Snake Bite

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  • Snake Bite

    1. 1. Snake Bite Harim Mohsin 02-13
    2. 2. Case <ul><li>A 55year old male, Ghulam Mustafa came to the ER on 12.8.08. </li></ul><ul><li>Presenting complaints: </li></ul><ul><li>Snake bite-3 dys ago. </li></ul><ul><li>Hemoptysis-3 dys. </li></ul>
    3. 3. <ul><li>HOPC : According to the patient he was alright before he was suddenly bitten while he was walking in Balochistan. The escaped snake was 1 ft long & black in color. The patient, went home & only bandaged the wound. In a few hours the pain got intense & the bleeding didn’t stop from the wound. There was difficulty in walking associated with the pain & he felt numbness in the left leg. </li></ul><ul><li>He also had hemoptysis several times a day containing fresh red blood of about 1tb each time. </li></ul><ul><li>There was no history of COPD. There are no associated features of hematomesis, melena, epistaxis or vomiting. </li></ul><ul><li>He received 1 st aid at a hospital in the periphery & was sent to Civil. His coagulation profile was deranged therefore he was sent to ziauddin after being given 16U of anti venom & 120ml of FFP. </li></ul>
    4. 4. <ul><li>Past medical/surgical: </li></ul><ul><li>Angiography & angioplasty: 5yrs ago. </li></ul><ul><li>Personal hx: appetite-N, micturation-N </li></ul><ul><li>bowels-constipation, sleep-disturbed. </li></ul><ul><li>Drug hx: none. </li></ul><ul><li>Family hx: not significant. </li></ul>
    5. 5. Physical examination <ul><li>Patient was stable, lying comfortably on the bed, well conscious in time/place/person. </li></ul><ul><li>Vitals: Bp-120/80, pulse-82 bpm, R/R: 21/min </li></ul><ul><li>GPE: J † A† C˚ K˚ E† L˚ </li></ul><ul><li>General impression: swelling on left leg from the foot to the knee. </li></ul>
    6. 8. Examination <ul><li>CNS- sensory was bilaterally equal except on the lateral aspect of left foot, where it was slightly decreased. </li></ul><ul><li>Tone, power & reflexes were bilaterally equal & normal. </li></ul><ul><li>Abdomen- firm, non tender, no visceromegaly </li></ul><ul><li>Cvs- s1 + s2, no murmurs </li></ul><ul><li>Resp- Normal vesicular breating, no additional sounds </li></ul>
    7. 9. Investigations <ul><li>Report at CIVIL </li></ul><ul><li>Hb-7.1 </li></ul><ul><li>Plt-30,000 </li></ul><ul><li>INR-5 </li></ul><ul><li>PT/APTT- Prolonged </li></ul><ul><li>Creatinine- Raised. </li></ul><ul><li>Total bilirubin- Normal </li></ul>
    8. 10. Investigations <ul><li>Coagulation profile: </li></ul><ul><li>PT-48 (control 9-13) </li></ul><ul><li>INR-4.53 (2.0-4.5) </li></ul><ul><li>APTT-98 ( <7) </li></ul><ul><li>Biochemistry: </li></ul><ul><li>Urea: 22 (10-50) </li></ul><ul><li>Creatinine: 0.68 </li></ul><ul><li>Albumin: 4.17 (3.8-4.4) </li></ul><ul><li>Electrolytes: </li></ul><ul><li>Potassium : 2.28 (2.7-4.5) </li></ul><ul><li>Calcium : 8.17 (8.1-10.4) </li></ul><ul><li>Magnesium: 1.92 (1.58-2.55) </li></ul><ul><li>Sodium: 141 (136-140) </li></ul><ul><li>Chloride: 100 (98-104) </li></ul><ul><li>Bicarbonate: 27 (22-29) </li></ul>
    9. 11. Investigations <ul><li>LFTs: </li></ul><ul><li>Bilirubin Total: 2.08 (<1.3) </li></ul><ul><li>Bilirubin direct: 0.47 (<0.3) </li></ul><ul><li>SGPT: 21 (upto 31) </li></ul><ul><li>Alk Phosphate: 62 (39-117) </li></ul>
    10. 12. Investigation
    11. 13. DIC Disseminated intravascular coagulation
    12. 14. Snake venom <ul><li>Venom is produced and stored in paired glands below the eye & delivered through the fangs. </li></ul><ul><li>Venom is mostly water. Enzymatic proteins in venom impart its destructive properties. Proteases, collagenase, and arginine ester hydrolase have been identified. </li></ul><ul><li>Specific details are known for several enzymes as follows: </li></ul><ul><li>(1) hyaluronidase allows rapid spread of venom through subcutaneous tissues by disrupting mucopolysaccharides; </li></ul><ul><li>(2) phospholipase A2 plays a major role in hemolysis secondary to the esterolytic effect on red cell membranes and promotes muscle necrosis; and </li></ul><ul><li>(3) thrombogenic enzymes promote the formation of a weak fibrin clot, which, in turn, activates plasmin and results in a consumptive coagulopathy and its hemorrhagic consequences. </li></ul>
    13. 15. <ul><li>It is the widespread generation of fibrin within blood vessels caused by initiation of the coagulation pathway by activation or injury due to toxic substance of the monocytes & endothelial cells. There is consumption of platelets & coagulation factors, & secondary activation of fibrinolysis leading to production of fibrin degradation products (FDPs) which contribute to coagulation by inhibiting fibrin production. </li></ul>DIC
    14. 16. DIC <ul><li>Consequence is a mixture of initial thrombosis followed by a bleeding tendency due to consumption of coagulation factors & fibrinolytic activation. </li></ul>SYSTEMIC ACTIVATION OF COAGULATION Intravascular deposition of fibrin Depletion of platelets and coagulation factors Thrombosis of small and midsize vessels Bleeding Organ failure DEATH
    15. 17. Coagulation pathway
    16. 18. <ul><li>Tissue factor pathway </li></ul><ul><li>The main role of the tissue factor pathway is to generate a &quot;thrombin burst,&quot; a process by which thrombin , the single most important constituent of the coagulation cascade in terms of its feedback activation roles, is released instantaneously. FVIIa circulates in a higher amount than any other activated coagulation factor. </li></ul><ul><li>Contact activation pathway </li></ul><ul><li>There is formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein , and FXII (Hageman factor). Prekallikrein is converted to kallikrein and FXII becomes FXIIa. FXIIa converts FXI into FXIa. Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which activates FX to FXa. </li></ul><ul><li>Final common pathway </li></ul><ul><li>Thrombin has a large array of functions. Its primary role is the conversion of fibrinogen to fibrin, the building block of a hemostatic plug. In addition, it activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin ), and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers. </li></ul>
    17. 19. <ul><li>Cofactors </li></ul><ul><li>Calcium, Vit K </li></ul><ul><li>Inhibitors </li></ul><ul><li>Three mechanisms keep the coagulation cascade in check. Abnormalities can lead to an increased tendency toward thrombosis: </li></ul><ul><li>Protein C which degrades the co-factors FVa and FVIIIa </li></ul><ul><li>Antithrombin i that degrades the serine proteases; thrombin and FXa, as well as FXIIa, and FIXa </li></ul><ul><li>Tissue factor pathway inhibitor (TFPI) inhibits F VIIa-related activation of F IX and F X </li></ul><ul><li>Protein S </li></ul><ul><li>Fibrinolysis </li></ul><ul><li>The main enzyme responsible for this process ( plasmin ) is regulated by activators (TPA) and inhibitor (Antiplasmin) & forms the FDPs. </li></ul>
    18. 21. Hemostatic Balance ATIII Clotting Factors Tissue factor * PAI-1 Antiplasmin TFPI Prot. C Prot. S Procoagulant Anticoagulant Fibrinolytic System
    19. 22. Pathophysiology of DIC <ul><li>Activation of Blood Coagulation </li></ul><ul><li>Suppression of Anticoagulant Pathways </li></ul><ul><li>Impaired Fibrinolysis </li></ul><ul><li>Cytokines </li></ul>
    20. 23. Pathophysiology of DIC <ul><li>Activation of Blood Coagulation </li></ul><ul><ul><li>Tissue factor/factor VIIa mediated thrombin generation via the extrinsic pathway </li></ul></ul><ul><ul><ul><li>complex activates factor IX and X </li></ul></ul></ul><ul><ul><li>TF </li></ul></ul><ul><ul><ul><li>endothelial cells </li></ul></ul></ul><ul><ul><ul><li>monocytes </li></ul></ul></ul><ul><ul><ul><li>Extravascular: </li></ul></ul></ul><ul><ul><ul><ul><li>lung </li></ul></ul></ul></ul><ul><ul><ul><ul><li>kidney </li></ul></ul></ul></ul><ul><ul><ul><ul><li>epithelial cells </li></ul></ul></ul></ul>
    21. 24. Pathophysiology of DIC <ul><li>Suppression of Anticoagulant Pathways </li></ul><ul><ul><li>reduced antithrombin III levels </li></ul></ul><ul><ul><li>reduced activity of the protein C-protein S system </li></ul></ul><ul><ul><li>Insufficient regulation of tissue factor activity by tissue factor pathway inhibitor (TFPI) </li></ul></ul><ul><ul><ul><li>inhibits TF/FVIIa/Fxa complex activity </li></ul></ul></ul>
    22. 25. Pathophysiology of DIC <ul><li>Impaired Fibrinolysis </li></ul><ul><ul><li>relatively suppressed at time of maximal activation of coagulation due to increased plasminogen activator inhibitor type 1 </li></ul></ul>
    23. 26. Pathophysiology of DIC - Cytokines <ul><li>Cytokines </li></ul><ul><ul><li>IL-6, and IL-1 mediates coagulation activation in DIC </li></ul></ul><ul><ul><li>IL-10 may modulate the activation of coagulation </li></ul></ul><ul><ul><li>TNF-  </li></ul></ul><ul><ul><ul><li>mediates dysregulation of physiologic anticoagulant pathways and fibrinolysis </li></ul></ul></ul><ul><ul><ul><li>modulates IL-6 activity </li></ul></ul></ul>
    24. 27. Causes of DIC <ul><li>Malignant disease </li></ul><ul><li>Septicemia (gram –ve & meningococcal) </li></ul><ul><li>Hemolytic transfusion reactions </li></ul><ul><li>Obstetric causes (abruptio, amiotic fluid embolism) </li></ul><ul><li>Trauma, burns, surgery </li></ul><ul><li>Other infections (eg. Malaria falciparum) </li></ul><ul><li>Liver disease </li></ul><ul><li>Snake bite </li></ul><ul><li>Hypothermia/Hyperthermia </li></ul><ul><li>Severe acidosis </li></ul><ul><li>Collagen vascular disease </li></ul>
    25. 28. Clinical features <ul><li>Patient is acutely ill & may present with shock. </li></ul><ul><li>Features vary from no bleeding to severe hemorrhage with widespred hemostatic failure. </li></ul><ul><li>Bleeding from mouth, nose, venepuncture site </li></ul><ul><li>Ecchymoses </li></ul><ul><li>Thrombotic events may occur, mostly involving brain, skin & kidney but may happen anywhere. </li></ul><ul><li>Ischemic tissue </li></ul><ul><li>Myocardial dysfunction </li></ul><ul><li>Any visceral organ infarct </li></ul>
    26. 29. Laboratory Tests Used in DIC <ul><li>D-dimer * </li></ul><ul><li>Antithrombin III * </li></ul><ul><li>F. 1+2* </li></ul><ul><li>Fibrinopeptide A* </li></ul><ul><li>Platelet factor 4* </li></ul><ul><li>Fibrin Degradation Products </li></ul><ul><li>Platelet count </li></ul><ul><li>Thrombin time </li></ul><ul><li>Prothrombin time </li></ul><ul><li>Activated PTT </li></ul><ul><li>Protamine test </li></ul><ul><li>Coagulation factor levels </li></ul><ul><li>*Most reliable </li></ul>
    27. 30. Laboratory findings <ul><li>Thrombocytopenia </li></ul><ul><ul><li>plat count <100,000 or rapidly declining </li></ul></ul><ul><li>Prolonged clotting times (PT, APTT) </li></ul><ul><li>Presence of Fibrin degradation products or positive D-dimer </li></ul><ul><li>Low levels of coagulation inhibitors </li></ul><ul><ul><li>AT III, protein C </li></ul></ul><ul><li>Low levels of coagulation factors </li></ul><ul><ul><li>Factors V,VIII,X,XIII </li></ul></ul><ul><li>Fibrinogen levels not useful diagnostically </li></ul>
    28. 31. Microscopic findings in DIC <ul><li>Fragments </li></ul><ul><li>Schistocytes </li></ul><ul><li>Paucity of platelets </li></ul>
    29. 32. Differential Diagnosis <ul><li>Severe liver failure </li></ul><ul><li>Vitamin K deficiency </li></ul><ul><li>Liver disease </li></ul><ul><li>Thrombotic thrombocytopenic purpura </li></ul><ul><li>Congenital abnormalities of fibrinogen </li></ul><ul><li>HELLP syndrome </li></ul>
    30. 33. Treatment of DIC <ul><li>Stop the triggering process . </li></ul><ul><ul><li>The only proven treatment! </li></ul></ul><ul><li>Supportive therapy </li></ul><ul><li>No specific treatments </li></ul><ul><ul><li>Plasma and platelet substitution therapy </li></ul></ul><ul><ul><li>Anticoagulants </li></ul></ul><ul><ul><li>Physiologic coagulation inhibitors </li></ul></ul>
    31. 34. Plasma therapy <ul><li>Indications </li></ul><ul><ul><li>Active bleeding </li></ul></ul><ul><ul><li>Patient requiring invasive procedures </li></ul></ul><ul><ul><li>Patient at high risk for bleeding complications </li></ul></ul><ul><li>Prophylactic therapy has no proven benefit. </li></ul><ul><li>Fresh frozen plasma(FFP): </li></ul><ul><ul><li>provides clotting factors, fibrinogen, inhibitors, and platelets in balanced amounts. </li></ul></ul><ul><ul><li>Usual dose is 10-15 ml/kg </li></ul></ul>
    32. 35. Platelet therapy <ul><li>Indications </li></ul><ul><ul><li>Active bleeding </li></ul></ul><ul><ul><li>Patient requiring invasive procedures </li></ul></ul><ul><ul><li>Patient at high risk for bleeding complications </li></ul></ul><ul><li>Platelets </li></ul><ul><ul><li>approximate dose 1 unit/10kg </li></ul></ul>
    33. 36. Blood <ul><li>Replaced as needed to maintain adequate oxygen delivery. </li></ul><ul><ul><li>Blood loss due to bleeding </li></ul></ul><ul><ul><li>RBC destruction (hemolysis) </li></ul></ul>
    34. 37. Coagulation Inhibitor Therapy <ul><li>Antithrombin III </li></ul><ul><li>Protein C concentrate </li></ul><ul><li>Tissue Factor Pathway Inhibitor (TFPI) </li></ul><ul><li>Heparin </li></ul>
    35. 38. <ul><li>The major inhibitor of the coagulation cascade </li></ul><ul><ul><li>Levels are decreased in DIC. </li></ul></ul><ul><ul><li>Anticoagulant and antiinflammatory properties </li></ul></ul><ul><li>Therapeutic goal is to achieve supranormal levels of ATIII (>125-150%). </li></ul><ul><ul><ul><li>reduced DIC scores, DIC duration, and some improvement in organ function </li></ul></ul></ul><ul><ul><li>Clinical trials have shown laboratory evidence of attenuation of DIC and trends toward improved outcomes. </li></ul></ul><ul><ul><li>A clear benefit has not been established in clinical trials . </li></ul></ul>Antithrombin III
    36. 39. Protein C Concentrates <ul><li>Inhibits Factor Va, VIIa and PAI-1 in conjunction with thrombomodulin. </li></ul><ul><li>Protein S is a cofactor </li></ul><ul><ul><li>Protein C levels are low in DIC due to sepsis. </li></ul></ul><ul><ul><li>Levels correlate with outcome. </li></ul></ul><ul><ul><li>Clinical trials show significantly decreased morbidity and mortality in DIC due to sepsis. </li></ul></ul>
    37. 40. Tissue Factor Pathway Inhibitor <ul><li>Tissue factor is expressed on endothelial cells and macrophages </li></ul><ul><li>TFPI complexes with TF, Factor VIIa,and Factor Xa to inhibit generation of thrombin from prothrombin </li></ul><ul><li>TF inhibition may also have antiinflammatory effects </li></ul><ul><li>Clinical studies using recombinant TFPI are promising. </li></ul>
    38. 41. Heparin <ul><li>Use is very controversial. </li></ul><ul><li>May be indicated in patients with clinical evidence of fibrin deposition or significant thrombosis. </li></ul><ul><li>Generally contraindicated in patients with significant bleeding and CNS insults. </li></ul><ul><li>Dosing and route of administration varies. </li></ul><ul><li>Requires normal levels of ATIII. </li></ul>
    39. 42. Antifibrinolytic Therapy <ul><li>Rarely indicated in DIC </li></ul><ul><ul><li>Fibrinolysis is needed to clear thrombi from the micro circulation. </li></ul></ul><ul><ul><li>Use can lead to fatal disseminated thrombosis. </li></ul></ul><ul><li>May be indicated for life threatening bleeding under the following conditions: </li></ul><ul><ul><li>bleeding has not responded to other therapies and: </li></ul></ul><ul><ul><li>laboratory evidence of overwhelming fibrinolysis. </li></ul></ul><ul><ul><li>evidence that the intravascular coagulation has ceased. </li></ul></ul><ul><li>Agents: tranexamic acid, EACA </li></ul>
    40. 43. Summary <ul><li>DIC is a syndrome characterized systemic intravascular coagulation. </li></ul><ul><li>Coagulation is the initial event and the extent of intravascular thrombosis has the greatest impact on morbidity and mortality. </li></ul><ul><li>Important link between inflammation and coagulation. </li></ul><ul><li>Morbidity and mortality remain high. </li></ul><ul><li>The only proven treatment is reversal or control of the underlying cause. </li></ul>

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