ECC Environmental Emergencies

sihirlifil's version from 2018-05-02 15:18

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!)
Factors affecting resp heat lossHumid climate, confinement w/ poor ventilation (hot car), URT abnorm (brachycephalic)
Factors affecting radiation & convection heat lossBlood doesn’t get to skin (poor cardiac output, hypovolemia
Skin cant transfer heat (obesity, thick fur coat)
Acclimitization to heat: takes up to 60d to physiologically acclimate to climate change
Most dangerous time of year for heat strokeHottest humidest day of SPRING
dogs and cats dissipate heat by PANTING. if they are panting...They are exhibiting an imbalance between heat generation and dissipation
(+/-) 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)
Systems involved in heat strokeCVS
**Initial patient assessment: TriageVitals: TPR, mm, CRT, PQ
Asses airway, mentation, brief neuro exam
Brief hx
explain cardiovascular effects of heat stroke (progression)EARLY ON: Present in HYPERDYMANIC state! Hyperemic mm, CRT <1s, weak pulses (hypovol 2’ to fluid loss, v/d, evaporation) 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 resp effx like w/ heat stroke?Most present tachypneic, rapid panting, short breaths (r/o upper airway abnorm/obstxn)
Assess for hypoxemia & auscult for crackles: aspiration pneumonia, parenchymal hge, edema. May need tracheostomy!
CNS effects of heat stroke: what’s happening in the brain?Poor cerebral perfusion
Direct thermal dmg
Cerebral edema
CNS hge
Metabolic changes (hypoglycemia)
CNS clinical signsMentation changes first! (alert to comatose)
Pupillary abnormalities: Symmetric (mydriasis, miosis) or asymmetric (anisocoria)
Cortical blindness, ataxia
Renal effects of heat strokeAKI from decreased perfusion, pigmenturia (hburia, myoglob)
Palpate bladder size (should fill if blousing fluids), US can help assess UOP before it comes out. Fluid therapy & monitoring UOP vital! (can devp hours-days later)
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
*******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.
PATIENT MONITORING for coag?Petechiae, ecchymosis; melena, hematuria, hemoptysis
LAB MONITORING for coag?Platelet count, D-dimers, FDPs, PT/PTT
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. 20ml/kg or 1/3 shock dose, reassess, repeat if needed
Factors associated w/ prognosisDuration of exposure
Highest body temperature reached
Pre-existing conditions (brachy, larpar)
2’ complications (DIC, sepsis, etc)
Rapidity of tx
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
Effects of smoke inhalationThermal (upper & lower airway), CO toxicity, 2’ bacterial pneumonia
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)
Steam > dry heat
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 & laryngeal edema
What emergency tx may be needed if laryngeal edema?Tracheostomy (edema can occur 1-3d post-presentation)
upper vs lower airway damage?UPPER= thermal! Lower= direct chemical injury
explain lower airway damage with smoke/CO inhalation Reduced lung compliance occurs minutes-24h post-exposure
Caused by alveolar atelectasis, pulmonary edema, reduced pulmonary surfactant --> massive neutrophil migration to lungs --> impaired gas exchange (V/Q mismatch). Acute lung injury +/- ARDS
explain the lung parenchymal damage with smoke/CO inhalationAirway dmg & obstruction = reduced lung compliance, mucociliary dysfxn, mucosal edema, sloughing --> membrane casts, increased secretions
Results in tracheobronchitis, necrotizing bronchitis, hyaline mb formation & hge in alveoli
Sequelae of lower airway effxDMg, obstruction, increased secretions, decreased mucociliary escalator, decreased pulmonary compliance --> 2’ bacterial bronchopneumonia
If DERMAL BURN also present, HIGHER MORBIDITY & MORTALITY assoc w/ smoke inhalation (norm bacteria aren’t cleared)
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
Patient eval: what tests?Rads (70% have pulmonary abnorm w/in 24h, may not show up until 72h) (severity of CS & Rads don’t correlate!!)
Acid/base: acidemia can be resp, metabolic, or mixed. Hyperlacatemia
medical mgmt for smoke inhalation?Fluid balance, analgesia, Oxygen, mechanical ventilation (resp musc fatique), IV fluids (CAREFUL b/c can leak & cause edema)
Treatments that are NOT RECOMMENDEDGlucocorticoids, prophylactic antibx
What can we do for airway management for smoke inhalation?Tracheostomy, bronchodilators, humidified O2, coupage, mucolytics
Why sedate a smoke inhalation pt?Anxiety increases resp effort, increases edema
(+/-) 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?NO 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
Alternative tx for smoke inhalationHyperbaric O2 therapy
If cyanide poisoning (silks, other fibers): IV sodium thiosulfate
**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 inhalation will kill them?HYPOXIA to brain or heart
what long lasting damage might result from CO inhalation? Delayed neurologic sequelae (DNS)
Prognosis of ‘uncomplicated’ cases(No CNS signs) = good w/ tx
Prognosis if improving w/ tx? Declining?Within fist 24 h improvement = good. Poor if decline
What’s mortality like?46% in dogs w smoke exposure & acute CNS signs, better (60%) if delayed CNS signs (don’t go away)
Guarded if dermal burn injury

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