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Proceedings of the Burns CME by Dr Suhas Abhyankar

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CME 23/04/2022 Summary

Systemic enzyme therapy with Trypsin, Bromelain and Rutoside Combination in Burns MODERATOR SPEAKER

Dr. Suhas Abhyankar MBBS, MCPS, MS - General Surgery, MCh - Plastic Surgery, DNB - Plastic Surgery

Dr. Arvind Vartak MBBS, MS – Gen Surgery, MS- Plastic Surgery

• Burns – A major public health problem worldwide • Main target in burns management – preventing complications, assisting physiological recovery • Targeting unchecked inflammation – key in faster recovery Case – High voltage electric flash injury → Thermal 3rd degree burns on dorsal aspect of left hand • Best modality - Conservative management with anti-inflammatory enzymes, and autograft after good granulation • Less effective modalities – i) Management with NSAIDs, and autograft after good granulation; ii) Tangential excision and cover with cadaveric graft followed by autograft Most common causes of failed or compromised skin graft • Poor vascularity • Hematoma or seroma, i.e., collections of blood or fluid • Infection at graft site • Mechanical shearing rd

Case – flame burns on dorsal aspects of right hand - 3 degree burns • Autograft after conservative management with NSAIDs → lot of swelling with impaired graft uptake • NSAIDs not effective in reducing edema; compromises graft uptake Risks with use of NSAIDs • Gastro-intestinal irritation • Renal disturbances (burns patients have hypovolemia) • Cardiovascular events • Potential hepatotoxicity • Marked negative impact on wound healing; may increase scar formation rd

Case - flame burns on right hand - 3 degree burns • Good recovery with anti-inflammatory enzymes; potentially due to: • Reduced edema; promoting healing • Local epidermal growth factor activation • Enhanced perfusion; better healing • Reduced edema & fibroblastic activity → better functional results in case of small hand joints


Comparison of mechanisms of NSAIDs & Systemic enzyme therapy with Trypsin, Bromelain and Rutoside

CME 23/04/2022 Summary

Tissue injury Coagulation

Vascular response

Secondary vasodilation ↑vascular permeability (plasma leakage)

Platelet aggregation Coagulation cascade initiation

(mediated by histamine, bradykinin, FDPs, NO)

Cyclo-oxygenase enzyme

Leucocyte activation & migration T cells

M1 macrophage

Phagocytosis

Cytokines+GFs

Neutrophil

Fibrin clot

Thromboxanes

Prostaglandins

Growth factors, Inflammatory cytokines, polyphosphates

Platelet activation Polyphosphates

Initial vasoconstriction

Inflammatory infiltrate

Proteases

M2 macrophage ROS, RNS

Tissue repair

Inhibition

Arachidonic acid Lysis

FDP: Fibrin Degradation Products ROS: Reactive oxygen species RNS: Reactive nitrogen species GFs: Growth Factors NO: Nitric Oxide

Bradykinin

NSAIDs Kininogen

Plasmin

Plasminogen

(non steroidal anti inflammatory drugs)

Multi-pronged action of systemic enzyme combination Tissue injury Coagulation

Vascular response Initial vasoconstriction Secondary vasodilation ? vascular permeability (mediated by histamine, bradykinin, FDPs, NO)

Eicosanoids (PG, TX)

Inflammatory infiltrate Growth factors, Inflammatory cytokines, chemokines

Platelet activation factor

Leucocyte activation & migration

Platelet aggregation Coagulation cascade initiation

Neutrophil

Fibrin clot

Proteases

T cells

M1 macrophage

Phagocytosis

Cytokines+GFs

Inhibition1

Arachidonic acid

Inhibition5 Kininogen

Plasminogen Depletion

Activation

↓ levels 8

Inhibition6

Plasmin

Tissue repair

1– by alteration of adhesion molecules on the platelet surface

Lysis

Bradykinin

ROS, RNS

↓production7

↑activation threshold

Inhibition2

M2 macrophage

↑availability 3

Potentiation4

2– by alteration of cell surface molecules involved in leucocyte activation and adhesion 3 – by displacing “bound” plasmin from plasma proteins 4 – by the activation of PAR1 and PAR2 receptors on macrophages 5 – by decreased production of iNOS-mediated NO 6 – by inhibiting intracellular Ca2+ mobilization in platelets

Bromelain

Trypsin

Rutoside

7 – by inhibiting the transcription of genes encoding for pro-inflammatory cytokines 8 – by scavenging action & iNOS inhibition

Trypsin, Bromelain and Rutoside in Burns

Take-home message Systemic anti-inflammatory enzymes – multi-pronged action Advantages of anti-inflammatory enzymes (trypsin, bromelain, rutoside) over NSAIDs • Reduction of edema; putting extra-vascular fluid back in circulation • Enhanced/quicker mobility • Enhanced wound healing • No nephrotoxicity


Link to CME & full length article on Burns

To access the CME ‘Potential role of systemic enzyme therapy with trypsin, bromelain and rutoside combination in burns’ please click on the youtube link.https://youtu.be/xRdLoSOo_NM

To access the full length article of ‘Potential role of systemic enzyme therapy with trypsin, bromelain and rutoside combination in burns’ Abhyankar, Suhas & Vartak, Arvind & Daftary, Gautam. (2021). International Surgery Journal 2021 Jul;8(7):2254-2259

https://www.ijsurgery.com/index.php/isj/article/view/7601/4791


An Aksigen Initiative

In the management of

BURNS S

disperse away the worry of inflammation, oedema & pain

Only dispersible enzyme trio…. Ensures faster recovery

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DCGI APPROVED BRAND 1 Trypsin, Bromelain & Rutoside

DCGI – Drugs Controller General, India; 1. Approval based on CTRI/2017/12/010804


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