CRITICAL CARE IN BURNS PLATIC SURGERYpptx

CRICAL CARE IN BURNS

1. CRITICAL CARE IN BURNS Dr.  S. V. NARAYANA

2. Critical care 2

3. Burn Intensive Care Unit Organization PHYSICAL PLANT BICU should exist within a designated burn center , ideally verified by the American Burn Association (ABA), and in conjunction with a recognized trauma center , thus providing the capability to treat both thermal and nonthermal injuries.    The optimal number of beds in the unit should be calculated by the incidence of moderate to severe burns in the referral area which in the United States is approximately 20 per 100,000 people per year. 3

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5. Multiply-resistant bacteria and fungi are commonly encountered in the BICU due to the presence of open wounds.   To prevent transmission of these organisms to other patients, isolation of burned patients from all other patients is recommended .   Single rooms with negative pressure ventilation are advisable.   In addition, strict guidelines for contact precautions in wound care and interventions, and hand-washing are standard. 5

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8. EQUIPMENT 8

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13. Hemodynamic Monitoring in the Burn Intensive Care Unit CARDIOVASCULAR MONITORING Arterial Lines   Hemodynamic monitoring is directed at assessing the results of resuscitation and maintaining organ and tissue perfusion.   Measurement of arterial blood pressure is the mainstay for the assessment of tissue perfusion.   T his measurement can be made using cuff sphygmomanometers; in practice this technique is not useful because the measurement is episodic and placement of these cuffs on burned extremities is problematic.   13

14. Diastolic pressures   can also be artificially elevated in the elderly and obese.  Instead continuous monitoring for hemodynamic instability   through the use of intraarterial catheters is generally preferable when the patient is in the BICU for a prolonged period.  Lines are typically placed in either the radial or the femoral artery.  The radial artery is the preferred site for critically ill patients because of safety, with the dual arterial   supply to the hand.  14

15. However radial artery catheters are inaccurate in the measurement of central blood pressure when vasopressors are used.   Furthermore femoral cannulation sites are often unburned due to the insulation provided by undergarments, and they do not preclude mobilization with physical therapy or rehabilitation goals.   For these reasons, we recommend femoral arterial blood pressure measurement in most burned patients . 15

16. Complications   Distal ischemia associated with vasospasm and thromboembolism, Catheter infection, and arterial damage/pseudoaneurysm   Complications are uncommon, the results can be devastating. Physical evidence of ischemia in the distal hand or foot should prompt immediate removal of the catheter and elevation of the extremity.   If improvement in ischemic symptoms is not seen promptly (within an hour), angiography and intervention must be considered. 16

17. Thromboembolism be found, the clot can be removed with operative embolectomy or clot lysis. If, during angiography, extensive arterial damage is found with ischemia, operative repair may be indicated. Evidence of catheter infection hallmarked by purulence and surrounding erythema should instigate removal of the catheter. If a pseudo-aneurysm is encountered after arterial catheterization and removal without signs of distal ischemia, injection of thrombin or compression with a vascular ultrasound device until no further flow will often alleviate the problem without operative intervention. 17

18. Cardiac Output Measurement Pulmonary artery catheters placed percutaneously through a central vein (internal jugular, subclavian, or femoral) and “floated” into the pulmonary artery through the right heart have been used extensively in hemodynamic monitoring in BICUs.   By measuring the back pressure through the distal catheter tip “wedged” into an end-pulmonary branch, an estimate of left atrial pressure can be measured.   In addition, dyes or isotonic solutions injected into a proximal port can be used to determine cardiac output from the right heart. 18

19. Arterial Waveform Analysis 19

20. The transpulmonary thermodilution technique provides an even more complete hemodynamic dataset without the use of a pulmonary artery catheter.  Using only a central line and central arterial line, thermodilution allows monitoring of preload with global end-diastolic volume index, intrathoracic blood volume, continuous cardiac output, and extravascular lung water index.  20

21. Echocardiography 21

22. Laboratory Estimates of Perfusion 22

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26. Critical Care Interventions Critical care of a burn patient in the modern era is predicated upon seven key factors:   ■ Sufficient goal-directed fluid resuscitation ■ Early burn excision and grafting ■ Aggressive antimicrobial and source control of sepsis ■ Aggressive and sufficient nutritional support ■ Active warming ■ Aggressive physical, occupational, and respiratory therapy ■ Aggressive and continuous support of organ failures 26

27. Various formulas to predict fluid requirement, balances between crystalloid versus colloid, and resuscitation endpoints have been advocated.   Early in resuscitation it is critical to provide sufficient volume to maintain preload and perfusion in the setting of fluid losses into burn edema and distributive shock   while avoiding over-resuscitation, with the resultant costs such as heart failure, liver failure, and compartment syndromes. 27

28. Early burn excision and grafting   The overriding principle is to remove inflammatory and diseased burned tissue to break the hyperinflammatory state underlying burn shock.   Early grafting reduces the inflammatory load on the patient, fluid loss, heat loss, the area susceptible to infection, and the total length of critical care. Collectively it reduces the exposure time available for MOF to occur. 28

29. TOXICOLOGICAL BURN CRITICAL CARE Many toxins can affect the burn-injured patient, particularly with occupational injuries and require appropriate decontamination, antidotes .    However the most common toxins are cyanide and carbon monoxide.     Cyanide can be elaborated from the combustion of various plastics, and significant exposure can result   from smoke inhalation.   cyanide toxicity is clinically significant in inhalation injuries, being found at clinically significant levels in up to 76% of inhalation injury patients.   29

30.  Hydroxycobalamin is the first-line antidote for cyanide toxicity and has a very mild side effect profile of transient hypertension, bradycardia, and urine discoloration. Carbon monoxide (CO) should be considered in any inhalation injury, enclosed fire, or patient with altered mental status.   Patients with carboxyhemoglobin ( COHb ) levels above 25% should be mechanically ventilated on 100% FIO2, which reduces the half-life from 4 hours to 1 hour.   Hyperbaric oxygen (HBO)   can reduce the CO half-life to 15 minutes, particularly in the setting of pregnancy or seizures. 30

31. NEUROLOGICAL BURN CRITICAL CARE The main aspects of neurologic management of burn patients are pain control, sedation, delirium management, and management of acute stress disorder or posttraumatic stress disorder (PTSD).   An important component of neurological care is early mobilization; physical/ occupational therapy should be performed unless firmly contraindicated.   Pain control is the most common neurologic intervention in the burn patient.   31

32. Basal pain management with narcotics such as morphine is administered as needed to maintain comfort, while taking care to avoid oversedation that can prevent achieving physical therapeutic goals. ​ Methadone can help by providing basal pain coverage and weaning of narcotics.  ​ For more extensive procedures ketamine is a safe, effective, and recommended agent.  ​ 32

33. Propofol, ketamine, and remifentanil have been increasingly used as alternatives to the formerly standard benzodiazepine-based therapies.   When compared to midazolam, patients sedated with the α -adrenergic agonist dexmedetomidine have required less sedation and have less hypotension.   Dexmedetomidine is associated with less time to extubation and higher rates of bradycardia, well tolerated in burn patients due to their hyperdynamic state and tachycardia.   Ketamine infusion is safe and effective in continuous BICU sedation. 33

34.  Psychiatric and psychological care is a critical component   of BICU care.  The critical care team can help prevent delirium and PTSD by avoiding benzodiazepine, minimizing sedation, treating pain first, limiting sleep disturbances, encouraging mobility,   reorientation, and avoiding prolonged infusion of sedatives. Haloperidol remains in   use in critical agitation and delirium settings and has documented   safety in  pediatric  and adult burn populations.   34

35. CARDIOVASCULAR BURN CRITICAL CARE 35

36. Preload Preload is the force that stretches the cardiac muscle before contraction. This force is composed of the volume that fills the heart from venous return.   Preload is estimated clinically by central venous pressure, pulmonary artery wedge pressure, echocardiography, or transpulmonary thermodilution.   These measures can be used to optimize preload, balancing vascular volume loading and cardiac performance against interstitial and pulmonary edema . 36

37. Cardiac  Contractility The force with which the heart contracts is referred to as cardiac contractility. It is directly related to the number of fibers contracting, their preload and afterload.   Contractility is diminished in patients with low preload or high afterload, in coronary artery disease with loss of myocardium from infarction and ischemia, in burned patients during the acute resuscitation due to myocardial depressant factor, in septic shock with Takotsobu cardiomyopathy, or severely Malnourished patients.   37

38. Afterload Afterload is the force impeding or opposing ventricular contraction and, in conjunction with cardiac output, creates blood pressure.   This force is equivalent to the tension developed across the wall of the ventricle during systole.   38

39. Heart Rate and Rhythm For the heart to function properly, the electrical conduction   system must be intact to provide rhythmic efficient contractions   to develop sufficient force to propel blood through the   circulatory system.  Heart rate and rhythm are monitored continuously as routine in every critically ill patient using   electrocardiography.  A combination of sympathetic and   adrenergic tone, combined with high atrial stretch, can predispose burn patients to atrial arrhythmias, such as atrial fibrillation (AF).  39

40. Effects of Burn on Cardiac Performance The first is to reduce preload to the heart through volume loss into burned and non burned tissues. It is for this reason that volumes predicted by resuscitation formulas must be used to maintain blood pressure and hemodynamics .   severe burn induces myocardial depression characterized by a decrease in tension development, and velocities of contraction and relaxation.   40

41. Hemodynamic Therapy: Preload Augmentation. 41

42. Hemodynamic Therapy: Inotropes and Vasopressors. If preload optimization is insufficient to improve hemodynamics , patients may require inotropes to increase cardiac output and/or vasopressors to increase afterload. .   Inotrope classes include phosphodiesterase inhibitors, digoxin, and adrenergic agonists.   Phosphodiesterase inhibitors like milrinone increase contractility and decrease afterload without increasing myocardial oxygen demand.   42

43. Digoxin increases   contractility and decreases heart rate without increasing   myocardial oxygen demand.  Dobutamine is a commonly used inotrope with effects   limited to  β -adrenergic stimulation, thereby increasing CO and causing vasodilation.  The associated vasodilation may be useful in perfusing peripheral vascular beds, as in threatened skin. 43

44. Catecholamines, the most commonly used medication to augment blood pressure, are considered “ inoconstrictors ” because they have both inotropic and vasoconstrictive properties.   Pure vasoconstrictors have a very limited role in burn care because concomitant inotropic support is advisable due to the patient’s hyperdynamic state. Phenylephrine is a pure α -agonist, and can decrease CO and perfusion. 44

45. These agents are effective in septic shock or neurogenic shock to increase vascular tone. However, in burned patients, it is believed that these agents will cause vasoconstriction of the skin and splanchnic circulation, thereby redistributing blood flow.  This can cause grafts to fail and conversion of partial-thickness skin injuries to full thickness, as well as resulting in ischemic injury to the gut. 45

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47. PULMONARY BURN CRITICAL CARE Lungs can be injured from inhalation injury, infection, inflammatory mediators, heart failure, or a sequela of critical care interventions, such as fluid overload or ventilator injury.   Minor pathology can be treated with supplemental oxygen, diuresis, bronchodilators, or mucolytics. However mechanical ventilation is an essential treatment to manage pulmonary failure.   Mechanical ventilation in the severely burned generally occurs for three reasons:   Airway control during the resuscitative phase,   Airway management for smoke inhalation,and   Support during acute respiratory distress syndrome (ARDS).   47

48. The first indication is for airway control early in the course, with the development of massive whole-body edema associated with the great resuscitative volumes required to maintain euvolemia.   In this situation, the need for mechanical ventilation is not due to lung failure per se, but rather to maintain the airway until the whole-body edema is resolved.   Once this occurs, usually 2–3 days into the course, extubation can be accomplished with minimal sequela. Ventilator management during this phase is routine.   48

49. The second indication is airway management early in the course of smoke inhalation,   Which is a direct toxic injury to the airways and alveoli resulting in mucosal sloughing, loss of mucociliary escalator function, airway narrowing and edema , loss of surfactant, weakening of cartilaginous support of the airways, and fibrinous exudation into the airways. 49

50. The third indication is the development of hypoxemia or hypercarbia due to a high alveolar-arterial (A-a) gradient, shunting, ventilation/ perfusion (VQ) mismatching, poor compliance, or high resistance.   Severe burns are known to be associated with hypoxemia and the development of ARDS.   The clinical manifestations are dyspnea , severe hypoxemia, and decreased lung compliance, with radiographic evidence of diffuse bilateral pulmonary infiltrates. 50

51. GASTROINTESTINAL SYSTEM BURN CRITICAL CARE Pathophysiologic Changes in the Gut After Burn The gut, including the stomach, intestines, liver, and pancreas, plays six critical roles after burn injury:   A bsorption of nutrients M ucosal barrier to invasive microbes   Elimination of hydrophobic wastes   C learance of lactate   Production of acute-phase proteins and coagulation factors A n endocrine function able to drive toward anabolism.   51

52. Clinical Changes in the Gut After Burn Given these changes in the gut from burn, it is commonplace to observe some evidence of gut dysfunction after burn, as evidenced by feeding intolerance and mucosal ulceration and bleeding, particularly in the stomach and duodenum Enteral feeding is an important means of providing nutrition to burned patients and has led to a decrease in mortality, but on occasion the gut will not cooperate.   At present there is no specific treatment for burn-induced ileus, but early enteral feeding prevents some of these potential complications.   feeding the gut promotes mucosal barrier function, nourishes the patient, and promotes bile flow, elimination of hydrophobic wastes, and an anabolic hormonal release from the gut and pancreas. 52

53. Stress ulceration of the stomach and duodenum, on the other hand, can be prevented effectively with antacid therapy.   Abdominal compartment syndrome has proved a significant risk. This is associated with massive volume resuscitation, inducing generalized edema in a relatively limited abdominal compartment.   It eventuates in decreased gut blood flow and renal blood flow causing oliguria and bowel ischemia. 53

54. RENAL BURN CRITICAL CARE Pathophysiology Acute kidney injury (AKI) is a potentially lethal complication of burns. Of note, AKI has supplanted the prior term (acute renal failure [ARF]). Despite substantial technical developments in dialysis to replace the function of the kidneys, mortality meets or exceeds 50% for all critically ill patients who develop ARF.   With the advent of early aggressive resuscitation after burn, the incidence of renal failure coincident with the initial phases of recovery has diminished significantly in the severely burned.   54

55. Another period of risk for the development of renal failure 2–14 days after resuscitation is still present and is likely related to the development of sepsis. Transient hypotension, nephrotoxic medications   such as antibiotics, hypovolemia from insensible fluid losses,   and rhabdomyolysis are all also significant  etiologies  of AKI   in the BICU.  In burned patients, the causes can be generally   narrowed to renal hypoperfusion, nephrotoxic insults from   pharmacologic treatments (e.g., aminoglycosides or intravenous   contrast agents), or sepsis.  55

56.   Ischemic renal failureis the more common of the three causes and is induced by hypoperfusion from an imbalance between vasoconstrictive and vasodilatory factors acting on the small renal vessels during low-flow states.   The initial care of patients with AKI is focused on reversing the underlying cause and correcting fluid and electrolyte imbalances.     A decrease in urinary output heralds renal failure . Volumes of urine of less than 1 mL/kg per hour may indicate the onset of AKI.   All   nephrotoxins should be discontinued or avoided. 56

57. Hyperkalemia may develop and can be treated with resins, glucose and insulin, and sodium bicarbonate in the presence of metabolic acidosis. Reducing the volume of fluid given can also alleviate volume overload in burned patients.   I t is important to continue sufficient nutritional delivery to the patient and balance this against the renal function, utilizing diuretics and even dialysis to ensure an excessive nutrient debt does not develop.   Reducing potassium administration in enteral feedings and giving oral bicarbonate solutions can minimize electrolyte abnormalities. 57

58. THANK YOU 58