Snake Bite
Upcoming SlideShare
Loading in...5
×

Like this? Share it with your network

Share
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
  • I wonder how much this movie made, its such a great film, I could see it over and over again, Watch the full movie at movies-play dot com
    Are you sure you want to
    Your message goes here
No Downloads

Views

Total Views
6,618
On Slideshare
6,591
From Embeds
27
Number of Embeds
2

Actions

Shares
Downloads
189
Comments
1
Likes
1

Embeds 27

http://www.slideshare.net 26
http://translate.googleusercontent.com 1

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

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