This document provides an overview of burn injury management. It discusses the epidemiology, pathophysiology, classification, and treatment principles for burns. The key aspects of management include initial resuscitation using fluid replacement formulas to prevent shock, wound care, infection prevention, and long-term rehabilitation to address physical and psychological impacts of severe burns. Proper management requires a multidisciplinary team to address the many systemic effects of serious burns.
A burn is a type of injury to skin, or other tissues, caused by heat, cold, electricity, chemicals, friction, or radiation. Most burns are due to heat from hot liquids, solids, or fire. While rates are similar for males and females the underlying causes often differ.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
polytrauma lecture prepare by three medical student in Kerbala university / college of medicine department of surgery to presented as seminar
for download as ppt
https://drive.google.com/open?id=1bc3HMEeJyhrOwag-AvTFMmPVKi12O1PU
Surgical management of burn injuries by Varun Harish.
From #CodaZero Live, Varun Harish provides an overview of the surgical management of burn injuries.
He talks us through how surgeons make decisions regarding burn management, including the importance of early assessment and intervention.
Burns evolve, what you see at the beginning is going to be very different in 24 hours and different again in three days.
Importantly, the management and principles of intervention differ for minor burns compared to severe burns.
For smaller burns, the golden rule is two weeks. If there is a good chance that the burn will heal in two weeks, intervention is avoided. If this is not the case, intervention in the way of a skin graft or other surgical procedure is usually the best option.
Varun details how the management priorities shift for larger burns. Larger burns significantly increase the chances of infection, making it important to intervene earlier rather than later.
Tune in to an interesting talk on the Surgical management of burn injuries by Varun Harish.
This topic is oriented mainly on the Bailey & Love - 26th edition.
This will be of immense help for the MBBS - Students for the Theory as well as Clinical application.
A burn is a type of injury to skin, or other tissues, caused by heat, cold, electricity, chemicals, friction, or radiation. Most burns are due to heat from hot liquids, solids, or fire. While rates are similar for males and females the underlying causes often differ.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
polytrauma lecture prepare by three medical student in Kerbala university / college of medicine department of surgery to presented as seminar
for download as ppt
https://drive.google.com/open?id=1bc3HMEeJyhrOwag-AvTFMmPVKi12O1PU
Surgical management of burn injuries by Varun Harish.
From #CodaZero Live, Varun Harish provides an overview of the surgical management of burn injuries.
He talks us through how surgeons make decisions regarding burn management, including the importance of early assessment and intervention.
Burns evolve, what you see at the beginning is going to be very different in 24 hours and different again in three days.
Importantly, the management and principles of intervention differ for minor burns compared to severe burns.
For smaller burns, the golden rule is two weeks. If there is a good chance that the burn will heal in two weeks, intervention is avoided. If this is not the case, intervention in the way of a skin graft or other surgical procedure is usually the best option.
Varun details how the management priorities shift for larger burns. Larger burns significantly increase the chances of infection, making it important to intervene earlier rather than later.
Tune in to an interesting talk on the Surgical management of burn injuries by Varun Harish.
This topic is oriented mainly on the Bailey & Love - 26th edition.
This will be of immense help for the MBBS - Students for the Theory as well as Clinical application.
Burn and burn rehabilitation includes patho physiology of burn, types or causes of burn, acute management of burn, rehabilitation of burn, surgical management, grafting, complication of burn etc.
Brief description about what are burns, structure of skin, how we can classify burns based upon mechanism and differential diagnosis ,pathophysiology of burn, rule of 9, general and systemic response to burns, complications, fluid resuscitation, parkland formula, monitoring of resuscitation
Acute management in burns
Types of burns
Admission criteria in burns
Fluid management in burns
Early surgical management in burns
Facial burn
Chemical burn
Eye burn
Ear burn
Hand burn
Electrical burn
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
1. MANAGEMENT OF BURN INJURIES
Dr. LAWAL G.D
Registrar, dept. of Surgery, NHA
2. OUTLINE
• INTRODUCTION
• EPIDERMIOLOGY
• AETIOPATHOGENESIS
• MANAGEMENT - Initial Assessment and Resuscitation
-Management of Inhalational injury
-Wound Care
-Nutritional Support
-Pharmacological Support
-Rehabilitation and Re-integration
• COMPLICATIONS
• PROGNOSIS
• EMERGING TRENDS
• CONCLUSION
3. INTRODUCTION
• Burns are one of the most devastating conditions
encountered in medicine.
• The injury represents an assault on all aspects of the
patient, from the physical to the psychological
• >90% of burns are caused by carelessness or
ignorance and are completely preventable.
4. INTRODUCTION (contd)
• Burns patient often require years of supervised
rehabilitation, reconstruction and psychosocial support.
The quality of burn care is no longer measured by only
survival but also by long-term function and appearance.
• The goal for any burn management is a well healed
durable skin with a normal function and near normal
appearance.
5. DEFINITION:
• A burn is tissue injury from thermal (heat or cold)
application or from the absorption of physical energy
or chemical contact. More than 90% of burn injury is
from thermal application
• It can also be defined as the coagulative necrosis of
skin ( and sometimes deeper tissues ) following
contact with injurious agents
6. EPIDEMIOLOGY
• Varying incidence worldwide
• Incidence Increasing in the last 3 decades- a major cause being
terrorists activities in recent times .
• In the United Kingdom about 250 000 people are burnt each year.
Of these, 175 000 attend accident and emergency departments,
and 13 000 of these are admitted to hospital.
• Mortality and Morbidity: Reducing in developing countries. This is
due to reduction in poverty, ignorance, illiteracy, and the advances
in technology; No real change in sub-Saharan Africa and other
poor nations
7. EPIDEMIOLOGY (contd)
PREDISPOSING FACTORS:
• Extremes of age (<3yrs, >60yrs)
• Male sex/adolescence
• Compromising factors such as alcoholism, epilepsy,
chronic psychiatric or medical illness/disability
8. AETIOPATHGENESIS
The common burns are :
• scald- hot water, hot soup, hot oil, hot tar/asphalt etc.
• flame/dry heat- house fire, petroleum product
explosion, road traffic accident, bomb blasts etc
• contact with-hot metals, hot plastic, hot objects, caustic
chemicals, electricity etc
10. EFFECTS OF THESE MEDIATORS
• Alter vascular permeability
• Catabolism of muscle
• Production of anaemia
• Initiate wound healing
• Produce fever
• Cause RBC haemolysis
• Disrupt interstitial matrix
11. THE BODY’S RESPONSE TO A BURN
Extent of initial burn injury is determined by ;
• The temperature of the burning agent
• The duration of contact with agent
• The consequent inflammatory reaction
Effect on the skin (Local Injury):
Coagulative necrosis, Disruption of basement membrane,
Blistering, Vascular changes, 3 zones (Jacksons burn zones of
injury)- coagulation, stasis, hyperaemia
13. REGIONAL INJURY
• Usually seen in circumferential burns (eschars)
• Mainly vascular (direct vascular injury is rare)
• Venous obstruction due to gross oedema
• Poor regional circulation may lead to ischaemia
14. SYSTEMIC INJURY
A. Fluid loss
• Initial vasoconstriction followed by vasodilation and increased
capillary leakage.
• Mediated by vasoactive agents and oxygen radicals
• There is extravasation of fluids, electrolytes and plasma to the
interstitial space- hypovolemia, (shock if severe),
Haemoconcentration-sluggish blood flow (stasis) may predispose to
thrombosis
• Fluid loss is fastest in the first 8 hours and tapers off within 24 -48
hours
• Without infection the reabsorption of oedema fluid is complete in 5-7
days
15. B. Renal dysfunction
• This is secondary to hypovolaemia- reduction in renal
perfusion → ↓GFR →acute tubular necrosis
• In deep burns haemoglobinuria and myoglobinuria may occur
leading to damage of the distal convoluted tubules
C. Gastrointestinal
• Mucosal damage – due to hypoperfusion →Loss of mucosal
integrity (Curling’s ulceration, GI bleeding), Ileus, Gastric
dilatation
• Translocation of gut bacteria via the portal system and
lymphatics- risk of sepsis
16. D. Anaemia
• Early anaemia is usually due to direct destruction
of red blood cells by heat
• Sludging from haemoconcentration or red cell
trapping following vessel thrombosis may also
contribute.
• Red cell loss is also noted following wound
dressing or bone marrow depression due to
infection
17. E. Inhalational injury
• Due to inhalation of noxious , irritant fumes (e.g. CO, hydrogen
cyanide )
• Acute inflammatory reaction → vasodilation, exudation and
oedema → separation of cilia from the basement membrane
→ ulceration
• Protein in the exudate form fibrin casts which adhere to the
bronchi and prevent expiration
• Release of oxygen free radicals TNF and interleukins also
damage the lung tissue
• During healing there may be loss of pseudostratified ciliated
epithelium
18. F. Adrenal changes
• Increased catecholamine release which helps with the
cardiovascular response to burns . They also cause
increased gluconeogenesis, glycolysis and lipolysis
G. Other systemic effects
• Increased production of ACTH and glucagon
• Negative nitrogen balance
19. H. Increased susceptibility to infections
• Presence of reactive free oxygen radicals destabilizes cell
membranes including the leucocytes
• Destruction of mechanical barrier
• Reduced peripheral lymphocytes
• Reduced NK cell activity
20. CLASSIFICATION
According to depth -based on Appearance, Blanching/Capillary refill,
Pain sensation (needle prick)
• SUPERFICIAL (EPIDERMAL)- erythema
• PARTIAL THICKNESS-
1.superficial partial thickness-blisters, pink, moist, good capillary
refill and blanches,
2.deep dermal partial thickness-dry, poor/absent capillary refill,
impaired sensation
• FULL THICKNESS- charred, densed white or brown leathery,
absent capillary refill, absent sensation
21.
22.
23.
24.
25. TREATMENT
Principles: Resuscitation, Repair, Rehabilitation, Re-
integration
CRITERIA FOR ADMISSION
• Burns >10% TBSA in children and >15% in adults
• Full thickness burns >5% in children and 7.5% in adult
• Inhalation injury
26. CRITERIA FOR ADMISSION (contd)
• Burns affecting hands, feet, face, perineum, joint surfaces
• Electrical burn
• Chemical burns
• Infected burn wounds
• Any suspected case of abuse or neglect
• Burns with other diseases
• People of extremes of life-young children and the aged
28. INITIAL ASSESSMENT AND RESUSCITATION (contd)
B. Assess the % Burnt area (helps to estimate the severity of
burn and in calculating the fliud requirement)- commonly used
method:
-Patient’s palm which is 1% of his or her body
-Wallace’s rule of 9
-Lund & Browder chart
C. Assess burn depth as discussed above
31. D. Fluid therapy
• Amount required in the resuscitative process estimated using
formulae.
• Various formulae available.
• Based on use of crystalloids or colloid in the resuscitative
process.
• The time-dependent variables for all of these formulas begin
from the moment of injury, not from the time the patient is
seen in the emergency department.
• Calculations for the rate of fluid resuscitation should take this
into account and reflect the decreased or increased starting
IV fluid rate.
32. Ringers Lactate solution
• Ideal crystalloid solution
• Preferable to normal saline for large-volume
resuscitations because its lower sodium
concentration (130 mEq/L vs 154 mEq/L) and higher
pH concentration (6.5 vs 5.0) are closer to
physiologic levels
• Has buffering effect of metabolized lactate on the
associated metabolic acidosis seen in burn injury.
33. Parkland formula
• commonly used
• fluid requirements estimated at approximately 4 mL/kg body weight ×
percentage burnt TBSA
• half the calculated volume given in first 8 hours post burn, with the
remaining delivered over 16 hours
• Next 24hrs: Colloids given as 20-60% of calculated plasma volume.
Dextrose in water is added and titrated in amount require to maintain a
hourly urine output of 0.5-1ml/kg/hr in adult and 1-2ml/kg/hr in children
NB: daily maintenance fluild in the form of 4.3% D/S is added in children-
they have a large surface area to body mass ratio and low glycogen store
34. Patients in need of higher fluid calculated from Parkland formula:
• electrical burns
• inhalational injury
• those on home diuretics
• presence of escharotomy or fasciotomy
Other formulae: Muir and Barclay ‘s, Modified Brookes; Evans;
Monafo; Shriner’s Cincinnati and Galveston (latter two formulae
being developed especially for children)
35. Antioxidant therapy: use of Zinc, Selenium, Vit. E and Vit. C etc have
been shown to help recovery in burn patients by stabilizing cell
membranes
E. Monitoring
-Hourly urinary output- aim for output of 1-2ml/kg/hr[n children and
0.5-1ml/kg/hr (or ≈30-50mls/hr) for adult
-vital signs temperature, pulse rate, blood pressure
-pulse oximeter
-continuous ECG monitoring in major burns
-serial determination of haematocrit, Serum electrolytes, glucose and
albumin
-doppler monitoring for compartment syndrome
36. MANAGEMENT OF INHALATIONAL INJURIES
Best managed in an ICU under the care of the anaesthesiologist,
burn surgeon and the chest physician
CLINICAL INDICATION FOR INTUBATION
ABSOLUTE:
-Burn of the palate, tongue and pharynx,
-Oedema of the posterior pharynx and upper glottis
- Burn of vocal cords.
RELATIVE:
- Hoarseness
- Facial burn
- Sooty sputum
38. WOUND CARE:
• Determination of depth of burns is critical
• Dressing could be by exposure or occlusive .
• Superficial partial thickness burn usually heals in 14-21 days
• Deep partial thickness burns heals in 2-6 weeks with some
scarring
• Full thickness burns takes longer to heal- complications
• Initial wound care aims to reduce bacterial load, remove dead
tissue, and prevent wound infection
• Topical antibiotic agents (Silver sulphadiazine, 0.5% silver
nitrate, povidone iodine, honey etc) are useful in preventing
wound sepsis
39. BURN WOUND / DONOR SITE DISCREPANCY
• Temporary skin graft- human allograft, xenograph (porcine
skin) , Biobrane etc
• Permanent skingraft- Integra, alloderm,
• Staged skin grafting
• Meshed skin grafting- allows for larger surface area to be
covered, allows for escape of bllod/plasma from beneath the
grafted skill thus reducing chances of graft uptake failure
• Biologic membranes such as amniotic membranes
• Cultured keratinocytes (skin culture)
41. Treatment by exposure
• Areas that are difficult to dress: face, genitalia and perineum
• Minimally discharging wound
• To allow for frequent monitoring: finger tips
• To allow for joint movement (polythene bag on the hand)
43. NUTRITIONAL SUPPORT
• Patient is in a catabolic state with negative nitrogen balance.
• Necessary to enable the body to repair the damaged tissue and to combat
infection.
• This is only feasible when the patients are stabilized
• Immediate commencement of oral feeding in the absence of ileus
• TPN only when enteral route impracticable
• Daily energy requirement may be calculated using the Curreri formula- 25 ×
wgt(kg) + 40 × TBSA
(Other formulae includes: Harris-Benedict, the Toronto formula, the Davies etc)
• The protein intake should be approximately 2-3g/kg/day
• Trace elements, vitamins and essential proteins are also given
44. • ANTI TETANUS
• ANTI ULCER
• ANTICOAGULATION
• ANTIBIOTICS
• ANALGESICS
45. REHABILITATION AND RE-INTEGRATION
• Physiotherapy- Very aggressive therapy sessions; Full ROM early-
Elevation hands and lower extremity
• Prophylactic splinting
• Occupational therapy
• Psychotherapy
• Early wound closure
• Early institution of pressure therapy
• Silicone gel therapy
• Anti itch therapy
• Management of abnormal scarring, and contractures
50. NEW AND EVOLVING MEANS OF MANAGEMENT
• Skin culture (Cultured Epidermal Autograft [CEA]) i.e growing
sheets of epithelium and applying it to the burn wound.
• Orcel temporary dressing- a marterial made up of layers of human
skin cells (from someone other than the donor0 and collagen from
cows. Use to dress burn wound and graft donor site for 2-3 weeks
then removed
• Tissue expanders made up of specialized balloon and inflated with
normal saline – use to cover areas burns injury
• Polychromatic light emiitting diodes use to stimulate healing of
burn wound in diabetics
51. PROGNOSIS
• age <3yrs, >60yrs
• TBSA >60%
• Inhalational injury
• % of full thickness burns
• Prognostic burns Index (PBI) = (age + %TBSA +
Grade of inhalational injury)- >140 unsurvivable
52. CONCLUSION
• A burn is the coagulative necrosis of tissue
• Proper rehydration in the first 24 hrs is important in the
management of this patient as this affects treatment
outcome and limits complications
• Good nutrition and proper wound care are essential
• The patient should be rehabilitated post burns treatment
• Giant strides being made in the search for treatment options
that will improve outcome
53. REFERENCES
• Grabb and Smith’s Plastic surgery 6th ed.
• Barret JP; Burns resuscitation BMJ; 392; 246-7
• Heimbach DM; Early burn excision and skin grafting
• Principles and Practise of surgery including pathology in the tropics by Badoe et al. 4th ed.
• Schwartz’s principle of surgery; 9th ed.
• emedicine.medscape.com/article/1277360/
• ncbi.nlm.nih.gov/pmc/articles/pmc30384061
• ncbi.nlm.nih.gov/pmc/articles/PMC31882641