DATA interpretation on coagulation

A 44 year old man presents with dyspnoea and is diagnosed as having multiple pulmonary emboli on CTPA. He is commenced on heparin 1000 units/hr after a 5000 unit bolus. During the night his heparin has increased to 1500 units/hr. The blood results are from the next morning:

PT 12, APTT 38.3
Fibrinogen 3.8g/L
D-dimer (latex immunoassay) > 20.0 mgh/ml (normal < 0.5)

1. Give two reasons for the low APTT despite heparin
2. List causes for an increased predisposition to venous thromboembolic disease?

Answer 1
Inadequate heparinisation, AT-III deficiency, increased heparin clearance, increased heparin binding proteins

Note: Heparin resistance is a term used to describe patients who require unusually high doses of heparin (>35,000u/day), and can be attributable to antithrombin deficiency, increased heparin clearance, elevation in heparin-binding proteins, elevation in factor VIII, and elevation of fibrinogen.
Heparin protocols are more effective in achieving goal in anticoagulation than ad hoc approach.

Heparin is a natural gycosaminoglycan that is extracted from procine intestinal mucosa. Intravenous administration results in immediate onset of action with t1/2 of 60secs-90 minutes. Liver and renal disease results in prolonged t1/2. When heparin combine with antithrombin III (heparin cofactor), thrombosis is blocked through inactivation of activated factor II, IX, X, XI and XII. Heparin also binds to platelets, both inhibiting and promoting their function.
Coagulation test findings: increased APTT, mildly increased PT, increased TCT, normal protamine corrected APTT test, normal reptilase time
TCT: thrombin clotting time -   test of the traditional final common pathway of the coagulation cascade which converts fibrinogen to fibrin.
Reptilase time - assist with the differentiation of causes of an increased TCT. Reptilase is a thrombin -like molecule that converts fibrinogen to fibrin but is not inhibited by antithrombin III.
Protamine corrected APTT: the APTT after protamin is added to the patient's blood.


Answer 2
1. anti-thrombin III deficiency
2. protein C and S deficiency
3. Factor V Leiden gene mutation
4. Lupus anticoagulation and anti-cardiolipin
5. malignancy
6. hyperhomocysteinemia

QUESTION 2

A 54 year old man post CABG is bleeding briskly into the chest drains
INR 1.4, PT 16, APTT 55, TT 17, fibrinogen 1.2 and Platelet 65

1. How would you correct this man's coagulation?
Answer: The TT is normal, so coagulopathy is not due to heparin. Consumptive or dilutional coagulopathy and needs platelets, FFP, and cryoprecipitate.

QUESTION 3

A 24 year old woman has the following haematology and coagulation profile post admission to ICU after post partum haemorrhage.
WCC 5.6, Hb 6g/dL, Platelts 30, PT 30.6, APTT > 150, fibrinogen 0.8, D-Dimer > 10 (normal < 0.4)
1. What is the likely cause of these abnormalities?
Answer: DIC
2. In this context list 3 likely causes of this coagulation profile
-preeclampsia, AF embolism, sepsis
-intrauterine fetal death
-massive or mismatched transfusion
3. What does an elevated D-dimer indicate?
Answer: Tests fibrinolysis (breakdown of the X linked fibrin)

QUESTION 4

A 54 year old woman presented to the ED after having been unwell for 4 days. Her FBC report is:
Hb 12.8 g/dL, WBC 56.5, Platelet 347, Hct 41.4%
Neutrophil 96.3%
Lymphocyte 2.8%
Mono 0.7%, Eosin 0.1%, Baso 0.1%
Moderate rouleaux. Marked neutrophilia. Dohle bodies present, toxic granulation present.
1. What likely hematological process is revealed by the abnormal white cell count?
Answer: Acute leukemoid reaction.
-> 50,000 cells, normal baso and eosinophil counts, Dohle bodies, toxic granulation

Data Interpretation

A previously well 54 year-old man presents with confusion. On examination a rash is noted. Temperature 37.1. The initial blood results are provided below.

Venous biochemistry
Na 135
K 3.8
Urea 18 mmol/l -*
Creatinine 177 micromol/l-*
Bilirubin 45 micromol/l -*

Hematology:
Hb 99 g/l
WBC 10.8 x 10(9)/L
Platelet 26 x 10(9)/L-*
Blood film: Schistocytes-*

Coagulation
PT 10 s
APTT 29 s
Fibrinogen 3.0 g/L

What is the most likely diagnosis?
Thrombotic thrombocytopenic purpura

What treatment needs to be instituted urgently?
Plasmapheresis

TTP shows a classic pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia, and renal and neurological defects. This is thought to be related to an abnormal metalloproteinase (ADAMST 13). The condition is seen with certain infections, drugs (e.g. calcineurin antagonists, clopidogrel), pregnancy, systemic lupus erythematosus and graft versus host disease.
The labarotary findings in this condition are:
-low platelets
-reduced hemoglobin level with polychromasia, shictocytes and spherocytes
-increased reticulocytes
-reduced haptoglobin and increased lactate dehydrogenase levels
-unconjugated hyperbilirubinemia with urinary urobilinogen
-variable neutrophilia
-increased urea and creatinine levels (greater in hemolytic uremic syndrome)

Hematology question

Question 1

A man with fractured ribs following a fall has the following results:

Hb: 10.9 g/dL
PCV: 39%
MCHC: 30g/dL
WBC: 12.8 x 10 (9)/L
Neutrophils: 64%
Lymphocytes: 27%
Monocytes: 3%
Myelocytes: 2%
Metamyelocytes: 4%

Nucleated RBCs, slight poikilocytosis, slight anisocytosis

1. What is this type of blood picture?
A: Leukoerythroblastic picture
leukoerythroblastic picture on blood film can be the bone marrow response to any irritation including marrow infiltration (causing immature red cells). Marrow infiltrative disorders include myelomas, malignancy, myelofibrosis, Gaucher's disease etc. It can also occur as a response to severe critical illness such as trauma, sepsis, massive hemolysis or severe megaloblastic anemia. Leukoerythroblastic change refers to the presence of nucleated red blood cells and primitve white blood cells.

Peripheral blood smear showing the presence of nucleated red blood cells and immature white cells.

2. List four possible underlying causes?Marrow infiltration, overwhelming sepsis, major blood loss and marrow hypoxia

3. What is meant by the terms anisocytosis and poikilocytosis?
Anisocytosis is excessive inequality in the size of red blood cells
Poikilocytosis is increase in number of abnormally shaped red blood cells on film

Question 2

A 78 yr old man presented after a fall resulting in a bruised hip. His Full blood count is the following:

Hb 12.0 g/dL
WBC: 1.9 x 10 (9) --> low
Platelet: 28 x 10 (9) --low
RBC: 3.01 x 10 (9)--low
HCT: 0.358 --low
MCV: 118.9 fL --high
MCH: 39.9 pg --high
MCHC: 335 G/L --normal
Neutrophils 79.6%
Lymphocyte 17.3%
Monocytes 3.1%
Eosinophils 0.0%
Basophils 0.0%

Moderate anisocytosis, marked macrocytosis

List causes for the raised MCV?
Answer:
-B12 deficiency
-folate deficiency
- myeodysplastic syndrome
- therapy with cytotoxics or immunposuppressants
- alcohol
-hypothyroidism
- alcohol and hypothyroidism do not produce such high levels of MCV usually but anwers accepted.

Note: macrocytosis - describe erythrocyte that are larger than normal, typically reported as MCV greater than 100 fL. Because the amount of Hb in the cell increases proportionately with the increase in size, MCHC remains within normal limits.
Causes of macrocytosis are many and range from benign to malignant; thus a complete work up to determine etiology is essential. Macrocytosis can occur at any age, but it is more prevalent in older age groups because the causes of macrocytosis are more prevalent in older persons.