Small Ani. Med- Enviro Emergencies 1

wilsbach's version from 2016-05-02 05:18

Heat Stroke (Multiple Organ Dysfunction Syndrome=MODS)

Question Answer
There are 3 types of heat induced illness, not all are true heat stroke! what are the 3 heat induced illnesses? What is going on with them? (1) Heat cramp: Muscle spasms secondary to NaCl depletion (2) Heat exhaustion: See GI signs (V/D), weakness, mm tremors. (3) Heat stroke: CNS signs!!! Multiple Organ Dysfunction Syndrome= MODS
explain classical vs exertional heat strokeClassical= high environmental temp. Exertional= strenuous exercise.
hallmark symptoms of heatstroke? (what's the temp for this definition?)***Core body temperature >104’F (remember we usually measure peripheral. sometimes peripheral can be a bit hotter, but if peripheral is 105/106 you can pretty much assume it's 104 at the core) *CNS~ dysfunction, Varying degrees of organ dysfunction
protective mechanisms for heat stroke? Thermoregulation, Acute Phase Response (happens when exposed to high temps), Intracellular Heat Shock Proteins (prevent cell death when exposed to high heat)
So heat stroke occurs when there are abnormalities with...(1) Thermoregulation (2) Acute phase response (3) Acclimatization (4) Production of heat shock proteins
predisposing factors for heat stroke?Conformation: brachycephalic. Body condition: obesity. Diseases that prevent normal evaporative cooling: neuro, resp... Age: geriactric. Hair: darker fur, thicker coat
*what are the 4 ways an animal thermoregulates?? (mechanisms)Convection, Conduction, Radiation heat transfer, Evaporative heat transfer
*what is convection? (part of thermoregulation) transfer from body surface to air (fan)
*what is conduction? (part of thermoregulation) transfer to surfaces/objects in contact with (table, kennel, ground) (lay on cool ground)
*what is Radiation heat transfer? (part of thermoregulation)Loss to surrounding structures not directly in contact (walls)
*what is Evaporative heat transfer? (part of thermoregulation)Loss from moisture on body surfaces (respiratory tract) to envt (panting!)
dogs and cats dissipate heat by PANTING. if they are panting...They are exhibiting an imbalance between heat generation and dissipation
what is the acute phase response?A systemic coordinated reaction Activated by inflammation (heat causes inflammation) and meant to protect against tissue injury & promote repair. You will see Acute phase proteins (Proteins released during an acute trigger event) which May be both Pro and Anti Inflammatory (aka cytokines). Cytokines can... Activate WBCs, Stimulates synthesis of more acute phase proteins, Stimulates H -P-A axis (stress!!), Activates endothelial cells (clotting & coagulation) (albumin is neg acute phase protein. globulin is positive) So basically acute phase is MAKING PROTEINS to try to protect body. (she said just know acute phase response is an endogenous protective mechanism we have)
what are heat shock proteins? what do they help prevent? what do they maintain?*Protect against heat insult to cells!! PREVENT: Apoptosis, oxidative stress, Multiple organ dysfunction, cell death. MAINTAIN: protein structural integrity
what is acclimation?A physiologic process that allows the body to adapt to environmental or climatic changes. Partially complete 10-20 days, but takes 60d for whole process!! While they are acclimating, they depend on Water conservation mechanisms to not go into heat induced illness. these include: Aldosterone & Anti-diuretic hormone: conserve water during elevating temperatures, Without adaptive mechanisms dehydration & hypovolemia occur
***at _________*F, critical enzyme systems are denatured!109 (peripheral)
explain cardiovascular effects of heat stroke (progression)EARLY ON: Renal/splanchnic vasoconstriction, cutaneous dilation---> inc CO, dec vascular resistance. EVENTUALLY LEADS TO: Splanchnic vasodilation: Venous pooling and decreased cardiac output. This causes HYPOVOLEMIA. Eventually you will see sinus tachycardia as the heart tries to compensate. VPCs= worst prognosis
*******what are coag effects like with heat stroke?HUGE DISK FOR DIC!! Both clotting & breakdown of clots occurring at same time. Heat is activating clot formation and fibrinolysis at same time-- BLEED AND CLOT AT SAME TIME! Usually see lots of bleeding, can see signs of thrombosis too. But usually see petechiation-- suffering from effects on coag system! HArd to manage- try to treat based on what signs theyre showing. FRESH FROZEN PLASMA can help.
GI effects of heat stroke?Vomiting (can be hematemesis), Diarrhea (hemorrhagic, mucoid, intestinal sloughing)--> this is usually happening due to changes in perfusion from the CV effects (dec perfusion bc shock) can lead to ischemia and organ death. GI ulceration, perforation, and necrosis can occur within a few hours (look out for bacterial translocation!-->prophy broad spectrum abx like metro(ana), ampi(+), enro aka baytril(-) aka BAM therapy) consider: Protectants –H2 blockers, Sucralfate, anti-emetics
CNS effects of heat stroke?(true heat stroke case need CNS signs) Seizures on presentation or shortly after, often due to Cerebral edema (because fluid shifts) (so think hyperosmotic like hypertonic saline/ mannitol), Electrolyte imbalances, Blindness (+/-) (direct thermal damage to CNS), Head bobbing, tremors, comatose (Poor cerebral perfusion, direct thermal damage, cerebral edema, hemorrhage, metabolic abnormalities)
therapies for heat stroke? When do you wanna STOP cooling? what should you NOT DO?DONT FORGET THE ABC'S FIRST!! (airway, breathing, cardiovascular), then think about COOLING-- Rapid evaporative cooling (fans, wet fur, wet towels)-- Stop cooling at **103.5’F to prevent rebound hypothermia! Also, NEVER PUT THEM IN AN ICE BATH. intense vasoconstriction prevents heat release. also dont forget to provide fluids IV!! crystalloids +/- colloid<---if think there is cerebral edema. but can mess with coag.
survival at _________ hours indicates a greater chance of survival, what trend is there with non-survivors?If alive at 48hrs= greater chance of survival. Blood glucose significantly lower in NON - SURVIVORS

Smoke inhalation/ carbon monoxide

Question Answer
how common is smoke inhalation?Fires are common, inhalation cases are NOT!
take hx to try to fig out..exposure time and extent of damage
CSs are often dependant on Intensity of exposure, duration, heat generated, and components of smoke, but common signs at the scene are... Stupor, coma (47%), Coughing, gagging (35%), Respiratory difficulty (35%)
what are the 3 main body systems affected, and most of the signs stem from what probs?main body systems affected are Respiratory, Ocular, Neurologic and these signs are generally the result of Result of tissue hypoxia, thermal damage, chemical irritation
If there is chemical inhalation, how might you be able to predict which part of the airway is harmed?has to do with water solubility of chemical- highly watersoluble chemicals will damage upper airway, low water solubility will mean it will travel farther down to lower airway.
UPPER (pharynx, larynx) airway generally damaged due to....heat (burns, sloughing, inflammation)
what usually causes airway compromise is ...edema & swelling which cause airway occlusion! This happens bc inflammatory cascade: Epithelial cell death--> Sloughing (can form casts in lower airways) & further inflammation--> inc capillary permeability--> Congestion & edema
upper vs lower airway damage?UPPER= thermal! Lower= direct chemical injury
explain lower airway damage with smoke/CO inhalation Not thermal --> closing of epiglottis, heat dissipation prevent this type of injury. Rather, it is the Result of direct chemical injury as well as Cast formation & migration (dead epithelial cells from heat damaged upper airway sloughing downwards=casts). ex of chem injuries: Formation of acid or alkali burns, Free radicals, protein denaturation, Low water soluble irritants (cyanide, soot), Particulate materials, Reflex bronchoconstriction (<--wheezy and dyspnea)
explain the lung parenchymal damage with smoke/CO inhalationhappens because of Direct epithelial damage and Recruitment of inflammatory mediators (Growth factors, cytokines, neutrophils--> ROSs). Also can get Pulmonary dysfunction from Apoptosis of epithelial cells, there can be dec surfactant production (-->atelectasis), Reduced pulmonary compliance, and V/Q(ventilation/perfusion) mismatches.
smoke inhalation pts are at risk for developing ARDS- what is going on with this?basically its an animal that suddenly develops a significant amount of pulmonary edema throughout the airways due to inc vascular permeability and inflammation (so not only thermal, cell, chemical irritation-- also have ARDS) MASSIVE INFLUX OF FLUIDS INTO PULM INTERSTITIUM
why are smoke inhalation pts at inc risk for pneumonia?Mucociliary apparatus dysfunction, Trapped particulate matter, Migration, Continued inflammatory reaction, Leakage of plasma into parenchyma, Denuded serosal surfaces, Ventilation and intubation. Basically, jack up resp immune system and then damage it--> breeding ground for bact
medical mgmt for smoke inhalation?Fluid balance, analgesia, Oxygen, mechanical ventilation
what is a Endoscopic intervention, why might you do this for a smoke inhalation pt?can do a Laryngoscopy & bronchoscopy: Helps gauge injury, prognosticate, can also do Endotracheal suctioning, physiotherapy
****should you give ABX to a smoke inhalation pt?N O BENEFIT prophylactically!!! (only if see signs which would indicate need it- and then culture too!! )
should you give steroids to smoke inhalation pts? NOT indicated currently
**what is the most common cause of death from fires?inhaled carbon monoxide
what does CO do in the lungs? result in?higher affinity for heme than O2, displaces the O2 and impairs its delivery, and shifts O2Hb curve and Interferes with mitochondrial enzymes. Results in: Cellular & tissue acidosis (lactic acidosis), Cellular dysfunction & organ failure
CSs of CO inhalation? How do you tx?Lower body temperature, inc RR, Abnormal respiratory auscultation, **Altered neurologic status IS THE BIG ONE. TO TX: O2 therapy resulted in rapid COHb decline (partial pressures will eventually push it off) (hyperbaric O2 chamber also help but expensive and rare)
will spO2 help you dx CO inhalation?pulse ox tells us saturation of Hgb. saturation of normally O2. but all it does it that Hgb is saturated with sthing. in these cases its CO tho. so will get false decent reading bc picking up there is saturation
**What odd symptom might stick around for a while even after full recovery from CO inhalation?transient hearing loss might happen
3 possible clinical outcomes of CO inhalation?(1) Complete recovery (+/- transient hearing loss) (2) Recovery with permanent CNS dysfunction (Delayed neurologic sequelae (DNS), After transient period of improvement) (3) death from cerebral hypoxia or myocardial hypoxia
what about CO inhalatin will kill them?HYPOXIA to brain or heart
what long lasting damage might result from CO inhalation? Delayed neurologic sequelae (DNS)


Question Answer
what is dry drowning?victims who do not aspirate liquid into lungs (10% of the time)
hypoxemia can result from what two different processes with drowning? Laryngospasm from dry drowning –no aspiration of water. Loss of surfactant –aspiration of water (alveoli stick together). Also risk bronchospasm, atelectasis, and ARDS(<--LOTS OF INFLAMMATION-->leaky capillaries-->pulm edema)
does fresh vs salt water make a difference?nope-- pathophys is the same. WASHOUT OF SURFACTANT-->atelectasis-->Intrapulmonary shunt--> Global hypoxia--> Tissue injury--> Neurologic damage--> Cardiovascular collapse--> death
why are there neuro signs with drowning?BC HYPOXIA! hypoxia-->Induces brain injury ( Severity of injury depends on duration of hypoxia)
what are the CV effects of drowning?Cardiac arrhythmias & dysfunction because of HYPOXIA-->ischemia-->acidemia-->E’lyte abnormalities-->Hypothermia
does water type or water temp affect survival more?salt vs fresh doesnt matter, TEMP DOES
*explain how temperature of water has effect on survival ratesIf there is ICE COLD WATER (<5*C), it will INC your chances of survival, because there is a diving reflex where as cold water hits your face, the trigeminal nerve causes bradycardia, hypertension, Preferential shunting of blood to cerebral & coronary circulation----> essentially, BRAIN AND HEART PROTECTION
explain drowning txGOAL is improve tissue oxygenation. Do CPR if indicated and able. Oxygen, intubation, mechanical ventilation. Artificial surfactant?, Antibiotics? If BAL supports. Fluid therapy? YES-- they are in SHOCK, whether it is distributive or hypovolemic. So want to restore effective circulating volume, correct acid-base abnormalities, and improve tissue perfusion. Hyperosmotic fluids if indicated based on neuro
prog of drowning?Unknown in veterinary patients but in humans 100% mortality if Submersion > 25 minutes/CPR > 25 minutes/ Pulseless cardiac arrest on presentation to hospital (Vtach, Vfib, tachycardia, fixed pupils, respiratory arrest)