The document defines different types of burns including ordinary, scald, electric, chemical, radiation, and cold burns. It describes the pathology of burns which can be local or systemic. Locally, it affects severity, extent, vascular changes and risk of infection. Systemically, it causes shock, biochemical changes, changes to blood and organs. Treatment involves shock management, fluid resuscitation, airway support, escharotomy/fasciotomy, antibiotics, nutrition and skin grafting. The goal is to prevent infection and promote wound healing.
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
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
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
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Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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2. Defination : A burn is a wound in which there is
coagulative necrosis of the tissue.
The various types of burns are as follows ;
1 . ORDINARY BURNS – are usually caused by dry heat with fire, open
flame, hot metal or aeroplane crash in civil life and bomb injuries in war
time.
2. SCALDS are caused by moist heat e.g. Hot liquid or steam.
3. ELECTRIC BURNS.— Low-voltage electrical sources produce direct injury
at the point of contact.
- most commonly skin and subcutaneous tissue.
- high voltage not only injury to the point of contact but also damage to
the tissue by tharmal burn.
- Majority of electric bums are caused by high-voltage electric current.
3. 4. CHEMICAL BURN is caused by strong acid or base which comes in contact with skin
or any other tissue.
- severity of the damage concentration of chemical, duration of contact , amount
of chemical
5. RADIATION BURNS are usually caused by X-rays or radium.
- This is in fact a type of inflammation of the skin which can be regarded as burn.
Include in freezing and non freezing.
6. COLD BURNS are caused by exposure to cold
Ex. Chilblain , trench foot
- FROSTBITE results in actual freezing of tissues with the formation of ice crystals.
- Mostly commonly skin and subcutaneous tissue of the hands, feet, ears and nose
are affected.
5. A.Local Changes:-
• These can be described under 4 change:-
1. Severity of burn,
2. The extent of burn,
3. Vascular changes and
4. Infection.
6. 1.Severity of burns:-
• Burns are classified into 3 grades or degrees according to the depth of necrosis.
1. first-degree burn in involved superficial layers of the epidermis , hyperaemia
of the skin with slight oedema of the epidermis.
- healing of the few days. Replace to the epithelium layer , so That is not
scaring.
- avoids further exposure to source of heat
2. Second degree burn in involved superficial layer of epidermis and first part of
dermis layer, hyperaemia of the skin with Blebs or vesicles are formed
between the separating epidermis and dermis.
3. third-degree burn there is complete destruction of the
epidermis and dermis with including the sensory nerves.
• Second and third degree burn in skin grafting required.
7. • Another type of classification 1. Partial thickness of burn, 2. Full thickness of
burn.
1. Partial thickness of burn – in burn only superficial layer of the skin ,e.g.
The whole of epidermis and sometimes the superficial part of the dermis become
destroy.
Surrounding the hair follicles or sweat glands from which regeneration of
epithelial cell may take place.
-skin grafting is not necessary.
2. Full thickness of burn – in whole superficial layer of epidermis and dermis
layer are complete destroyed.
- Development of scar. Skin grafting is required.
- As sensory nerves are also destroyed in full thickness burn , sensation is lost.
8. 2.Extent of burn:-
• The length and width of the burn wound is expressed as a
percentage of the total surface area displaying either second or
third-degree burn.
• The extent of burn is most commonly estimated by the
‘rule of nines’.
9. • Rule of nines’ for estimating percentage of body surface involved in bums
are as follows:—
• Anatomic area Percentage of body surface
Head, face and neck 9%
Right upper extremity 9%
Left upper extremity 9%
Right lower extremity (thigh – 9%, leg and foot-9%) 18%
Left lower extremity 18%
Anterior trunk ( chest – 9%, abdomen – 9% ) 18%
Posterior trunk ( upper half – 9%, lower half – 9%) 18%
External genitalia 1%
10. 3.Vascular Changes:-
• There is dilation of large vessels due to direct
injury of vessels wall and local liberation of
histamine that increases the blood flow to the
injured part.
• Due to inflammatory changes in burn area the
capillary permeability increases in great extent so a
large amount of fluid exudate in blisters along with
plasma protein. Body losses a good amount of
plasma protein to cause hypoproteinemia in large
body surface area burn.
• Later on these blisters dried and forms the brown
crust which protects the wound.
Crust
11. 4.Infection:-
• As we know the skin is our first line protection from
infection, so in second and third degree burn skin is
destroyed so these burn always have great risk of
infection.
• Because of malnutrition, loss of plasma protein,
blood volume and anemia body’s defense mechanism
become week to resist any infection.
• Burn patient should kept in special design burn ward
in sterilized environment to protects from infection.
13. 1.Shock:-
• This is the most important effect of bums.
• Various types of shock are come across in burns such as
1. Oligaemic shock
2. Neurogenic shock
3. Cardiogenic shock
4. Bacteriaemic shock
14. 1. Oligaemic shock:-
• The direct effect of heat as well as liberation of vasoactive materials from the area of
injury increases capillary permeability, which permits loss of fluid and protein from
the intravascular compartment into the extravascular tissue. These volume shifts occur
in direct proportion to the extent of burn and are clinically apparent as oedema and
blebs.
• Owing to the outpouring of fluid there is remarkable concentration of blood as shown
by haemoglobin concentration. This leads to olegaemic shock and oxygen starvation of
the tissues.
• The intense heat destroys the red blood cells and causes haemolysis which may be
massive and accompanied by haemoglobinuria.
• These factors may result in ischaemia of important organs particularly the liver and
kidney, so that acidosis and uraemia may develop.
• This leads to stimulation of adrenal cortex with immediate rise in urinary excretion of
17-Ketosteroids.
15. 2. Neurogenic shock :-due to severe pain and apprehension.
3. Cardiogenic shock:- Cardiac output falls in the early postbum
period initially as a result of marked increase in peripheral
resistance and later on as a result of decreased blood volume and
also increased viscosity. The increase in blood viscosity results from
the combined effect of increased haematocrit and aggregation of
red cells, white cells and platelets.
4. Bacteriaemic shock is mainly due to infection and release of toxic
material absorbed from the burnt area.
16. 2.Biochemical changes:-
1. Electrolyte imbalance becomes obvious in the form of low sodium
and chloride concentration and high potassium level in the blood.
2. Hypoproteinaemia is obvious due to excessive loss of plasma
protein.
3. Hyperglycemia may often develop.
4. There will be rise in blood urea and creatinine level due to
kidney damage in extensive burns.
17. 3.Changes in Blood:-
1.Haemoconcentration is due to outpouring of serum and Haemoglobin
level may rice to 150% in severe burns.
2.Increase number in the Red cell is also due to outpouring of plasma.
3. Sludging of blood may occur due to intravascular agglutination of RBCs
4. There is sudden fall in the Eosinophil count during The first 12 hours is
very characteristics of burn , in the course of 24 hour the count should
begin to rise may give an indication to the prognosis of case.
5. Aggregation of red cell , white cell and platelet is common finding in
burns and it increases blood viscosity.
6. Anemia due to immediate red cell destruction in the early post burn
period and there is also continuous red cell loss during first 5 to 7 postburn
days . And 8 to 12% loss of red cell mass per day is general measurement.
7. Alteration of the coagulation system is also seen in burns and there is
early marked decreased level of platelets and fibrinogen level.
18. 4.Systemic Lesions:-
1. The liver may show numerous area of focal necrosis. In the necrotic areas the cells may
contain intranuclear inclusion which is only bordered by nuclear membrane. In majority of
cases of burns is detected with liver necrosis.
2. Kidney is often involved due to low blood perfusion. In severe cases there may be
haemoglobinuria. Gradually oliguria and Anuria may develop and patient may die of
uraemia.
3. Adrenal glands become slightly enlarged. In severe burns there mat be petechial
haemorrhages and small areas of focal necrosis. In the post mortem examination. there may
find shrunken glands with necrosis and haemorrhage.
4. Gastrointestinal tract also respond to burn injury. Gastric and duodenal mucosal changes
indicative of focal ischamia observed as early as 3 to 5 hours after burns. This is due to less
mucosal blood flow. Acute ulceration of the stomach and duodenum has been noticed as a
common complication of major thermal injury. These ulcer were first described by Curling in
1842. Acute ulceration of the colon has been appeared in severe burns patients.
19. 5. Alteration of pulmonary functions:-The actual changes in pulmonary function
following burns are hyperventilation and pulmonary insufficiency which may e
require of mechanical ventilators support .
6. A change in endocrine pattern is seen in burn patient. There is elevated
glucagon , cortisol and catechplamine levels. Insulin and triiodothyronin levels are
depressed. These cause a change in metabolic rate , glucose flow and negative
nitrogen balance.
7. Neurogenic changes are not commonly seen in burn injuries. There may be
some delirium and disorientation due to less blood flow to brain. Specifically
neurological changes are most commonly seen in patient with high voltage
electrical burn.
8. Immunologic impairment is often seen in patient with burns over 50% of total
body surface. And in this condition this patient is having high chances of
infection. There is depression of the immunoglobulin level in the early postburn
period. There is lymphocytes level is also depressed with decreased in T cells and
increased in B cells.
20. • This is conveniently described under three headings:-
I. Treatment of shock,
II. General treatment and
III. Local treatment of burn wound.
Treatment:-
21. I. Treatment of Shock:-
• 1. Sedation.—
• Sedative and analgesic medications are required in burn patients.
• Sedatives should be given during the first 4 to 5 days by intravenous
route and at an absolute minimum dosage.
• The dosage should be minimal to prevent depression of cardiopulmonary
function and to allow evaluation of the sense of the patient.
• The dosage is reduced markedly after 48 hours.
• Barbiturates are preferred in the case of children.
22. • 2. Fluid resuscitation.—
• Indications: -in all adults with burns of 15% or more
-in children with burns above 10%
• Blood transfusion is required when burns involve more than 20% of full thickness
or 40% of partial thickness of total body surface.
• There is conflict of interest for:
use of colloid containing fluid during first 24 hours as it is not retained within the
circulation and exerts greater restorative effect on cardiac output than an equal.
volume of colloid-free electrolyte containing fluid such as Ringer's lactate solution.
• Studies have shown that the colloid solutions not only restore cardiac output more
rapidly but also is more efficient in adequate organ perfusion due to more rapid
replacement of plasma volume deficits.
23. • Moore’s Formula:
• In 1st 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and
normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid-
containing fluid in the form of plasma or plasma substitutes 7.5% of body
weight.
• In 2nd 24 hours: Ringer's lactate solution is given 1000 to 4000 ml and
normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid-
containing fluid in the form of plasma or plasma substitutes 2.5% of body
weight.
24. • Evan’s Formula:
• In 1st 24 hours normal saline is given 1 ml/kg/% burn, 2000 ml of 5%
dextrose and colloid-containing fluid 1 ml/kg/% burn.
• In 2nd 24 hours normal saline is given Vi the amount of 1st 24 hours
requirement, colloid-containing fluid is also given the Vi the requirement
of 1st 24 hours, whereas 5% dextrose is given 2000 ml.
25. • The rate and amount of transfusion are assessed by:
• -repeated red cell volume and haematocrit estimations
• -hourly monitoring of vital signs
• -general condition
• -urinary output.
• Urinary output is a good reflection of adequacy of resuscitation.
26. • Patients usually do not require any diuretic except in 4 categories —
(i) high voltage electrical burn
(ii) associated mechanical soft tissue injury
(iii)deep burns involving muscles
(iv) extensive burns
• In first 3 conditions there is chance of heavy loads of haemochromogens
in urine and are prone to develop acute renal failure unless the urine
output is maintained with diuretic.
• Fluid should be infused at the rate needed to achieve an hourly urinary
output of 75 ml to 100 ml.
27. • 3. Maintenance of airway.—
• Patients with burns exhibit signs and symptoms of hypoxia.
• It ranges from pronounced tachypnoea to respiratory arrest and coma.
• Diagnosis confirmed by analysing the concentration of carbon dioxide in the blood.
• Treatment:
1. Ventilatory support.
2. Endotracheal intubation
3. Tracheostomy
28. II. General Treatment:-
• These include —
1. Escharotomy and fasciotomy,
2. Tetanus prophylaxis,
3. Antibiotics,
4. Nutritional support,
5. Gastric decompression and
6. Treatment of G.I. complications.
29. 1.Escharotomy and fasciotomy:-
• Eschar: an unyieldingcrust formed due to circumferential third-degree or full thickness burns of the extremities or
thoracicwall.
• It exerts pressure on the blood vessels causingdiminished peripheralpulses and decreased skin temperature with
oedema.
• The clinical signs includes:
- cyanosis
- impaired capillaryrefilling
- progressiveneurologicsigns (paresthesia).
• Indication:Restriction ofchest wall motion to the point at which ventilatory
exchange is impaired.
• Escharotomyis performed as a ward procedure without anaesthesia
• The eschar, which is insensitive,is incised on either midlateral or midmedial line.
• The incision shouldextend alongthe entire length of the burned area and carried down deep through the eschar and
the superficial fascia to a depth sufficient to allowthe cut edges of the eschar to separate.
• The bleedingis usuallyminimal and can be controlled byelectrocoagulation.
• Coveringthe escharotomywound with a topical antimicrobial agent is essential.
30. • Fasciotomy is indicated when escharotomy may not result in improvement of blood flow
to the peripheral part. In these cases fasciotomy is required.
• Fasciotomy is performed under general anaesthesia and the fascia of all involved
compartments is adequately released.
• It is indicated in severe bums with extensive damage to the underlying fat and muscles.
• Also required in the treatment of electrical bums where there is
extensive muscle injury
31. 2.Tetanus prophylaxis:-
• All burn injuries should be considered contaminated and tetanus
prophylaxis is obligatory. Intramuscular administration of tetanus
toxoid in the dose of 0.5 ml usually provides adequate
prophylaxis.
32. 3.Antibiotics:-
• In burns, microorganisms contaminate the wound. These organisms
will proliferate if topical chemotherapeutic agents are not
applied. Usually gram-positive organisms colonize in the burn
wounds.
• The most common site of involvement in the burn patient is the
lungs. Bronchopneumonia in burn patients is commonly caused by
opportunistic organisms especially gram-negative bacteria.
• Bronchial secretions should be cultured and antibiotic treatment is
begun on the basis of the sensitivity test.
33. 4.Nutritional Support:-
• In case of all major injuries increased metabolism or
hypermetabolism takes place.
• Such hypermetabolism is also manifested by increased oxygen
consumption, elevated cardiac output, increased core
temperature, wasting of body mass and increased urinary nitrogen
excretion.
34. III. LOCAL TREATMENT:-
1. First aid measure
2. Wound care
• Open method
• Closed method
3. Skin grafting
4. Physiotherapy and Rehabilitation
35. 1. First Aid Measure:-
• The patient should be immediately removed from source of heat.
• Cold clean water should be applied to the burned area
immediately and is continued every 5 minutes.
36. 2. Burn Wound Care:-
• After proper resuscitation, attention should be directed to the
burn wound.
• It should be cleansed with a surgical detergent and all loose
nonviable skin should be trimmed away.
• Silver nitrate must be used soon after injury, before bacteria have
proliferated on the wound.
39. Complications of Thermal Burn:-
1. Curling Ulcer :-
• Curling’s ulcers are often multiple and are found simultaneously
in the stomach and duodenum.
• Until the burn wound is healed, 30 ml antacid is administered
each hour through nasogastric tube to maintain the gastric pH
above 5.
40. 2. Acute Pancreatitis:-
• The peculiarity is that the abdominal pain is often absent and this
condition is only suggested by increasing fluid requirement and new
onset of hyperglycaemia.
3. Acute acalculous cholecystitis:-
• This complication occurs occasionally in burned patients in two forms.
• In one form, the gallbladder is infected by haematogenous seeding from
a primary source in the septic burn wound.
• The other presentation occurs in critically ill patients with marked
dehydration, ileus, hypematraemia and hyperosmolarity.