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
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
