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Khaled Halima
Lecturer of chest diseases AlAzhar University
Personal history:
► Male patient.
►53 years old .
►Born, living in Eldarrasa .
►Married for 20 year.
►Electrical engineering .
►Heavy Smoker .
Stages
1/11/2009 …. 31/3/2010
I
II
III
VI
2 Months
1.5 Months
1Month
2 Weeks
Stage 1
1/11/2009----1/1/2010
►Swelling of both lower limbs up to
both knees.
►Bluish discoloration of skin .
►Pain in both heels.
Treated with :
1) Brufen
2) Augmentin
400mg
625mg
1x2
1x3
Referral to vascular
physician
Received the following medications :
1)
2)
3)
4)
5)
Colchicine tab 1x3
Marevan 5mg tab 1x1
Aspocid 75mg 2x1
Anti-cox cap 1x2
Thrombophob cream 1x2
New symptoms:
-Increased bluish discoloration
skin up to the thighs.
of
-Migrating
pain
and
bluish
discoloration of the skin appeared
in both upper limbs.
What are the possibilities?
1- Cellulitis?
2- Vasculitis?
3- Local cause?
Trauma
V.V.
4- Burger’s Disease?
I.V. Inject.
What investigations do you suggest?
1-X-ray for both feet
Normal
2-Duplex for both LL.
Superficial thrombophlibitis in GSV ( Great
Saphenous Veins ) in both limbs more in left
side with no evidence of DVT.
3-ESR.
125
4 . ANA, ANCA, AntiDS DNA
Negative
5-Complete blood count.
6-Liver function test.
7-Renal function test.
HB 13.4
PLT 507
TLC 14.7
I
Superficial
Thrombophlibitis
2 Months
Partial improvement
Stage II
1/1/2010-------20/2/2010
Haemoptysis.
Pleuritic chest pain in left side.
Referral to chest physician
What Investigations do you suggest?
■ Coagulation profile.
Coagulation profile
Complete blood count
Liver, Renal function test
■ Chest X Ray P.A View
21/1/2010
4/2/2010
CT Pulmonary Angiography
Pulmonary embolism involving the left
lower lobar pulmonary artery & its
anterior & lateral segmental branches
with consequent left lower lobar
pulmonary consolidation (likely an
infarction & left sided mild pleural
effusion).
CT Pulmonary Angiography
10/2/2010
- Pulmonary emboli at the posterior
& medial segmental branches of the
right lower lobar pulmonary artery.
Decision:
Pulmonary Embolism.
I
Superficial
Thrombophlibitis
II
Pulmonary
Embolism
2 Months
1.5 Months
Stage
III
20/2/2010----18/3/2010
Fever .
Productive Cough.
Dyspnea of gradual onset, progressive
course, increased with mild exertion .
20/2/2010
Developed:
Marked Dyspnea.
Fever Subsided.
7/3/2010
Before Aspiration
8/3/2010
After Aspiration
Simple aspiration was done >>
Haemorrahgic in nature.
New Symptoms
Marked loss of weight.
Haemoptysis.
Dyspnea at rest.
Chest pain, severe back pain that
decreased with potent analgesics.
Decision???
investigated by :
1- (INR: 9) So oral anti-coagulant was stopped.
2- X-ray: Massive left sided pleural effusion.
15/3/2010
So thoracocentesis was done
4400 ml was aspirated by multiple sessions
What the cause of pleural effusion??
1-Pulmonary embolism?
2-Pneumonia?
3-Marevan toxicity?
4-Trauma ?
5- Non of the above?
I
Superficial
Thrombophlibitis
II
Pulmonary
Embolism
III
Pleural
Effusion
2 Months
1.5 Months
1Month
Reevaluation
Stage IV
18/3/2010……31/3/2010
progression of the previous symptoms
Thoracoscope was done
Result
(multiple pleural nodule was seen &
taken as biopsies) & another 1500 ml.
of
haemorrahgic
effusion
was
aspirated) .
18/3/2010
New symptoms
Marked loss of weight.
Loss of appetite , cachexia .
Marked dyspnea , orthopnea, cyanosis.
Psychological depression.
Generalized bone ache.
Malignant infiltrating adenocarcinoma versus
epithelial mesothilioma for immunophenotyping .
Immunophenotyping reaveled that it
is adenocarcinoma.
Immunophenotyping reaveled that it is
adenocarcinoma
I
Superficial
Thrombophlibitis
II
Pulmonary
Embolism
III
Pleural
Effusion
VI
Adenocarcinoma
2 Months
1.5 Months
1Month
2 Weeks
How???
Adenocarcinoma
Pulmonary
Embolism
Superficial
Thrombophlibitis
Massive
Pleural effusion
CAUSES OF SUREFICIAL THROMBOPHELEBITIS
HEMATOLOGIC SYNDROMES:
Most hematologic syndromes associated
with lung tumors are not as well
characterized as the endocrine syndromes,
because the ectopic hormone responsible
for the syndrome has not been identified in
most tumor tissues.
In many of the hematologic syndromes,
such
as
granulocytosis
and
thrombocytosis, clinical sequelae are
often absent. As with the endocrine
paraneoplastic syndromes, the most
appropriate therapy for the hematologic
syndromes is the treatment of the
underlying neoplasm.
Granulocytosis
Non–small-cell lung cancer is the most
common
cancer
associated
with
granulocytosis. Twenty percent of patients
with non–small-cell lung cancer have
granulocytosis, with absolute white blood
counts ranging from 10,100 to 25,000
(normal range is 4000 to 10,000).
Although granulocyte colony– stimulating
activity can be demonstrated in serum
and/or urine in 80 percent of patients, the
specific peptide hormone causing the
syndrome has not been identified.
Tumor production of granulocyte colony–
stimulating factor (G-CSF), granulocytemonocyte colony–stimulating factor (GMCSF), and interleukin-6 (IL-6) has been
shown in a minority of patients.
Clinical:
All patients with lung cancer who present
with tumor - associated granulocytosis are
asymptomatic.
Diagnosis:
- The diagnosis is suggested by the
presence of an increased white blood count
in which neutrophils predominate without
immature forms, in the absence of non
neoplastic causes.
An
increased
leukocyte
alkaline
phosphatase score and a normal bone
marrow are consistent with this diagnosis.
Thrombocytosis:
Thrombocytosis is common in patients with
lung cancer, afflicting 40 percent of patients
with both non–small-cell and small-cell
tumors.
Pathogenesis:
The pathogenesis of thrombocytosis in
patients with lung cancer has not been
totally explained.
IL-6,
which
is
a
cytokine
for
megakaryocytes, has been demonstrated in
cell lines from patients with lung cancer and
thrombocytosis, and increased levels of IL-6
have been demonstrated in the plasma of
such patients.
The
recent
identification
of
the
thrombopoietin gene should lead to a better
understanding of the role of this protein in
paraneoplastic thrombocytosis.
Clinical:
Patients with thrombocytosis are nearly
always asymptomatic and do not have an
increased incidence of thromboembolism.
The
diagnosis
of
cancer-associated
thrombocytosis
is
suggested
by
an
increased
platelet
count
(above
500,000/mm2) in a patient with newly
diagnosed lung cancer.
A primary myeloproliferative disorder can
be excluded only by a bone marrow biopsy.
Thromboembolism:
Twenty percent of patients with lung
cancer develop venous thrombo embolism
during the course of their disease. Twenty
percent of patients who present with
recurrent idiopathic venous thrombosis are
found to have an underlying diagnosis of
cancer.
THANK YOU