Burns, Shock, & Sepsis Flashcards
Epidemiology of Burns
65+ is highest in mortality
18-35 years old 2:1 (M:F)
Cellular Changes in Burns
Intracellular influx of Na/H2O
Extracellular migration of K
Disruption of cell membrane function
Failure of “sodium pump”
Hematologic Changes in Burns
Increased hematocrit
Increase in blood viscosity
Anemia due to RBC destruction
At what temperature does cell damage occur?
113+ F
Denatures protein
What happens to the zone of coagulation with a burn?
Irreversibly destroyed
What happens in the zone of stasis with a burn?
Stagnation of microcirculation
Can/will extend if not treated appropriately
What occurs in the zone of hyperemia with a burn?
Increase blood flow
How to Determine What Percentage of Patient is Burned
9%: each arm 9%: front of each leg 9%: back of each leg 9%: chest 9%: abdomen 18%: back 9%: head 1%: genitals
1st Degree Burn
Erythema of skin
Minimal surrounding edema
Minimal pain
2nd Degree Burn
Partial thickness Painful Red or mottled skin Blisters with broken epidermis Edema Wet/weeping surfaces Sensitive to air
3rd Degree Burn
Full thickness Damage to all skin layers, subQ tissues, & nerve endings Pale white or charred appearance Leathery Broken skin with fat exposed Dry surface Painless to pinprick Edema
Specific Issues with Burn Management
Carbon around nose Burns involving the mouth Significant respiratory problems Fires in enclosed places CO exposure Toxic gases from combustion (cyanide) Intubate early
Chemical Burns
Irrigate
Alkali burns more serious
Why are alkali burns more serious than acid burns?
Alkali’s penetrate deeper
Electrical Burns
Always more serious than they appear
Deeper structures have more damage
Rhabdomyolysis -> acute renal failure
Dark urine: assume rhabdomyolysis
What can you do to help clear up the urine from rhabdomyolysis?
Increase fluids to achieve a UO of 100 mL/hr
Mannitol if necessary
ABCDE of Burn Patients
A: airway B: breathing C: circulation or control of hemorrhage D: disability (neurologic) E: environmental control/exposure
What needs to be observed in a burn patient?
Eyes: corneal ulcers
Need 2 large bore IVs
Estimate depth & extent of burn
Management of the Burn Victim
20%+ BSA partial thickness burn: NG tube placement CBC, CMP ABGs, carboxyhemaglobin level CXR & EKG on suspected inhalation injury Urine: myoglobin & CPK Tetanus status Remove jewelry Foley placement Pain control
Dressings for Burn Victims
1% silver sulfadiazine (sivadene)
Re-evaluate every 24 hours until full extent is known
Dressing changes BID until weeping stops
Honey shown to be effective
Guidelines for Transferring Burn Patients
Partial thickness >10% BSA
Burns involving the face, hands, feet, genitalia, perineum, or major joints
Third-degree burns in any age group
Electrical burns
Burns with complicated co-morbidities
Children with significant burn that are not in a children’s hospital
Define Shock
Inadequate tissue/organ perfusion
Reasons for Shock
Pump failure
Decreased peripheral resistance
Hemorrhage
Cardiac Response to Shock
Tachycardia
Increased myocardial contractility/oxygen demand
Constriction of peripheral blood vessels
Renal Response to Shock
Stimulating an increase in renin secretion
Vasoconstriction of arteriolar smooth muscle
Stimulation of aldosterone secretion by the adrenal cortex
Neuroendocrine Response to Shock
Increase in circulating antidiuretic hormone
Types of Shock
Hypovolemic
Septic
Cardiogenic
Neurogenic
Reasons for Hypovolemic Shock
Decreased vascular volume
Hemorrhagic
Reasons for Septic Shock
Systemic infections lead to hypotension & decreased vascular volume
Reasons for Cariogenic Shock
Some abnormal cardiac function
Reasons for Neurogenic Shock
Disruption of the autonomic pathways within the spinal cord
Signs of Shock
Tachycardia
Hypotension
Decreased urine output
Altered mental status
Reversal of Hypovolemic Shock
Fluids: isotonic saline
Colloids: albumin, hespan
Systemic Physiologic Responses to Hemorrhagic Shock
Increased HR
Cardiac contractility issues
Blood shunted to vital organs
Conservation of water & sodium
Local Physiologic Responses to Hemorrhagic Shock
Local activation of coagulation system
Affected vessels contract
Activated platelets adhere to damaged vessels
Activated platelets release Thromboxane A2
Thromboxane A2 increases vessel contraction
Clinical Presentation of Hemorrhagic Shock
Tachycardia Tachypnea Narrow pulse pressure Decreased output Cool clammy skin Poor capillary refill Decreased CVP Hypotension Altered mental status
Treatment for Hemorrhagic Shock
2 large bore IVs
Give 1-2 L as rapidly as possible (3 mL/ 1 mL blood loss)
Monitor urine for adequate fluid (30-50 cc/hr)
Blood transfusion based on response to fluid bolus
Monitor ABGs
Monitor calcium
Monitor for coagulopathy (DIC)
Prevent hypothermia
Vital Signs Return to Normal After Fluid Bolus in Hemorrhagic Shock
Type, cross, hold
Monitor urine output & vitals
Vital Signs Return to Normal then Drop Again After Fluid Bolus in Hemorrhagic Shock
Give type specific blood
Plan to go to OR
Treatment for Severe Hemorrhagic Shock
Replace blood (PRBCs)
Possible replacement of platelets & FFP
Reversal of clinical manifestations often adequate to guide resuscitation
Identify source of bleeding
Goal of Therapy in Hemorrhagic Shock
Restoration of organ perfusion & adequate tissue oxygenation
How is organ perfusion & adequate tissue oxygenation assessed?
Appropriate urine output
CNS function
Skin color
Return of pulse & BP towards normal
Define Cardiogenic Shock
Shock resulting from some abnormal cardiac function (MI)
Hallmark Sign of Cardiogenic Shock
Hypotension
Signs of increased peripheral vascular resistance
How to Determine Inadequate Organ Perfusion
Altered mental status
Decreased urine output
Treatment of Cariogenic Shock
Identify abnormality
Address abnormality
Define Septic Shock
Sepsis induced with hypotension despite adequate resuscitation along with the perfusion abnormalities
Perfusion Abnormalities in Septic Shock
Lactic acidosis
Oliguria
Acute alteration in mental status
What is septic shock usually due to?
Gram negative bacteria
Predisposing Co-Morbid States with Septic Shock
DM
Immunosuppression
Leukemia
Why does relative hypovolemia occur?
Pooling of blood in microcirculation & loss of fluid into the interstitial spaces (leaky capillaries)
Toxic Shock Syndrome
Diffuse red rash
Thrombocytopenia
Usually within 5 days of menses
Common Bugs of Sepsis from GU Origin
E. coli
Klebsiella
Proteus
Pseudomonas
Common Bugs of Sepsis from Respiratory Origin
Strep pneumoniae
Staph aureus
Common Bugs of Sepsis from Below the Diaphragm
Aerobic gram negative bacilli
Clostridium
What is neurogenic shock most often caused by?
Spinal cord injury
Special Considerations for Shock
Do not use colloids in septic shock
Cardiogenic & Septic: can use inotropic medications
All other shock: can use inotropic medications IF CVP monitoring shows patient to be normovolemic & they remain hypotensive
No substitute for blood in hemorrhagic shock
Define Sepsis
Presence of bacteria or other infectious organisms or their toxins in the blood or other tissues of the body
Clinical Manifestations of Sepsis
Fever/chills
Malaise
Hypotension
Mental status changes
Etiology of Sepsis from the GI Tract
Enterobactericeae
Pseudomonas
Anaerobes
Etiology of Sepsis from the Skin
Staphylococcus
Beta hemolytic streptococci
Etiology of Sepsis from the GU Tract
Enterobactericeae
N. gonorrhea
Etiology of Sepsis from the Respiratory Tract
Pneumococcus
Hemophilus
Viruses
Etiology of Sepsis from the Oral Cavity
Alpha-hemolytic streptococci
Anaerobes
Risk Factors for Gram Negative Bacillary Bacteremia
DM CA Cirrhosis Burns Invasive procedures/devices Neutropenia
Risk Factors for Gram Positive Bacteremia
Vascular devices
Indwelling mechanical devices
IV drug administration/use
Burns
Risk Factors for Fungemia
Immunosuppressed with neutropenia
Broad-spectrum antibiotic therapy
Risk Factors for Severe Sepsis
Age 50+
Primary pulmonary disease
Abdominal infection site
CNS infection
Clinical Signs of Sepsis
Fever Leukocytosis Tachycardia Tachypnea Reduced vascular tone Organ dysfunction
Define Systemic Inflammatory Response Syndrome (SIRS)
Infectious or non-infectious etiology with the presence of 2+ of the following
Fever or hypothermia
Tachypnea
Tachycardia
Leukocytosis, leukopenia, or neutrophilic bands
Non-Septic Causes of SIRS
Pancreatitis Burns Trauma Adrenal insufficiency Pulmonary embolism Dissecting or ruptured aortic aneurysm MI Occult hemorrhage Cardiac tamponade Post-cardiopulmonary bypass surgery Drug overdose Anaphylaxis
Skin Manifestations of Sepsis
Acrocyanosis
Peripheral ischemic necrosis
Dermatologic lesions
Define Acrocyanosis
Cyanosis of the extremities with mottled discoloration of skin of the digits, wrists, ankles, and profuse sweating & coldness of the digits
Dermatologic Lesions of Sepsis
Cellulitis
Pustules
Bullae
Hemorrhagic lesions
Pathogens with Petechiae/Purpura in the Presence of Sepsis
N. meningitis
H. influenza
Pathogen of Petechiae in Tick Bite Endemic Areas in the Presence of Sepsis
Rocky mountain spotted fever
Pathogen with Erythema Gangrenosum Lesions in the Presence of Sepsis
Pseudamonas aeruginosa
GI Clinical Manifestations of Sepsis
N/V
Diarrhea
Ileus
Cholestatic jaundice
Major Cardiopulmonary Complications of Sepsis
Hypotension secondary to abnormal distribution of blood fluids/volume
Hypoxemia
Hypercapnia
Acute respiratory distress syndrome (ARDS)
Major Renal Complications of Sepsis
Oliguria Azotemia Proteinuria Non-specific urinary casts Polyuria Renal failure secondary to acute tubular necrosis induced by hypotension & capillary injury
Other Major Complications of Sepsis
Thrombocytopenia
DIC
Neurologic complications
Define Severe Sepsis
Sepsis with 1+ signs of organ dysfunction
OR
Hypotension
Signs of Organ Dysfunction
Metabolic acidosis Acute encephalopathy Oliguria Hypoxemia Disseminated intravascular coagulation (DIC)
Define Septic Shock
Severe sepsis with hypotension that is unresponsive to fluid resuscitation
Define Refractory Septic Shock
Septic shock that lasts for 1+ hour & does not respond to fluid or pressor administration
Define Multiple Organ Dysfunction Syndrome (MODS)
Dysfunction of more than one organ requiring intervention to maintain homeostasis
Mechanisms of Cell Injury/Death
Cellular necrosis
Apoptosis
Leukocyte mediated tissue injury
Cytopathic hypoxia
Pathophysiology of Sepsis-Induced Ischemic Organ Injury
Cytokine production leads to massive production of endogenous vasodilators
Structural changes in endothelium result in extravasation of intravascular fluid into interstitium
Plugging of microvascular beds with neutrophils, fibrin aggregates, & micro thrombi impair microvascular perfusion
Organ-specific vasoconstriction
Therapeutic Strategies in Sepsis
Renal placement therapies: dialysis Surgical intervention Drainage Cardiovascular support Culture directed antimicrobial therapy Mechanical ventilation Transfusion for hematologic dysfunction Enteral/parenteral nutritional support Minimize exposure to hepatotoxic & nephrotoxic therapies Optimize organ perfusion Expand effective blood volume Hemodynamic monitoring
