A 75 y/o woman with past medical history of CVA, HTN, DM type II is sent to the Emergency Room from Nursing home for evaluation of fever and altered mental status. Vitals reveal a temperature of 101F, BP 100/60, RR 22, HR 110. Physical examination reveals an elderly woman not respond…ing to verbal stimuli but moans in response to deep pain. Echymoses are seen on lower extremities. A foley catheter is present draining cloudy urine. Lab studies show Hgb of 8.6, WBC 12K, Platelets 15k, BUN 48 and Creatinine 3.2. Prothrombin time is 14.8 and Partial thromboplastin time is 58. LDH level is elevated at 600. A peripheral blood smear is shown.
Which of the following features would most likely help in identifying the etiology of this patient’s thrombocytopenia?
A. Fragmented Red Blood Cells ( Schistocytes)
B. Decreased Fibrinogen and Increased D-dimer
C. Elevated LDH
D. Decreased Reticulocyte Count
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b
B
a
Ans. B.
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The patient presents with fever and possible sepsis. Cloudy urine indicates that UTI is the possible source of sepsis. Recognize that severe sepsis can lead to multi-organ dysfunction such as hypotension, encephalopathy. Disseminated… intravascular coagulation and renal insufficiency. The latter three are seen in this patient.
Recognize that the important difference between DIC and TTP is that DIC is a consumption coagulopathy i.e; it consumes the entire coagulation factors along with platelets. Hence, PT and PTT are elevated and fibrinogen is decreased in DIC but not in TTP. The intravascular thrombi in DIC are fibrin thrombi – the lysis of these lead to increased D-Dimer and Fibrin Split products. TTP is a consumption thrombocytopenia and is composed of platelet thrombi not fibrin – so, D-dimer is usually normal in TTP.
Increased LDH suggests hemolysis here and is non-specific. MAHA is associated with increased reticulocyte count not decreased retic.
The distractors in the question are typical TTP like pentad and scistocytes on the smear. However, realize that severe sepsis can have all these features ( Fever, thrombocytopenia, DIC leading to MAHA, altered mental status and renal failure). So, the entire clinical scenario should be put together in arriving at the diagnosis.
The peripheral blood smear shows Schistocytes.
Recognize that schistocytes are not specific for TTP. Schistocytes can occur in any condition that is associated with Microangiopathic Hemolysis (MAHA). MAHA can occur in conditions where intravascular thrombi rub against RBC in tiny capillaries leading to RBC fragmentation and hemolysis eg: MAHA can be seen in TTP, HUS, DIC, HELLP Syndrome and Malignant Hypertension.
Key Concepts:
1. DIC is a consumptive coagulopathy-thrombocytopenia and occurs secondary to several causes.
2. TTP is non-immune consumptive thrombocytopenia. PT and PTT are usually normal.
3. Severe sepsis can resemble TTP. Full clinical picture should be considered in decision making. Source of sepsis should be sought and ruled out in suspected cases before making a diagnosis of TTP
4. MAHA is not specific for TTP. Recognize other causes of MAHA are DIC, HUS, HELLP and Malignant Hypertension.
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awesome explanation!
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nice one
DIC is a complex syndrome in which there is pathological generation of thrombin and diffuse intravascular clot formation.[6] It is known to occur as acute decompensated or chronic compensated form. The underlying disease that sparks off DIC determines the clinical presentation. In acute decompensated DIC, there is a sudden massive exposure of tissue factor over a brief time period; it is beyond the capacity of control mechanisms and there is no time for generation of coagulation factors.[7] Chronic DIC, also known as compensated DIC, results from a persistent weak or intermittent activating stimulus. Under such conditions, destruction and production of coagulation factors and platelets are balanced.[1]
Bleeding is a universal manifestation of DIC, but most of the morbidity and mortality of DIC is due to microvascular thrombosis.[7] Thrombosis is witnessed essentially in the form of renal failure, coma, liver failure, respiratory failure, skin necrosis, gangrene and venous thromboembolism.[2] In chronic DIC, there may be very minimal or no clinical features or there may be only laboratory evidence of DIC.[7] Thus, we see marked heterogenicity in clinical manifestations, and the etiologic factor is the major predictor of the clinical events.[1]
In our case, perhaps an unspecified trivial trauma has instigated osteomyelitis of the tibia which remained undiagnosed till there was sepsis. A small post-traumatic right renal hematoma has gradually enlarged due to chronic DIC.
Though the pathophysiology is identical to acute DIC, clinical picture and laboratory findings in chronic DIC may be wavering. Here, nearly all of the global tests like platelet count, fibrinogen, PT and PTT may be normal. FDP, fibrinopeptide A and D dimer are usually raised and diagnostic.[7] Chronic DIC is usually associated with carcinomatosis, retained dead fetus, liver disease, aneurysm or hemangioma.[2] Sepsis usually causes acute DIC but nonovert chronic DIC is also observed.[1] Liver hematoma, subdural hematoma[3,4] and post-biopsy renal hematoma due to chronic DIC have been reported.[5]
Critical point in the management of DIC is to eradicate the primary disease and treat the concomitant causes.[8] Patients usually require treatment for thrombotic obstruction of the vasculature and subsequent multiorgan failure.[8] Theoretically, interruption of coagulation should be of benefit in patients with DIC. Heparin has been shown to have a beneficial effect in small, uncontrolled studies of patients with DIC, but not in controlled clinical trials.[9] The cornerstone of management of DIC is the treatment of the underlying disorder. Most often, these cases can be managed with blood and coagulation factors if the underlying cause is treated as in our case.
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