4 levels of consciousness
- Obtunded: unconscious but rousable with NON-noxious stim (yelling, clapping, etc)
- Stuporous: unconscious, rousable with NOXIOUS stim (pain, etc)
- Comatose: unconscious, unrousable
Triage primary survey - 4 parts
Triage primary survey - neurologic (3)
- Consciousness: normal, obtunded, stuporous, comatose
- CN: menace, palpebral, PLR
Triage primary survey - Respiratory (2)
- Rate and effort: eupneic, tachypneic, dyspneic (DISTRESS), apneic
- ascultation: crackles and wheezes
Triage primary survey - Cardiovascular (4)
- Heart sounds: loud and distinct, muffled and distant (Pleural effusion, pericardial effusion), symmetrical or asymmetrical
- HR: tachy vs bradycardic
- regularity of rhythmpresence of pulse deficit
Triage primary survey - perfusion (4)
- Pulse quality: strong, fair, poor, bounding (vasodilation or hypovolemia)
- MM: pink, red (vasodilation, distributive shock), pale/white (anemia or vasoconstriction/shock), cyanotic (VERY big deal, O2! SpO2<80)
- CRT: <1 is hyperdynamic, 1-2s is normal, >2s is poor perfusion, undetectable
- temp: elevated (fever or hyperthermia), low (poor perfusion or environment), cold in periphery (poor perfusion)
Triage secondary survey
- AFTER starting resuscitation phase/stabilization PRN.
- Full PE
- additional diagnostics and tx plans. Be able to JUSTIFY
Triage tertiary survey
- sequential PE
- lab data and imaging studies
- 12-24h after presentation and throughout hospitalization
- goals: ID things you missed when emergent, monitor progression, find cause of emergent probs to plan definitive tx
shock definition (5)
- widespread failure of energy production at the cellular level causing decreased cellular ATP levels
- Increased PVR, Decreased CO, decreased circulating blood volume, decreased tissue perfusion
Stages of shock (3)
- early: compensation working. Catecholamine release, tachycardia, increased contractility, increased CO. Relatively stable
- middle: beginning to decompensate, perfusion to vital organs okay, non-vital organs are suffering.
- late: severe decompensation (decreased CO, bradycardia, severe hypotension), IMMINENT danger
Types of shock (4)
- Hypovolemic: decreased intravascular volume
- distributive: maldistribution of blood flow
- cardiogenic: cardiac pump failure
- Other: failure of energy production at cellular level (tissues can't USE O2, delivery okay)
hypovolemic shock - def, where did it go?, signs, PE findings
- MOST COMMON TYPE
- critical loss of circulating volume. State depends on volume lost
- Where did it go!?: hemorrhage (internal or external), dehydration (loss of extravascular volume will eventually lead to intravascular volume), third-spacing, urinary, GI
- signs: weakness/collapse, depression, rapid shallow breaths, cold extremities
- PE findings: Pale mm, prolonged CRT, weak peripheral pulses, tachycardia
Distributive shock - def, pathology, ddx, signs of 2 phases
- inappropriate vascular tone: vasoconstriction in some places, vasodilation in others
- Microcirculation: sluding of blood, platelet and coag activation, neutrophil activation
- ddx: sepsis/SIRS, anaphylaxis, adverse drug rxn, severe acidosis, electrolyte derangements, trauma, neurogenic
- signs of hyperdynamic (early): hyperemic mm, fast CRT, tachycardia, normo or hypertension, bounding pulses (vasodilation)
- signs of hypodynamic (late): like hypovolemic shock. Pale mm, prolonged CRT.
Cardiogenic shock - def, ddx in dogs vs cats, signs
- heart "pump" failure - decreased forward flow out of heart.
- ddx in dogs: valvular disease or arrhythmias. Much less = DCM
- ddx in cats: HCM, rarely DCM
- signs: like hypovolemic. Pale mm, poor pulse, tachycardia. Also listen for murmur/gallop (gallop = HCM), arrhythmia, resp distress (Pulm edema or pleural effusion), elevated CVP (distended jugular, ascites)
Pathophys of shock and what determines it (2)
- inadequate delivery of O2 to tissues
- determined by CO (determined by preload, contractility, afterload) and Arterial oxygen content/CaO2 (hemoglobin concentration or PCV, and PaO2/SPO2)
How to ID tissue O2 delivery (DO2) deficits (2)
- Central Venous O2 Saturation (ScvO2): decreased DO2, increased fraction of O2 extraction = decreased ScvO2. Global picture, normal >70%
- Lactate: product of anaerobic metabolism.
Differentiate the three types of telephone triage calls and how to handle each
- Obvious emergencies: recommend first aid in transport, then come in now! No need for extensive conversation
- obvious non-emergencies: go to rDVM. Discuss routine services. What changed today?
- everything else: explore current complaint and ppHx. When in doubt, come in.
- TOTAL BLOOD VOLUME
- cat: 60ml/kg
- dog: 90mL/kg
- isotonic crystalloids
- TITRATE. 1/4 to 1/3 over 15-20min, reasses. Some need multiple.
5 determinants of O2 delivery (DO2) that can be manipulated clinically, how to dx deficits in each and how to tx P with those deficits
- SPO2: O2! Don't tolerate hypoxemia!
- Preload: hypovolemia = decreased preload. Decreased CVP, Atrial or ventricular size on echo. Isotonic crystalloids (SHOCK DOSE). NEVER hypotonic!!! Hypertonic IF HYDRATED
- hemoglobin concentration: blood loss = loss of RBC. Treat clinical signs that don't improve from fluids with transfusion. 1mg/kg pRBC improves HCT by 1%. 2ml/kg whole blood.
- Afterload: nitroglycerine
- Contractility: positive inotropes
Initial diagnostic, therapeutic and monitoring plan for hypovolemic shock (2)
- By definition decreased preload
- Isotonic crystalloids (60mL/kg for cats, 90mL/kg for dogs, give 1/4-1/3 over 15-20min, REASSESS). NEVER hypotonic, hyperosmotic ONLY if hydrated. Plasma or albumin maybe?
- hypoxemia common
- O2! - DO NOT TOLERATE HYPOXEMIA
Initial diagnostic, therapeutic and monitoring plan for distributive shock
tx priorities (2) and options (1:2, 2:3)
- preload deficits. Vasodilation causes decreased effective circulating volume, or IV fluid losses from sepsis/SIRS etc. Maldistribution, poor cardiac contractility.
- Tx priorities: same as hypovolemic. Vasopressors for vasodilation (IF HYDRATED), positive inotropes
- Vasopressors: catecholamines (stim alpha1 for vascular smooth muscle contraction. Acidemia inactivates. Arrhythmogenic). Vasopressin (ADH) - stimulates V1 receptors for vascular smooth muscle contraction, not affected by acidemia and not arrhythmogenic, but $$$
- Inotropes: for contractility. Dobutamine (beta1 receptors, as CRI), Digoxin (poison Na/K ATP-ase? PO or IV), Pimobendan (Ca channel sensitizer. PO). RULE OUT HYPOVOLEMIA FIRST
Initial diagnostic, therapeutic and monitoring plan for cardiogenic shock.
Tx options (3) +1
- decreased forward flow due to DECREASED CO. Backup of blood from INCREASED PRELOAD. Often caused by CHF
- Treatment options: decrease preload, decrease afterload, maybe increase contracility. Treat arrhythmias. May resolve when perfusion restored. ALL ANTIARRHYTHMICS ARE ARRYTHMOGENIC
- Decrease preload: Furosemide to inhibit Na/K/2Cl pump in ascending loop of Henle.
- Increase forward flow: decrease afterload (nitroglycerin topical or nitroprusside CRI ($$)) or increase contractility ONLY if THIS IS THE PROB (positive inotropes like dobutamine, pimobendan, digoxin).
resuscitation endpoints you would use to determine efficacy of P in shock you're stabilizing (7)
- Pink mm
- CRT <2sec
- improved pulse quality
- normal RH
- Systolic >120 mmHg
- resolution of hyperlactemia, metabolic acidosis, anemia
initial stabilization general approach (7)
- provide supplemental O2
- establish venous access
- collect and evaluate MDB
- collect additional pretreatment samples
- optimize DO2
- reassess frequently
- DOCUMENT EVERYTHING.
larger gauge and short catheter due to Poiseulle's Law
MDB for ER (4)
- PCV: low = blood loss. High = normal vs splenic contraction
- TP: <6 = hemorrhage. High = unlikely hemorrhage
- BG: Low = sepsis, metabolic. High - stress, metabolic.
- BUN ESTIMATE (Azo): high = pre, renal or post
Pulse Oximetry: principles, indications, interpretation, limitations
- Principles: views only pulsatile. 660nm is oxyhemoglobin and 940 is reduced hemoglobin - measures both wavelengths. Math determines %
- indications: hypoxemic, on life-monitor (circulatory/perfusion or critically ill), anesthesia
- interpretation: must be in place 30s, check good wave form, pulse form and matching HR. Dyshemoglobinemias falsely elevate (can't differentiate)
- Limitations: poor perfusion (hypotension, hypothermia, peripheral vasoconstriction), dark pigmentation, motion
- AB: exhalation of gas contained in dead space at beginning of exhalation
- BC: emptying of connecting airways and beginning of emptying of alveoli
- CD: emptying of alveoli
- D: end-tidal CO2 level - best approx of alveolar CO2 level
- DE: P begins to inhale fresh gas
- EA: inspiratory pause
end tidal capnometry: principles, indications, interpretation
- Principles: Infrared passed through air to photo-detector. Intensity of light is inversely proportional to CO2 (CO2 bounces light?). Mainstream vs sidestream
- indications: P at risk of ventilatory failure (Cardiac, resp, NMJ, neuro), PPV, anesthesia, CPR
- interpretation: increased ETCO2 - hypoventilation, increased metabolism, IPPV (increased CO). Decreased ETCO2 - hyperventilation, hyperthermia, IPPV (reduced CO). Rise in both baseline and ETCO2 (rebreathing of CO2). Sudden fall in ETCO2 (airway leak, ventilator malfunction, IPPV (cardiac arrest)
arterial blood gas sampling: principles, limitations
FiO2 x 5
PaO2 x FIO2
- Principles: 45-60 degree angle with heparinized syringe, expel air and cap. Analyze immediately or on ice in 1-2h.
- Limitations: exposure to room air or bubbles, excess heparin. Different O2 in dif places, dif with different temps!
- PaO2: partial pressure of O2 dissolved in plasma. <85-90 = hypoxemia.
- Alveolar-arterial oxygen difference
- FiO2 x 5: Expected PaO2 = FIO2 x 5. Room air ~ 105mmHg. On 60% O2 ~ 300mmHg
- PaO2 / FIO2: >500 is normal, <300 is bad. Room air of PaO2 of 97 = 97/0.21 = 462. On 100%O2 = 97/1.0 = 97 = abnormal.
Stages of hypothermia
- Change in setpoint - P will resist warming!!
- mild (98-99.9): Normal to increased HR, normal MAP, RR and mentation
- moderate (96-98): hypotension, HR (cats decrease, dogs increase), mental dullness
- severe (92-96): bradycardia, hypotension, resp depression, severe CNS depression
- Critical (<92): moribund, may appear dead, high mortality rate
Tx and goals for hypothermia
- Goals: rewarm to 98.5. Avoid rebound hypothermia (vasodilation, distributive shock)
- passive surface warming: insulation to prevent heat loss! for MILD hypothermia with adequate circulatory volume
- active surface warming: provide a heat source. Focus on thorax. In moderate, severe or critical hypothermia. MUST provide volume support to prevent distributive shock from vasodilation. Monitor to avoid burns!
- active core warming: in severe/critical hypothermia, reduces peripheral vasodilation (use WITH surface warming). Heated, humidified inhaled air, warm saline lavage (peritoneal, pleural, gastric, bladder), warm water enemas, warm IV fluids
- tissue freezing: EC vs IC ice crystals, cellular dehydration, denaturation of membrane lipid-protein complexes. Vasoconstriction causing tissue hypoxia, endothelial injury, release of inflammatory mediators, local thrombosis.
- cats: tail, pinnae, footpads
- dogs: external genitalia, footpads
- superficial: freezing skin and SQ, erythema with central white plaque. Full recovery
- deep: death of skin, SQ, muscle, hemorrhagic blisters, black eschar, px guarded.
- tx: warm rapidly (104-108 water bath for 15-30mins if refreezing can be avoided). Debride blisters (contain inflamm mediators), aloe vera q6h. Wrap in loose bandage, consider NSAIDs. Parentaral narcotics. Staged debridement--more appears damaged later.
Types of hyperthermia and physio response
- pyrogenic (febrile): thermoreg mediation. Pyrogens (IL-1, TNF-alpha). Set point > normal body temp. THINK THEY'RE FINE
- non-pyrogenic: heat producing mech > heat dissipating mech. Temp > normal set point. FEEL HOT
- cutaneous vasodilation and elevated CO, increased RR and panting, compensating mech fail in extreme temps and high humidity
3 stages of heat illness
- heat cramps: muscle cramps, salt depletion, hypotonic fluid replacement. Not recognized in d/c
- heat exhaustion: lethargy, weakness, v/d, excessive panting
- heat stroke: CNS signs, DIC/platelet dysfunction, hypovolemic shock, cardiac arrhythmia.
Types of heat stroke
- classic (non-exertional): overheated enclosure, outdoors with no water/shade, vehicular entrapment (most common)
- exertional heat stroke: late spring or early summer before acclimation to increased temps. Predisposed by obesity, lar par, brachycephalic. Eclampsia or status epilepticus cause this, too.
Pathophys of severe hyperthermia and clinical signs
- pathophys: cellular necrosis (denature proteins and inactivate enzymes), global ischemia (microvascular thrombosis, hypoxemia), multiorgan failure
- signs: core temp >106 (did O tx?), excessive panting (tachy mm), hyperemia = fast CRT, hypersalivation, tachycardia, neuro signs (ataxia, altered mentation, sz), petechiae/ecchymoses, melena/hematochezia/mucosal sough/hematemesis, icterus (hemolysis vs hepatic dysfunction), dark urine (myoglobinuria, glucosuria, casts).
Clin path of heat stroke
- more nRBC = more likely to develop organ dysfunction, watch the trend!
- hemoconcentration, elevated liver enzymes, electrolyte changes (hypernatremia and hyperkalemia from cell damage), prolonged PT/PTT, azotemia, hypoglycemia (sepsis)
first aid for heatstroke
rapid cooling! Hose off with room temp water before transport to vet! Don't use ice or ice water - vasoconstriction stops them from being able to release heat, just evaporation.
tx, px for heatstroke
- external cooling: soak with water, put in front of fan.
- internal cooling: cold water enemas, gastric lavage, room-temp IV fluids.
- STOP WHEN TEMP = 103 to avoid afterdrop. MONITOR
- tx dangerous effects
- px: if going to die, do so in 24h. Bad if hypothermic on presentation, refractory hypotension, DIC, persistent hypoglycemia, organ dysfunction
Snakes - elapidae vs viperidae
- elapidae: coral snakes, cobras. Neurotoxic venom to immobilize. Minimal pain/swelling, flaccid paralysis to resp failure. Signs can be delayed 3-12h
- viperidae: rattlesnake, copperhead. Proteolytic and hemotoxic venom. Strike and release and then wait to die. Edema, swelling.
- ECHINOCYTES in first 48h and thrombocytopenia
tx for snake envenomation
- secure airway
- tx shock
- analgesics - not NSAIDs.
- KNOW your local snakes and whether there are antivenins. Steroids if no antivenins.
- abx esp with local tissue necrosis. May also need debridement (may have to stage, takes a while to declare itself).
insect bites - perpetrators, types of rxn and clinical signs
- most are bees, yellow jackets, wasps, hornets, fire ants
- types of rxn: allergic (type I hypersensitivity) vs toxic (cytotoxic and vasoactive).
- local toxic: swelling, redness, pain, self-limiting
- local allergic: edema/swelling, often on face and feet
- generalized toxic: fever, depression, weakness, shock, resp distress, neuro, GI, coag
tx for insect bites (3 dif types)
- local toxic: remove stinger and scrub
- local allergic: usu outpatient but hospitalize airway compromise. Antihistamines (diphenhydramine) +/- corticosteroids if really severe.
- generalized toxic: tx for shock (O2 and fluid), antihistamines, steroids, blood products.
- OK to tell O to use OTC benadryl if no noisy breathing, but warn of dangers
- Black widow/Latrodecus: SNS, PNS, neuromuscular. Opens cation channels. Fatal in cats. central pale area surrounded by erythema. Vocalization, hypersalivation, intense abdominal pain, muscle spasm/rigidity, resp paralysis. Antivenin (test dose), Ca Glc if hypocalcemic, ventilator, px guarded.
- brown recluse/Loxosceles: necrotizing, bullseye lesion with black center, white around that then red around that. May spread or heal. Sx debride, abx. Px good, may need flaps etc.
smoke inhalation dangers
- CO: Hb affinity, displaces O2, tissue hypoxia, brain damage.
- CO2: displaces O2, enhances toxicity of other gasses
- HCN: rapidly translocated into brain, rapid CNS depression, can't use O2, cellular hypoxia.
- irritant gasses: pulm irritation, alveolar damage, pulm edema. Soluble = immediate, insoluble = delayed
Stages of clinical signs of smoke inhalation (4)
- 1: during inhalation. hyperventilation and hypoxemia. CO tx common = hypoventilation/apnea
- 2: 0-30mins later. hypercapnea + hypoxemia, compensatory hyperventilation
- 3: 2-4h later. increasing hypoxemia, worsening alveolar damage, pulm edema
- 4: 24h later. Development of bacterial pneumonia. Failure = poor px. No pneumonia = good px.
smoke inhalation tx
- establish airway (bronchodilators vs suction vs intubation).
- Fluids (shock, but NOT overhydration)
- DON'T use corticosteroids
- abx only if penumonia
- CO: O2!
- CO2: drops quickly once out, pulm dysfunction if stays high
- HCN: O2, sodium nitrate NOT RECOMMENDED. thiosulfate to cause renal excretion
- PORCUPINES CAN'T SHOOT
- specialized hairs with barbs on end, WILL migrate so don't leave any in! FIND them - palpate tongue, everywhere
- HEAVY sedation, grasp at base and pull straight out, wrap hemostat for deeply embedded
- vax for rabies!
- pain meds but not abx.
4 initial steps in trauma patient management
- triage: ABC(CD) - airway, breathing, circulation, consciousness, disability (CNS, peripheral nerves, MS)
- primary survey: the rest, include US, rads PRN
- stabilize: O2, shock, protect CNS, analgesia, minimal stress
- secondary survey: what body systems and how affected? Dx plan, Tx plan
- focus on cardio, resp, neuro because they are most likely to be/indicate life-threatening
4 things a TFAST can ID
What can an AFAST ID?
- TFAST: (rib fx), pneumothorax, hemothorax, pleural effusion, pericardial effusion. B-lines (vertical, comet tails or search lights rather than horizontal A lines. Indicate pulmonary contusion or pulm edema) and glide sign (side-to-side moving of lung, means no pneumothorax. Ants on a washing line. Mvmt of lung when P breathes. disappearing suggests pneumo).
- AFAST: free fluid - hemoabdomen vs something with a smooth outline. Check between liver lobes - spiky is free, rounded is in a viscus.
5 principles of initial stabilization of trauma patient
- ensure adequate oxygen
- treat shock
- protect the brain and SC - neuro injury until proven otherwise!
- provide analgesia - pain complicates assessment
- minimize stress
role of fluids in tx of shock
- crystalloids: 15mL/kg/15min then reassess. Cheap, familiar, minimal effects.
- hypertonic saline: minimize cerebral edema, short-term augmentation of blood volume. For head trauma. 2-5mL/kg/15min, follow with crystalloids
- blood products: whole blood vs component (usu reconstitute whole blood by giving all products). Autotransfusion from hemoab - don't need anticoagulant unless active bleed.
analgesia for trauma
- opioids, ketamine, locals
- dex (not at first)
- NOT NSAIDS - usu volume depleted.
which types of injury are most commonly reported to trauma centers?
- #1 Penetrating trauma 50.2% (bites are 69% of these)
- #2 blunt trauma 46.8%, vehicle collisions are 41% of these
- combined mechanism 3%
Recognize common patterns of injury inflicted by bites
- Usu soft tissue trauma, then intercostal avulsion, sternebrae fx/lux, rib fx, laryngeal.
- Watch for airway trauma - emphysema, pneumo-anything, flail chest or intercostal, penetration etc, bladder rupture.
- Teeth are meant to rip and tear, damaged tissue may not declare itself right away
- Hemorrhage leading to shock, SIRS/Sepsis leading to shock. Iceberg effect!
recognize common patterns of injury from blunt force trauma
- often HBC
- watch for repeated, or the story doesn't fit. Keep an eye out for abuse.
- pneumothorax, pulmonary contusions, rib fx, diaphragmatic rupture (usu in tendon, not muscular part in center), hemoperitoneum, fx in general (pelvic! Often in many places - check the other side! Limb).
- Resp distress may develop later, resolves in a few days. FLAIL UNCOMMON.
recognize common patterns of injury inflicted by falls from height.
- Safter from 6th and 2nd floors - time to right themselves!
- limb fx, spinal injuries, pneumothorax, palatine injuries, mandibular fx
definition and veterinary criteria for sepsis
- life-threatening organ dysfunction due to a dysregulated host response to infection
- SIRS + Infection
- defined by mortality using retrospective data
- infection + 2(+) point increase in Sequential Organ Failure Assessment (SOFA) score or quick SOFA points (Hypotension<100, altered mental status<15, tachypnea>22)
definition and veterinary criteria for SIRS
- Systemic Inflammatory Response Syndrome
- signs of systemic inflammation in response to pathological insult (trauma, pancreatitis, burns, snakebite, neoplasia, heat stroke)
- Dog: temp high or low (99-102.5), HR >140, RR >30, WBC <6, >19 or >10% bands
- cats: temp high or low (100-103.5), HR high or low (140-225), RR >40, WBC <5, >19.5, or >5% bands
definition and veterinary criteria for severe sepsis
- ELIMINATED! ALL sepsis is severe!
- OR sepsis complicated by disfunction of one or more organs
definition and veterinary criteria for septic shock
- Sepsis-associated circulatory failure, with hypotension despite volume resuscitation.
- subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality
- Consists of sepsis, ADEQUATE volume resuscitation, vasopressor dependent hypotension (required to maintain MAP), lactate >2
- SAP <90, MAP <60, fall in SAP >40 (systemic arterial pressure)
causes of vasodilatory shock in sepsis (3)
- failure of vascular smooth muscle to contract
- inappropriate vasodilation despite hypotension
- poor response to vasopressors
Low ATP, high H+ and high lactate causes K+ to leave cells, which changes how Ca comes into cells which stops contraction.
common sources of infection in patients with SIRS/sepsis (7 with examples)
- Peritoneal cavity: GI perf, liver abscess etc
- Resp: pneumonia, pyothorax
- GI: enteritis
- Repro: pyometra, prostatitis
- Urinary: pyelonephritis, cystitis
- Soft tissue or bone: trauma, osteomyelitis, bite wounds
- CV: endocarditis
common physical exam abnormalities of SIRS/sepsis (early and late)
- Early: tachypnea, bounding pulses, CRT <1, Red mm, depression, hyperthermia
- late: tachypnea, thready pulses, CRT >2, pale mm, stupor/coma, hypothermia, organ failure.
Most important treatment paradigms for patients with SIRS/sepsis (5)
- CV support: optimize preload (venous return and volume), maintain perfusion pressures (MAP >65-75 for kidneys)
- early, effective antimicrobials
- source control
- adjunctive therapy for organ function support
patterns of organ dysfunction and how they can be scored (6...or 7)
- CNS: altered consciousness, confusion, psychosis
- Resp: tachypnea, AsO2 <70, SaO2 <90%, PaO2/FiO2 <300
- hepatic: jaundice, increased liver enzymes, decreased albumin, increased PT
- CV: tachycardia, hypotension, altered CVP, Altered PAOP, arrythmias, increased troponin etc
- renal: oliguria, anuria, increased creatinine
- Coag: decreased platelets, increased PT/APTT, decreased protein C, increased D-dimers
- SOFA scores, but we don't really use them? CV = MAP, Resp = PaO2/FiO2, Neuro = glasgow coma scale, renal = creat, hepatic = bilirubin, hematologic = platelets
How major organ systems can be supported in sepsis (4)
- resp: O2, minimize stress, antimicrobials, bronchodilators, nebulized furosemide
- kidney: fluids, diuretics, acid-base/electrolytes, mgmt of GI signs, dialysis PRN
- hematologic: transfusion!
- GI: enteral nutrition if possible! Low-dose to start. IV glc with enteric is better
- NOT HIGH DOSE STEROIDS
10 tips for sepsis managment
- be suspicious - recognize early
- early appropriate abx save lives
- measure lactate
- give fluid but not too much
- think about vasopressors early
- ID source and control if you can
- watch for organ dysfunction
- use adjunct therapy where appropriate
- monitor, monitor, monitor
- refer early if really sick!
- serious allergic reaction that is rapid in onset and might cause death
- severe, potentially fatal, systemic allergic reaction that occurs suddenly after contact with an allergy-causing substance
- a systemic, immediate hypersensitivity reaction most commonly caused by IgE-mediated immunologic release of mediators from mast cells and basophils
3 classifications of anaphylaxis (causes, Igs, PAF, Histamine)
- IgE: insect stings/bites, reptile venom, food, medications. Histamine and PAF, cytokines
- IgG: Immune aggregates, complement system activation, coag system activation, autoimmune mech. PAF, NO HISTAMINE
- non-Ig-mediated: physical factors (cold, water exposure, heat, exercise), certain meds (opioids), chemotherapeutic. PAF, Histamine, cytokines
which effector cells and vasoactive mediators are involved in pathogenesis of anaphylaxis (3 kinds)
- IgE: mast cells and basophils (histamine) (Bcells release IgE to bind to mast or basophils). Histamine, PAF and cytokines
- IgG: neutrophils, macrophages (needs more Ag-Ab) PAF and cytokines
- non-immunologic: mast cells and basophils, triggered by something other than Ig
which antigens are common in anaphylaxis in cats/dogs (5/10)
- insect and reptile venom
- radiocontrast agents
- transfusion products
pathology of anaphylaxis and how it leads to clinical signs
- vasodilatory and maldistributive shock
major organ systems affected by anaphylaxis
clinical signs of analphylaxis: skin
- generalized erythema, urticaria, pruritis, facial angioedema
- milder than humans, harder to ID due to fur and pigmented skin
clinical signs of analphylaxis: CV
- maldistributive shock
- increased vascular permeability (fluid extravasation, inappropriate vasodilation)
- altered CRT (slow/rapid)
- poor pulse quality
- depression to dull mentation
clinical signs of analphylaxis: resp
- dyspnea, tachypnea
- stridor, bronchospasm, cough
- pharyngeal edema, laryngeal edema, bronchoconstriction, excessive mucus production
clinical signs of analphylaxis: GI
- hypoperfusion, splanchnic congestion
- nausea, vomiting, diarrhea (hemorrhagic)
timeframe of anaphylaxis
- typically acute (5-30), rapidly progressive, but can be biphasic
- sometimes doesn't develop for several hours or could last up to 32h
how to diagnose anaphylaxis and biomarkers that help. Role of allergy testing in dx and mgmt
- hard to dx. Pattern recognition, hx, clincal signs.
- people have biomarkers, not useful in vet.
- "halo sign" around gallbladder on US and elevation of alanine transaminase
- allergy testing (IgE has short half life, so IgG?, or ID skin testing) within 4-6weeks.
Tx of choice in anaphylaxis, and supportive therapy, ancillary therapy
- tx: epinephrine! Not sure of optimal tx but this is big.
- supportive: ABC, stabilization HUGELY important. O2
- ancillary: antihistamines (cutaneous and nasal, not CV, GI, resp), glucocorticoids (for later or prevent biphasic, don't help with current, can CAUSE anaphylaxis), bronchodilators (albuterol, aminophylline)
Triage a P with suspected toxicity
- Primary survey: resp, cardio, perfusion, CNS
- Triage history
- IMMEDIATE triage to tx area for decontamination!
- tx goals: stabilize vital signs, clinical eval, prevent continued exposure, facilitate removal, administer antidote, provide supportive therapy
principles for preventing further exposure to a toxin. Topical, ocular, GI
- Topical: if wet, bathe. If dry, brush off
- Ocular: irrigate with water or saline (syringe into sclera!) for 20-30mins, examine for corneal damage, monitor for redness, lacrimation and pain, tx with ocular lubricant.
- GI: emesis (most effective), gastric lavage, activated charcoal (always first dose with cathartic at first to prevent it from detaching), cathartic
describe methods used to induce emesis in both dogs and cats
- emesis causes 40-60% of gastric emptying. Generally more effective than gastric lavage
- dogs: apomorphine, 3% H2O2
- cats: alpha-2 agonist (xylazine reversed with yohimbine, medetomidine reversed with atipamezole - 50-70%), 3% H2O2 and apomorphine (not usually effective)
List contraindications to inducing emesis in SA (6)
- >4-5h since ingested
- corrosive: alkaline, acids, hydrocarbons, petroleum
- unable to guard airway: abnormal neuro, resp distress, lar par/dysfunction, megaesophagus
- CV compromise: severe bradycardia, too - vomiting causes vagal response
- recent abdominal surgery: even a hernia may prevent adequate pressure
- already vomiting: get a history!
Describe how to perform a gastric lavage
- if can't induce emesis or planned intubation already
- consider risk of toxic vs risk of procedures: aspiration, soft tissue edema of esophagus or stomach
- Steps: intubate with inflated cuf
- premeasure from tip of nose to last rib
- lubricate and pass tube (with soft tip, not freshly cut). Use roll of tape or kong toy as speculum
- ensure correct placement (get gastric contents)
- instill water, lower free end and drain
- repeat until reflux is clear
MOA of activated charcoal - limitations, side effects and contraindications
- large surface area for adsorption
- Binding may be reversible - use a cathartic! Adsorbs many organic compounds (but not all)
- administer after emesis or gastric lavage. Give an emetic or wait an hour or two.
- effects: constipation/diarrhea (cathartic), black stool (stains!), hypernatremia or dehydration (pulls water into GI), elevated lactate (glycerol or propylene glycol)
- repeat if toxin undergoes enterohepatic recirculation (will re-tox when bile acids used again - need repeated doses of AC to adsorb. cholestyramine is a bile binder, may also help. Send home?)
Hasten a drug's eliminination
- IV Lipid Emulsion: lipid phase in aqueous portion of blood, preferentially pulls lipophilic drugs, keeps out of tissues. 1.5mL/kg IV for a min, then 0.25mL/kg/min for 30-60
- Urinary: fluid diuresis (2-3x maintenance), bladder catheterization to drain (prevents resorption)
Emergency database of suspected toxicity patient and why
- MDB: QATs, acid/base, electrolytes, maybe lactate, coag, UA
mechanism of toxicity, generations, effects, dx, tx, antidote for anticoagulant rodenticide
- MOA: inhibits vitamin K epoxide reductase, which is necessary for activation of vit K. (coags 2, 7, 9, 10). Prevent recycling. Lag time of 48-72h before depletion.
- Extrinsic prolongs first (VII shortest half life) but by the time you see them, it's both.
- 1st gen - warfarin, not used
- 2nd gen - tx 4-6wks. Bromodialone, brodifacoum
- Indandiones - tx 4-6wks. Chlorophicinone, diphacinone.
- effects: lethargy, anorexia, weakness to collapse, anemia, hypoproteinemia, thrombocytopenia due to hemorrhage. Bleed into body cavities, hematomas, fascial planes or muscle bellies. Resp common.
- test: PT and aPTT. Can test with PIVKA or find rodenticide in blood/serum or liver.
- tx for ACUTE ingestion: decontaminate with emesis and AC if <6h, check PT in 2d and vit K PRN. >6h = vit K PO 4-6wks, maybe AC, check PT 2d after last dose and prolong PRN.
- tx for CLINICAL: IVF, O2, FROZEN PLASMA (V and VIII not there), pRBC if needed, thoracocentesis just until comfortable, Vit K x 4wks, recheck 2s post-therapy. 24h before Vit K works, so plasma may be given even if stable.
- antidote: vitamin K1
antidote for acetaminophen
- antidote: pamidronate, calcitonin
- rodenticide that has something to do with Ca regulation.
dose, mechanism of toxicity, signs/effects, therapy and px for bromethalin
- 0.1mg/kg, cats worse than dogs
- MOA: uncouples oxidative phosphorylation (decreased ATP, failure of Na/K/ATPase, cells can't maintain osmotic control and swell.
- signs: worst in CNS due to cerebral and SC edema and increased CSF pressure
- rapidly absorbed (4-36h), N-demethylation in liver, biliary excretion, enterohepatic recirculation.
- effects: paralytic or convulsant. Cats always paralytic.
- tx for acute: decontaminate!! mannitol, sz control, nutrition, nursing care
- px: signs resolve in several weeks-months if mild. More serious have grave px.
mechanism of toxicity, antidote, therapy and px for NSAID
- MOA: prevent PG production, cause gastric irritation and ulceration, decreased renal perfusion, platelet dysfunction
- signs: anorexia, vomiting, abdominal pain, melena, peritonitis (perf), azotemia
- tx: <4-5h, emesis/gastric lavage, AC (first iwth cathartic). >5-6h, AC but no emesis. Antiemetics, antacids, cytoprotective (misoprostal, sucralfate), renal (diuresis, watch), hepatic (N-acetylcysteine, SAMe, silymarin)
antidote for Ethylene glycol
antidote: 4-methypyrazole, ethanol
mechanism of toxicity, therapy and px for chocolate
- MOA: methylxanthines - theobromine and caffeine. Varies between type of chocolate, even crop, individuals.
- signs: v/d, polydipsea, cardiotoxic, sz with increasing dose. Up to 72h
- tx: emesis, AC with cathartic. Methocarbamol for tremors, anti-sz, B-blocker for tachyarrhythmias, lido for ventricular arrhythmias, fluid diuresis, walk frequently or UA catheter, monitor
therapy for permethrin
- tx: methocarbamol for tremors, supportive
dx, therapy and px for marijuana
- dx: signs and client Hx (urine tests don't work). There are better tests but take too long, no point.
- tx: decontaminate before clinical, but CNS so once clinical no emesis or AC. IV lipid emulsion, supportive care (even ventilation, can be cost-prohibitive).
- Px: good.
therapy for tremorgenic mycotoxins
tx: methocarbamol for tremors, supportive
mechanism of toxicity, therapy and px for xylitol
- just dogs, not cats?
- MOA: recognize xylitol as glc, huge release of insulin. Collapse, weakness, sz. Can happen in minutes to 12-18h PI.
- Also hepatic insufficiency or failure, not sure why. enzymes in 8-12h, signs in 24-48h.
- RAPIDLY absorbed
- tx: Emesis and AC are not helpful (emetic if REALLY early). >75mg/kg can cause hypoglycemia, hospitalize with glc. Higher doses monitor for LIVER, check q3d. Hepatoprotectants (N-acetylcystein, SAMe, silymarin, Tx coag etc PRN).
- Px: if liver failure, poor. But hypoglycemia or mild liver enzymes are good.
mechanism of toxicity, therapy and px for grapes and raisins
- MOA unknown, dogs only, causes tubular necrosis and renal failure.
- tx: emesis, AC, fluid diuresis, resp watch, monitor renal panel.
- Px: excellent if tx before failure. Grave after failure
mechanism of toxicity, therapy and px for lillies
- entire plant toxic (lillium and hemerocallis - peace lillies okay, lily of the valley is cardiotoxic), MOA unknown. Renal tubular epithelium
- signs: acute kidney injury (tubular necrosis). Cats only.
- azotemia - signs related to this. Chem, CBC, UA.
- tx: emesis, AC (ONE dose). Fluid diuresis, resp watch, monitor renal panel.
- Px: excellent if fluid diuresis started before renal failure. Grave once renal failure.
things you need to know when you suspect a toxic dose
- weight of animal in kg
- total amount missing
- percentage of toxin in substance
- toxic dose reported
- if in multiple pets, assume the SMALLEST consumed ALL the toxin
three components of Virchow's triad and be able to give examples of disease processes that affect each of these components
- Flow stasis from impaired circulation: vascular anomalies, cardiomyopathy, hyperviscosity, hypovolemia, neoplasia (reduced velocity = congestion)
- Endothelial damage from systemic inflammation: anaphylaxis, pancreatitis, heat stroke, sepsis (activated by inflammatory cytokines, release vWF)
- hypercoagulable state from hemostatic imbalance: IMHA, PLN/PLE, neoplasia, pancreatitis, cardiomyopathy, hepatobiliary disease (activated coags or reduced anticoags, thrombocytosis, platelet activation, reduced fibrinolysis) (microparticles shed from WBC, RBC, platelets, endothelial, etc., express PS)
- any one alone is probably not enough
Four proposed steps to enable dx of thrombosis, and give examples of tests and methods for each step
- ID risk factors: signalment/Hx/PE/CBC/Chem for underlying (DM, IMHA, etc)
- hemostasis testing: shortened PT/aPTT, D-Dimers, evidence of consumption (thombocytopenia, reduced fibrinogen). NOT PFA-100 or flow cytometry. Maybe thrombin generation or OHP assay.
- quantify consequences of thrombosis: CNS (altered), resp (tachy, low PaO2, SaO2, PaO2/FiO2), hepatic (jaundice, high enzymes, low albumin, high Pt), CV (tachycardia, hypotension, etc), Renal, Coag etc.
- definitive thrombus imaging: thrombus visible on US, can use contrast and see contrast in some vessels and none in others
pros and cons of thrombolysis
- converts plasminogen to plasmin. Fibrin-specific
- cons: risk of hemorrhage and ischemia reperfusion injury (esp cats in aortic thrombi - washes out scary nastiness into circulation). Maybe breaking up clot could embolise into other parts. MUST catch early - more risk and less benefit the longer you wait.
difference between fibrin-rich and platelet-rich thrombi
- fibrin-rich is low shear for venous clots
- platelet-rich is high shear for arterial
Four classes of antithrombotic drugs
- parenteral anticoagulants: potentiate antithrombin (unfrac. or low molecular weight heparin) or directly inhibit thrombin.
- oral anticoagulants: direct Xa inhibitors or direct thrombin inhibitors. Not VKOR (warfarin) - the rest are safer and just as effective
- parenteral antiplatelet agents:
- oral antiplatelet agents: COX inhibition, PDEi/Adenosine Ri, P2Y12 receptor antagonists, aspirin, clopidogrel
diaphragmatic hernia in LA
- colic and dyspnea
- acquired from blunt trauma
- rads, US, thoracocentesis
- tx: primary closure via midline ceiliotomy, rib resection, thoracoscopy or laparaoscopy
3 types of pneumothorax in LA
- open: open chest wound. Air enters pleural space during inspiration
- closed: lung laceration. Air enters pleural space from lung
- tension: worst. Chest wound becomes one-way valve that lets air in but not out, causes severe tension in pleural space. severe hypoxemia, air rushes out when cannula goes in.
- Usu bilateral in horses (fenestrated mediastinum unless inflamed), but 50:50. Unilateral usu pleuropneumonia (px worse), but bilateral can be fatal.
- cause: pleuropneumonia, open thoracic wounds, closed thoracic trauma, sx of resp tract.
Treatment of thoracic trauma in horses
- PATIENT STABILIZATION: REMOVE PLEURAL AIR - convert tension pneumothorax to open, then close or bandage. Prevent tension, control hemorrhage, fluids, blood, abx, O2
- Conservative mgmt: keep stable and prevent tension pneumo. This may be it for simple rib fractures or wounds without severe lung lacerations continued hemorrhage, deep penetration and abdominal cavity.
- sx exploration: not required for all. Deep penetrating wounds, lung lacerations, complicated rib fractures (flail chest), GA with + pressure ventilation. Round rib pieces, warm saline detects bronchiole damage - warm saline to find and close. Splint for flail. Remove air from pleural cavity, place drains, close.
Emergency thoracocentesis in horses
- teat cannula or catheter
- high in 12-15th intercostal space
- extension set + 3-way stopcock
- 60mL syringe or suction pump
importance of endotoxemia in LA
- 10-40% of colicky horses, 50% of septic neonatal foals.
- life-threatening sequelae: CV, coag, laminitis, kidney, liver, repro
- mortality strongly associated with degree of endotox
Most common reasons for LA endotoxemia (6)
- intestinal damage (lots of endotox in LI. Damaged barrier like strangulation, enteritis, colitis)
- foal sepsis
- septic peritonitis
clinical picture of LA endotoxemia
- Early HYPERDYNAMIC response: increase HR, RR, fever, red mm, increased CO, decreased SVR, hyeprmetaboism
- late HYPODYNAMIC response: hypovolemia (pooling decreases preload), myocardial depression (decreased BP, cold extremities), peripheral vascular constriction/sludging, pale or cyanotic membranes, anuria, tissue hypoxia, V/Q mismatch, mental confusion
- massive dysregulated, inflammatory response to endotoxin.
- CV: early vasoconstriction, develops into vasodilation, hemodynamic shock
- pulmonary hypertension and hypoxia: tachypnea, resp distress
- vascular permeability: neutrophil activation (leukopenia)
- GI: hypoperfusion of SI, decreased intestinal motility, decreased gastric acid, diarrhea
- lab: increased PCV, lactate, increased PAI (inhibits fibrinolysis), leukopenia, hyperglycemia.
most sensitive species to endotoxemia
- humans and horses
- pulmonary intravascular macrophages of some domestic animals (horses, cattle) may become pro-inflammatory. Equine platelet activation.
Systemic Inflammatory Response System in LA - criteria for dx
- 1. hypothermia, hyperthermia
- 2. tachycardia, tachypnea, hypocapnea
- 3. leukocytosis, leukopenia, increased number (>10%) of immature leukocyte forms
- 4. evidence of sepsis in foals
- 2 required for dx!
Pathophys of endotoxemia in LA
where it comes from
- path: LPS induces excessive inflammation, proinflammatory mediators (PGs, histamine, serotonin, kinins, PAF)
- location: endotoxin liberated from cell wall of G-bacteria (from cell death or rapid proliferation).
- components: LPS = O-polysaccharide, core-oligosaccharide, Lipid A (anchors LPS into membrane)
- LPS defense mech: mucosal epithelial cells (barrier), lysozymes/enzymes/abx, resident bacteria, kupffer cells (hepatic macrophages), antiendotoxin abs
therapy for LA endotoxemia
- address multiple levels: complex inflammatory response with feedback loops and cytokine redundancy (one site not enough!)
- monitor: Perfusion, O2 most important. Organ function, sepsis containment/inflammation, electrolytes/acid base, meatbolism/nutrition, complications
Goals of therapy for LA endotoxemia (4)
- eliminate LPS source: treat underlying disease, remove damaged tissues
- supportive care: fluids (to combat hemodynamic effects of LPS) - crystalloids, colloids, hypertonic saline. Abx, prevent laminitis
- prevent LPS binding and reduce inflammation: Polymixin B, NSAIDs, DMSO and pentoxifylline, lidocaine and ketamine
- future directions: hemofiltration, detergents and phospholipid emulstion, LPS pathway or cytokine antibodies
Eliminate LPS source in LA endotoxemia, reduce translocation
- find primary site and remove infected tissues!
- Abx (ID organism).
- Reduce endotoxin translocation with lidocaine (prokinetic, anti-inflammatory, anti-ischemic, negates flunixin adverse), bismuth subsalicylate, AC/biosponge,
- Misoprostal (mucosal barrier, improves blood flow), glutamine/acetylcysteine (mucosal integrity)
Supportive care in LA endotoxemia
Fluids, coags, anticoags, pressors, LPS scavengers, endotoxin binders, NSAIDs, steroids, antioxidants
- crystalloids: for shock, hypertonic saline! then crystalloids.
- 20L bolus vs 10-20ml/kg/hr (=5-10L/hr) or 10mg/kg bolus every 30min until normal values (>65MAP, 7-12CVP)
- colloids: sustained blood volume expansion. Hetastartch or pentastarch or tetrastarch (vWf with high dose - 10mg/kg/day)
- hyperimmune plasma: fresh frozen, antiendotoxin (abs against LPS, replenish coags), anticoag (protein C and S, ATIII, heparin to prime)
- unfractionated heparin: decrease coag, but watch for increased bleeding, anemia, thrombocytopenia
- low molecular weight heparin: dalteprin
- Clopidogrel: plavix, reduce platelet activation by binding ADP receptor
- Vasopressors: for P with inadequate tissue perfusion after restoration of circulatory volume.
- LPS scavenger: antiendotoxin abx (plasma, serum, hyperimmune plasma, vax)
- endotoxin binding drugs: polymixin B (nephrotoxic!)
- NSAIDs: bute blocks LPS increase in GI blood flow, ketoprofen (blocks leukotriene pathway). FLunixin best
- steroids: decrease cytokines and ROS
- antioxidants: DMSO
- new, future: phospholipid emulsions to bind, tyloxapol to remove from circu, ketamine, omega-3, hemofiltration
Flunixin in LA endotoxin
- improves clinical signs, increases survival
- improves BP/tissue perfusion
- Reduces cytokine release and free radical scavenging
- prevents hypoxemia, lactic acidosis
- reduces endothelial damage
future directions in LA endotoxemia
- hemofiltration: dialysis to pulll out cyokines. Didn't help in horses. POlymixin B filter?
- detergents and phospholipid emulsion: binds and neutralizes endotoxin (hemolysis?). Tyloxapol (like a bile acid)
- LPS pathway or cytokine antibodies: ?
four types of hypersensitivity rxns, examples and Ig involved in LA
- adaptive immune system - protective and pathologic
- allergy (immediate): anaphylaxis, atopy. IgE
- cytotoxic (Ab dependent): AIHA, M. gravis. IgM/IgG
- immune complex: serum sickness, rheumatoid A. IgG
- delayed hypersensitivity (cell-mediated): contact dermatitis like poison ivy. T cells
anaphylaxis in LA
- most severe systemic allergic rxn
- type I hypersensitivity rxn (IgE), seconds to minutes, faster is more severe.
- Mild, moderate or severe
- increased secretions from mm, increased bronchial smooth muscle tone, decreased vascular smooth muscle tone, increased vascular permeability, urticaria, erythema, pruritis
- caused by foods, drugs, latex, venoms, vaccines
anaphylactoid reaction (anaphylactic-like) in LA
- not immune - no IgE involved. May happen on first exposure. Direct effect on mast and basophils.
- Effects, signs, tx are the SAME as anaphylaxis.
causes of non-IgE-mediated anaphylaxis (5)
- exercise-induced (exercise dependent food allergy)
- IV contrast materials
- beta blockers
3 timings of anaphylaxis
- uniphasic: most common, resolution of signs within hours
- biphasic: second phase occurs in 1-8h (24h) after asymptomatic period. Only in 20% of cases but 1/3 are more severe than initial. Occasionally fatal. More common in humans, SA
- Protracted: profound hypotension that may last beyond 24h.
shock organs of the horse (2)
- resp tract, GI tract
- systemic anaphylaxis has clinical signs relating to these organs Watch for dyspnea, hypotension.
clinical signs of LA anaphylaxis (6)
- airway obstruction: angioedema, nasal congestion, laryngeal edema, pulm edema, bronchoconstriction, dyspnea, cyanosis
- cardiac collapse: tachycardia (brady in severe), cardiac arrhythmia, hypotension (vasogenic shock), myocardial ischemia (hypoxia and hypotension)
- angioedema, uritcaria, erythema, pruritus
- sz (rare), shock and death
ddx of anaphylaxis in LA (7)
- vasovagal reaction: following painful, pallor and hypotension, bradycardia leading to poor perfusion, nausea, diaphoresis, syncope, absense of uritcaria/pruritis, angioedema, bronchospasm, tachycardia. Improve in 20-30mins without tx
- myocardial infarct
- severe asthma
- FB aspiration
- pulmonary embolism
Tx of anaphylaxis in LA (4)
immediate, refractory hypotension, adjunctive, or if on beta blockers or ACE inhibitors
- immediate: ABC - intubate or maks, tracheotomy. Epi for breathing and circulation. O2, IV fluids, bronchodilators.
- refractory hypotension: repeated epi, dopamine.
- adjunctive: steroids to prevent 2nd phase, antihistamines, observation for 24-48 for biphasic
- If on beta blockers or ACE inhibitors: need higher doses of epi, glucagon, dopamine, isoproterenol
dx of LA anaphylaxis
- based on hx/clinical signs - sudden resp distress, hypotension, urticaria and collapse.
- Rule of twos: begin from 2mins to 2h following injection, infusion, ingestion, contact or inhalation
most common "drugs" that cause anaphylaxis in horses (9) and how to prevent a reaction if we need to use them
- whole blood
- vaccines (chronic laminitis, ERU)
- ceftiofur (rare)
- iron and copper products
- B vitamins
- insect bites
NSAID or antihistamine pre-tx
routes for epi administration in LA anaphylaxis (4)
Prevention of anaphylaxis in LA: desensitization
- injection of allergen in increasing amounts, SQ
- very small risk of anaphylaxis (but there is a risk)
- induces IgG response instead of IgE
summary of LA anaphylaxis ER Tx (6)
- rapidly assess ABC
- secure airway, check HR, RR, BP
- tracheotomy for resp distress
- administer epinephrine (1:1000 = 1mg/mL)
- administer oxygen
- administer IV fluids
human criteria for anaphylaxis
- acute onset illness - involvement of skin or mucosa together with RESP DISTRESS or HYPOTENSION
- two or more of following occuring rapidly after exposure to likely antigen - skin/mucosa involvement, resp distress/hypotension, persistent GI symptoms
- reduced BP after exposure to known allergen
LA anaphylaxis testing (4)
- serum tryptase: mast cell tryptase in serum or plasma, released in anaphylaxis or anaphylactoid. Increased after rx, peak in 1h. Confirms dx.
- urine methylhistamine: measured in urine, 2nd sample after rxn
- specific IgE
- skin tests
appropriate choices for red, yellow and green CPR codes
- Red: progressive irreversible underlying disease, reluctance to pursue aggressive treatment or financial concerns.
- yellow: <10kg dogs or cats and keel-chested larger dogs.
- green: pleural space disease, pericardial disease, already in surgery, or giant-breed with round chest.
good chest compressions generate __________ of normal stroke volume
cardiac pump theory
- ventricles are compressed between ribs during CPR compressions (or sternum to spine)
- pressure and elastic recoil causes the valves to open at the right times
- forward flow of blood accomplished by direct compression of the heart (small dogs/cats and keel-chested dogs), so compressions right over heart.
- not good for older, large, obese, pleural space, etc - too stiff
thoracic pump theory
- external chest compressions raise overall intrathoracic pressure and push blood from aorta into circulation. Valves don't close, and elastic recoil pulls blood through circulation.
- Aorta is compressed, casing vasoconstriction and forward flow. Veins are collapsed, preventing backflow.
- Compress over widest part of chest.
- larger dogs with round chests, obese dogs and pleural space disease etc.
Chest compression details
- 1/3-1/2 the width of chest
- 100-120 compressions per minute
- takes a minute for aortic BP to reach a steady state to provide perfusion to heart and tissues
- If you're alone, 30 compressions then 2 breaths
non-shockable arrest rhythms
- Pulseless electrical activity (PEA): <200/min, coordinated and repeated, but no pulse. Often <50/min and narrow QRS
- Asystole: flat line. Make sure your compressions are causing waves, or ECG just may not be attached
Shockable arrest rhythms
- Pulseless VT: organized, repeated, wide QRS complexes at >200/min without pulses. RATE separates this from PEA
- VFib: wavy chaotic line - lack of consistent repeated waveforms.
ETCO2 in CPR
- amount of CO2 in inhaled air at end of breath.
- determined by minute ventilation and blood returning from tissues to the lungs.
- Can be used to monitor quality of chest compressions (NOT PvCO2) (should be >15, make sure breathing is 10 breaths/min)
- Sudden increase to >30 = return of spontaneous circulation. Palpate for pulse and look for signs of consciousness
IO catheters: location, equipment
- sites: humerus, femur, tibia. Humerus gets things to heart the fastest
- equipment: adults need bone marrow needle or needle with stylet. Puppies and kittens could use an 18-20g needle, or spinal needle with stylet. There are drills, too.
IT drug administration: drugs, how to dose/deliver.
- epinephrine, atropine and vasopressin
- NEVER sodium bicarb
- STOPGAP - re-dose IV once you have access
- 2-10x the normal dose, diluted with 5-10ml of sterile water or saline
- feed a long catheter through the ET tube, administer, then pulse air to blow fluid out. Give 2 rapid breaths.
Fluids in CPR
Huge benefit to giving fluids in hypovolemic. Don't give to euvolemic - decreases preload (increases pressure in tissue bed by pooling in veins)
- for pleural space disease, pericardial effusion, P under anesthesia for thoracic or abdominal surgery and giant breeds with round chests
- lateral thoracotomy between 4th and 5th ribs on left side of chest where elbow reaches. Try to avoid internal thoracic, 1/3 of the way up the chest.
- Rib spreaders
- remove pericardium, don't cut the phrenic
- compress from ventral to dorsal (apex to base)
- 100 compressions/min
- leave chest open for 10-15 mins following ROSC to ensure it continues.
- Flush chest copiously and close. Abx and thoracostomy tube
Treatment for VF and Pulseless VT
- Shockable rhythms
- make sure you can't palpate a pulse (and that the animal is collapsed and unresponsive).
- aka accelerated idioventricular rhythm (AIVR)
- ventricular arrhythmia that generates blood flow sufficient for O2 delivery to tissues of body (= normal BP)
- <180 bpm, often alternates with sinus rhythm, possible R on T.
- May not need tx, but myocardial ischemia or injury and possible decompensation into unstable.
- generating insufficient blood flow, causes arterial hypotension (MAP <80)
- usu >180 bpm
- may include R on T ("sine wave")
- may be due to systemic disease or CV disease, causes myocardial ischemia
- tx with antiarrhythmic drugs: lidocaine, amiodarone, procainamide
perfusing VT in cats
- from severe systemic or cardiac disease
- careful -- similar signs to hyperkalemia
epinephrine in CPR
- alpha-1, beta-1, beta-. Positive inotrope and chronotrope
- low-dose: 0.01mg/kg IV (= 0.1mL/10kg), first-choice vasopressor in non-shockable (PEA, Asystole) and in PROLONGED VF/pulseless VT
- high-dose: 0.1mg/kg (= 1mL/10kg), used after 10min. Higher rate of ROSC but significant effects like neuro and reduced discharge rates (extreme vasoconstriction = acidosis and increase myocardial oxygen demand). Last ditch in asystole/PEA due to acidosis from prolonged CVA (alpha-1 more responsive to catecholamines at 7.40)
- affected by pH, doesn't work in acidosis
- administer every 2 cycles of BLS (3-5min) in catheter CLOSEST TO HEART
vasopressin in CPR
- stimulates V2 receptors in renal collecting ducts (water balance) and is a vasopressor
- 0.8 U/kg IV/IO
- used as an alternative to epi during CPR
- for non-shockable (PEA, asystole) and PROLONGED VF/Pulseless VT
- not affected by pH like epi so better for acidotic cases
- administer every 2 cycles of BLS (3-5min) in catheter CLOSEST TO HEART
parasympatholytics in CPR
- useful in cardiac arrest caused by high vagal tone, which can be caused by severe GI (v/d), coughing/resp, ophtho sx, laryngeal manipulation (intubation), or opioids. bradycardia or pronounced sinus arrhythmia.
- Atropine most common. Glycopyrrolate is less potent and longer lasting.
- IV atropine will start with paradoxical slowing of HR, then overwhelm vagal and increase HR.
- 0.04mg/kg every 2 cycles or 3-5min, IV/IO/IT into catheter CLOSEST TO HEART
- also causes pupils to dilate and block PLR.
consequences of prolonged CPA (4)
- prolonged asystole and PEA have grave px if not tx - metabolic derangements
- acidosis: from lactate can cause pH <7.0, which limits effects of catecholamines
- hyperkalemia: due to acidosis and ischemia, increasing cardiac dysfunction (tx with CaGlc in >7.5)
- hypocalcemia: common, causes cardiac and vascular tone issues (tx iCa <0.9)
- myocardial ischemia and necrosis: can develop, cause arrhythmias that make the heart resistant to defibrillation
bicarbonate therapy in CPR
- when blood gas shows pH <7.0 (prolonged CPA)
- Can cause increased serum osmolarity, alkalemia and paradoxical cerebral and metabolic acidosis
- used to maximize effect of epinephrine and prevent systemic vasodilation, enzyme issues.
- but too much can cause alkaline pH and cause post-CPR cerebral depression (difference between CNS and arterial pH)
- 1mg/kg IV/IO
differentiating pulseless VT from perfusing VT (2)
- palpating a pulse!
- pulseless VT should be collapsed and unresponsive, perfusing VT will be conscious (if weak or pale)
categories of perfusing VT (2) and what to do with them (and what they mean)
- stable VT: accelerated idioventricular rhythm. Sufficient blood flow generated, normal BP. HR <180, often alternates with sinus rhythm. Often no need to treat but may degenerate into unstable VT
- unstable VT: insufficient blood flow, arterial hypotension (<80), usu >180. R on T (sine wave). Can be systemic or cardiac. Treat with drugs.
- both indicate underlying ventricular myocardial ischemia or disease, so SA node is not driving. Usually due to systemic disease, but can be cardiac
- stable often needs no therapy. Unstable should be treated with drugs to improve perfusion
treatment of unstable or rapid stable VT (3)
- lidocaine: 2mg/kg slow IV over 1-2min, up to 3 times
- amiodarone: 0.5mg/kg, diluted 1:10 with D5W slow IV over 1-2min, can cause allergic rxn.
- procainamide: 2-6mg/kg slow IV over 1-2min
- all slow the rate of ventricular myocardial cells
goal of defibrillation and types (3, 2)
- depolarize as many myocardial cells as possible to send them into refractory period and let SA node take back over. Most effective tx for V-fib and pulseless VT
- Electrical: electric shock via paddles or adhesive patches externally or internal paddles directly on ventricles.
- mechanical: precordial thump. MINIMAL effect, only if you don't have an option.
- chemical: ACh/KCl, bretylium tosylate, lidocaine and Mg. Experimental but not successful in real life. Reduce efficiency of electrical defibrillation. Not recommended.
- monophasic: unidirectional current
- biphasic: bidirectional current, preferred.
- use appropriate dosing chart for charge!
when to defibrillate
- usu ASAP, but wait 1 cycle of BLS if arrest was unwitnessed (in circulatory or metabolic phase of CPA). An ischemic heart with no ATP is unlikely to ROSC and shock will cause more injury.
- If in electrical phase (witnessed arrest), BLS until charged and go
- THEN RESUME BLS. Check at end of next BLS cycle unless ETCO2 jumps or pulse is palpated.
- at end of next cycle, if still in VF or pulseless VT, increase defibrillator dose by 50% and tyr again. Max dose 10 J/kg.
- repeat until ROSC, conversion to non-shockable rhythm or CPR abandoned.
Phases of CPA (and ischemia etc) (3)
- electrical phase: in first 4 min after onset of CPA. ATP stores are still enough to sustain, minimal ischemic damage.
- Circulatory phase: next 6 mins (up to 10min after CPA onset) reversible ischemic injury due to ATP depletion.
- metabolic phase: after 10mins without perfusion, potentially irreversible ischemic injury.
tx for prolonged VF or pulseless VT
- prolonged if >10min
- antiarrhythmics: amiodarone (best) and lidocaine
- Vasopressors: ONLY in prolonged - constriction increases afterload which may decrease CO (so make make arrhythmia worse). Vasopressin best (no Beta-1), low-dose epi if you have to.
Amiodarone in CPR
- class III antiarrhythmic agent
- prolongs repolarization
- beta blockade
- potassium channel blocking in SA and AV nodes (slows).
- for stable VT, prolonged VF/pulseless VT (with defibrillation)
- IV/IO 5mg/kg over 1-2mins. Dilute with D5W. NOT IT.
- anaphylactic - give diphenhydramine
Lidocaine in CPR
- for tx of stable VT, prolonged VF/pulseless VT (with defibrillation). In unstable, increases fibrillation threshold to prevent deterioration.
- 1B antiarrhythmic, blocks fast Na channels in myocardium to shorten action potential and slow rate.
- makes higher energy needed in monophasic defibrillator. NOT in biphasic.
- sudden fall in ETCO2: airway leak, ventilator malfunction or IPPV - cardiac arrest
- decreased ETCO2: hyperventilation, Hypothermia, IPPV - reduced CO
- Increase in ETCO2: hypoventilation, increased metabolism (fever), IPPV - increased CO
- rise in both baseline and ETCO2 - rebreathing of CO2 gas
- indications: blunt trauma, penetrating injuries with possible perforation, shock with no obvious cause, or suspicion of post-op leakage of sx site.
- Blind is easy but many false negatives
- single just lat to umbilicus vs in 4 quadrants, or US guided.
Diagnostic peritoneal lavage
- indications: acute abdominal pain and unexplained fever with negative 4-quadrant abdominocentesis
- WILL DILUTE CELLS AND CHEM
- clip and prep, local, incision, catheter (peritoneal with J wire vs reg 14-18g with holes cut in it). Add 22mg/kg of warm saline, rock then gravity or aspirate back out
- indications: diminished cardioresp sounds, tachypnea with shallow chest wall excursions, rad evidence of pneumothorax or pleural effusion.
- butterfly vs needle with extension set, + 3-way stopcock and syringe. Sternal or standing. Usu don't need analgesia or sedation.
- 6-8 intercostal near costochondral (or top 1/3 for air, bottom for fluid). Poke cranial to rib. Aspirate while advancing to stop immediately. Put needle against wall with bevel inward. US helps. Catheters tend to kink.
tracheostomy tube placement
- indications: upper airway obstruction, trauma, laryngeal or pharyngeal collapse, long-term PPV
- clip mandible to Thoracic inlet.
- incision on ventral midline, blunt dissection to trachea. Visualize neurovascular bundles then get a hemostat under to elevate.
- incise transverse between 4-5 or 5-6, NOT MORE THAN 50%
- incise longitudinal through rings 3-6
- Insert tube.
- Stay sutures on each side, LABEL
- umbilical tape and wrap
thoracostomy tube (3 kinds)
- indications: ongoing accumulation of air or fluid causes resp distress, or for thoracic lavage, or post-op.
- Usually GA. Lateral
- Argyle trocar: incision at 10th or 11th space, pull forward to 7th (SQ tunnel). Measure tube, hold the bottom and tap the top in, remove stylet and slide in, purse string, finger trap (aspirate and clamp).
- red-rubber: with hemostat. Incision at 10, pull to 7, push in with hemostat, let skin return for SQ tunnel. Purse string and finger trap.
- Mila fenestrated chest tube: no need to pull skin. Cather, J wire, remove catheter, chest tube, remove wire. Suture wings.
Open-chest CPR process
- large or obese patients, pleuroal effusion, pneumothorax, pericardial tampanade, penetrating thoracic injuries, rib fractures like flail, diaphragmatic hernia (where closed chest fails).
- R lat, incision at 5th to intercostals, stab with blunt scissors (at exhale!), extend until you can reach in. Rib spreaders. Careful of phrenic! Incise pericardium
- Squeeze apex to base. Don't twist!
- Could occlude descending aorta to maximize cerebral blood flow
physio causes of metabolic acidosis (1.4 and 1.2) and alkalosis (2), and lab changes differentiate
- metabolic acidosis due to increased acid: low bicarb and increased anion gap. Lactic, uremic (sulfate and phosphate), ketones/DKA or exogenous (ethylene glycol)
- metabolic acidosis due to lost bicarb: small bowel diarrhea vs renal tubular acidosis (no azotemia), normal anion gap.
- metabolic alkalosis: iatrogenic (sodium bicarb vs furosemide = loss of Cl for bicarb) or upper GI obstruction/vomiting (loss of H+ and Cl and H2O, retain Na but no Cl, so waste K+ and H+ and keep bicarb. Paradoxic aciduria with hypochloremia, hypokalemia)