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College of Allied Medical Professions

Department of Medical Technology

Angeles University Foundation
Angeles City

A Formal Written Report for

Hematology 2 Laboratory:
Case Analysis 2
(Preliminary Period)

Submitted by:
Fajutagana, Maria Clarice D.
Lusung, Joana Marie C.
Maniego, Ann-Clarisse L.
Sumera, Jayvee T.
Group 7

Submitted to:
Mrs. Mariecel B. Quiambao
Dr. Tristan Angelo Calaquian
(Hematology 2 Lab Professors)

November 10, 2015


A 60-year-old man with a prolonged history of esophagitis and now
esophageal obstruction was found to have adenocarcinoma of the distal
esophagus and uneventfully underwent esophagectomy, relieving obstruction but
having positive margins for tumor.
A few days later, his right leg began to ache and became swollen;
appropriate studies revealed a substantial deep vein thrombosis (DVT) in that
leg. He was treated with heparin infusion and warfarin therapy was initiated. Six
days later when his INR was 2.7 for the second consecutive day, heparin therapy
was stopped and he was discharged.
Within hours, the right leg slowly became significantly worse, and now his left
arm, at the site of a recent IV line, quickly became painful and swollen. He was
readmitted. His platelet count, which had been 300,000/L preoperatively and
had remained at that level at discharge, was 160,000/L on readmission. His PT
was 16.7 seconds, PTT 68 seconds and analysis for D-dimer tests returned
markedly positive.


1. What most likely is the diagnosis for this patient? Explain why.
The most likely diagnosis for this patient is Disseminated Intravascular
Coagulation. Blood tests show that the number of platelets in a blood sample
has dropped and that the blood is taking a long time to clot. The diagnosis of
DIC is confirmed if test results show large quantities of plasma D -dimer
(indicating that more clots are being produced and broken down than usual, )
and often a low or decreasing level of fibrinogen (a protein produced when
blood clots).
This bleeding disorder is characterized by low platelet and fibrinogen
levels; prolonged prothrombin time (PT), partial thromboplastin time (PTT),
and thrombin time; and elevated fibrin degradation products (D-dimers).
2. What are the causes of this disorder?
DIC is not a disease but a sign of an underlying condition. It may be
triggered by sepsis, trauma, cancer, shock, abruptio placentae, toxins or
allergic reactions. In DIC, normal hemostatic mechanisms are altered. The
inflammatory response generated by the underlying disease initiates the
process of coagulation within the vasculature. The natural anticoagulant
pathways within the body are simultaneously impaired, and the fibrinolytic
system is suppressed so that a massive amount of tiny clots forms in the

It is also caused by an organ function or failure, usually a result of

excessive clot formation (with resultant ischemia to all or part of the organ)
or, less often, bleeding. Patient may bleed from mucous membranes,
venipuncture sites, and gastrointestinal and urinary tracts.
In this case, DIC develops more slowly, as in people with cancer, then
clots in veins are more common than bleeding. If clots form in veins (usually
in the legs), the person may have swelling, redness, or pain in the area.

3. What treatment can be given to the patient?

The most important management issue is treating the underlying
cause of DIC. A second goal is to correct the secondary effects of tissue
ischemia by improving oxygenation, replacing fluids, correcting electrolyte
imbalances, and administering vasopressor medications. If serious
hemorrhage occurs, the depleted coagulation factors and platelets may be
replaced (cryoprecipitate to replace fibrinogen and factors V and VII; freshfrozen plasma to replace other coagulation factors).
A heparin infusion, which is a controversial management method, may
be used to interrupt the thrombosis process. Other therapies include
recombinant activated protein C and AT infusions.

Turgeon, M. (2012). Clinical Hematology. 5th ed.
Smeltzer, S. (2010). Brunner & Suddarth's Textbook of Medical-surgical
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Keohane, E. (2012). Rodak's Hematology: Clinical Principles and