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Case Management

Conference
Objectives
At the end of this session, the class should be able to
Utilize history and PE to be able to form a sound working
impression
Formulate a wide spectrum of differential diagnosis
Rationalize each use of diagnostics and therapeutics
Correlate and anticipate clinical signs symptoms with
diagnostics
CASE
H.J.
34 year old, Female
Married
Filipino
Born Again Christian
Dasmarinas, Cavite
Chief complaint
Abdominal pain
History of Present Illness
Known case since 2013
Dexamethasone 10mg OD, Celecoxib 100mg OD
SLE

loss of appetite, weight loss


occasional, intermittent non-productive cough
2 months (-) nausea, vomiting, diarrhea, nor chest pain
PTA (-) consult done

loss of appetite, weight loss persisted


change in bowel habits, 3 times per week
1 month (-) dyspnea, nausea, vomiting, cough, colds, nor fever
PTA (-) consult done
History of Present Illness
Recurrence of intermittent, non-productive cough
(+) associated generalized body weakness, dyspnea,
occasional palpitations
1 week (-) nausea, vomiting, abdominal pain, and fever noted
PTC (+) weight loss and loss of appetite

Epigastric-periumbilical pain, VAS 10/10 , burning in


character, non-radiating
8 hours (+) 2 episodes of non-bilious, non-projectile vomiting
PTA (+) chest heaviness, dyspnea

Consult
Past Medical History

Opted alternative herbal medicine 3 months PTA


Green Leaf capsule 4 doses ODHS, Alkaline capsule,
Calcium phosphate 1 tab SL for 3 doses, Kaliphos 1 tab
SL for 3 doses and MX3 capsule OD

Diabetes Mellitus (2016)


Glimeperide/Metformin 2mg/500mg OD, stopped after 6
months
Family Medical History
Hypertension- both sides
No history of other heredofamilial diseases noted
No known history of connective tissue disease
Personal Social History
Non smoker
Non alcoholic beverage drinker
No history of illicit drug use
Previously worked as an employee at an electronics
company
OB-Gyne History
G1P1 (1001) Male, 2013, LTCS at DLSUMC
LNMP: February 2017
Regular monthly cycles, 3-5 days duration, using 2-
3 moderately soaked pads/day
Review of Systems
General: (-) weakness, (-) weight loss (-) loss of
appetite, (-) easy fatigability
Integument: (-) wounds, (-) nail clubbing, (-) rashes, (-)
pallor
Head & Neck: (-) headache (-) dizziness (-) mass, (-)
distension of veins, (-) stiffness
Eyes: (-) pain (-) redness, (-) discharge, (-) use of
corrective lenses
Ears: (-) otalgia, (-) discharge (-) vertigo (-) tinnitus
Nose & Sinuses: (-) nasal congestion (-) colds (-)
epistaxis, (-) watery discharge, (-) obstruction
Mouth & throat: (-) sore throat (-) ulcers, (-) dysphagia,
(-) tongue fasciculation
Review of Systems
Respiratory: (+) shortness of breath (-) hemoptysis,
(+) pleuritic chest pain
Cardiovascular: (-) chest pain, (-) murmur (-) palpitations
GIT: (-) epigastric pain, (-) Nausea (-) Vomiting, (-) diarrhea, (-)
hematochezia, (-) melena, (-) abdominal distention
GUT: (-) frequency, (-) dysuria, (-) polyuria
Vascular: (-) ulcers, (-) varicose veins
Hematologic: (-) easy bruising, (-) bleeding, (-) pallor
Endocrine: (-) polyuria, (-) polyphagia, (-) polydipsia
Musculoskeletal: (-) fractures, (-) joint pains, (-) edema
Nervous: (-) seizures, (-) tremors
Physical Examination
Poorly nourished, fairly developed
awake, conscious, and coherent, oriented to time,
place, and person.

Weak-looking, appears her older than her stated


chronological age of 34

in mild cardio-respiratory distress.


Physical Examination
Blood Pressure: 110/60 mmHg
Heart Rate: 118 bpm
Respiratory Rate: 25 cpm
Temp: 36.3oC
O2 sat: 98% on nasal cannula 2-3 lpm
Weight= ~40kg Height= 52 BMI= 16.1
Physical Examination

Skin
Pallor, but no jaundice or erythema, edema
Warm to touch with prompt return of skin, no excessive
dryness or moisture, soft and resilient.
There are hypopigmented patches on the dorsal
aspect of both hands.
Hair is limp but in normal amount and black in color. No
nail dystrophies or deformities, no changes in shape and
color.
Mucosa is pink and moist.
Physical Examination
Eyes
Eyes are symmetrical, with pale palpebral conjunctiva,
anicteric sclerae, direct and consensual reflex. Pupils were
equally and briskly reactive to light. There are no noted corneal
or lens opacities. Extraocular muscles are intact.

Nose
The external nose is symmetrical, aligned vertically with the
midline and free of any masses, deformities. The external
nares are equal in size and shape. The vestibule and the rest
of the visible nasal cavity are free of masses, ulcerations or
discharge.
Physical Examination

Ears
The pinna is mobile and devoid of masses, ulcerations or
tenderness. The periauricular areas likewise have no swelling
or tenderness. The canal is patent and devoid of masses,
discharge or excessive epithelial debris.
Physical Examination

Oral Cavity and Pharynx


Lips are symmetrical, pale and devoid of masses or
ulcerations at the time of examination. The oral mucosa and
gums are pale, smooth, free of masses or ulcerations. The
tongue is mobile. The dorsum of tongue is pale pink and free
of masses or ulcerations. The palate is smooth and without
lesions.
Physical Examination

Head and Neck


Hair of normal pattern, texture; scalp/head symmetrical, no
mass nor tenderness. No cervical lymph nodes palpated. Neck
veins are not distended. JVP was measured at 10cm H2O.
Thyroid gland not palpable, no tenderness noted. Thyroid
cartilage prominence moves with deglutition. Trachea is in
midline.
Physical Examination
Chest and Lungs
Chest is symmetrical, without deformities nor lesions
Respiratory rate is at 25cpm, regular,
(+) use of accessory muscles but no abnormal
intercostal retractions
Decreased breath sounds on the right mid-base.
Occassional crackles were heard at the left mid-base
lung fields.
Dullnesss on percussion of the right lung field
Physical Examination
Cardiovascular
No precordial bulging
Point of maximal impulse is at the 5th ICS LMCL
The apex beat is found at the 5th ICS LMCL with heaves but no
thrills.
Heart rate is tachycardic at 118 bpm, regular rhythm,
S1>S2 at the apex, S2>S1 at the base, (+) S3, no S4
no murmurs appreciated.
Physical Examination
Abdomen
The contour of abdomen is slightly globular,
symmetrical, with a midline hard, non-movable, and
hypertrophic CS scar from the infraumbilical to the
hypogastric area. No discolorations, visible peristalsis, or
pulsations appreciated. Low-pitched bowel sounds are heard
at an average of 7 per minute. The abdomen is
hypertympanitic all over. Abdomen is soft, with direct
tenderness on the epigastric and periumbilical area. The
liver, spleen, and kidneys are not palpable
Physical Examination
Musculoskeletal
There are tolerable joint pains noted on the knees,
shoulders, and elbows, and patient is able to move
extremities against gravity.

Gait is not observed.

There is no tenderness, redness, mass, swelling


deformity, crepitus, nor limitation of motion noted on the
temporomandibular joint.

The extremities are atrophic, with noted muscle rigidity


on both biceps. No limitation of motion in the upper or
lower extremities.
Physical Examination
Neurologic

The patient is bed-ridden, neat, dressed appropriately


according to age and occasion. Stream of talk is quite
racing and appropriate mood are noted. There are no noted
thought disturbances. She appears with average intellectual
capacity. She is awake, conscious, oriented to place and
person, with vague time orientation. She has fair attention
span and good remote and recent memory.
Physical Examination
Neurologic

CN I not assessed
CN II (+) direct and consensual light reflex
CN III, IV, VI full EOMS
CN V (+) equal facial sensation
CN VII symmetric facial expressions
CN VIII intact gross hearing
CN IX, X speech was of normal tone of voice,
able to swallow and cough
CN XI Good shoulder shrug
CN XII Tongue is midline, (-) fasciculation
Physical Examination
Meningeals (-) nuchal rigidity, (-) Brudzinkis sign (-) Kernigs
sign

Cerebellar testing (-) nystagmus, (-) dysmetria (-)


dysdiadochokinesia

Higher Cortical Function Testing The patient has no


expressive aphasia.

4/5 4/5 100% 100% ++ ++

4/5 4/5 100% 100% ++ ++


Salient Features
34 y/o Female
Weak looking, BMI 16.1
Known SLE for 3 years, lost to follow up
Known chronic steroid and NSAID user
Sudden severe epigastric-periumbilical pain, burning
character, non-radiating, (+) 2 episodes vomiting
Decreased breath sounds on the right mid-base,
Occassional crackles at the left mid-base, Dullness
on percussion of the right lung field
Dyspnea, Tachycardia, Anorexia, Weight loss, Pleuritic
chest pain
Working Impression
Peptic Ulcer Disease Community Acquired
secondary to Chronic Steroid Pneumonia- Moderate Risk
and NSAID use, secondary Acute cough
to SLE Tachypnea
Epigastric-periumbilical pain Tachycardia
Burning in character Adventitious breath sounds
(+) vomiting (crackles)
3 year history of steroid and Probable pleural effusion
NSAID use (decreased breath sounds on
the right, dullness on
percussion on the right)
DIFFERENTIAL DIAGNOSIS
PULMONARY
DIFFERENTIALS
Pulmonary Tuberculosis
Likely Due To: Not Likely Due To:
2 month history of cough Cannot totally rule out, need for
sputum microscopy or Gene
anorexia and weight loss Xpert study
easy fatigability
dyspnea
immunocompromised state
Community Acquired
Pneumonia
Likely Due To Not Likely Due To
Dyspnea Cannot be totally ruled out
Occasional intermittent cough
Generalized body weakness
Co-morbidities (e.g. SLE, and
Diabetes Mellitus)
Increased respiratory rate
Presence of crackles on left mid-
basal lung field
Dullness on percussion of the
right lung field
Primary Spontaneous
Pneumothorax
Likely Due To Not Likely Due To
Dyspnea Patient had a 2 month history
of cough
Occasional intermittent
cough Absence of pleuritic chest
pain
Decreased breath sounds
No noted lagging on
inspiration
Dullness on percussion
(should be hyperresonant)
Interstitial lung disease
Likely Due To Not Likely Due To
Working for an electronics Cannot be totally ruled out in
company the absence of CXR. CSR
should show an evidence of
History of SLE structural lesion consistent
Dyspnea with the interstitial process
depending on the agent
Cough
Pulmonary Hypertension
Likely Due To Not Likely Due To
Working for an electronics Cannot be totally ruled out in
company the absence of CXR. CXR
should show an evidence of
History of SLE structural lesion consistent
Dyspnea with the interstitial process
depending on the agent
Cough
CARDIOVASCULAR
DIFFERENTIALS
Myocarditis
Likely Due To Not Likely Due To
Ruled in due to the presence Absence of evidence for a
of dyspnea and weakness recent viral infection with
fever and myalgia
Chest heaviness
Dyspnea not noted to be
progressive
Congestive Heart Failure
Likely Due To Not Likely Due To
Ruled in due to the presence Cannot be totally ruled out
of dyspnea, intermittent
cough, and dyspnea on
effort.
Chest heaviness
Noted S3 on auscultation
Tachycardia (118 bpm)
Crackles on the left mid-
basal lung field
GASTROINTESTINAL
DIFFERENTIALS
Inflammatory Bowel Disease
Likely Due To Not Likely Due To
Abdominal pain Absence of diarrhea
Pallor Absence of hematochezia
Tachycardia (118 bpm) Non-distended abdomen
Acute Pancreatitis
Likely Due To Not Likely Due To
Sudden epigastric pain, radiating Cannot totally rule out,
to the back
request for Amylase or
Nausea and vomiting Lipase (more specific)
Anorexia
may also request for BUN,
Tachycardia Calcium, ABG, and CBC
Dyspnea after 48 hours to determine
severity of pancreatitis and
Corticosteroid use
predict mortality
Direct and rebound tenderness of
epigastric area
History of SLE
NEOPLASTIC
DIFFERENTIALS
B Cell Lymphoma
Likely Due To Not Likely Due To
Weight loss Absence of
lymphadenopathies
Pallor
Tachycardia Absence of purpura,
petechiae, and ecchymoses
Tachypnea
Dyspnea
Shortness of breath
Decreased breath sounds,
right mid-base
Course in the Wards
Course at the Wards
At the ER Uric acid

Diagnosics: ESR
12L ECG CRP
CBG
CBC PT/PTT
Na
K
C3
BUN Albumin
Creatinine
Chest Xray AP blood CS
Chest Ultrasound Ionized calcium
Chest apical series
Therapeutics:
Omeprazole 40mg IV
Tramadol 50mg IV
Upon admission:
Diagnostics:
Fecalysis with fecal occult blood test
Anti-dsDNA
Pleural fluid analysis
Serum LDH and total protein
Abdominal ultrasound

Patient was referred to Surgery and


Rheumatology for co-management.
Upon admission:
Therapeutics:
Tramadol 50mg IV q8 RTC
Ceftriaxone 1g IV OD
Azithromycin 500mg IV
N-acetylcysteine 600mg/tab 1 tab OD
Duavent neb q8 and prn
Omeprazole 40mg IV OD
Dexamethasone (DECILONE FORTE) 1 tab ODPC
CaCO3 1 tab
Lantus 15u ODPM
Apidra 6u TID premeals
05-09-2017 05-09- 05-09-2017
2017
Hemoglobin 127 Na 137
PT Patient 16.2
Hematocrit 0.40 BUN 5.2
PT Control 13.4
WBC 20.4 Trop I 6.6
PT INR 1.24
RBC 4.9 Albumin 22
% Activity 69
Segmenters 0.95 Uric Acid 0.71
Lymphocytes 0.04 Creatinine 66.3
Eosinophils 05-09- K 3.6
Basophils 2017 Procalcitonin 0.42
Platelet 708 C- Lipase
reactive 57.4
MCV 82.6 protein LDH
MCH 25.9 C3 1500 Total Protein
MCHC 314 Ionized
1.72
RWD 22.3 calcium
Chest Ultrasound
Right: 317.4cc anechoic fluid, Loculated pleural
effusion

Left: 4.1cc
05-09-17
Day 1 (05/10/17)
S O A P
Problem: BP: 100/60 mmHg Community Give Apidra
Increased blood HR: 128 acquired (Insulin glulisine)
glucose RR:25 pneumonia 6 units TID and
O2 Sat: 99% moderate risk; Humulin R 15
CBG= 240- (-) CRD DM type II units OD PM
270mg/dL (+) pallor uncontrolled
(+) decreased For CBG
No new breath sounds on monitoring q1
subjective right base
complaint
WHOLE ABDOMEN
Fecalysis ULTRASOUND (05/10/2017)
05/10/2017 IMPRESSION:
Color Brown -Ascites
Consistency Formed -Consider focal pancreatitis of the
Occult Blood Negative body of the pancreas. Clinical
WBC None correlation with serum
RBC None parameters (I.E. Amylase and
Fats Lipase) is suggested for further
Bacteria +3 evaluation
Ascaris -Urinary sediments
Trichuris -Unremarkable ultrasound study
Hookworm of the liver, gallbladder, spleen,
abdominal aorta and kidneys
-Normal-sized retroflexed uterus
with an intact endometrial stripe
PLEURAL FLUID ANALYSIS (05/10/2017)
Negative for atypical cells
Color: Reddish yellow
Character: Cloudy
Specific gravity: 1.020
pH: 8.0
WBC Count: 10/cumm
Segmenters: 28%
Lymphocytes: 72%
RBC Count: 6,192/cumm
Sugar: 6.12 mmol/L
Protein: 48 g/L
GRAM STAIN PLEURAL FLUID
(05/10/2017)
Epithelial cells: few
PMNs: +1
Gram (+) Cocci Seen Singly: Few
Day 2 (05/11/17)

S O A P
BP: 100/60 mmHg
HR: 128
RR:25
O2 Sat: 99%
Problem: General: awake,
Increased blood conscious, not in Dulcolax 2
glucose cardiorespiratory Community suppositories
distress acquired
CBG=? Skin: (+) pallor pneumonia CBG monitoring
No new Chest/Lungs: moderate risk was decreased
subjective decreased breath with pleural to TID
complaint sounds on right effusion, right;
base DM type II, Thoracentesis
controlled was done
05-
12-17
Day 3 (05/12/17)
S O A P

BP: 100/60 mmHg


HR: 128
RR:25
O2 Sat: 99%
General: awake,
conscious,
disoriented not in
cardiorespiratory
distress Dulcolax 2
Problem: Increased Skin: malar rash suppositories
blood glucose Chest/Lungs: Fine
crackles were still Community CBG monitoring
CBG=? heard at mid-base acquired pneumonia was decreased to
No new subjective bilateral lung moderate risk; SLE TID
complaint fields. in flare; DM type II,
Extremities: controlled Thoracentesis was
arthritis done
Hospital Day (05/13/17)
S O A P
problem # 1 BP: 110/70 Community acquired Fluimucil was increased
occasional DOB HR: 126 pneumonia moderate to BID
no chest pain, no RR: 20 risk; SLE in flare; DM type
fever, no T: 36.8 II, controlled Clindamycin 300mg IV q6
desaturation O2 Sat: 98% was started

SHEENT: (+) malar rash, Apidra was


oral ulcers discontinued.

Chest and Lungs: Fine CBG monitoring was


crackles right mid-base decreased to Q12.

Heart: (+) tachycardic

Abdomen: soft non-


tender abdomen was
noted.

Extremities: (-) edema, (-)


joint pains

CTT output was 300 cc.


Hospital Day (05/14/17)
S O A P
No new subjective BP: 110/70 mmHg Community acquired Present management
complaints HR: 116 pneumonia moderate continued
RR: 26 risk; SLE in flare; DM
No fever, no DOB Temp: 37.2 type II, controlled
No chest pain O2 Sat: 97%

Chest and Lungs: (+)


fine crackles right mid
base

Heart: Normal rate and


rhythm.

Extremities: Grade 1
non pitting edema, (+)
joint pains

CTT output: 200cc


Hospital Day (05/15/17)
S O A P
No new subjective BP: 110/70 mmHg Community acquired Clindamycin IV was
complaints HR: 99 pneumonia moderate shifted to oral
RR: 20 risk; SLE in flare; DM 300mg/capsule 1
No fever, no DOB Temp: 36 type II, controlled capsule q6
No chest pain O2 Sat: 96%
Sultamicillin 750mg tab
Chest and Lungs: CBS BID was started.

Heart: Normal rate and Hydrocortisone was


rhythm, (+) S3 shifted to
Methylprednisolone
Extremities: Grade 1 (Mepresone) 16mg tab
non pitting edema, (+) BID.
joint pains

CTT output was 100 cc.


CULTURE AND SENSITIVITY (05/15/2017)
Blood culture Left arm: No aerobic growth after 5 days
incubation

Pleural Fluid: No aerobic growth after 4 days incubation


Hospital Day (05/16/17)
S O A P
Problem 1: patient was BP: 120/70 mmHg Community acquired
noted to have febrile HR: 102 pneumonia moderate
episodes of 38.4 C RR: 19 risk with pleural Paracetamol given
Temp: 36.4 effusion, bilateral; SLE
O2 Sat: 98% in flare. DM type II,
Problem 2: lower controlled
extremity edema. SHEENT: (+)malar rash Peptamen 6 scoops in
and oral ulcers 250cc water TID
Chest and Lungs: Clear
breath sounds
Heart: tachycardic and Bumetanide 1g tab
OD were given

Extremities: (+) Grade 1 For repeat chest xray


non pitting edema, (+) PA upright/high sitting
joint pains

CTT output was 100 cc.


05-16-17
Hospital Day (05/17/17)
S O A P

patient did not have BP: 110/60 mmHg


any febrile episodes HR: 98
RR:
Temp: 36.4
Problem 1: 4 pm, O2 Sat: 98%
patient was noted to Community acquired
have difficulty of Extremities: Grade 1 pneumonia Ipratropium +
breathing and oxygen non pitting edema, (+) moderate risk with Salbutamol (Duavent)
saturation was at 91%. joint pains pleural effusion, 500mgc/2.5mg for 3
bilateral; SLE in flare doses
CTT output was 200 DM type II, controlled
cc.
S O A P
ACLS + chest
compressions + manual
respirations

Problem 2: Epinephrine 1mg


4:20pm, patient q3mins > subsequently
was referred due intubated
to Dopamine drip 400mg
unresponsiveness D5W 250cc x 10cc/hr
and HR = 0 and
BP= 0 Diagnostics ordered 12L
ECG, ABG 1 hour post
mechanical ventilation,
Return of CXR portable, blood CS
spontaneous x 2 sites, and ETA
circulation with GS/CS. Indwelling foley
catheter and
sinus rhythm was nasogastric tube were
noted after 3 also inserted.
cycles of ACLS,
with a BP of 60 Enoxaparin 0.6cc SQ
BID was ordered.
palpatory,
at around 5:00pm, PEA was again noted in the patients
cardiac monitor. ACLS was again rendered but patient was
persistently on PEA after 10 cycles of ACLS. Patient was
pronounced clinically dead at 5:54pm after noting asystole
on the cardiac monitor.

Immediate cause of Death: Acute Pulmonary Embolism


Antecedent cause of Death: Pneumonia in the
immunocompromised host
Underlying cause of death: Systemic Lupus
Erythematosus in flare
PLEURAL EFFUSION
PLEURAL EFFUSION
Accumulation of Pleural fluid when pleural fluid formation
exceeds pleural fluid absorption.
This condition can develop when there is excess pleural
fluid formation or when there is decreased fluid removal by
the lymphatics
May be transudative or exudative
Distinguished from each other using Lights Criteria
Pleural fluid protein/serum protein >0.5
Pleural fluid LDH/serum LDH >0.6
Pleural fluid LDH more than two-thirds the normal upper limit for
serum
PLEURAL EFFUSION
CLINICAL MANIFESTIONS
Pleuritic chest pain, cough, and dyspnea
Decreased breath sounds
Decreased or Absent tactile fremitus
Dullness on percussion
Tracheal deviation
X-RAY
PLEURAL EFFUSION
UNDERLYING ETIOLOGIES
CARDIAC
GASTROINTESTINAL
INFECTION
MALIGNANCY
PULMONARY TUBERCULOSIS
CHYLOTHORAX
HEMOTHORAX
MISCELLANEOUS CAUSES
PLEURAL EFFUSION
Transudative Exudative
Parapneumonic Effusions
Congestive Heart failure
Malignant tumors
Cirrhosis
Infectious diseases
Other transudative effusions
Nephrotic Syndrome Collagen Diseases
Peritoneal dialysis
Chylous Pleural Effusion
Superior vena syndrome
Myxedema
Urinothorax
TRANSUDATIVE PLEURAL
EFFUSION
Effusion due to Heart
Failure
The most common cause of pleural effusion is left
ventricular failure.

Increased amounts of fluid in the lung interstitial spaces


exit in part across the visceral pleura that overwhelms
the capacity of the lymphatics in the parietal pleura to
remove fluid
Hepatic Hydrothorax
Cirrhosis and Ascites
The predominant mechanism is the direct movement of
peritoneal fluid through small openings in the
diaphragm into the pleural space

Usually on the right side


Other transudative
effusions
Nephrotic Syndrome
Peritoneal dialysis
Superior vena syndrome
Myxedema
Urinothorax
EXUDATIVE PLEURAL
EFFUSION
Parapneumonic Effusion
Bacterial Pneumonia
Lung abscess
Bronchiectasis
Empyema
Effusion due to Malignancy
Pleural effusion is often bloody
Can result from primary cancer of the lungs, pleural
mesothelioma, leukemia lymphoma or metastatic
spread of another tumor to the lungs.
Effusion due to Pulmonary
Embolism
Dyspnea is the most common symptom
If the pleural effusion increases in size after
anticoagulation, there is recurrent emboli or another
complication, such as a hemothorax or a pleural
infection.
Tuberculous Pleuritis
TB pleural effusion is straw colored fluid containing
fibrin and comprises 70% lymphocytes

Associated with primary TB due to a hypersensitivity


reaction to tuberculous protein in the pleural space
Chylous Pleural Effusion
Thoracic duct is disrupted and chyle accumulates in
the pleural space.
Hemothorax
thoracentesis reveals bloody pleural fluid
hematocrit is more than one-half of that in the
peripheral blood
Miscellaneous causes of
Pleural Effusion
Pancreatitis
Systemic Lupus
Erythematosus
SLE
This is a chronic autoimmune disease. There is
production of autoantibodies and subsequently
deposited in tissues.

More common in women.


SLE is higher among Asians, African Americans,
African Caribbeans, and Hispanic Americans
Pathogenesis
Lupus Serositis
Immune Complex deposition in the Pleural vessels

Inflammation of the Pleural vessels

Increased Permeability of the microvascular circulation

Fluid and Protein leak


Pulmonary Embolism
Virchows Triad
(Inflammation, Hypercoagulability and endothelial inflammation)

Recruitment of Activated platelets, releases microparticles

Binding of proinflammatory mediators to neutrophil

Stimulate platelet aggregation and


promote platelet dependent thrombin generation

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