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Snake Bite

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Information about Snake Bite

Published on August 20, 2008

Author: blackempress

Source: slideshare.net

Description

snake bite leadin to dic
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Snake Bite Harim Mohsin 02-13

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.

A 55year old male, Ghulam Mustafa came to the ER on 12.8.08.

Presenting complaints:

Snake bite-3 dys ago.

Hemoptysis-3 dys.

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.

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.

Past medical/surgical: Angiography & angioplasty: 5yrs ago. Personal hx: appetite-N, micturation-N bowels-constipation, sleep-disturbed. Drug hx: none. Family hx: not significant.

Past medical/surgical:

Angiography & angioplasty: 5yrs ago.

Personal hx: appetite-N, micturation-N

bowels-constipation, sleep-disturbed.

Drug hx: none.

Family hx: not significant.

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.

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.

 

 

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

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

Investigations Report at CIVIL Hb-7.1 Plt-30,000 INR-5 PT/APTT- Prolonged Creatinine- Raised. Total bilirubin- Normal

Report at CIVIL

Hb-7.1

Plt-30,000

INR-5

PT/APTT- Prolonged

Creatinine- Raised.

Total bilirubin- Normal

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)

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)

Investigations LFTs: Bilirubin Total: 2.08 (<1.3) Bilirubin direct: 0.47 (<0.3) SGPT: 21 (upto 31) Alk Phosphate: 62 (39-117)

LFTs:

Bilirubin Total: 2.08 (<1.3)

Bilirubin direct: 0.47 (<0.3)

SGPT: 21 (upto 31)

Alk Phosphate: 62 (39-117)

Investigation

DIC Disseminated intravascular coagulation

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.

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.

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

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 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

Consequence is a mixture of initial thrombosis followed by a bleeding tendency due to consumption of coagulation factors & fibrinolytic activation.

Coagulation pathway

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.

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.

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.

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.

 

Hemostatic Balance ATIII Clotting Factors Tissue factor * PAI-1 Antiplasmin TFPI Prot. C Prot. S Procoagulant Anticoagulant Fibrinolytic System

Pathophysiology of DIC Activation of Blood Coagulation Suppression of Anticoagulant Pathways Impaired Fibrinolysis Cytokines

Activation of Blood Coagulation

Suppression of Anticoagulant Pathways

Impaired Fibrinolysis

Cytokines

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

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

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

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

Pathophysiology of DIC Impaired Fibrinolysis relatively suppressed at time of maximal activation of coagulation due to increased plasminogen activator inhibitor type 1

Impaired Fibrinolysis

relatively suppressed at time of maximal activation of coagulation due to increased plasminogen activator inhibitor type 1

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

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

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

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

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

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

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

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

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

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

Microscopic findings in DIC Fragments Schistocytes Paucity of platelets

Fragments

Schistocytes

Paucity of platelets

Differential Diagnosis Severe liver failure Vitamin K deficiency Liver disease Thrombotic thrombocytopenic purpura Congenital abnormalities of fibrinogen HELLP syndrome

Severe liver failure

Vitamin K deficiency

Liver disease

Thrombotic thrombocytopenic purpura

Congenital abnormalities of fibrinogen

HELLP syndrome

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

Stop the triggering process .

The only proven treatment!

Supportive therapy

No specific treatments

Plasma and platelet substitution therapy

Anticoagulants

Physiologic coagulation inhibitors

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

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

Platelet therapy Indications Active bleeding Patient requiring invasive procedures Patient at high risk for bleeding complications Platelets approximate dose 1 unit/10kg

Indications

Active bleeding

Patient requiring invasive procedures

Patient at high risk for bleeding complications

Platelets

approximate dose 1 unit/10kg

Blood Replaced as needed to maintain adequate oxygen delivery. Blood loss due to bleeding RBC destruction (hemolysis)

Replaced as needed to maintain adequate oxygen delivery.

Blood loss due to bleeding

RBC destruction (hemolysis)

Coagulation Inhibitor Therapy Antithrombin III Protein C concentrate Tissue Factor Pathway Inhibitor (TFPI) Heparin

Antithrombin III

Protein C concentrate

Tissue Factor Pathway Inhibitor (TFPI)

Heparin

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

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 .

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.

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.

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.

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.

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.

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.

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

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

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.

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.

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