Anesthesia for Burn Patient dictated slides 26-49

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Carbon monoxide (CO) poisoning:

Carbon monoxide (CO) poisoning Results from inhalation of CO produced by fires, exhaust from internal combustion engines and cooking and charcoal stoves Produces tissue hypoxia by its 200-300 times affinity for Hgb compared to oxygen Direct myocardial depression Oxyhemoglobin curve shifts to left Cytochrome inhibition CO combines w/ Hgb  COHgB formed Pulse oximeter may display higher than actual O2 saturation ABGs must have co-oximetry to determine true O 2 saturation S/S Tachypnea, headache, irritability Respiratory failure, myocardial ischemia Seizures, coma, death Cherry red color of blood (only when COHgB >40%)

Clinical manifestation of CO exposure:

Clinical manifestation of CO exposure CO HgB level (%) Manifestations 0-5 None 5-10 Mild H/A, confusion 11-20 Severe H/A, blurred vision 21-40 Disorientation, N/V, irritability, syncope 41-60 Tachycardia, tachypnea, agitation >60 Death

CO poisoning:

CO poisoning Treatment: 100% O2 immediately R educes CO half-life from 4-4.5hrs to 40-50min Hyperbaric oxygen therapy (HBO) may be initiated if symptoms not abating

Cyanide Poisoning:

Cyanide Poisoning Highly toxic compound that forms in high temperature combustion of synthetic materials Cyanide binds to cytochrome oxidase and inhibits tissue utilization, producing tissue hypoxia and metabolic acidosis Produces high mixed venous O2 and low arterial-venous O2 content difference because of impaired O2 use Does not affect SpO2 Sx: coma, apnea, cardiac dysfunction, severe lactic acidosis Tx: may be difficult; check cyanide level to confirm Should have cyanide antidote kit in ER The Cyanide Antidote Kit contains amyl nitrite pearls, sodium nitrite, and sodium thiosulfate Hydroxocobalamin


Frostbite Local freezing of tissue Ice formation in the extracellular space Appears waxy / white Extent of damage may be hidden for days to weeks Numbness & Pain (upon thawing) Upon thawing Severe hyperemia, edema, blistering RBC & Platelet dumping = circulatory stasis / ischemia (gangrene) Treatment Rapid re-warming decreases extent of the damage Emersion in warm water

Pathophysiology of burns:

Pathophysiology of burns Skin is largest organ in body Contains majority of sensory nerve endings Major role in thermoregulation and maintains body temperature within narrow range Prevents loss of body fluids and barrier to microorganisms When skin damaged: Hypothermia Capillary integrity compromised leading to large fluid losses Skin barrier compromised  infection, sepsis

Tissue response to injury:

Tissue response to injury Burn  fluid rapidly accumulates in would Burn of 15-20% or greater BSA will cause hypovolemic shock if not adequately resuscitated Edema response most rapid in first 6-8 hours postburn and continues for 18-24 hours Locally released inflammatory mediators (platelets, macrophages, leukocytes) contribute to hyperpermeability of microcirculation Regional blood flow increasesrise in capillary pressure Denatured protein (coagulated by heat) may further worsen wound edema via osmotic and hydrostatic gradients

Stages of Thermal Injuries:

Stages of Thermal Injuries 1 st Stage – Edema 2 nd Stage – Diuresis

1st Stage: Edema:

1 st Stage: Edema First 24 hours Fluid leak: vascular space  interstitial space  osmotic pressure  capillary permeability Vasoactive substances released  interstitial edema and intravascular hypovolemia occurs

1st Stage Con’t:

1 st Stage Con’t Burns >30% BSA cause capillary changes in both burned and non-burned tissue Burned tissue edema Direct thermal injury to endothelial cells and  burn tissue osmolarity Non-burn tissue edema Severe hypoproteinemia Small wound Edema greatest 8-12 hrs post injury Large wound Edema greatest 18-24 hrs post injury

2nd Stage: Diuresis:

2 nd Stage: Diuresis 24-36 hours after burn, fluid and electrolytes begin to remobilize back into intravascular space Capillary seal reestablishes Diuresis occurs due to  GFR in response to  intravascular volume May see hypernatremia and hypokalemia Cardiac output may  200-300% normal  O 2 consumption

Impact on Systems:

Impact on Systems Immune System Alters immune cells ability to function  killing power of neutrophils Macrophages and lymphocytes do not work well Hematologic System Destruction of RBCs Hemoglobinuria  Hgb level  viscosity  WBC level Coagulation altered

Impact on Systems:

Impact on Systems Cellular Response  tissue oxygen tension Na and H 2 O shift into cell  intracellular swelling Possible cell death  K+ level intravascularly  O 2 level Anaerobic metabolism begins  Lactic acid levels Metabolic acidosis occurs

Impact on Systems:

Impact on Systems Endocrine System Massive release of catecholamines, glucagon, ACTH, ADH, Renin, Angiotensin, & Aldosterone Hyperglycemia Neurological System  cerebral perfusion Cerebral edema occurs from Na shifts Carbon monoxide or associated head injury may cause neuro changes

Impact on Systems:

Impact on Systems GI System  HCL acid secretion from stress response Narcotics for pain management further slow peristalsis Hepatic System Decreased hepatic synthesis Decreased metabolic function Slow peristalsis and possible ileus

Impact on Systems:

Impact on Systems Renal System RBF & GFR Activation of RAS Release of ADH retain water & Na lose of K, Ca, & Mg ARF Acute Tubular Necrosis 2 o hemoglobinuria & myoglobinuria d/t hemolysis & tissue necrosis Maintain high u/o (2ml/kg/hr) w/ fluids / osmotic diuretics

Impact on Systems:

Impact on Systems CV System (first 24 hrs) Activation of CNS system and catecholamine release: Tachycardia Vasoconstriction During early phase: Classic S/S of compensated shock Dramatic decrease in cardiac output Volume loss and decreased venous return:  preload  cardiac filling pressure  CVP and PCWP After 24hrs = increased blood flow to tissues, HTN

Impact on Systems:

Impact on Systems Respiratory System Upper airway injury Involves all of airway to level of true vocal cords Initially due to inflammation from heat of inspired smoke Exacerbated by accumulation of excess interstitial fluid Major airway injuries Involves trachea and bronchi Parenchymal injury Involves entire respiratory tract down to, and including, alveolar membrane Commonly lethal within first few hours after injury due to profound bronchospasms and hypoxia

Impact on Systems:

Impact on Systems Respiratory System Con’t 0-24hrs Edema Obstruction Carbon Monoxide Poisoning 2-5 Days May develop ARDS Signs & Symptoms Stridor / Hoarseness / Facial burns / Singed nasal hairs / Carbonaceous sputum / Impaired level of consciousness S/S of deteriorating ABGs & increasing respiratory distress

Overview of Thermal Injuries:

Overview of Thermal Injuries General Management ABC’s Stop the burning Supportive care Oxygen (intubation) Fluid replacement Electrolyte management Escharotomies / Fasciotomies Wear isolation materials with patient contact Do NOT institute broad spectrum antibiotics or steroids!!!

Rapid Evaluation of Burn Patient:

Rapid Evaluation of Burn Patient A= Airway assessment B= Breathing C= Circulation D= Neurological deficit E= Exposure to environment (heat loss) F= Fluid resuscitation

PowerPoint Presentation:

Figure 68-1 Algorithm for the primary survey of a major burn injury. O 2 , oxygen. (From Hettiaratchy S, Papini R: Initial management of a major burn I: overview. BMJ 328:1555–1557, 2004.)

Preoperative Evaluation & Testing:

Preoperative Evaluation & Testing Initial evaluation of the burn patient Time of the injury* Type (electrical / chemical), depth, & extent of burn Airway / pulmonary damage Age, allergies, medications Associated trauma Co-existing medical conditions Anesthetic history

Preoperative Testing:

Preoperative Testing Diagnostic Testing ABG (w/ co-oximetry)  acid-base balance Electrolytes  imbalances (hyperkalemia) Serial Hct  ongoing blood loss or erythrocyte destruction / volume status Coagulation Profile  rule out a bleeding diathesis Urine Myoglobin (electrical injuries or pigmented u/o) CXR

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