Rosen & Barkin's 5-Minute Emergency Medicine Consult (216 page)

Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
11.43Mb size Format: txt, pdf, ePub

Potential – MS, MG, stroke, aneurysm, SAH, lymphocytic meningitis, Wernicke encephalopathy

CODES
ICD9
  • 368.2 Diplopia
  • 368.15 Other visual distortions and entoptic phenomena
ICD10

H53.2 Diplopia

DISSEMINATED INTRAVASCULAR COAGULATION
Steven H. Bowman

Ernesto J. Romo
BASICS
DESCRIPTION
  • Normal coagulation: Series of local reactions among blood vessels, platelets, and clotting factors
  • Disseminated intravascular coagulation (DIC) is systemic activation of coagulation and fibrinolysis by some other primary disease process.
  • Coagulation system activation results in systemic circulation of thrombin and plasmin.
  • Role of thrombin in DIC:
    • Tissue factor/factor VIII(a) activate the extrinsic pathway, leads to thrombin formation.
    • Thrombin circulates and converts fibrinogen to fibrin monomer.
    • Fibrin monomer polymerizes into fibrin (clot) in the circulation.
    • Clots cause microvascular and macrovascular thrombosis with resultant peripheral ischemia and end organ damage.
    • Platelets become trapped in clot with resultant thrombocytopenia.
  • Role of plasmin in DIC:
    • Plasmin circulates systemically converting fibrinogen into fibrin degradation products (FDPs).
    • FDPs combine with fibrin monomers.
    • FDP-monomer complexes interfere with normal polymerization and impair hemostasis.
    • FDPs also interfere with platelet function.
  • Role of impaired anticoagulation in DIC.
    • Failure of physiologic anticoagulation is necessary for DIC to occur.
    • Antithrombin III, protein C system, and tissue factor pathway inhibitor all impaired.
  • Acute DIC—uncompensated form:
    • Clotting factors used more rapidly than body can replace them
    • Hemorrhage
      predominant clinical feature, which overshadows ongoing thrombosis
  • Chronic DIC—compensated form:
    • Body able to keep up with pace of clotting factor consumption
    • Thrombosis
      predominant clinical feature
ETIOLOGY
  • Precipitated by many disease states
  • Complications of pregnancy:
    • Retained fetus
    • Amniotic fluid embolism
    • Placental abruption
    • Abortion
    • Eclampsia
    • HELLP syndrome
  • Sepsis:
    • Gram negative (endotoxin-mediated meningococcemia)
    • Gram positive (mucopolysaccharide-mediated)
    • Other microorganisms (e.g., viruses, parasites)
  • Trauma:
    • Crush injury
    • Severe burns
    • Severe head injury
    • Fat embolism
  • Malignancy:
    • Solid tumor or metastatic disease
    • Hematologic malignancy (e.g., leukemia)
  • Intravascular hemolysis:
    • Transfusion reactions
    • Massive transfusion
  • Organ destruction:
    • Severe pancreatitis
    • Severe hepatic failure
  • Vascular abnormalities:
    • Kasabach–Merritt syndrome
    • Large vascular aneurysm
  • Thrombocytopenia:
    • Thrombotic thrombocytopenic purpura
    • Idiopathic thrombocytopenic purpura
  • Miscellaneous:
    • Snake bites
    • Recreational drugs
DIAGNOSIS
SIGNS AND SYMPTOMS
  • Excessive bleeding:
    • Petechiae
    • Purpura
    • Hemorrhagic bullae
    • Wound bleeding
    • Bleeding from venipuncture/arterial lines
    • Epistaxis
    • Hemoptysis
    • GI bleeding
  • Excessive thrombosis:
    • Large vessels
    • Microvascular thrombosis and end organ dysfunction
    • Cardiac, pulmonary, renal, hepatic, CNS
    • Thrombophlebitis
    • Pulmonary embolus
    • Nonbacterial thrombotic endocarditis
    • Gangrene
    • Ischemic infarcts of kidney, liver, CNS, bowel
  • Acute DIC:
    • Hemorrhagic complications predominate.
  • Chronic DICL:
    • Thrombotic complications predominate.
History
  • Previous history of bleeding disorder
  • Pregnancy/last menstrual period
  • History of malignancy or immunocompromised
Physical-Exam
  • Neurologic:
    • Altered MS, confusion, lethargy
  • Cardiovascular:
    • Hypotension, tachycardia
  • Respiratory:
    • Tachypnea, rhonchi, rales
  • GI:
    • Upper or lower GI bleeding, abdominal distension
  • GU:
    • Oliguria, hematuria
  • Skin:
    • Petechiae, purpura, jaundice, necrosis
ESSENTIAL WORKUP
  • Depends on precipitating illness
  • Diagnosis generally not made in ED
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Platelet count:
    • Important to note rapid decrease
    • <100,000/mm
      3
    • May be normal in chronic DIC
  • Prothrombin time (PT)/partial thromboplastin time (PTT):
    • Increased
    • May be normal in chronic DIC
  • Fibrinogen:
    • Decreased
    • <150 mg/dL in 70%
    • Low sensitivity, as levels can remain normal
    • May be normal in chronic DIC
  • FDPs:
    • Increased
    • >40 μg/mL
  • D-dimer increased
  • CBC/peripheral smear:
    • Red cell fragments
    • Low platelets
    • Peripheral smear confirms disease in chronic DIC
  • Electrolytes, BUN, creatinine, glucose:
    • Elevated BUN, creatinine owing to renal insufficiency
  • ABGs:
    • Oxygen, acid–base status
  • ISTH scoring system
    • Underlying disorder associated with DIC
      • no = 0, yes = 2
    • Platelet count
      • >100 = 0, <100 = 1, <50 = 2
    • Fibrin markers (D-dimer, FDP)
      • Normal = 0, moderate increase = 1, strong increase = 2
    • Prolonged PT
      • <3 = 0, >3 but <6 = 1, >6 = 2
    • Fibrinogen
      • 1 g/L = 0, <1 g/L = 1
    • Score >5 overt DIC, associated with increased mortality.
Imaging
  • CXR for suspected pneumonia
  • Head CT for altered mental status
  • OB US in pregnant patients
DIFFERENTIAL DIAGNOSIS
  • Inherited coagulation disorders:
    • Factor deficiencies
  • Other acquired coagulation disorders:
    • Anticoagulant therapy
    • Drugs
    • Hepatic disease
    • Vitamin K deficiency
    • Massive blood loss
  • Platelet dysfunction:
    • TTP/HUS
    • HIT
    • ITP
  • Platelet dysfunction:
    • TTP/HUS
    • HI
TREATMENT
INITIAL STABILIZATION/THERAPY
  • Airway management and resuscitation measures:
    • Control bleeding
    • Establish IV access
    • Restore and maintain circulating blood volume.
  • Initiate therapy of precipitating disease:
    • Antibiotics in sepsis
    • Evacuate uterus of retained products of conception
    • Chemotherapy in malignancy
    • Débridement of devitalized tissue in trauma
ED TREATMENT/PROCEDURES
  • Therapy of DIC is controversial and should be individualized based on:
    • Age
    • Hemodynamic status
    • Severity of hemorrhage
    • Severity of thrombosis
  • Involve admitting service before initiating specific DIC therapy.
  • Replace depleted blood components:
    • Fresh frozen plasma (FFP):
      • For prolonged PT
      • Provides clotting factors and volume replacement
      • Dose: 2 U or 10–15 mL/kg
    • Platelets:
      • If platelet count <20,000 or platelet count <50,000 with ongoing bleeding
      • Dose: 1 U/10 kg body weight
    • Cryoprecipitate:
      • Higher fibrinogen content than whole plasma
      • For severe hypofibrinogenemia (<50 mg/dL) or for active bleeding with fibrinogen <100 g/dL
      • Dose: 8 U
    • Recombinant factor VIIa
      • Successful use reported, benefit and safety unknown.
    • Washed packed cells
    • Albumin
    • Nonclotting volume expanders
  • Inhibit intravascular clotting with heparin:
    • Use is controversial.
    • Consider when thrombosis predominates.
    • May be effective in mild to moderate DIC
    • Efficacy undetermined in severe DIC. Possible indications:
      • Purpura fulminans (gangrene of digits, extremities)
      • Acute promyelocytic leukemia
      • Dead fetus syndrome—several weeks after intrauterine fetal death
      • Thromboembolic complications of large vessels
      • Before surgery with metastatic carcinoma
    • Administer activated protein C (controversial):
      • No mortality benefit.
    • Antithrombin
      • No mortality benefit found in patients also receiving heparin.
      • Lack of evidence to support use at this time.
  • Inhibit fibrinolysis:
    • Block secondary compensatory fibrinolysis that accompanies DIC
    • Use complicated by severe thrombosis
    • Use only when DIC accompanied by primary fibrinolysis:
      • Promyelocytic leukemia
      • Giant hemangioma
      • Heat stroke
      • Amniotic fluid embolism
      • Metastatic carcinoma of prostate
    • Initiate in extreme cases only:
      • Profuse bleeding not responding to replacement therapy
      • Excessive fibrinolysis present (rapid whole blood lysis/short euglobulin lysis time)
      • E
        -
        aminocaproic acid (EACA)
      • Tranexamic acid

Other books

The Challenge by Hart, Megan
Devil’s in the Details by Sydney Gibson
Conagher (1969) by L'amour, Louis
Bound to the Abyss by Vernon, James
Buffalo Palace by Terry C. Johnston
Skin by Kathe Koja
Seven Words of Power by James Maxwell