ANZCVS 2014 Flashcards
a) List the tendons that comprise the common calcaneal tendon.
Gastrocnemius
Superficial Digital Flexor
Common tendon (Gracilis, Biceps Femoris and Semitendinosus)
b) Name and draw three (3) suture patterns commonly used for tenorrhaphy.
- Locking Loop Pattern
- Three-Loop Pulley
- Bunnell Suture
c) Describe the process of tendon healing following surgical apposition with minimal (less than one millimeter) gap. (10 marks)
1) Inflammatory phase (first 14 days): Hemostasis (platelet clot), Cell Migration (Leukocytes, Monocytes and lymphocytes), release of histamine and bradykinin improve vascular permeability. Fibroblasts from MSC produces a fibrin scar.
2) Proliferative phase (2 to 4 weeks): Fibroblast, myofibroblast and endothelial cell proliferation replace inflammatory tissue with granulation tissue. Tendon-bone adhesion improves. Fibroblasts begin to produce Collagen Type III after second week.
3) Maturation/Remodeling (4 to 12+ weeks): Collagen III gradually replaced with Collagen I, forming dense connective tissue. Tendon is integrated within bone.
d) State the approximate strength (expressed as a percentage of original tendon strength) attained in a surgically repaired tendon by:
i. 6 weeks following repair (1 mark) : 56% (Dueland, R et al. J Am Anim Hosp Assoc. 1980)
ii. 12 months following repair. (1 mark): 79% (Dueland, R et al. J Am Anim Hosp Assoc. 1980)
e) Discuss appropriate post-operative management and rehabilitation of a 30 kg dog following surgical repair of a common calcaneal tendon rupture. Include the rationale behind each recommendation. (9 marks)
The tendon will only regain 56% of its original strength in the first 6 weeks, so the tarsus must be strongly supported during this phase to prevent full dorsal flexion. Options include external coaptation (Splint) + Calcaneo-tibial screw or external fixation. Hinged splints and external fixators can be constructed in such way as to allow limited tarsal extension (not flexion) for the first 3 weeks. Tarsal range of motion can be gradually increased over 2 to 10 weeks. Activity is limited to brief leash walks for the first 10 weeks. Therapeutic ultrasound or extracorporeal shock wave therapy may improve tissue perfusion and stimulate faster healing.
Gastric dilatation-volvulus (GDV).
In your answer consider the sequence of events that results in dilatation and volvulus of the stomach (7 marks) and the specific pathophysiologic consequences that GDV has on the circulatory system (8 marks),
Pathoanatomy: The pylorus and proximal duodenum move ventrally and then cranially, stretching the hepatogastric ligament. The pylorus continues to move from right to left, creating a fold in the stomach, and eventually coming to rest on the left side of the abdomen dorsal to the esophagus. This movement creates traction on the gastrosplenic ligament and short gastric vessels, which eventually rupture.
Circulatory consequences: As the stomach dilates with fluid and especially gas it applies pressure upon the caudal vena cava, significantly decreasing cardiac preload. Poor coronary blood flow and production of myocardial depressant factor lead to myocardial ischemia and cardiogenetic shock. Resultant cardiac arrhythmias are observed in 65% of cases (first 72 hours post-op) and further decrease systemic perfusion. Concurrent compression of the portal vein results in portal hypertension and venous stasis, decreasing tissue perfusion throughout the entire GI tract and creating mucosal death and bacterial translocation.
Gastric dilatation-volvulus (GDV).
In your answer consider the consequences that GDV has on the gastrointestinal system (8 marks),
Gastrointestinal consequences: Gas distension compress and collapse gastric capillaries, leading to mucosal necrosis. This is compounded by systemic hypotension due to cardiogenetic shock, often leading to full-thickness gastric wall necrosis. Gastric mucosal necrosis allows bacterial translocation into the bloodstream,
Gastric dilatation-volvulus (GDV).
In your answer consider the consequences that GDV has on the respiratory system (8 marks),
Respiratory system: Gastric distension applies pressure on the diaphragm, making inspiration more difficult and further decreasing oxygen delivery.
Gastric dilatation-volvulus (GDV).
In your answer consider the systemic consequences of GDV
Systemic effects: Hypovolemia, metabolic and respiratory acidosis, hypoxemia and the creation of oxygen-reactive species (reperfusion injury) lead to oxidative damage to kidneys and central nervous system. The role of reperfusion injury remains debatable and further studies are needed to determine when and how it is most severe.
a) List the major types of burn injuries experienced in small animals (2 marks) and explain the basis by which burns cause damage to tissue (2 marks).
Thermal burns: Exposure to temperature extremes, either high or low, sufficient to cause cellular damage. This damage occurs when heat is transferred via conduction, convection or radiation.
Chemical burns: Exposure to chemicals that cause tissue necrosis, either directly via chemical reactivity or indirectly via secondary thermal effects.
Electrical burns: Exposure to electrical current of sufficient energy that passes through the patient and causes cell necrosis along its path.
Radiation burns: Exposure to ionizing radiation at levels that cause acute cell death, such as solar radiation or radiation therapy for neoplastic disease.
b) Describe the common classification system of burns used in small animal patients. (5 marks)
Two common classification schemes exist:
Five-degree classification scheme based on depth:
- Overall it can be said that the amount of heat transfer into tissues, rather than its source, determines the degree of the burn
First degree: superficial. Only the epidermis is affected. No scarring
Second-degree: full thickness epidermal necrosis that extends into the underlying dermis, with resultant fluid exudation and occasionally blistering (more common in humans).
Third degree: burn extends through the dermis and into underlining subcutaneous tissue
Fourth degree: burn extends through the underlining muscle or fascia
Fifth degree: burn extends into bone.
c) Explain the ‘rule of nines’ in relation to burn injuries. (3 marks)
The Wallace’s “rule of nines” was adapted from human medicine for use in veterinary burn victims. It divides the body into regions which are multiples of 9% of total body surface area.
The head and neck are counted as one “nine”, or 9%. Each forelimb is another 9% and each hindlimb is “two nines”, or 18%. The dorsal and ventral halves of the trunk are another 18% each.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at a local level
At a local level the severity of a burn injury radiates outward from the greatest point of energy delivery to the tissue. This leads to the formation of three distinct zones: Zone of Coagulation (inner-most zone, with no viable tissue), Zone of Stasis (reduced tissue perfusion due to increased vessel permeability, with fragile but viable cells) and Zone of hyperemia (area of inflammatory response). Local perfusion is upregulated immediately after the burn by postganglionic autonomic stimulation and NO synthesis upregulation. The inflammatory response is characterized by vasodilation, increased capillary permeability, edema and influx of inflammatory cells. Wound healing is significantly slower than surgical wounds, presumably due to very low levels of fibroblast growth factor (FGF-2, less than 5% normal).
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the pulmonary system
- Pulmonary System (smoke inhalation): Consists of two components, thermal and toxic. The thermal component is limited to the upper airways, therefore the majority of the injury is toxic. Housefire smoke contains more than 250 toxic compounds, like carbon monoxide (from incomplete carbon combustion), hydrogen cyanide (from nitrogen-containing products like nylon, formica, melamine, wool) and inorganic acids from Teflon, neoprene and plastics (hydrochloride, hydrogen fluoride, etc..).
Carbon monoxide reduces tissue oxygen delivery by direct binding to hemoglobin, by promoting carboxyhemoglobin formation and by binding to myoglobin.
Hydrogen Cyanide binds to mitochondrial cytochrome oxidase, preventing cell respiration.
Inorganic acids, like hydrochloride, are intensely irritating to respiratory mucous membranes promoting laryngospasm and bronchospasm.
The lung’s response to smoke inhalation consists of increased pulmonary vascular permeability, venoconstriction, rapid accumulation of fluid, mucous and neutrophils within the alveoli and airways, hallmarks of pulmonary edema. These are combined with atelectasis, deactivation of pulmonary surfactant and decreased ling compliance, resulting in Acute Respiratory Distress Syndrome. Cytokines, eicosanoids and substance P are produced by damaged tissue and the GI tract, reaching the lungs via the lymphatic system. Eicosanoid Thromboxane A2, synthesized by pulmonary macrophages, causes marked pulmonary vasoconstriction and increased vascular resistance.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the general cardiovascular system (not heart)
- General Cardiovascular System (hypovolemia, vascular disfunction, generalized edema): Consists of fluid extravasation, evaporation, blood hyperviscosity and vasoconstriction. The end result being tissue hypoxia and metabolic acidosis.
Fluid extravasation into the extravascular space begins within 10 min of a burn, and is mediated by histamine, complement activation and oxygen free radical activation of myosin-contraction of endothelial cells and endothelial cell damage. Systemic extravasation rapidly overwhelms the lymphatic system and hypovolemia/edema ensue as protein-rich fluid accumulates in the interstitial space.
Evaporation through burned skin is 3 to 20% higher than through intact skin. Even a partial thickness burn (second degree) can increase evaporation by 35%.
Hyperviscosity occurs as a result of decreased erythrocyte deformability, which in combination with hypovolemia leads to hyperviscosity and compromises blood flow characteristics.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the cardiovascular system (heart)
- Cardiovascular System – Heart (myocardial effects): large burns (50% total body surface) leads to oxidative injury to the sarcoplasmic reticulum, inducing calcium leakage into the cytoplasm. Intracellular hypercalcemia significantly decreases myocardial contractility. Toxic effects of carbon monoxide, particularly the production of carboxyhemoglobin, leads to cardiomyocyte necrosis.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the Gastrointestinal system
- Gastrointestinal system: burn injuries significantly increase the apoptotic rate of gut mucosal cells, without a corresponding increase in mucosal proliferation, leading to loss of mucosal integrity. Translocation of endotoxins, gut bacteria and cytokines quickly lead to septic shock. Gastroenteric motility is also significantly impaired.
The liver is also significantly impaired by oxidative stress , leading to increased rate of apoptosis and proliferation. Acute phase protein production increases and albumin production decreases.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the renal, hemopoietic and immune systems
- Renal System: Acute renal failure may occur as a result of hypovolemia, hypoalbuminemia, hemoglobinemia, myoglobinemia, sepsis and the use of nephrotoxic antibiotics.
- Hematopoietic System: Burn injury produces an immediate and persistant reduction of circulating RBC’s, known as “burn anemia. This is a result of RBC loss and decreased erythropoiesis.
- Immune system: burns produce significant negative effects on lymphocyte production and function. Lymphocyte apoptosis is upregulated by TNF-a. Sympathetic nervous system-mediated inhibition of T-cells lead to increased susceptibility to sepsis.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the neurologic system
- Neurologic system: burns rapidly cause hyperalgesia through the release of prostaglandins and kinins by inflammatory cells. The resulting intense pain stimulates a massive sympathetic discharge responsible for the cardiovascular events of burn shock.
d) An adult male entire Labrador retriever is brought to your clinic following a house fire. He has sustained major burns to approximately 30% of body surface area and is suffering from smoke inhalation. Discuss the pathophysiology of these injuries at the neurologic system
- Metabolic and endocrine changes: immediately following a burn injury the body enters a hypometabolic phase (“ebb phase”), followed by a hypermetabolic phase (“flow phase”). Basal metabolic rate increases by 100% during the flow phase due to increased heat loss (evaporation, increased hypothalamic set point due to inflammatory cytokines and eicosanoids). The resulting nonproductive metabolic work produces the required additional heat at a significant energy cost to the patient. Aminoacids are utilized for energy production, leading to loss of lean body mass (poor prognostic indicator).