Environmental / Venomous (SACCM + Dobratz) Flashcards
Define primary vs secondary hypothermia
primary (aka. accidental): caused by excessive exposure to low environmental temperature without preoptic and anterior hypothalamic nuclei disease.
secondary: caused by disease, trauma, drug-induced, surgery.”
Define mild, moderate and severe hypothermia and what are the expected clinical signs for each
The main thermostat of the body is the hypothalamus, with temperature changes sensed by the ____________. Secondary temperature sensors are located within the skin and deep body tissues; namely, the ________________.
“preoptic and anterior hypothalamic nuclei
spinal cord, abdominal viscera, and great vein”
T/F The core is defined by well-perfused tissues in which the temperature remains relatively uniform, such as within the abdominal and thoracic cavities, or the cerebrum
TRUE
Describe the pathway of termoregulation
Temperature is sensed by the transient receptor potential channels (family of ion channels), which are activated at distinct temperature thresholds. This peripheral input from the skin travels to the spinal cord or trigeminal dorsal horn for passage to the midbrain and thalamus. This thermal information is then output to the sensory cortex, producing the sensation of hot and cold. The behavioral and autonomic responses are linked to the reticular inputs in the brainstem
In a normal body, the rate of heat production depends on:
Activity Enviromental temperature Age Food ingestion Circulating levels of thyroid hormones, epinephrine and NE
Shivering is characterized by involuntary oscillatory skeletal muscular activity and can increase the metabolic rate by a factor of ____________. The energy substrate for shivering is usually carbohydrate oxidation, but in glycogen- depleted patients, _________ reserves need to be used. Therefore this method of heat production may be diminished in the cachectic, the very old, and the very young
four to ten
lipid and protein
The transfer of heat from the body surface to the air surrounding the body is known as:____________.
convection
The transfer of heat from body surface to objects that come into contact with the body, such as the ground, examination tables and kennels is known as: _________________.
Conduction
Immersion hypothermia is an example of which heat loss mechanism?
Conduction
Increasing air circulation is an example of which heat loss mechanism?
Convection
Heat loss to surrounding structures that do not come into direct contact with the body, such as walls; is know as:____________This heat transfer is independent of the termeprature of the intermediary substance (ex. Air).
radiation
The loss of heat from moisture on the body surface or through the respiratory tract to the environment is know as: _____________
Evaporation
Give an example of evaporation heat loss that could be relevant in VM
Wet patients (incidentally or in preparation for surgery)
What makes neonates more prompt to heat loss?
larger body surface area
hypothermia shifts the oxygen-dissociation curve to the _______.
left (more affinity, less O2 delivery)
Why hypotension develops after a prolonged state of hypothermia
Initially there is a sympathetic response but as hypothermia progresses, vascular responsiveness to norepinephrine begins to decrease.
what is the initial dysrhythmia seen in hypothermic patients and how does it progress?
Iinitially atrial fibrilation, which can progress to Vtaq and Vfib.
**As CBT (core body temperature) approaches 23.5C –> 50% of dogs demonstrate vfib
Why tidal volume and respiratory rate decreases with hypothermia
Decreased metabolism –> decreased CO2 production –> decreased stimulus for respiration
Loss of airway protective reflexes and a reduction
in ciliary clearance in a hypothermic patient may predispose the patient to ______________.
aspiration pneumonia
At temperatures below 34° C, the sensitivity to partial pressure of carbon dioxide _______, and carbon dioxide production decreases by_____% with an 8° C fall in body temperature
Decreases
50%
What are neuromuscular effects of hypothermia
Decreased cerebral blood flow (by 6-10% per each 1C of Core body temperature decrease in humans) Increased ICP --> ""cold edema"" Muscle stiffness Ataxia hyperreflexia followed by hyporeflexia pupillary dilation
List causes of acidosis in hypothermic patients
- Increased CO2 in blood due to hypoventilation
- CO2 more soluble in low T –> increases CO2 in blood
- Decreased hepatic clearance of lactate
- Increased lactate production due to shivering and tissue hypoperfusion
- Decreased acid excretion by kidneys
- Decreased buffering capacity of cold blood
List effects of hypothermia on primary hemostasis
- PLT sequestration in liver and spleen (thrombocytopenia).
- Decreased PLT agreggation due to decreased production of thromboxane A2.
- Decreased granule release of platelets (thrombopathia).
- Attenuation of P selectin expression.
- Decreased expression of vWF receptor.
Your hypothermic patient is showing signs of a coagulopathy but your PT, PTT came back as normal. Why?
Kinetic coagulation tests are performed on warmed blood. Therefore the standard clotting tests performed in the laboratory at 37° C will not reflect the effects of hypothermia on the patient’s clotting cascade
What is cold diuresis? How does it happen?
Diuresis, regardless of hydration status.
initial renal effect observed in mild to moderate hypothermia,why? –>
** initially sensed increase in blood volume caused by peripheral vasoconstriction
** As the CBT drops, there is a decreased response to vasopressin at the level of the distal tubule
can cause significant hypovolemia and subsequent hypotension.
List mechanism of hyperglycemia in hypothermic partients
- Decreased glucose excretion due to decreased GFR
- Insulin resistance
- Decreased insulin production by pancreatic b cells
- Cathecholamines/stress?
Why hypothermia can contribute to increased post-anesthetic recovery time?
Decrease hepatic enzyme activity and decreased perfusion to the liver –> decreased metabolism and clearance of substances/medications
medications that have shown increased potency/reduced clearance with hypothermia –> fentanyl, morphine, midazolam, pentobarbital, phenobarbital, propofol, volatile anesthetics.
How can hypothermia affect the immune system
- Decreased chemotaxis
- Decreased phagocytosis
- Leukocyte depletion
- Decreased mobility of macrophages
- Impaired oxydative killing by neutrophils
T/F Rectal temperatures are useful in steady-state conditions but are slow to change and can read slightly high (by 0.4° C) in a patient with hypothermia
TRUE
Describe the rewarming techniques (recommendations/basis, applications and complications for each one)
Passive external rewarming
** usually used only to assist in diminishing further CBT drops
Active external rewarming
Active core rewarming
Which complications during rewarming can develop if the extremities are warmed before the core
- Rewarming shock –> vasodilation, hypotension
- Afterdrop -> colder peripheral blood return to vital organs and drops more the CBT
- Rewarming acidosis –> returning colder blood and lactate to core organs
give an example of forced air surface rewarming
3M bair hugger –> convective transfer of heat to the patient
give an example of resistive heating rewarming
Hot dog warming blancket –> conductive transfer of heat
Airway rewarming can be accomplished through delivery of warmed (__ to __ C) humidified air via a face mask or endotracheal tube
40° to 45°
Provide the rewarming rate (C/hour) for each rewarming method
How would you perform a peritoneal lavage to rewarm a patient
With heated (109.5°F - ~43C) isotonic dialysate (normal saline, lactated Ringer’s solution, or 1.5% dextrose dialysate solute) infused via a peritoneal catheter at 10 to 20 ml/kg. A dwell time of 20 to 30 minutes is allowed and then the fluid is aspirated and the procedure repeated
**Normosol and plasmalyte appear to be painful when placed in the abdomen!!
what is a less invasive alternative to peritoneal lavage to actively rewarm a patient?
saline irrigation (109.5F - 43C) of the urinary baldder via urinary catheter.
What is considered a safe and steady rewarming rate?
0.5 to 2C/h
** in severe hypothermia, it may be impossible to achieve complete stability without significant rewarming. Therefore the aggressiveness of rewarming will need to be altered appropriately
Hct increases by __% for every 1C drop in CBT
2%
T/F Because return of spontaneous circulation may not occur until severe hypothermia has been addressed, the duration of CPR may depend on the length of time it takes to warm the patient
TRUE
How can hypothermia offer neuroprotective support in patients following ROSC?
- Decreased cerebral O2 demand
- Slow down destructive enzymatic reactions
- Suppresion of free radical reactions
- Prevent apoptosis after celullar injury
What is the conclusion of the RECOVER initiative regarding therapeutic hypothermia after ROSC
Data suggest a beneficial effect on neurologically intact survival when the hypothermia is instituted as soon as possible after ROSC and maintained for longer than 12 hours; however, the practical aspects of its clinical application with regard to onset, level, and duration still need to be determined
It is recommended to cautiously place the rectal probe in at least __cm ; however, this is patient size dependent
15cm
T/F Electrocardiogram changes related to body temperature can be seen. At approximately 32 °C (90 °F), the Osborn J wave may appear. The J waves are usually upright in aVL, aVF, in leads II and V6, at the junction of the QRS complex and ST segment
TRUE
Splanchnic blood flow and gastrointestinal motility diminish as the core temperature approaches ______. Ileus develops when the temperature drops below ________.
34 °C (93 °F)
30 °C (86 °F)
T/F Severe hypothermia often induces a hemorrhagic pancreatitis as a consequence of depressed pancreatic perfusion
TRUE
Hyperglycemia despite effective rewarming can indicate:
DKA, hemorrhagic pancreatitis
Why extremely gentle care of severely hypothermic patients is recommended?
Vfib can be triggered by mere handling of the patient or mechanical irritation such as placing a central line. Also if CPR is intiated wihtout making sure patient was in CPA
T/F The hypothermic heart is unresponsive to pacing and cardioactive drugs
TRUE
Basic cardiopulmonary resuscitation should be performed, if cardiac arrest diagnosed, until the temperature is _______ when advanced cardiac life support (the use of medication) can be added if required. Administration of normal doses, and repeat doses of any medication, will lead to accumulation and be toxic to the patient when rewarmed.
≥32 °C (90.3 °F)
T/F Canine studies indicate that a pH >7.4 was cardioprotective during rewarming of extreme hypothermia
TRUE
What are the 4 degrees of frostbite?
- First degree manifests as erythema after warming.
- Second degree leads to blistering.
- Third degree is skin necrosis.
- Fourth degree devitalization of the whole part (gangrene).
Explain pathophysiology of frostbite
- Extracellular water crystallizes, decreasing the interstitial water in the liquid phase with subsequent increased osmolarity.
- In response, water moves out of cells, affecting intracellular electrolyte concentrations and modifying cellular protein structure.
- In addition, diversion of oxygen and nutrients away from the periphery due to vasoconstriction and hypoperfusion predisposes to cell death.
- The associated vasculitis, exacerbated by hemoconcentration, hyperviscosity, platelet sequestration/dysfunction and cold-induced inhibition of coagulation cascade enzymes, predisposes to thromboembolism.
- This may also cause bleeding, which becomes evident on thawing of the tissues.
- As tissues thaw, marked edema occurs because of melting of water crystals, cellular damage, loss of endothelial integrity, and thrombosis.
- Over a few days, the degree of necrosis + /- gangrene
will be established. - Local production of prostaglandins and thromboxanes enhances the degree of injury.
Describe management of a frostbite injury
- Thaw –> immerse body part in water (104-108F / 40-43C) for at least 20min.
- Protective bandage around and in between digits prn.
- Drainage of blisters and cover with Aloe Vera q8h (ANTIPROSTAGLANDIN AND THORMBOXANE EFFECTS)
- Pain meds –> NSAID can help decrease TXA production.
- Daily bandage change/ topical honey if ruptured blisters/necrosis.
- +/- topical antiseptics if necrotic at risk tissue.
- Cage rest
- Elevation of affected area to avoid reperfusion edema.
- Surgical management should be delayed until spontaneous amputation of necrotic tissue has occurred and is complete.
List the conditions associated with worse prognosis in heat stroke
NRBCs Hypoglycemia hypocholesterolemia hypoalbuminemia Increase TBil Increased creatinine Increased PT and APTT -> DIC Seizures Obesity Timefrom event to medical attention Ventricular arrhythmias
The hallmark of heat stroke is severe ___________, and it is often associated with multiple organ dysfunction
CNS disturbance
Define heat stroke
Hyperthermia associated with a systemic inflammatory response leading to a MODS in which encephalopathy predominates.
In dogs, it is characterized by core temperatures above 41 °C (105.8 °F) with central nervous system (CNS) dysfunction
Heat dissipation may occur via four mechanisms:
convection, conduction, radiation, and evaporation.
70% of heat loss in dogs and cats occurs by
radiation and convection through the skin.
Increased body heat induces three protective mechanisms:
Thermoregulation –> heat dissipation via the 4 mechanisms in respose to hot enviroment or excercise
Acute-phase response –> involves a variety of pro- and anti- inflammatory cytokines.
Increased expression of intracellular heat shock proteins.
What is the function of the heat shock proteins (HSP72)?
HSP72 protect the cell and the body against further heat insults;
- Protect against denaturation of intracellular proteins.
- Help to regulate the baroreceptor response during heat stress -> preventing hypotension and conferring cardiovascular protection.
Why heat stroke develops? Describe the suggested pathophysiology
- Failure of thermoregulation, followed by an exaggerated acute-phase response and alteration of heat shock proteins.
- Additionally, absorption of endotoxin from the GI tract may fuel the inflammatory response because intestinal mucosal permeability is increased during heat stress.
- suggested patophysiology –> initial production and release of interleukin-1 and interleukin-6 from the muscles into the circulation and increased systemic levels of endotoxin from the GI tract –> excessive activation of leukocytes and endothelial cells, which results in release of numerous proinflammatory and antiinflammatory cytokines as well as activation of coagulation and inhibition of fibrinolysis –> Direct endothelial cell injury due to the heat, combined with an initial hypercoagulable state, results in microthrombosis and progressive tissue injury –> MODS
What type of shock is usually seen in heats troke
Vasodilatory -> most dogs arrive for treatment in a hyperdynamic state. The mucous membranes are usually hyperemic and the capillary refill time is very short.
List differentials for a patient with heat stroke and pulmonary crackles
- DIC –> pulmonary parenchymal hemorrhage
- Aspiration pneumonia (if vomited before)
- Pulmonary edema
List causes of neurologic anormalities during heat stroke
- Poor cerebral perfusion.
- Direct thermal damage.
- Cerebral edema.
- CNS hemorrhage.
- Metabolic abnormalities such as hypoglycemia or hepatoencephalopathy, although the latter has not been documented in clinical cases of dogs with heat stroke.
In one canine heat stroke study, a value of ____ or more NRBCs per 100 leukocytes at presentation had a sensitivity and specificity of 91% and 88%, respectively, for predicting death. The NRBC level typically decreases rapidly over the first ___ hours
18 NRBCs
24 hours
In general, how many platelets should be visualized in a well-executed blood smear?
there should be at least 8 to 15 platelets per 100× oil immersion field
What cooling method would you recommend for a heat stroke patient
evaporative method –> wetting patient with tepid water and blowing fans over the body
Why whole body alcohol should be avoided in a heat stroke patient?
because not only is this noxious to the animal, but it may present a significant fire hazard should defibrillation be required in dogs that experience cardiac arrest
List 3 mechanisms of heat stroke development in dogs
- Classic heat stroke: exposure to a hot and humid environment
- Exertional heat stroke: voluntary strenuous physical exercise
- Severe, uncontrolled tremors or seizures
The most common hematological findings in canines with heat stroke are:
- Thrombocytopenia
- Increased PCV and Hb
Why thrombocytopenia occurs in heat stroke?
- Splenic sequestration
- Vasculitis
- GI bleeding
- Hyperthermia-induced platelet aggregation
Why nRBCs are abundant on peripheral blood smears of heat stroke dogs
- Heat-induced damage to the bone marrow.
- Could also be mediated by the action of cytokines.
Most common biochemical abnormalities in heat stroke:
Increased AST, ALT, CK, GGT, ALP, hypoglycemia
Rhabdomyolysis and liver damage are prominent features in heat stroke
What is the reported mortality rate in dogs suffering from severe heat stroke, and what is it in dogs suffering from heat-induced illness?
40-50% - severe heat stroke
35% heat-induced illness
What is electroporation
Is the development of momentary holes in cellular membranes induced by electrical shock. The holes allow passage of macromolecules across membranes which causes osmotic damage to cells
Describe the initial pathophysiology of electrical injury
- Electrical current is transformed into heat.
- Intracellular and extracellular fluids may become superheated.
- Results in coagulation of tissue proteins leading to thrombosis of small vessels, and degenerative changes in small arterial walls.
- Necrosis of the superheated tissues and those tissues that become ischemic from the vascular consequences.
Direct thermal injury may also occur from arcing of a current that leaves the electrical source, crosses an air gap, and strikes tissue.
what does the severity of electrical injury depend on?
- Electrical resistance of the part of the body that is struck
- nature or the current (alternating vs direct)
- intensity of the current (amperage)
T/F Wet skin and moist mucous membranes have high electrical resistance; therefore one can expect low flow of electricity in these tissues and a propensity for minimal tissue damage
FALSE - Wet skin and moist mucous membranes have low electrical resistance; therefore one can expect high flow of electricity in these tissues and a propensity for maximal tissue damage
T/F Alternating currents tend to cause more severe injury than direct currents at the same amperage.
TRUE - Higher exposure may occur with alternating current electricity than with direct current because the former elicits muscular contractions that prevent the victim from releasing the power source. For this reason, the exposure time is typically longer with alternating current than with direct current. Direct current electricity does not usually cause muscular tetany
Amperage is a funtion of _____ divided by _______. This is known as _______law.
Voltage divided by resistance
Ohm’s law
Sudden death from electrical shock is likely due to ventricular fibrillation caused by _____-voltage current, as with most household exposures. _____-voltage exposure may cause asystole.
low- voltage
high-voltage
Causes of respiratory distress after lightning/electrycal injury include:
Respiratory arrest from tetanic contractions of respiratory muscles occurs during contact with the electrical source, but breathing typically resumes when the victim is separated from the source of electricity
Causes of repiratory distress afterwards:
Facial or nasopharyngeal edema
diaphragmatic tetany
neurogenic pulmonary edema.
Define neurogenic pulmonary edema
is a form of NCPE –> results from massive symphathetic outflow that causes pronounced vasoconstriction and systemic hypertension –> marked elevation of left ventricular afterload, decreased LV stroke volume –> increased pulm. Capillary pressure and subsequent edema
T/F Respiratory distress is less severe with pulmonary edema induced by electrical cord shock than with other causes of noncardiogenic pulmonary edema
TRUE. There is often radiographic evidence of resolving pulmonary infiltrates within 18 to 24 hours
What are the proposed mechanism for acute and delayed neurological injury in electrical injury patients
Acute neurological injury: due to direct CNS stimulation upon electrical contact.
Electrically induced neural activity
Hypoxia due to excess energy consumption could play a rol
Delayed neurological injury:
Electroporation and free radical mechanisms
What are ocular manifestations of electrical injury? When are noticeable?
- Cataracts
- Usually noted several months after the episode.
Which consideration would you keep in mind regarding fluid therapy in a patient after electrical injury?
Fluids that typically are given in low volumes (e.g., hypertonic saline, synthetic colloids) are recommended
Animals in shock are treated with intravenous fluids to expand intravascular volume because the mechanism of shock is likely a relative hypovolemia. However, because there may be a cardiogenic component to the shock from arrhythmia and subsequently decreased stroke volume, and because neurogenic pulmonary edema may develop quickly, the volume of fluids administered should be strictly controlled.
List medications/procedures that can be considered for treatment of electrical injury
- Low volume resuscitation
- Antiinflammatories
- Pain management
- Temporary tracheostomy
- O2 supplementation
- Bronchodilators
- Furosemide
- PPV
- Wound management of burned tissues PRN
- Antiarrhythmics PRN
- Benzos if seizures
- Early nutrition
T/F It is possible that small dogs are less susceptible to lightning injury than larger dogs
TRUE
Which are the five possible mechanisms by which lightning can deliver electrical energy to a victim:
(1) direct lightning strike
(2) direct strike of an object that the victim is touching (contact injury)
(3) side flash from a struck object (splash)
(4) step voltages produced by current flowing through the soil beneath (ground potential)
(5) an upward streamer that does not connect or complete a full lightning strike
Which additional type of injury can be expected in a patient with lightning injury vs electrical injury. What are consequences of this type of injury reported in other species?
In addition to electrical and thermal injury, mechanical energy can be imparted to the lightning victim. A blast effect from rapid air movement caused when superheated air is then cooled may result in physical injury. consequences: spinal fractures, spinal cord injury (pigs, pond fish) lumbosacral fractures (pigs) Muscle pain (people) vestibular injury (horses, humans)
Which changes can be seen in bloodwork and urinalysis secondary to tissue necrosis?
hyperkalemia (not just due to necrosis but also due to excessive muscle activity after electrical shock)
myoglobinemia/myoglobinuria
hemoglobinemia/hemoglobinuria
Hypoproteinemia if severe burns
All submersion victims experience hypoxemia, either from________ in which no aspiration occurs or from __________resulting in loss of surfactant that causes atelectasis and intrapulmonary shunt. Most submersion victims (about 85%) that survive are thought to have aspirated less than 22 ml/kg of water
laryngospasm
aspiration of fluid
List all contributors of hypoxemia due to intrapulmonary shunting of blood in a submersion injury
- Washout of surfactant by water inhalation –> atelectasis
- ARDS
- Infectious or chemical pneumonitis (from gastric content/dirt/sand)
- Bronchospasm
- Decreased surfactant production due to alveolar damage
Explain why submersion in ice-cold water (<5C) increases the chances of survival
Diving reflex –> Within seconds after a victim’s face contacts cold water and before unconsciousness ensues, a reflex mediated by the ophtalmic division of the trigeminal nerve (when face is immerse in cold water) sends impulses to the CNS that cause bradycardia, hypertension, and preferential shunting of blood to the cerebral and coronary circulations. This reflex acts to protect the brain and heart from hypoxia-induced injury. Hypothermia also causes a decrease in metabolic need, which protects the brain from injury.
T/F Hypothermia in patients injured by submersion in warm water is a negative prognostic sign indicating poor peripheral perfusion and longer submersion times
TRUE
Elevations in arterial PCO2 causes cerebral _____, which contributes to _________ in ICP and creates the potential for ____________.
vasodilation
an increase
CEREBRAL EDEMA
What is the difference between immersion and submersion?
- Immersion - the victim’s body being immersed but maintaining the airway above the surface of water.
- Submersion - the airway is under water.
Describe pathophysiology of submersion injury
- The hydrostatic pressure exerted upon the body causes –> increased venous return, CO, L to R shunting and increased WOB –> body senses “hypervolemia” –> increased diuresis, kaliuresis, natriuresis
- Water enters oropharynx -> is spat out or swallowed and victim hold breath –> once not sustainable, water enters airways –> cough reflex, laryngospams, hypoxemia (1-2.2ml/kg of water can cause significant hypoxemia)–> hypercapnia, acidosis –> critical levels of hypoxemia –> laryngospasm abates –> additonal water into the lungs and GI
- Hypoxia –> cerebral hypoxia –> apnea, unconsciousness –> cardiac deterioration follows (tachycardia–> bradycardia –> PEA –> asystole)
What is the cold- shock response?
pattern of reflexes driven by cutaneous cold thermoreceptors –> characterized by sympathetic meditated tachycardia, uncontrollable hyperventilation, respiratory gasp, peripheral vasoconstriction and hypertension. –> seems to be responsible of innablity to swim in cold water
What would be an indication of corticoid use in a submersion injury patient?
Bronchospasm refractory to bronchodilators.
Active rewarming after submersion injury should be stopped when core temperature reaches:
37C to avoid rebound pyrexia
List conditions that can be associated with air embolism
IV catheter
laparoscopy
hyperbaric treatments
surgeries/biopsies
Which is the most sensiive tool for detection of air embolism
transesophageal echocardiography
Explain pathophysiology of air embolism
Air emboli wedge into pulmonary vessels –> V/Q mismatch –> pulmonary hypertension
air emboly can enter systemic circulation –> blocking blood flow to critical organs –> The cerebral vasculature and coronary artery are vulnerable locations, and emboli in these locations have the most severe consequence
T/F in massive air embolism in the heart –> Because the heart is full of air, resuscitation using standard cardiopulmonary resuscitation techniques is not usually successful in the case of air embolism
TRUE
T/F Factors that increase the risk of air embolism include use of a venous access site at a level that is gravitationally higher than the heart. This can occur in standing dogs and cats during jugular catheterization or puncture, or when ear catheters are used
TRUE
large volumes of air may be mistakenly administered via intravenous tubing or extension sets that were not appropriately primed before use. Standard intravenous tubing holds more than ___ ml, and a standard extension set holds __ml, which is enough air as a bolus to cause arrest in a ___kg or ___kg animal, respectively
10mls
4mls
5kg
2kg
Which condition can make a patient more prompt to become symptomatic for air embolism even at low volumes or air?
right-to-left cardiac shunt–> the lungs may not filter out air bubbles; consequently these individuals may experience focal cerebral infarcts when even the smallest air bubbles are administered or allowed to form.
which inflation gas is generally used during laparoscopy to minimize the impact of gas bubble formation? Why?
carbon dioxide is generally chosen as the inflation gas –> Carbon dioxide can still form emboli, but because it is absorbed rapidly into tissues, it seldom causes clinical problems (0.001% to 0.59% incidence in humans). Carbon dioxide has an additional advantage over nitrogen: it does not produce bronchoconstriction or changes in pulmonary compliance to the same degree as nitrogen
how can an air embolism develop in a patient during laparoscopy?
- Insufflated gas can gain entry into the vascular system by mistaken placement of the needle into an artery, vein, or solid organ.
- It can also happen simply because of the positive intraabdominal pressure. In theory, for an embolus to enter the venous system during laparoscopy there would have to be a defect in a vein or other vascular bed. If the intraabdominal inflation pressure matched the intravenous pressure, air could gain access to the circulation. If the inflation pressure were high enough to collapse the vein, air entrainment would cease, and if the inflation pressure were lower than venous pressure there would be hemorrhage from the vein without air entrainment
In general, inflation pressures higher than _____mm Hg are not recommended during laparoscopy. Under normal conditions veins collapse at _____ mm Hg. Therefore, when recommended inflation pressures are used, transected vessels should hemorrhage rather than entrain gas.
15mmHg
20 to 30 mmHg
What is the recommended rate of abdominal insuflation during laparoscopy to reduce incidence of massive embolism?
< 1L/min
** However, it is still very close to the insufflation rate capable of causing arrest in 60% of dogs studied (1.2 ml/kg/min) –????? No tiene sentido, el perro tendria que pesar 800kg……..
What precautions can be taken to avoid gas embolization during surgery
- more likely when surgical site is hiigher than the heart
- surgical positioning –> avoid excessive elevation of surgical site –> if not possible, keep surgical site filled with isotonic fluids
- elevation of CVP, use of PEEP
what is the normal % of dead space from the tidal volume
~30%
what happens with the dead space if a patient suffers air embolism. Write the formula that explains this
new region of dead space is created –> acute fall in the ETCO2 and increase in the PaCO2
% dead space = ((PaCO2-ETCO2)/PaCO2)x100
during air embolism –> blood flow will be routed through regions of the lung that are less ventilated, which _______ physiologic shunt and decreases oxygenation.
Increases
What is a grade III air embolism
When half of the right ventricle, right atrium, and right ventricular outflow tract are filled with air
List therapeutic options for management of air embolism
- Supplemental oxygen
- Removal or air emboli by manual reduction if possible –> with a catheter and aspiration
- Elevate apex of the heart (dorsal recumbency) –> controversial
- Hyperbaric oxygen chamber
**HBOT can compress the bubble size (more relevant with air than with carbon dioxide due to solubility)
**A reduction in intracranial pressure and increased dissolved oxygen in the plasma are additional positive effects of HBOT - Deinsuflation of abdomen (if applicable)
- Stop usage of Nitrogen gas
- Ligate any non-ligated vasculature that can be allowing entry of air
increase CVP - fluorocarbons are solutions with high gas-dissolving capability. When administered intravenously these compounds could improve oxygenation and simultaneously help shrink gas emboli
T/F porcupine quills have antimicrobial properties, as self-quilling in falls is not uncommon in porcupines
TRUE
When would you consider a rabies booster in a dog that has been quilled?
A rabies booster vaccine is therefore not necessary after a dog attacks a porcupine, unless there is some other reason for considering rabies infection, such as a true porcupine attack during daylight hours. Rabies has not been reported after a quilling.
What are possible complications after a dog has been quilled?
Migration:
- eyes
- CNS
- Joints
- Thorax –> pneumothorax –> surgical removal required
- Heart/pericardium
T/F quills are easily recognized with advanced diagnostic imaging (CT)
FALSE - Quills are hard to find with diagnostic imaging, although experienced and patient radiologists may be able to localize some migrating quills, particularly with ultrasound
List the Pit vipers in the USA (Crotalinae)
- Rattlesnakes (Crotallus spp)
- Copperheads and water moccasins (aka cotton mouth) (Agkistrodon spp)
- Pygmy rattlesnakes and massasaugas (Sistrurus spp).
Vipers are _________ which indicates they have movable fangs
Elapids are _________ which indicate they have fixed fangs
solenoglyphic
proteroglyphic
What controls the ammount of venom injected with a snake bite?
o Snake’s last meal - longer it’s been > venom
o Size of the snake’s venom glands -> larger > venom
o Ability to voluntary compress the venom glands - adults have more control
o Nature of the bite –> there is a percentage of bites without measureable venom delivery, and there may be a trend toward lower volumes injected with defensive bites
- 25% are dry bites
**All pit vipers control the amount of venom injected during a bite.
What are the published mortality rates for Crotalinae envenomation in dogs and cats?
1.8% to 24% in dogs
6% to 18% in cats
What are factors associated with non-survivors after a Crotalinae snake bite
- Envenomations to the head, including the eye and tongue (may provide a more direct route to the CNS or predispose to asphyxiation)
- Intra-arterial envenomation.
- Advanced age
- Increased time from envenomation to treatment
What’s the composition of crotalinae venom?
Mixture of water, proteins, and peptides.
*Most of the proteins are enzymatic, while the peptides exert organ toxicity.
Classically described enzymes include:
- *hyaluronidase –> facilitates rapid spread of the venom by breakdown of the connective tissues
- phospholipase A2 –> cytotoxicity –> echinocytosis and spherocytosis, anticoagulation via anti-Xa activity
- thromboxane –> partially responsible for the thrombocytopenia
- Metalloproteinases (SMVPs) –> contribute to platelet dysfunction
What are the effects of Crotalinae venom in the coagulation system?
thrombosis and hemorrhage –> these proteins can be broadly classified as FV and FX activators, activators of prothrombin, thrombin-like enzymes, anticoagulant factor IX/X binding proteins, activators of protein C, thrombin inhibitors, fibrinolytic enzymes as well as plasminogen activator
What are the effects of Crotalinae venom in the nervous system?
Some venoms contain potent neurotoxins
Mojave venom causes presynaptic inhibition and may lead to progressive paralysis. These toxins have been identified in the venoms of the Mojave rattlesnake (C. scutulatus), western diamondback (C. atrox), prairie rattlesnake (C. viridis) and southern pacific rattlesnake (C. helleri)
Explain why a snake bite patient can have hyperglycemia and hypokalemia
Hyperglycemia and hypokalemia may be appreciated as a consequence of catecholamine surge.
T/F Opioid administration is safe and should not be withheld for fear of exacerbating neurological symptoms in Crotalinae envenomation cases
TRUE
What is the difference between Antivenin (Crotalidae) Polyvalent (ACP) antivenom and Fab-based antivenoms
ACP –> comprised of whole IgG molecules, contains unwanted contaminants such as albumin, alfa and beta globulins, IgM
Fragment antigen binding (Fab) based –> enzymatic digestion of the whole IgG to cleave off the antigen (venom) binding region (Fab region), from the fragment crystallizable (Fc) portion.
Increase the volume of distribution and possibly result in a less antigenic product
What is the difference between a Fab monomer and a Fab dimer (F(ab)2) antivenom
F(ab’)2 antivenoms have a longer half-life and remain in the vascular compartment longer. They also have 2 antigen binding sites per molecule, compared to 1 antigen-binding site on the Fab monomer.
Fab-based antivenoms tend to have a relatively short half-life and move outside of the intravascular compartment faster than other antivenoms and may necessitate readministration if re- envenomation occurs.
T/F One vial has been shown to be sufficient to neutralize clinical signs of rattlesnake envenomation in most dogs.
TRUE
How many antivenom vials can be safely given to affected dogs?
A safety study reported that up to 6 vials could be administered intravenously within one hour safely to healthy dogs. Can give more, Silverstein mentions up to 10 vials.
It is reasonable to consider starting with two vials of F(ab’)2 antivenom in very small dogs or patients presenting with severe clinical signs.
How would you administer antivenom to your patient (dose, rate), dogs and cats?
Dogs –> 0.25–0.5 mL/kg/h –> If no reaction –> administer the rest within 30–60 minutes
Cats may be more likely to experience a reaction –> CRI can be considered 1–2 vials over 6 hours
Ideally given within 4 hours of accident but can be still effective up to 24 or longer
Which adjunctive therapies can be offered in addition to standard treatments for snake envenomation (antivenom, fluids, analgesia)
Local wound laser therapy (evidence lacking, no more often than q8h)
Would you recommend NSAIDS to provide analgesia on a snake bite patients?
Not recommended, these patients are at risk for kidney injury due to hypoperfusion, coagulopathy, nephrotoxins in the venom, and pigmenturia. Additionally, gastrointestinal ulceration is possible secondary to hypoperfusion and coagulopathy
T/F Hemolysis with spherocytosis may be observed, sometimes as late as 72 hours following initial envenomation. It is most likely that these patients are experiencing ongoing envenomation, and treatment with antivenom should be prioritized over immune suppression.
TRUE
(T/F) In patients experiencing hemorrhagic complications of envenomation, treatment with fresh frozen plasma is not indicated. The mechanism of coagulopathy in most cases is not due to factor deficiency, but rather a complex syndrome of factor inhibition, activation, platelet inhibition, and endothelial dysfunction. As such, neutralization of circulating venom with antivenom is the treatment of choice
TRUE
(T/F) CroFab (ovine origin) is a single Fab based antivenom that has 5.2 times the potency of the ACP which could possibly narrow the cost differentials and # of vials required
TRUE
List the broad category of toxins present in Elapid snake venom
Neurotoxins Procoagulant toxins Anticoagulant toxins Myotoxins Hemolytic toxins
What are the two categories of neurotoxins in elapid snake venom and how can that affect treatment?
Pre-synaptic: –> belongs to the phospholypase A2 group of toxins –> cause structural changes of the nerve terminal affecting release of Acethylcholine –> seems to be an irreversible binding –> antivenom might not help
Post-synaptic –> act as antagonist of acethylcholine –> there is no evidence of irreversible binding, so rapid response to antivenom should be expected
What are consequences of the myotoxic effect of some phospholipase A2 toxins
Severe rhabdomyolysis
AKI secondary to myoglobinuria
Megaesophagus
T/F Localized tissue reactions or injury around the bite site are a significant component of North American or Australian elapid envenomations
FALSE. In most cases the bite is difficult to identify in dogs and cats.
When are antihistamines recommended for snake envenomation?
Only when Hypersensitivity type 1 reaction occurs, which is mostly associated with the antivenom and not the venom itself.
Would you recommend the rartle snake vaccine? Why?
No:
Retrospective study in 2014 found no difference in mortality of morbidity in vaccinated vs unvaccinated dogs (total 82 dogs, 14 being previously vaccinated)
other study 272 dogs (15 previously vaccinated) –> no difference in mortality of morbidity
consider –> sample size is low
studies in mice show immediate death of some vaccinated mice upon exposure to venom
2 reports of dogs previously vaccinated having signs of severe anaphylaxis when biten by a snake –> suspected anaphylaxis to the rattle snake venom, with the initial sensitizing event being the rattle snake vaccine
What are the two most common clinical syndromes associated with spider bite worldwide? What are the general characteristics?
Loxoscelism:
- Spider from the genus Loxosceles (recluse, fiddle-back or brown spiders) –> violin shape mark
- Endemic in the central and southern USA/ South America
- Contains phospholipases, hyaluronidases, lipase, shingomyelinase D –> SxCx –> dermonecrosis, hemolysis
bite is not painful, most of the times self-limited mild edema, erythema.
- Asympthomatic or local irritation (95% of cases)
- Cutaneous loxoscelist (4% of cases) –> rarely skin necrosis and ulceration (after a few days), vomiting, fever
systemic loxoscelism (<1% of cases)–> rare –> IV hemolysis, AKI (humans), DIC
- excellent prognosis
Latrodectism
Widow spider group is the most relevant
the most clinically relevant toxin is alpha-latrotoxin –> acts on nerve endings –> first initial activation followed by depletion of neurotransmiters –> flacid paralysis
little or no pain at the time of the bite but in 5–60 minutes local pain develops with increasing intensity.
Pain is the dominant sign in systemic latrodectism: acute abdominal pain, muscle cramps, and/or spasms; muscle stifness –> then flacid paralysis and respiratory difficulty
there is antivenom available (Lyovac)
cats extremely susceptible
T/F There is considerable species variability in susceptibility to black widow envenomation. Guinea pigs and horses are highly susceptible, cats are moderately susceptible, and dogs are relatively resistant to the effects of the venom
TRUE
Spiders from the family Theraphosidae are commonly known as ______________, bird-eating, spiders or whistling spiders. Envenomation by these spiders has minor effects in humans but can have fatal effects in animals.
Tarantulas
What is the composition of scorpion venoms?
Mixture of toxicants that can vary between species:
Acethylcholinesterases
serotonin, histamine, proteases inhibitors
phospholipases
hyaluronidases
neurotoxins
Which component of scorpion venom has the greatest medical importance? Why?
Neurotoxins –> bind to Na, K, and Ca channels –> membrane hyperexcitability and repetitive uncontrolled axonal firing –> autonomic dysfunction and neuromuscular activity
This can also trigger massive catecholamine and vasoactive peptides release (neuropeptide Y and endothelin-1)
What are clinical signs in dogs after scorpion envenomation
An experimental study compared:
natural envenomation dose (0.4mg total) vs a much higher dose (0.25mg/kg)
natural dose –> local pain, hyperstesia, sialorrhea, vomiting, diarrhea, sneeze, postration
high dose –> caused acute and reversible cardiac injury in few days
List the two main components of bufo toad venom and the associated systemic effects
Biogenic amides
steroid derivatives
**Neurologic effects seem to be the most common in south FL, hypersalivation and red MM in Australia
What is the lethal dose of bufo toad venom?
0.1g/dog –> equals entire content of both parotids
What’s the hallmark clinical sign of bufo toad toxicosis?
hyperemic “brick red” MM
which animal-derived toxin resembles cardiac glycosides and digoxin toxicity?
Bufogenic toxins
Describe mechanism of action of bufotoxins/bufagenins
Cardioactive steroids, digitalis like substances, inhibition of Na/K/ATPase –> increased IC Na in myocardial cells –> increased IC Ca –> ventricular arrhythmias, Vfib
T/F Initial treatment of dogs and cats with bufo toxicosis consist on at home decontamination. This should be performed by lavaging the animal’s mouth with a hose or running tap water
False, at-home decontamination should be performed with a damp towel or damp clean rag used to wipe the oral mucous membranes and prevent further absorption of the toxins.
Several dogs that have died in hospital while being treated for Bufo toxicity died due to aspiration pneumonia caused by owners attempting to lavage the mouth with water or by administration of products such as milk or olive oil believed to decrease toxin absorption.
T/F Animals with mild signs of Bufo envenomation (hypersalivation and hyperemic mucous membranes) can be treated as outpatients after oral decontamination and owners should continue monitoring at home for development of neurological signs.
TRUE
List the different insects included in each of these families:
- Apoidea
- Vespoidea
- Formicidea
Apoidea –> honey bees, Africanized honey bees, bumble bees, solitary bees (social and herbivores)
Vespoidea –> wasps, hornets, yellowjackets (carnivores)
Formicidea –> ants –> clinically relevant are the black and red imported fire ants (Solenopsis invicta and S. richteria) (omnivorous)
What is the major component of Apoidea and Formicidea venom and what are the main effects
- Mellitin, the major component and the main cause of pain following a sting, is a detergent, which alters cell membrane integrity.
- Mellitin works synergistically with the primary allergen of venom, phospholipase A2, to cause red blood cell, platelet, leukocyte, and vascular endothelial cell lysis, and is suspected to cause myelinolysis of the spinal cord
who are responsible for the intense pain of wasps sting?
Wasp venoms are more heterogeneous but most contain three major allergenic peptides as well as vasoactive amines (serotonin, histamine, tyramine, catecholamines), wasp kinins, and acetylcholine. The vasoactive substances are responsible for the intense pain of wasp stings.
T/F Vespid venom does not contain mellitin
TRUE
Unlike the venom of other Hymenoptera, which are composed primarily of proteins in an aqueous solution, fire ant venom is composed of 95% __________.
Water-insoluble alkaloids –> primarily piperidines which have cytotoxic, hemolytic, antibacterial, and insecticidal properties.
T/F Fire ant venom produce an IgE-mediated reaction, which causes formation of pustules secondary to tissue inflammation and often secondary bacterial infection which are almost pathognomonic for fire ant stings
FALSE - They do not produce an IgE-mediated reaction, but instead produce sterile pustules secondary to tissue inflammation which are almost pathognomonic for fire ant stings
The lethal dose for bee, wasp or hornet enenomation is estimated to be ____stings/kg in most mammals
20 stings/kg
Describe the three subtypes of immune-mediated response to Hymenoptera envenomation and the main characteristics of each
- Regional reaction
IgE mediated
edema, erythema, regional reaction (can extend to the whole limb)
peak in severity at 48h after sting - Systemic anaphylaxis
Rare
IgE mediated
unlikely to occur if sigs are not noted within 30min
The time to onset of signs is directly proportional to the severity of the signs. - Delayed hypersensitivity reaction
within days to weeks
secondary to ag-ab complexes deposition –> complement binding –> formation of anaphylatoxin
end results can be –> vasculitis, polyarthritis, glomerulonephritis, myocardial lesions.
How would you treat a local regional reaction to Hymenoptera envenomation?
Ice/cold packs in affected region oral or injectable antihistaminics analgesia camphor and mentol lotion for fire ant stings \+/- abs if secondary infections develop
How can aminophylline help in the treatment of anaphylaxis?
- Smooth muscle relaxation
- Decreases release of histamine via phosphodiesterase inhibition
- Increases endogenous epinephrine release
How can refractory bronchospasm be treated during anaphylaxis?
- Glucagon –> glucagon has been found to have smooth muscle relaxant effects in the gastrointestinal, genitourinary, and cardiovascular systems.
- Glucagon-mediated smooth muscle relaxation in these organ systems utilizes the same cyclic adenosine monophosphate (cAMP) pathway that β-adrenergic agonists use in relaxing bronchial smooth muscle. This mechanism of action suggests that glucagon may have a useful role as a bronchodilator.
Inhaled ipratropium –> is an acetylcholine antagonist via blockade of muscarinic cholinergic receptors. Blocking cholinergic receptors decreases the production of cyclic guanosine monophosphate (cGMP). This decrease in the lung airways will lead to decreased contraction of the smooth muscles
What is a toxoid?
Toxin that has been denatured by being treated with formaldehyde –> render it nontoxic –> used for active immunization of animals in the process of antitoxins production
T/F The Intervet tetanus antitoxin is not recommended for use in cats because of the phenol ingredient, which has a high potential for causing anaphylaxis in cats
TRUE
T/F A commercially available Black widow spider antivenom made for use in humans has been shown to be very effective in a cat.
TRUE
What is the optimal time lapse for antivenom administration of Pit viper antivenom
Antivenom is optimally given within 4 hours after the snakebite, although it can still be effective up to 24 hours or longer after envenomation.
The molecular size of Fab molecules in pit vipers antivenom is
~50kDa
Serum sickness is a Type ____ hpersensitivity reaction
Type III –> is a delayed immune complex hypersensitivity response characterized by fever, malaise, nausea, diarrhea, lymph node enlargement, and dermatopathy that can occur over a period spanning 3 days to 2 weeks after antivenom administration.
What is CaO2?
Total oxygen content of arterial blood
CaO2 = mls of O2/dL of arterial blood
What is the formula of CaO2? Explain the components
CaO2= (1.34 x [Hb] x SaO2) + (PaO2 x 0.0031)
[Hb] = gr of Hg per dL of blood
SaO2 = saturation of Hg as a decimal
- 34 = mls of O2 per gr of Hb
- 0031= solubility constant of O2 in blood (ml O2/dL blood/mmHg)
Synthesis of the heme starts with the mitocondrial enzyme__________. Which is the limiting step of heme synthesis which is regulated in the presence of ___.
ala-synthase
iron
A series of 8 enzymatic reactions culminates in combining _______________with iron to form heme. Many of these enzymes are inhibited in ____ toxicosis
Protoporphyrin IX
lead
_____ toxicity can cause accumulaton of porphyrin precursors and photosensitivity
Lead
List pigments that are breakdown products of heme
Biliverdin -> bilirubin -> stercobilinogen
The binding of O2 at one heme increases the affinity of the other heme sites by ____fold. This phenomenon is called __________, and is what gives the Hb-O2 dissociation curve its distinctive sigmoidal shape.
150x
cooperativity
T/F while we commonly associate certain values of SPO2 and PaO2 together, the correlation of any individual’s value will depend on the P50 of that patient’s Hb-O dissociation curve
TRUE
A Hb type with a lower P50 will have a ____ affinity for O2 at a given PaO2 compared to one with a higher P50.
Higher affinity for O2 (left shifted) –> less delivery
What is the Hb p50 of humans, dogs and cats
Cat = 35 Dog = 29 mmHg Human = 26.6mmHg
In iron deficiency, the absense of ____ inhibits both the transcription and translation of ____
heme
globins
What is the bohr effect
States that O2 Hb affinity is inversely proporitonal to H+ and CO2 concentrations.
What is the Haldane effect
Describes Hb capacity to bind to CO2. (Oxygenated Hb displaces CO2, deoxygenated Hb binds more CO2)
List functions of Hb
O2 carrier
Buffer
CO2 transporter
Oxyhemoglobin reacts with NO to form_______, resulting in these three effects___________
Nitrate
Scavenging of NO
Vasoconstriction
Methemoglobin formation
T/F Hb within the erythrocytes may act as a producer and carrier of NO
TRUE – modulating vascular tone in the microcirculation
Methemoglobin results when the heme group is oxidized from_____ to ____
ferrous (Fe2) to ferric (Fe3)
MetHb shifts the curve to______
The left. Promotes the T State
List causes of methemoglobinemia
- Drug-related (Acetaminophen, nitroprusside, nitroglycerine, benzocaines, phenazopyridine).
- Enviromental exposures (skunk musk, aniline, hydroxicarbamide).
- Toxic plants (red maple toxicity, brassica).
- MetHb reductase deficiency
Why are cats more susceptible to RBC oxidative damage and MetHb
They have an increased number of -SH (sulfhydryl) groups on their globin molecules (8 rather than 4 in the dog)
T/F MetHb levels of >30% will cause pulse oximeters to read in the mid 80s regardless of SaO2
TRUE
CO has an affinity for Hb_____ times higher that O2
210-250x (230-270 silverstein)
T/F COHb should be considered a possible cause of clinical signs even if it’s slightly elevated (>5%)
TRUE
At 21% inspired oxygen, the half-life of carbon monoxide is ____hours. The half-life decreases to _____ at 100% oxygen and ____ with 100% hyperbaric oxygen therapy at 2.5–3 times atmospheric pressure
5 hours
1 hour
20 minutes
Mention two protective mechanisms from oxidative damage
- Proteins that act as free radical scavengers.
- Reducing agents that can remove the unpaired electron from an oxidized molecule.
What are two important reducing agents involved in reduction of oxidized glutathione and metHb back to functional molecules?
NADPH and NADH
What makes glutathione a powerful antioxidant?
Is a tripeptide produced in the erythrocyte and composed of glutamic acid, cystein and glycine and contains an easily oxidizable sulfhydril group (SH group). Potent antioxidant that operates as a free radical scavenger.
What are protective mechanism from oxidative damage in the eythrocytes?
superoxide bismutase catalase glutathione peroxidase glutathione metHb reductase
List oxidants continuously generated in vivo
Hydrogen peroxyde(H2O2) super oxide free radicals (O2-) hydroxil radicals (OH-)
How is MetHb produced?
Naturally, Hb undergoes an auto-oxidation as an electron is pulled off the Hb onto an O2 molecule. But this oxidation can happen with drugs, enviromental exposures, toxic plants
________________are aggregates of denatured, precipitated hemoglobin within erythrocytes that form as hemoglobin with oxidative damage is metabolized
Heinz bodies
How do ghost cells form?
Numerous HzBs can disrupt the membrane sufficiently to result in “ghost” cells, empty red blood cells with just a cell membrane and HzB remaining, which are associated with oxidation-induced intravascular hemolysis.
T/F feline spleens have an ultrastructural variation and impaired ability to catch and remove oxidized red blood cells.
TRUE - the combination of more SH groups available for oxidation on feline hemoglobin and the unique spleen in this species, healthy cats often have notable HzBs in circulation (with reports up to 96%).
T/F - Substances that cause metHb production are likely to cause HzB production, and potentially hemolytic anemia, in the days after the exposure.
TRUE
____________, a component of over-the-counter drug formulations, is metabolized rapidly to acetaminophen and also could result in toxicity in small animals
Phenacetin
blood with more than ___% metHb remains dark with a brown discoloration upon exposure to room air
10%
T/F The presence of metHb distorts this ratio. If metHb levels exceed 30% the pulse oximeter reading plateaus at about 85% regardless of the true oxygen content.
TRUE
What are findings of oxidative damage in a blood smear?
HzBs, eccentrocytes, and “ghost” cells.
What are side effects of rapid NAC IV administration
Hypotension, bronchospasm and phlebitis if it leaks perivascularly.
___________ is a nonirritant gas that interferes with the utilization of oxygen by cellular cytochrome oxidase and thereby causes histotoxic hypoxia
Hydrogen cyanide
T/F Direct thermal injury caused by hot, dry air is highly unusual distal to the larynx because heat is dissipated effectively by the thermal regulatory system of the nasal and oropharyngeal areas
TRUE
List irritant gases that can result after combustion
short-chain aldehydes
gases that are converted into acids in the respiratory tract (e.g., oxides of sulfur and nitrogen)
highly water-soluble gases (e.g., ammonia, hydrogen chloride)
benzene (from plastics)
List complications that can develop with time after smoke inhalation
- Laryngeal edema and upper airway obstruction (needing tracheostomy)
- Pulmonary edema (up to 24h after)
- Neurological signs
- ARDS
- Bacterial pneumonia
Why morbidity and mortality associated with smoke inhalation are much greater when significant concurrent dermal burn injury is present?
Due to both the pulmonary pathophysiology
associated with dermal burns (pulmonary edema, bacterial pneumonia, acute lung injury, and acute respiratory distress syndrome) and to burn management requirements, including more aggressive fluid therapy and repeated general anesthesia.
T/F In smoke inhalation cases the use of B2 agonists is indicated
TRUE - to reduce bronchoconstriction-induced airflow resistance and improve dynamic compliance. Beta-2 agonists such as terbutaline (0.01 mg/kg IV, SC, IM, PO) or inhaled albuterol decrease histamine release, leukotriene levels, and TNF-alpha concentrations, thereby conferring an anti-inflammatory effect. There is also evidence that beta-2 agonists may improve fluid clearance within the respiratory tract and promote mucosal repair.
Is the use of glucocorticoids recommended in smoke inhalation patients? Justify
The use of glucocorticoids following smoke inhalation has been widely investigated. Experimental studies report variable effects associated with this treatment, but the vast majority of clinical reports point to an increased incidence of bacterial pneumonia with no clear clinical benefit. The use of glucocorticoids is therefore not recommended in these patients
What treatments would you recommend if you are suspicious of hydrogen cyanide toxicity
- Amyl nitrate and sodium thiosulfate may prove beneficial.
They oxidize hemoglobin to methemoglobin, which preferentially binds cyanide to create cyanomethemoglobin and allows free cyanide to be converted to thiocyanate by the liver and metabolized.
Since treatment of cyanide requires the formation of methemoglobinemia, the use of this antidote is controversial as it may worsen hypoxemia.
- Hydroxocobalamin (vitamin B12a) administration may also be considered since it binds cyanide to form cyanocobalamin which is excreted via the urine
What are the categories of the snake severity score?
- Cardiovascular (0-3)
- Respiratory (0-3)
- Gastrointestinal (0-3)
- CNS (0-3)
- Hematological system (0-4)
- Wound (0-4)
> 6 antivenin or if severe in 1 category
Common orla florin rattlesnakes
o Gram negative rods (Enterobacter, P. aeruginosa, Aerobacter, Proteus)
o Streptococcus and S. aureus
o Clostridium
o Bacteroides
