CPC 2

Case # 3
Done by:

Khaled Jaraq Ahmad AL Rasheed

Ali Abdullah Alaa Abul
Ali AL Jeraiwi Bodour Aburezq
Abdul Aziz AL Saad Amina AL Jasem
History
A 23-year old man sustained 30% total body surface area burns
in a gas explosion. He was admitted to the intensive care unit
(ICU) where he was intubated and supported He underwent
skin grafting. One week later, his clinical picture deteriorated:
Physical Examination
Vital signs
Temperature: 39.5o C ↑
Pulse Rate : 110 b/minute ↑ (60-100 b/minute)
BP : 80/50 ↓ (120/80 mmHg)

Skin : Donor sites became black and necrotic.

Generalized rash
Donor sites became black and necrotic
•Generalized rash
•Petechie (minute hemorrhage into skin – 1-2 mm )
Laboratory Investigations:
CBC
WBC: 20 x 109/L ↑ (4-11 x 109 )
HGB: 110 g/L ↓ (male: 140-180 g/L)
MCV: 82 fl N (male 80-92 fL)
PLATELETS: 30 x 109/L ↓ (130 -400 x 109/L)
Peripheral Blood Smear: Discussed in the next slide

Coagulation Profile
APTT: 50 seconds ↑ (30-40 sec) Fibrinogen: 0.8 g/L ↓ (200-400 mg/dl)
PT: 25 seconds ↑ (10-13 sec) FDP: > 1000 µg/L ↑ (<10 mcg/ml)

TT: 30 seconds ↑ (10-13 sec)

Laboratory Investigations (cont’d):
Renal Profile
S-Creatinine: 300 mmol/L ↑ (60 -120 mmol/L)
S-Urea: 20 mmol/L ↑ (3.3 -6.7 mmol / L)

Liver Profile
S-AST: 500 IU/L ↑ (10-50 IU/L)
S-ALT: 650 IU/L ↑ (<40 IU/L)

Blood Culture:
Klebsiella (Gram –ve) and Staphylococcus (Gram +ve) Bacteremia.
Progression
Despite antibiotic therapy, his clinical picture deteriorated and
biopsy
of the necrotic skin donor sites demonstrated fibrin thrombi within
dermal blood vessels. Generalized clinical bleeding developed
including bleeding from intravenous (i.v) puncture sites. He passed
away 2 days following his acute deterioration.
Post-mortem examination was performed to determine the cause of
death.
How would you explain the patient’s vital signs?

Temp. 39.5 o C ↑ Septicemia

BP: 80/50 ↓ Fever and vasodilation

Pulse Rate: 110 b/min ↑

Due to exotoxins produced by staphylococcus and
endotoxins from the klebsiella

Hypotension

Reflex tachycardia
What pathological process could
explain the clinical picture in
this patient?

Septic Shock
 What coagulation disorder did this patient
have?
Coagulation Profile
APTT: 50 seconds ↑ (30-40 sec) Fibrinogen: 0.8 g/L ↓ (200-400 mg/dl)
PT: 25 seconds ↑ (10-13 sec) FDP: > 1000 mg/L ↑ (<10 mcg/ml)
TT: 30 seconds ↑ (10-13 sec)
PLATELETS: 30 x 109/L ↓ (130 -400 x 109/L)
HGB: 110 g/L ↓ (male: 140-180 g/L)

Disseminated Intravascular Coagulopathy (DIC)

How would you explain the peripheral
blood smear finding?

•Thrombocytopenia due to DIC

•Shystiocytes (fragmented RBCs) due to the
passing of RBCs through fibrin clots produced
as a result of DIC
Comment on the renal and liver function
results.
High serum urea and creatinine levels
indicate renal failure because:

Sepsis or hypotension or embolism

Decreased renal blood flow

Hypoxia

Acute Tubular Necrosis (ATN)

[Coagulative Necrosis]

Renal Failure
High serum AST and ALT levels indicate
liver failure because:

Sepsis or hypotension or embolism

Decreased blood flow

Hypoxia

Coagulative Necrosis

Liver Failure
Describe the microscopic findings seen in
the images below .

ATN (coagulative
necrosis):
•Maintained architecture of
tissue
•Congested blood vessels
•No nucleus
•Amorphous cytoplasm
•PMNs
•Fluid between tubules
•More extensive necrosis (later stage)
•Notice: glomeruli are preserved while the
tubules are necrotized
What is the likely cause of the patient’s
deterioration.

•Septic Shock (leads to multi organ failure )

•DIC
What is the final diagnosis in this patient?

•Septic shock due to septicemia

•Septicemia also causes DIC

 Explain the pathogenesis of the condition.
Burn
Infection Septicemia Septic shock DIC

Graft

Klebsiella (G –ve) Staphylococcus (G +ve)

Endotoxins Exotoxins

Activate monocytes
to macrophages

TNF & IL-1

Activate endothelial cells to

produce IL-6 & IL 8

Vasodilation NO PAF Platelets activation

Blood vessel injurry,

Decrease CO & BP thrombosis, DIC