Disseminated intravascular coagulation and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome




















Disseminated intravascular coagulation
Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome
Meningococcemia, pneumococcemia, staphylococcemia, gonococcemia
Rocky Mountain spotted fever
Immune thrombocytopenic purpura
Henoch–Schönlein purpura
Hemorrhagic drug reaction
Stevens–Johnson syndrome/toxic epidermal necrolysis
Viral hemorrhagic fever (Hanta, Lassa, dengue)




Table 49.2. Conditions associated with DIC



























Severe infection/sepsis
Trauma (including neurotrauma)
Solid and myeloproliferative malignancies
Transfusion reactions
Rheumatological conditions (adult-onset Still’s disease, systemic lupus erythematosus)
Obstetric complications (amniotic fluid embolism, abruptio placentae, HELLP, eclampsia)
Vascular abnormalities (Kasabach–Merritt syndrome, large vascular aneurysms)
Liver failure
Envenomations
Hyperthermia/heatstroke
Hemorrhagic skin necrosis (purpura fulminans)
Transplant rejection





HELLP, hemolysis, elevated liver enzymes, and low platelet count.


Presentation


Classic presentation of DIC


  • DIC develops 6–48 hours after a physiological insult. Many of the patients developing this condition are already hospitalized.
  • Patients will have diffuse petechiae, purpura, bleeding from their mucous membranes, and oozing from intravenous or surgical sites.
  • Laboratory investigations will show:

    • Thrombocytopenia
    • Anemia
    • Increased international normalized ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (aPTT)
    • Increased D-dimer
    • Increased fibrin split products (FSP)
    • Decreased fibrinogen (may be normal since fibrinogen is an acute-phase reactant).

Critical presentation of DIC


  • Patients with DIC may present with life-threatening conditions associated with a coagulopathy:

    • Pericardial tamponade
    • Massive gastrointestinal bleeding
    • Pulmonary hemorrhage
    • Intracranial hemorrhage.

  • They may also present with life-threatening conditions attributed to a hypercoagulable state:

    • Cerebrovascular accident (CVA)
    • Mesenteric ischemia and thrombosis
    • Venous thromboembolic events (VTEs) such as pulmonary embolus (PE) or deep vein thrombosis (DVT).

Classic presentation of TTP/HUS


  • The classic presentation of TTP involves a pentad of symptoms that include fever, neurological signs, anemia, thrombocytopenia, and renal dysfunction. This collection of symptoms is only seen in 20–30% of cases and it is strongly recommended to suspect the condition and manage it as such if a patient exhibits three or more of those features (Table 49.3).
  • The disease is termed HUS when renal failure predominates over neurological symptoms.
  • HUS is most commonly seen in children and often follows an infectious illness, usually diarrhea. It is classically associated with E. coli O157:H7.


Table 49.3. Symptoms associated with TTP






















Finding Mechanism
Fever Acute-phase reaction
Altered mental status From cerebral microvascular thrombosis
Anemia From MAHA and thrombosis
Thrombocytopenia From direct platelet activation
Renal dysfunction From renal microvascular thrombosis



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Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Disseminated intravascular coagulation and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome

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