Polytruama Flashcards

Stem: A known hepatitis C patient suffered a traumatic splenic rupture with massive blood loss. Spleenectomy done and the patient reecieved a massive blood transfusion. Later, the patient developed epistaxis, bleeding in the NG tube and oozing from the surgical wound. Investigations showed sever thrombocytopenia and low fibrinogen with increased fibrin degradation products.

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Stem: A known hepatitis C patient suffered a traumatic splenic rupture with massive blood loss. Spleenectomy done and the patient reecieved a massive blood transfusion. Later, the patient developed epistaxis, bleeding in the NG tube and oozing from the surgical wound. Investigations showed sever thrombocytopenia and low fibrinogen with increased fibrin degradation products.

Q1: What’s your diagnosis?

A

DIC Dissemented intravascular coagulopathy

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2
Q

Define DIC?

A

Pathological Consumptive Coagulopathy due to activation of coagulation and fibrinolytic system leading to forming microthrombi with consmpution of clotting Fx and platlets. Chch by wide spread hge / Thrombocytopenia / consumption of coagulation factors

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3
Q

Q2: How to correct DIC?

A

Transfusion of FFP and platlet and cryoprecipitate(fibrin, fibrinogen, Fx 8, Fx 13, VWF) and desmopressin

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4
Q

Q3: What’s massive transfusion protocol? What are its complications?

A

rapid administration of large amounts of blood products (at least 6 units of PRBC) in fixed ratios (usually 1:1:1) for the management of hemorrhagic shock. Only a subset of patients with “massive transfusion” will receive a massive transfusion
protocol.

Complications; Volume overload, Hypothermia, Hyperkalemia, Hypocalcemia, platlet dysfunction, coagulopathy

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5
Q

Q4: How to minimize the need for blood transfusion?

A

-Maintain a hemoglobin concentration of 8 g/dL.
-Ensure platelets are at 10 × 10³/μL.
-Use fresh frozen plasma for proven coagulopathies.
-Avoid blood loss using diathermy and normothermia.
-Apply fibrin sealant or glue.
-Administer anti-fibrinolytic agents like tranexamic acid and aprotinin.
-Use haematinics and erythropoietin preoperatively, with iron and folate supplements.
-Use plasma expanders, such as crystalloids and colloids.
-Utilize autologous transfusion.

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6
Q

Q5: How platelets are formed? What’s its shelf life?

A

From megakrycytes by fragmentation
5-6 days

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7
Q

Q6: What’s the percentage of platelets and WBCs in packed RBCs?

A

Platlets; zero
WBCs; 5x106/L

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8
Q

Q7: What’s the life span of RBCs?

A

120 days

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9
Q

Q8: What would a hematologist ask F1 before ordering the blood transfusion?

A

Grouping and cross matching ABO / Rh

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10
Q

What’s cross matching? Which antigens are tested? what is meant by group and save?

A

Test donor RBCs against the recipient serum to detect any potentiality of incompatibility. As recipient ab may cause hemolysis of donor RBCs
ABO / RH
blood group and Ab screen

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11
Q

Q9: Why does this patient has bleeding tendency?

A

Liver dysfunction  Vit K definecy affecting production of coagulation Fx 1972

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12
Q

Q10: What are the late manfestations of HCV?

A

Cirrihosis and hepatocellular carcinoma

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13
Q

Q11: What activates intrinsic and extrinsic pathways? How can you test each?

A

Int; exposure of endothelial collagen / By APTT
Ext; Tissue Fx / By PT

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14
Q

Q12: The patient developed a hypersensitivity reaction during blood transfusion, what is the definition of hypersensitivity? What are its types?

A

Exaggerated immunological response to an Ag.
Types
I – immediate - IgE – Anaphylaxis
II- Cytotoxic – IgM / IgG – Hemolytic anemia
III- Immunocomplex – AgAb – SLE /RA
IV- Cell mediated – T cell – Contact dermatitis / TB
V- autoimmune – Grave’s Dis

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15
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Q13: The patient has sustained a long bone fracture, can you mention the different stages of bone healing?

A

Hemtoma Formation – Hrs to Days
Inflammatory Phase – Days to weeks
Fibrocartilagenous callus Formation – 2 wks
Hard Callus Formation – 2 wks to several months
Remodling – 7 mon – years

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16
Q

Q14: What are the effects of prolonged imobility on bone healing?

A

Immobilization impacts bone modeling and remodeling by increasing the activation of remodeling sites while decreasing osteoblastic activity. This dual effect results in a local reduction in bone mass. The heightened remodeling activity exacerbates the deficit in bone formation, leading to weakened bone structure and delayed healing.

17
Q

Fracture was treated by ORIF; then the wound started oozing yellow fluid
Q15: What’s the first test to be done to the fluid?

A

Swap for C&S

18
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Q16: Wound swab and culture revealed PVL, What does PVL stand for? What’s the effect of its cytotoxin?

A

Panton Valentine Leucocidin
Cytotoxin produced by S. Aureus cuase leucocyte destruction and tissue necrosis.
effect; cuase pores in the membranes and this will cause necrotic lesion like in skin or mecosa

19
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Q17: What would you like to do with the implant? Why?

A

Removing it as it become a septic focus.