2013 SA Benchmark Vignettes

Question 1

What are the two favored methods of burn classification in small animals?

Answer 1

Depth of tissue destruction
Total body surface area

Question 2

Explain the depth of tissue destruction classification

Answer 2

First degree burn –> Superficial: epidermis only. Erythematous, painful. Heals in <1 week with topical wound management. No systemic effects.

Second degree burn –> Superficial partial-thickness: epidermis to upper 1/3 of dermis. Erythematous, moist, painful. Hair follicles spared. Heals in 10-21 days with re-epithelialization also with minimal scarring. May have some systemic effects.

Second degree burn –> Deep partial-thickness: epidermis and all of the dermis. Skin may be black or yellow-white, and hair follicles are destroyed. Heals via contraction and epithelializlation within 2-3 weeks, DOES scar. Systemic effects expected.

Third and fourth degree burns –> Full-thickness: epidermis, dermis, and SQ tissues (4th degree extends into underlying muscle). Black insensitive eschar will form. Does not heal without intervention (flaps/grafts/surgical intervention). Systemic effects can be severe.

Question 3

Explain total body surface area

Answer 3

The rule of 9’s: head and neck is 9%, each arm is 9%, dorsal trunk 18%, ventral trunk 18%, each rear leg 18%

Burn card: a credit card equals approx. 45 cm^2 so compare size of a credit card to size of the burn, then use standard body weight to surface area chart to estimate the percentage of body surface area affected.

Question 4

What are the definitions of local burn injury and severe burn injury?

Answer 4

Local burn injuries involve <20% of TBSA; involvement of >20% TBSA constitutes a severe burn injury (SBI) (>second degree or higher).

SBI frequently results in severe systemic derangements requiring intensive care (burn shock).

Question 5

What are the expected homeostatic alterations that occur with SBI?

Answer 5

Capillary thrombosis and plasma leakage results in massive amounts of fluid being retained in the wound, leading to edema. This results in loss of fluid and electrolytes with the most dramatic losses occurring within the first 12 hours.
Anemia, hypoproteinemia, hypernatremia or hyponatremia, hyperkalemia or hypokalemia, acidosis, coagulopathy, oliguria and azotemia can ensue.

Hemoconcentration is initially noted because of the dramatic loss of plasma (anemia will likely develop later).

During the initial 24 hours after resuscitation for shock, typical fluid rates will be 1-4 mL/kg bw x TBSA burned

–> 4 mL/kg per percentage TBSA in the first 24 hours, with the first half of this amount administered in the first 8 hours. The remainder is then administered over the remaining 16 hours of the first day.

Question 6

What are the roles of caspases and MIF (macrophage migration inhibitory factor) in the cardiac output alterations that characterize the resuscitation phase of SBI?

Answer 6

Caspases (family of cysteine proteases) are activated early in SBI by ROS, increased intracellular calcium, and inflammatory cytokine production. Caspase activation causes myocardial apoptosis and contributes to the production of many inflammatory mediators.

MIF is released by skin and cardiomyocytes in response to burn injury. MIF is a mediator of late and prolonged cardiac dysfunction.

Vaughn et al. Severe burn injury, burn shock and smoke inhalation injury in small animal Part 1. JVECC 22(2) 2012; pp 179-186.

Question 7

What are three classifications of “burn pain”?

Answer 7

Procedural pain (bandage changes, surgery, debridement; stinging, burning- persists minutes to hours after intervention)

Background pain (at rest with normal daily activity; constant and throbbing)

Breakthrough pain (occurs with movement after being immobile; severe intensity, unpredictable)

Question 8

Intra-abdominal hypertension and abdominal compartment syndrome are common sequelae to SBI in people. Define ACS, and differentiate between primary, secondary and tertiary ACS.

Answer 8

ACS is a syndrome associated with a raised intra-abdominal pressure, abdominal distention and associated organ dysfunction (e.g., oliguria or anuria, decreased cardiac output, hypotension and reduced pulmonary compliance).
For humans, the definition of ACS is as follows: “a sustained or repeated IAP ≥ 20 mm Hg and/or abdominal perfusion pressure < 60 mm Hg in association with new-onset single or multiple organ system failure”.

Primary ACS– results from direct injury or disease of any organ located in the abdomino-pelvic region (e.g., fractured liver or spleen, penetrating foreign body, peritonitis, neoplasia, hepatic abscess)

Secondary ACS– results of conditions not originating from the abdomino-pelvic region (e.g., sepsis, capillary leak, major burns, massive fluid resuscitation)

Tertiary ACS – results from surgical and/or medical management of primary or secondary ACS

Question 9

What is normal IAP in dogs?

Answer 9

0-5 cm H2O (0-3.75 mm Hg); healthy dogs following OHE had postoperative IAP up to 15 cm H2O (11.25 mm Hg) with no clinical signs referable to IAH.

Question 10

List and briefly describe 4 organ dysfunctions that can occur associated with ACS

Answer 10

Hemodynamic effects:
Elevations in CVP, pulmonary artery pressure, right atrial pressure, pulmonary capillary wedge pressure, and systemic vascular resistance (SVR)
Ultimately, the patient will experience a reduction in cardiac output associated with impaired venous return and increased SVR.

Renal effects:
Reduction in GFR and urine output with resultant oliguria and/or anuria
This is thought to occur subsequent to both decreased cardiac output and direct compression of the renal vasculature and parenchyma.
Pulmonary effects:
Reduction in pulmonary compliance due to greater pressure on the peritoneal side of the diaphragm

CNS effects:
Increased intracranial pressure from reduced venous blood flow in the jugular system and reduced drainage from the head.

Visceral effects:
Hepatic, portal, intestinal and gastric blood flow is reduced. Bacterial translocation is one of the possible sequelae.

Hormonal effects:
Increased levels of antidiuretic hormone, renin, aldosterone, epinephrine and norepinephrine have been documented in experimental animal models.

Question 11

What is the formula for abdominal perfusion pressure?

Answer 11

APP = MAP - IAP

Question 12

List and describe the phases (3-4 phases) of wound healing

Answer 12

Inflammation – occurs in the first 5 days; early vasodilation allows for leakage of fibrinogen and clotting elements in plasma into the wound for clot formation. This clot serves as scaffolding for invading neutrophils, monocytes, fibroblasts and endothelial cells. Also in the plasma are inflammatory mediators (e.g., cytokines, leukotrienes, complement and growth factors).

Debridement – occurs simultaneously with inflammation; marked by entrance of WBCs into wound. Neutrophils appear in the first 6 hours to remove extracellular debris via enzymatic activity and phagocytosis. Monocytes follow at 12 hours, and become macrophages in the next 1-2 days. The monocytes stimulate fibroblast activity, collagen synthesis and angiogenesis. Macrophages remove necrotic tissue, bacteria and foreign material.

Depending on the source, inflammation and debridement may be combined as one phase.

Repair/proliferation – occurs 3-5 days post-injury and lasts 2-4 weeks. This healing phase is characterized by angiogenesis, granulation tissue formation and epithelialization. Granulation tissue is a source of myofibroblasts that play a role in wound contraction. New epithelium is visible by day 4-5 post-injury; wound contraction begins by 5-9 days after injury.

Maturation – starts 17-20 days after injury and can continue for years; characterized by wound contraction and remodeling of collagen fiber bundles; healed wounds only 80% as strong as original tissue

Caroline Carzotto. “Wound management” In: Silverstein, Chp 157
Fossum, 3rd Edition. “Surgery of the Integumentary System”, Chp 15
Karen Cornell. “Wound healing” In: Veterinary Surgery Small Animal, Volume 1 by Tobias and Johnston, 2012. Chp 9

Question 13

What are five contraindications for primary wound closure?

Answer 13

Foreign debris in a wound (significant contamination or tissue damage)

Need for continued debridement of wound

Dead space

Too much tension on the wound

Questionable blood supply

Wound location (some areas such as large wound on limbs are not amenable to closure)

Wound > 6 hours old

Maria Fahie. “Primary wound closure” In: Veterinary Surgery Small Animal, Volume 2 by Tobias and Johnston, 2012. Chp 75

Question 14

Provide a definition for nosocomial infection and list the 4 main sites of this type of infection in human (and likely veterinarian) patients.

Answer 14

Nosocomial infection: An infection that occurs more than 48 hours after admission to the hospital; an infection that occurs less than 48 hours after admission, IF the patient has been hospitalized within the last 2 weeks prior to the current hospital admission, or if an infection is transferred from another hospital or long-term facility.

Sites:
Bloodstream; catheter-related blood stream infections (CRBSI)

Respiratory (i.e., ventilator –associated pneumonia [VAP])

Urinary (UTI)

Surgical site infection (SSI)

Question 15

List at least 5 risk factors associated with nosocomial CRBSI

Answer 15

Immunosuppression
ICU hospitalization
Parenteral nutrition
Mechanical ventilation
Multi-lumen catheter
Site of catheter
Catheter dwell time
Failure to adhere to aseptic technique

Question 16

List 5 management strategies recommended to reduce the incidence of BSI in hospitalized patients.

Answer 16

Handwashing
Sterile precautions; thorough skin preparation
Decreased catheter manipulation
Single-lumen catheters; reduced access ports
Catheter fixation
Antiseptic-coated or antibiotic-coated catheters

Question 17

Describe how the CVP can be used to determine if the patient’s hypotension is due to hypovolemia?

Answer 17

A low CVP (<0 cmH2O) alone could indicate the presence of hypovolemia either due to fluid loss or vasodilation. If the CVP reading is questionable a test bolus (10-15ml/kg) of isotonic crystalloid solution can be given over a 5 minute period. If the patient has a low CVP from hypovolemia the reading will remain unchanged or increase slightly before returning to the baseline reading rapidly. If the patient is euvolemic a small increase will be seen (2-4cmH2O) followed by a slower return (15 minutes) to baseline. If the patient is hypervolemic or has reduced cardiac compliance the CVP will rise >4cmH2O with an even slower return to baseline (>30minutes)

Question 18

Briefly discuss the controversy surrounding the use of CVP in determining preload and/or predicting response to a fluid challenge.

Answer 18

This is a static variable that measures pressure, not volume. Many things influence this variable unrelated to patient volume status: e.g. venoconstriction, changes in RV compliance, obstruction of the major veins, tricuspid valve disease and other cardiac structural abnormalities (shunts). Increased intrathoracic pressure associated with positive pressure ventilation/PEEP, altered compliance of the chest wall (flail, pain), presence of pleural effusion/diaphragmatic hernia or increased IAP can also result in high CVP measurement in a volume-contracted patient.
Human studies have shown that CVP demonstrates a very poor relationship with blood volume status, and the CVP/change in CVP is inconsistently able to predict the hemodynamic response to a fluid challenge. There is an expanding body of evidence that recommends against the use of CVP in clinical decisions regarding fluid management in critically ill human patients. Fluid therapy guided by CVP may result in volume overload and pulmonary edema, or alternatively may lead to ongoing hypovolemia in patients with “higher” CVPs. Although CVP does not directly or accurately reflect preload, low serial CVPs evaluated in context with the PE and possibly thoracic radiography, may indicate a margin of safety for fluid challenges until more dynamic and reliable indices of preload become available to the veterinary practitioner.

Question 19

In what echo mode do you calculate fractional shortening, and what is the formula for it? What is a normal fractional shortening value in the dog?

Answer 19

M-mode
FS% = [(LVIDd-LVIDs)/LVIDd] x 100 = 11%

Normal FS% ranges from 25% -45%

Question 20

What are some mechanisms behind development of sepsis-induced myocardial dysfunction?

Answer 20

1. Timing of cardiac changes and recovery

–> Clinical studies indicate a reduction in systolic function is observed around day 2-4 after the onset of sepsis/SIRS. In patients that survive cardiac function returns to normal by days 7-10.

2. Myocardial depression

–> Several lines of evidence suggest that the ventricular myocardium is depressed during sepsis with features of diastolic dysfunction. Potential candidates responsible for septic cardiomyopathy include pathogen-associated molecular patterns (PAMPs), cytokines, and nitric oxide. Extracellular histones and high-mobility group box 1 that function as endogenous damage-associated molecular patterns (DAMPs) also contribute to the myocardial dysfunction associated with sepsis.

3. Diastolic and systolic dysfunction

–> Decreased systolic contractility during sepsis limits ventricular ejection and stroke volume. Initially, this effect is compensated for by increased diastolic filling during volume resuscitation. Reduced afterload due to arterial vasodilation also compensates so that cardiac output can be maintained or increased. Recent results recognize the importance of diastolic dysfunction, reduced ventricular diastolic compliance that impedes ventricular filling. Diastolic dysfunction becomes increasingly important as severity of septic shock increases. When impaired ventricular ejection is coupled with limited diastolic filling, stroke volume must decrease. Accordingly, diastolic dysfunction is more closely related to mortality than systolic dysfunction. Recent trials of beta-adrenergic agonists and levosimendan have been disappointing, while approaches to modulating the intramyocardial inflammatory response show promise.

Other potential reasons:

B-receptor hypo-responsiveness
Mitochondrial dysfunction
Dysregulated calcium homeostasis

https://web.archive.org/web/20190308231812id_/http://pdfs.semanticscholar.org/faf1/a568809918ebd378944a5257ecb29c7702b1.pdf

https://link.springer.com/content/pdf/10.1186/s40560-016-0148-1.pdf

Question 21

What is a biomarker?

Answer 21

A biomarker, or biological marker, is a substance used as an indicator of a biological state. It is a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.

Question 22

What is NGAL (neutrophil gelatinase-associated lipocalin)

Answer 22

NGAL (neutrophil gelatinase-associated lipocalin, lipocalin-2, siderocalin) is a small protein expressed in neutrophils and certain epithelia, including the renal tubules. Renal expression of NGAL is dramatically increased in kidney injury from a variety of causes, and NGAL is released into both urine and plasma. NGAL levels rise within 2 hours of the insult, making NGAL an early and sensitive biomarker of kidney injury. In people, urine and plasma NGAL measurements have been demonstrated to represent early biomarkers of AKI in a heterogeneous pediatric intensive care setting, being able to predict this complication approximately 2 days prior to the rise in serum creatinine, with high sensitivity and AUC-ROCs of 0.68–0.78..In a recent clinical study in dogs urinary NGAL was able to identify patients with AKI 12 hours before changes in serum creatinine or serum NGAL occurred. This study was designed to assess for post-operative AKI not AKI from sepsis but does show promise. It also highlights the need to assess urinary biomarkers in additional to serum biomarkers to enhance early detection.

Question 23

What is cystatin-B?

Answer 23

Cystatin B is an intracellular protein that is released into the urine following damage to renal tubular epithelial cells. Cystatin B can be used to identify kidney injury but does not evaluate kidney function.