-lactam and B- lactamase inhibitor If with complicated history and recent UTI
cephalosporin with or without (Ampi-sul, Tic-Clav, Pip-Taz);
aminoglycoside, carbapenem Carbapenem, (imipenem, cilastatin,
ertapenem, meropenem)

Non-pharmacologic:
Perineal hygiene, genital hygiene

Admitting Orders
Pyelonephritis
Admit to WARD
Diet REGULAR
Monitor VS Q4H
IVF D5NM 1 LITER FOR 8 HOURS
Diagnostics CBC. BLOOD GS/CS, URINALYSIS, URINE GSCS, RBS, BUN, CREATININE, KUB UTZ
Therapeutics
Ø ANTIBIOTICS (see table above)
o MODERATELY ILL/ NON SEPTIC (TREAT FOR 10-14 DAYS PO)
o SEVERLY ILL/ SEPTIC

§ CIPROFLOXACIN 200 -400 MG iv Q12H

§ CEFTRIAXONE 2 GM IV Q24H
Shift to PO drugs once afebrile
Ø SYMPTOMATIC
o Paracetamol 500mg PO for fever q4H
o Mefenamic acid 500mg PO for pain

References
th
Harrisons, UTI CPG 8 ED, IM Plat 2015, Extended Bluebook

107