1. MANAGEMENT OF BURNS PATIENT IN ICU
-DR. MUNIRA DILAWER GHEEWALA

2. APPROACH Primary survey : stabilization of patient
Evaluation of airway and securing it
Ventilation with high O2 concentration till risk of CO toxicity is excluded.
Appropriate Vascular access and fluid resuscitation
Secondary survey:
Determination of mechanism of injury
Evaluation for presence / absence of inhalational injury
Detailed assessment of burn wound
Consideration of possibility of abuse
Consideration of need for transfer to higher centre.
As high O2 conc will clear CO frm body more rapidly. Also CO toxicity can result in falsely elevated pulse oximetry saturation

3. CALCULATING TBSA INVOLVED
Initial burn chart / Lund Browder chart
Alternative and easier method in adults is Rule of Nine chart.

4. LUND AND BROWDER CHART

5. TBSA BY RULE OF NINE

6. OTHERS Arterial line for BP in radial or femoral artery.
Pulmonary artery/central venous catheter.
Lab studies: initial lactate is a strong predictor of mortality. Sr lactate trend provide greater information regarding the hemostatic status.
Electrolyte levels should be monitored and if required promptly corrected.

7. CLASSIFICATION OF WOUND
On basis of skin thickness involved:
- Superficial
Partial thickness
Full thickness
On basis of depth
First degree burns: red, dry & painful
Second degree burns: red, wet and very painful.
Third degree: leathery, dry, insensate, and waxy. These wounds generally donot heal except by contraction and limited epithelial migration.
Fourth degree burn: involve underlying subcutaneous tissue, tendon or bone.

9. BURN PHYSIOLOGY
Tissue burn involves direct coagulation and microvascular reactions in surrounding dermis which results in extension of injury.
Systemic response caused by
Loss of skin barrier
Release of vasoactive mediators
Subsequent infection
Decreased cardiac output
↓ plasma volume
↑ afterload
↓ contractility (sec. to ? Circulatory mediators, impaired Ca at cellular level)
Interstitial edema in soft tissue

10. PATHOPHYSIOLOGY CONTD…
Systemic microcirculation loses its vessel wall integrity and proteins are lost into interstitium. ↓
Intravascular colloid osmotic pressure drops
Fluid escapes from circulation
Decrease in interstitial pressure caused by release of osmotically active particles
Sucking in of fluid from plasma space
Marked increase in fluid flux into interstitium due to above imbalance in hydrostatic and osmotic forces
Marked fluid movement into interstitium

11. PATHOPHYSIOLOGY CONTD…
Loss of circulating plasma volume, hemoconcentration, massive edema, ↓ urine output and depressed cardiac functions. Interstitial + decreased cardiac = SHOCK edema output (distributive & hypovolemic) Functional plasma volume in burn can only be restored with expansion of the extracellular space.

12. FLUID RESUSCITATION Cornerstone of treatment in initial 48 hrs
Proper fluid resuscitation aims to anticipate and prevent rather than treat burn shock
Delay in fluid resuscitation >2 hrs of injury complicates resuscitation & increases the mortality.
Excessive resuscitation leads to fluid overload and then further complications : Pulmonary Edema, Myocardial Edema, Abdominal Compartment Syndrome.

13. A Lund-Browder chart is used to calculate the TBSA burn
Formulae should be regarded as guideline but fluid administration has to be adjusted to individual patient need.
Ringer’s lactate is the most commonly used as it most closely resembles normal body fluids.
Factors influencing fluid requirement: TBSA, depth of burn, age, inhalational injury, delay in resuscitation, etc.

14. FORMULAE FOR FLUID RESUSCITATION
Parkland formula: most widely used
4ml/kg body wt/% of TBSA burn hrs
Half of fluid volume is given in first 8 hrs, rest in 16 hrs.
Galveston regime : pediatric
5000ml /m² burned ml /m² total.
Modified Brooke’s formula:
First 24 hrs : RL 4ml/kg/% of TBSA burn (1/2 in 8 hrs)
Second 24 hrs : crystalloid – to maintain u/op
colloids – ml/kg/burns in 24 hrs
(albumin with RL)

15. Measure of adequate hydration:
Urine output – guidelines recommend
0.5ml/ kg/hr output in adults
ml/kg/hr in children > 30 kg wt.
lesser hourly u/op in first 48 hrs post burn almost always represent inadequate resuscitation.
A pulse rate < 110/min indicates adequate volume while > 120 usually indicates hypovolemia.
Narrowed pulse pressure provides an early indication of shock than systolic BP.

16. METABOLISM & NUTRITION
Ideally enteral feeds should be started with fluid resuscitation, except in pts with major burns or complications.
As there is hypermetabolism, there is increase in normal resting energy expenditure. Hence enteral feeds should be started as early as possible.
TPN is assoc with immunosuppression, and increase in infection.
Glutamine, arginine, omega 3 fatty acid supplements may improve immunity and gut function.
Strict glucose monitoring should be done. hyperglycemia should be avoided as it can lead to increased risk of infection

17. Hypermetabolism can lead to catabolic effect
Hypermetabolism can lead to catabolic effect. Hence anabolic steroids like Oxandrolone can be used in pts with severe burns. They promote protein synthesis, nitrogen retention, skeletal ms growth and decreased wound healing time.
Pts on Oxandrolone are found to regain weight and lean mass faster than with nutrition alone.
Vitamin C : studies have shown that high doses of ascorbic acid during initial 24hrs post burn reduced fluid requirement by 40% and burn tissue water content by 50%, decreasing ventilator days.

18. CARDIAC MANAGEMENT
Inotropic drugs can be used in patients with myocardial dysfunction
Most of these drugs cause vasoconstriction in burn wounds : not used till adequate fluid resuscitation is done.
Dobutamine which does not produce vasoconstriction can be used : preserves wound viability.

19. RENAL MANAGEMENT
Pigmented urine is commonly seen with deep thermal burns : It precipitates Renal Failure : Treatment is administration of crystalloids.
Bicarbonates may facilitate clearance of myoglobin by preventing its entry into tubular cells. Rarely loop diuretics or mannitol is used but this obscures u/op as an indicator for circulating volume.
Delayed renal failure is usually d/t sepsis and asso. with MODS.
Early renal support (hemodialysis/filtration) helps control electrolyte levels and accommodates the large volumes of nutritional supplements essential in burns.

20. ADDITIONAL THERAPIES Wound management Pain management Physiotherapy
Transfer to higher centre.

21. WOUND MANAGEMENT Goal : To close the wound as soon as possible.
Debride the non viable tissue leaving any newly formed dermis/epidermis
Topical application of silver sulfadiazine (antimicrobial)
Also silver containing sheets and compounds can be placed directly on partial thickness wounds.
Deep Burns of external ear are treated with mafenide acetate as it penetrates the eschar and prevents purulent infection of the cartilage

22. For pts with full thickness burns - prompt surgical excision of the eschar and allografting/ autografting can be done depending on wound size.
Circumferential or near circumferential wounds cause limb ischemia & interfere with perfusion as wound swelling occurs. Timely escharotomies is essential in such cases.

23. VARIOUS DRESSINGS USED IN BURN WOUND

24. PAIN MANAGEMENT
The main issue in burns patient is inconsistent and inadequate pain management.
Opioids - long acting analgesics can be used.
Ketamine is used for extensive burn dressing changes and procedures like escharotomies.
Anxiolytics like BZD’s can also be used.

25. PHYSIOTHERAPY
Rehabilitation therapy can be started right from admission to maximize functional recovery.
These patients require special positions, splinting, early mobilization, and exercise to avoid formation of contractures.

26. TRANSFER CRITERIA
Pts who should be acutely transferred to a burn centre
10% TBSA partial thickness burn
Any size full thickness burn
Burns to special areas of function or cosmesis
Inhalational injury, serious chemical injury
Electrical injury including lightning
Burns with trauma
Pediatric burns if hospital has no special pediatric department
Burns in pt with multiple co-morbidities.

28. COMPLICATIONS Inhalational Injury Compartment Syndrome
Infection / Sepsis
Hypothermia
Deep Venous Thrombosis
Neutropenia
Stress Ulcers
Adrenal Insufficiency

29. INHALATIONAL INJURY Warning signs of airway burns:
Burns in an enclosed space
Stridor, hoarseness of voice, cough
Burns to face, lip, mouth, pharynx
Soot in sputum, nose, or mouth
Dyspnea, decreased level of consciousness, confusion
Hypoxemia or raised carbon monoxide level(>2%).
Patients presenting with stridor should be intubated on presentation.
A carboxy-hemoglobin level taken within 1 hr after injury is strongly indicative of smoke inhalation if >10%.

30. TREATMENT OF INHALATIONAL INJURY
There is no specific treatment. Only ensuring adequate oxygenation and minimizing iatrogenic lung injury.
Aggressive airway toilet can be given. Nebulization with diluted heparin and acetyl cysteine may help.
Higher O2 conc. should be given as it will clear CO from body more rapidly. Also CO toxicity can result in falsely elevated pulse oximetry saturation
For pts requiring ventilator – mode that is capable of supporting oxygenation and ventilation is used. Plateau pressure should be <35 cm of H2O.
PEEP of appropriate level should be used
Prophylactic antibiotics have no role and actually increase the rate of infection.

31. MECHANISMS OF PULMONARY INSULT AFTER LOWER AIRWAY BURN:
Mucosal inflammation
Mucosal burn
Ciliary paralysis
Reduced surfactant
Obstruction by debris
Bronchospasm
Bronchorrhoea
Systemic inflammatory response.
Nearly 70% of pts on ventilator develop ventilator associated pneumonia. Prevented by head elevation, turning position of the patient, oral care and gastrointestinal prophylaxis.

32. COMPARTMENT SYNDROME
A life threatening complication caused by high volume resuscitation.
Abdominal compartment syndrome:
- Defined as abdominal pressure >20 mmHG plus atleast one new organ dysfunction. Assoc with renal impairment, gut ischemia, and cardiac & pulmonary malperfusion.
- c/f : tense abdomen, decreased pulmonary compliance, hypercapnia, oliguria.
- Mx - ↑ Intravascular vol, body positioning, pain Mx, nasogastric decompression, torso escharotomy are all interventions to increase abdominal wall compliance & decrease intra abdominal pressures.

33. Bladder pressure monitoring should be initiated in pts with >30% TBSA burn.
Patients who receive >250 ml/kg of fluids in first 24 hrs. likely require abdominal decompression.
Percutaneous abdominal decompression is a minimally invasive procedure that should be performed before undertaking laparotomy
Decompression laparotomy should be performed in pts with ACS that is refractory to other Rx : mortality rates are high.

34. INFECTION / SEPSIS Causative agents:
ß hemolytic streptococci – Cellulitis, TSS
Staphylococci – MRSA – abscess and sub eschar pus
Gm negative bacteria – P. Aeruginosa, Acinetobacter, Proteus spp.
Fungi – candida – MC
- Filamentous fungi – aspergillus, fusarium, phycomycetes.
Rx must include debridement of infected tissue.
- Viruses – herpes simplex – vesicular lesions.

35. Around 70% of mortality in burns patient is related to infection.
Infective pulmonary complications are the most common type of infections.
Deciding whether infection is present is difficult in burns as these pts have an inflammatory state from injury itself that can mimic infection.
Diagnosing infection :
Change in wound appearance – discoloration , offensive exudate.
Delayed healing
Graft failure
Conversion of partial thickness wound to full thickness
Wound biopsy and histopath examination
Culture and sensitivity of wound tissue

37. PREVENTION & TREATMENT
Preventing invasive wound infection :
Topical antimicrobial treatment
Early closure of burn wound
Prophylactic antibiotics are not advised.
Antibiotic based on C/S reports.
Aggressive surgery – extensive debridement of necrotic tissue.
Infection control can be achieved by strict isolation of the patient.

38. PREVENTABLE COMPLICATIONS
Hypothermia : metabolic responses can be minimized by treating the pt in a thermoneutral environment. A warmed room warmed inspired air, blankets can be used to prevent hypothermia
Deep venous thrombosis : prophylaxis to prevent DVT is routinely practiced in patients with burn.

39. OTHER COMPLICATIONS Neutropenia :
Transient leucopenia is seen primarily d/t decreased neutrophils.
Maximal decrease is seen several days after admission and rebound to normal a few days later.
Silver sulfadiazine has also been associated with transient leucopenia, resolution of which is independent of its use.
Stress ulcers : routine prophylaxis with PPI to prevent occurrence.
Adrenal insufficiency : those with massive burns have higher cortisol levels but may be resistant to serum cortisol increase in response to stimulation.

40. SPECIAL TOPICS Chemical burns :
immediate removal of clothing and chemicals.
Copius irrigation with tap water for atleast 30 mins
Adequate ocular irrigation
Agents with irritating fumes can cause airway compromise and may require intubation and ventilation.

41. THANK YOU