Acute Care Flashcards
What parameters can be adjusted to improve oxygenation
- FiO2
- PEEP
What parameters can be adjusted to improve ventilation
- minute ventilation (RR)
- tidal volume
Defn spinal shock vs neurogenic shock
spinal shock: loss of muscle tone and reflexes immediately after spinal cord injury; muscles can’t help constrict blood vessels (think about the flaccid part of UMN injury before they become hypertonic) (also its not really a type of shock - think of like spinal cord concussion)
neurogenic shock: must occur T6 and higher, loss of vasomotor tone due to loss of sympathetic innervation to the heart resulting in hypotension and bradycardia (UNABLE to mount tachycardia response). NOT reversed with fluid alone
What is a brown sequard lesion
- Hemi-transection of cord - injury on one side
- Often penetrating trauma
- Ipsilateral motor and position sense loss
-
Contralateral loss of pain & temperature 1-2 levels below injury site
-Can be associated with Horner’s syndrome if above T2 (ptosis, anhidrosis, miosis)
What is a chance fracture
- thoracic spinal fracture
- often from MVC inappropriately worn lap belt with forward flexion motion
- requires internal fixation (unstable fracture)
- often other internal organ injuries
Acute management of splenic sequestration in SCD
fluid resus for hypotension
blood to stop the sequestration - small 5ml/kg transfusions of RBCs and/or post-transfusion target of 80
avoid post transfusion hgb of 100 (risk hyperviscosity syndrome)
DDX wheezing in young children (CPS)
Infectious:
- bronchiolitis
- pneumonia
Inflammatiory:
- asthma
- allergic reaction
- cystic fibrosis
Structural:
- laryngotracheomalacia
- foreign body aspiration
- GERD
- TEF
- Vascular Ring
- Mediastinal Mass
Cardiac:
- CHF
consider alternate ddx if severe resp distress, no viral URTI dynptoms, and/or frequent recurrences
Diagnostic studies in suspected bronchiolitis ( CPS)
tests often unhelpful! no evidence to support diagnostic testing in typical cases of bronchiolitis
- CXR: non specific, patchy hyperinflation and areas of atelectasis, often misinterpreted as consolidation with increased innappropriate use of abx. consider cxr if diagnosis of bronchiolitis is unclear, rate of improvement is not as expected, or severity raises concern of bacterial pna
- NPA: dont alter management, not routinely recommended unless for infection control patients or in high risk patients (ex. if it will impact performing additional tests, hospitalization, or using tamiflu for influenza)
- CBC: not useful in predicting SBI
- Bacterial cx: incidence of SBI in febrile infants with bronchiolitis is low, UTI is the most likely SBI in infant with bronchiolitis but is still low. don’t routinely screen for SBI (urine or blood) in patients with bronchilitis
- blood gas: only if concerned about potential respiratory failure
Risk factors for higher risk severe bronchiolitis (CPS)
prematurity <35 weeks
<3 mo of age at presentation
hemodynamically significant cardiopulmonary disease
immunodeficiency
Phases of iron toxicity
Phases (5)
1. GI Phase (30min-6hr post)
- Abdo pain, vx/dx, melena
2. Latent Phase (6hr- 24hr)
3. Shock/Metabolic acidosis (6-72hr)
4. Hepatoxcity/hepatic necrosis (12-96hr)
5. Bowel obstruction (2-8wks)
- Strictures/scarring
Antidote for Iron toxicity
Deferoxamine (specific chelator of iron) is the antidote for moderate to severe iron intoxication.
○ Indications: serum iron concentration >500 μg/dL or moderate to severe symptoms of toxicity (e.g., acidosis)
○ Preferably given by continuous IV infusion at 15 mg/kg/hr.
○ S/E: Hypotension → managed by slowing rate of infusion, fluids, vasopressors
○ If >24H of deferoxamine → ARDS and Yersinia sepsis
○ Discontinue when clinical symptoms and acidosis resolve.
Hyperkalemia management
Stop all administration of potassium containing drugs/fluid
If K > 6.5, get an ECG
If ECG changes - goals to stabilize heart to prevent arrhythmia and to reduce K+
1. Calcium Gluconate (60mg/kg) IV over a few minutes (give slowly over 30 minutes if patient is on digitalis) (stabilizes cell membrane, works within a few minutes)
2. Bicarbonate (shifts K+ intracellularly, effective in patients with metabolic acidosis)
3. Insulin plus Glucose (shifts K+ intracellularly, works within 30 min)
4. Nebulized albuterol (ventolin) (stimulates B1 adrenergic receptors to shift K+ intracellularly, rapid)
5. Lasix (loop diuretic) (heps remove K+ from the body)
6. Kayexalate (Sodium polystyrene sulfonate) exchange resin to poop out K+
Hyperkalemia ECG changes
peaked T waves → prolonged PR interval → prolonged QRS → arrhythmia
Differentiating serotonin syndrome and NMS
both have same effect on vitals (high everything)
NMS:
- lead pipe rigidity
- hyporeflexia
- really high CK
- normal pupils
Serotonin syndrome
- hyperreflexia and clonus
- hypertonic but not as rigid
- small pupils
Serotonin syndrome diagnosis
exposure to serotonergic agents + one of the following
- spontaneous clonus
- inducible/ocular clonus AND agitation or sweating
- inducible/ocular clonus AND hypertonia AND high temp
- tremor and hyper-reflexia
Serotonin syndrome typical symptoms
SHIVERS mnemonic
- shivering
- hyper-reflexia
- increased
- vitals (HR, RR, BP, Temp)
- encephalopathy
- restlessness
- sweating
higher risk features of button battery ingestion
Highest risk batteries:
Larger diameter >20mm (more likely to get impacted)
Lithium cell (higher voltage)
Newer battery
age<5yr
Esophageal button battery
immediate endoscopy to remove within 2 hours
gastric button battery
Gastric or further down tract
If high risk (Age <5 AND button battery >/=20mm) then likely endoscopy within 24-48hr
If low risk Age >/= 5 and/or battery <20mm, consider outpatient observation only
- repeat xray in 48hr if >20 mm
- repeat xray in 10-14 days if <20mm if not found in stool
Button battery with esophageal injury on scope - next steps
NPO, IV abx, admit
CT angiogram to look at aorta
consider MR chest to look at distance from aorta
Splenic sequestration signs and symptoms
Signs and symptoms:
Rapid spleen enlargement
Left sided abdominal pain
Drop of hemoglobin at least 20 from baseline
+/- signs of hypovolemia (trapping blood in the spleen)
+/- severe anemia (<30)
+/- drop in WBC and platelets
Splenic sequestration acute management
- fluid resus with isotonic fluid if needed
- PRBC 5ml/kg transfusion - it may rise the Hgb quite a bit, risk of hyperviscosity symdrome
Splenic sequestration chronic management
Prophylactic splenectomy: perform after an acute episode has resolved, only effective strategy to prevent future life-threatening episodes (blood transfusions have been tried in the past to present sequestration, but evidence suggests that transfusions DO NOT reduce risk of recurrence compared to no transfusion therapy). Transfusions may be used as a short course bridge to splenectomy
Brain dead criteria
- Cause consistent with brain death
- Absence of confounding conditions: Paralysis, sedatives/significant drug tox, hypothermia (</= 34 degrees), extreme electrolyte derangement, un-resuscitated shock
- Absence of response to deep painful stimulus
- Absence of brainstem reflexes: Fully dilated pupils, absence of corneal, pupillary, gag, cough, suck/root, doll’s eyes, vestibulo-occular (COWS)
- Apnea test
- Increase CO2 >= 60, and increase by 20, absence of resp effort, pH <= 7.28 - Ancillary testing if unable to do apnea test: Brain perfusion scan
Brain dead defn
Brain death = Irreversible loss of the capacity for consciousness
Irreversible loss of all brainstem function, including the capacity to breathe
Cholinergic toxidrome
Cholinergic toxidrome - diarrhea, diaphoresis, hypersalivation, miosis
Muscarinic sx: SLUDGE = salivation, lacrimation, urination, diarrhea, GI upset, emesis
Nicotinic sx: Killer B’s = bronchorrhea, bronchospasm, bradycardia (muscarinic)
Example drugs:
- Organophosphates (insecticides, nerve agents)
- Nicotine/vape
- carbamates (physostigmine, neostigmine, pyridostigmine)
- alzheimer medications
- myasthenia treatments
Cholinergic toxicity antidote
atropine
CATCH CT Head rule
CATCH = Canadian Assessment of Tomography for Childhood Head Injury
CT head is required for children with a minor head injury plus any one of the following findings:
High risk (need for neurologic intervention):
- GCS < 15 at 2 hours after injury
- Suspected open or depressed skull fracture
- History of worsening headache
- Irritability on exam
Medium risk (brain injury on CT scan):
- Any sign of basal skull fracture - hemotympanum, racoon eyes, CSF otorrhea or rhinorrhea, battle’s sign
- Large boggy scalp hematoma
- Dangerous mechanism of injury - MCV, fall from 3 or more feet/5 stairs, fall from bicycle with no helmet
PECARN CT Head rule <2yo
High risk criteria: CT recommended if any single criterion present. (4.4% risk ciTBI):
- GCS 14 (<14 excluded from rule)
- Altered mental status (agitation,
somnolence, slow
response, repetitive
questioning)
- Palpable skull fracture
Low risk criteria: Observation vs CT recommended if any single criterion present. (0.9% risk ciTBI):
- Non-frontal hematoma
- Not acting normally per parent
- Severe mechanism: Fall >3 ft, MVC with ejection, death of passenger, or rollover, Unhelemeted pedestrian or bicyclist struck by vehicle, Head struck by high impact object
Avoid CT if no criteria present. (<0.02% risk ciTBI)
Sensitivity 100%
PECARN CT Head >/= 2 yo
High risk criteria: CT recommended if any single criterion present. (4.3% risk ciTBI):
- GCS 14 (<14 excluded from rule)
- Altered mental status (agitation,
somnolence, slow
response, repetitive
questioning)
- Signs of basal skull fracture
Low risk criteria: Observation vs CT recommended if any single criterion present. (0.9% risk ciTBI):
- history of Loss of consciousness
- history of vomiting
- severe headache
- Severe mechanism: Fall >5 ft, MVC with ejection, death of passenger, or rollover, Unhelemeted pedestrian or bicyclist struck by vehicle, Head struck by high impact object
Avoid CT if no criteria present. (<0.05% risk ciTBI)
Sensitivity 96.8%
Differences PECARN CT Head rule <2 or >/=2 yo
<2
- frontal hematoma
- not acting themself per parents
- palpable skull fracture
- fall >3ft
> /= 2
- loss of consciousness
- history of vomiting
- severity of headache
- signs of basal skull fracture
- fall > 5 ft
Pneumothorax size
For children >12 yrs only, a pneumothorax is considered ‘large’ based on the following measurements:
Measurement of the vertical distance between the lung and thoracic cage at the apex on CXR. If >3 cm, pneumothorax is large
OR
Measurement of the distance between the lateral lung edge and chest wall at the level of the hilum; >2 cm = (at least 50%)
Pneumothorax management
Small and asymptomatic: conservative
Small and any symptoms (chest pain, SOB): oxygen - helps resorb faster
Any resp distress/compromise or large - chest tube
Pediatric GCS
Motor
6 - Obeys commands
5- Localizes pain
4- Withdraws from pain
3- Decorticate (flexion)
2- Decerebrate (extension)
1- None
Voice
5- Oriented, answers questions
4- Confused
3- Inappropriate words
2- Incomprehensible sounds/groans
1- None
Eye response
4- Spontaneous
3- To speech
2- To pain
1- None
Indications for synchronized cardioversion
V-tach with a pulse
unstable SVT
begin with 0.5-1J/KG. can increase to 2J/KG
Sedate if needed but don’t delay cardioversion
Drug used to treat SVT
Adenosine
1st dose 0.1mg/kg (max 6mg)
2nd dose 0.2mg/kg (max 12mg)
Maxes out at 60kg
Acute managemenet hypercalcemia
Initial therapy of severe hypercalcemia includes the simultaneous administration of
- Intravenous (IV) isotonic saline,
- Lasix
- Calcitonin SC
- Bisphosphonate
The administration of calcitonin plus saline hydration should result in substantial reduction in serum calcium concentrations within 12 to 48 hours. The bisphosphonate will be effective by the second to fourth day and provide a more sustained effect, thereby maintaining control of the hypercalcemia.
Parkland formula
If TBSA >20% burn
4ml x weight (kg) x % Second degree or worse burns = total fluid volume over 24 hr Ringers Lactate
Divide by 2. Give first half of volume within 8 hours of the burn, the other half spread over the remaining 16 hr
For children <30kg, add maintenance fluids 4-2-1 rule with dextrose
Fluid replacements for mild/moderate/severe dehydration
Mild: ORS 50ml/kg over 4h
Mod: ORS 100ml/kg over 4h
Severe: IV 20-40ml/kg x1h
OR
Fluid deficit = 10 * weight * % dehydration
Treatment of agitate tox patient
Psychomotor agitation is treated with benzos as first line
Anaphylaxis criteria
Anaphylaxis criteria (need only one of three)
1. Acute onset after exposure to allergen with involvement of skin or mucosa and one of: resp compromise, hypotension, end-organ dysfunction
2. Two or more of: skin or mucosal involvement, resp compromise, hypotension or GI symptoms
3. Hypotension
Anaphylaxis management
0.01mg/kg IM epi (1:1000) every 5-15 mins as needed
Give up to 3 doses then do epi infusion 0.05mcg/kg/hr and titrate
Treatment high ICP
ABCs
Rapid treatment of hypoxia, hypercarbia, hypotension
Isotonic fluids to maintain MAP and CPP
If hypertensive, do not drop BP too quickly or will lose CPP (CPP = MAP – ICP)
Elevated head of bead 15-30 degrees
Maintain head midline
Get a glucose and correct hypoglycemia
Maintain normothermia
Correct anemia
Prophylactic anticonvulsants if high risk of seizures (ex. severe TBI)
Pain control
Neurovitals q1-2h
Hypertonic saline 3ml/kg
Osmotic diuresis: mannitol 1g/kg
Uncal herniation
Cushing triad = late sign of impending herniation
Hypertension
Bradycardia
Respiratory depression
Other signs of herniation: headache, altered LOC, anisocoria, Cheyne Stokes respirations, hemiplegia, decorticate or decerebrate posturing, coma
Impending herniation management:
Secure airway with RSI (FIRST STEP)
IV 3% saline 5ml/kg
Hyperventilation to PaCO2 30-35mmHg
Baseline stabilization
Emergency CT head
Bacterial tracheitis presenting features
Bacterial tracheitis = acute bacterial infection of upper airway that is potentially life threatening, mucosal swelling at level of cricoid cartilage with copious, thick, purulent secretions +/- pseudomembranes
Staph aureus = most common bug
Others: Strep pneumo, Strep pyogenes, Moraxella, non-typeable H. flu, anaerobes
Avg 4-8yrs old
Often follows a viral respiratory infection (esp laryngotracheitis)
More common than epiglottitis in vaccinated populations
Clinical manifestations: BT can be distinguished from croup as patients are often older and toxic appearing
Brassy cough
High fever
“Toxicity” with respiratory distress either immediately or after a few days of apparent improvement
Can lie flat, does not drool, no dysphagia (compared to epiglottitis)
Epi nebs ineffective
Tetanus indications
Tetanus toxiod booster (Td or Tdap) should be given if
Immunization status unknown or <3 doses
>10 years since last tetanus booster and minor wound
>5 years since last booster and major wound
For children under 7yrs, DTap should be given as choice booster, for children >7, Tdap is preferred method
Tetanus immune globulin should be given if someone has a serious wound and incomplete immunizations
Activated charcoal uses
ACE inhibitors
Antiepileptics
ASA
Beta blockers
Digoxin
NSaids
Tylenol
Antidiabetics
Neuroleptics
Opiates
Iron overdose pathophys
corrosive to the GI mucosa, leading to hematemesis, melena, ulceration, infarction, and potential perforation
Iron-induced hypotension is caused by volume losses, increased permeability of capillary membranes, and vasodilation mediated by free iron
Iron accumulates in tissues, including the Kupffer cells of the liver and myocardial cells, leading to hepatotoxicity, coagulopathy, and cardiac dysfunction
Metabolic acidosis develops in the setting of hypotension, hypovolemia, and iron’s direct interference with oxidative phosphorylation and the Krebs cycle
Moderate to severe toxicity is typically seen with ingestions >60 mg/kg
Management croup CPS
The clinical benefit of corticosteroids in croup is well established and should be considered for treating all children presenting with croup and symptoms ranging from mild to severe.
Improvement generally begins within 2 to 3 hours after a single oral dose of dexamethasone and persists for 24 to 48 hours
The dexamethasone dose used in most clinical trials is 0.6 mg/kg/dose
Timing of bloodwork for tylenol ingestion
must wait 4 hours before obtaining labs, then do ASAP
Acute management presumed metabolic new diagnosis
Bottom line for acute treatment of metabolic problems is Dextrose 10% (to prevent catabolism) and saline fluids (to prevent hyponatremia and dehydration)
NPO is safest to avoid adding more substrate when you don’t know what type yet (organic aciduria/amino acidopathies/urea cycle, do not want to consume proteins; fatty acid oxidation- avoid lipids)
Pancreatitis diagnosis and initial management
NASPGHAN Guidelines
Diagnosis: INSPPIRE criteria- at least 2 of : (1) abdominal pain compatible with AP (2) serum amylase and/or lipase values >=3 times upper limits of normal, (3) imaging findings consistent with AP
Management:
Early IV fluids- crystalloid volus then 1.5-2 x maintenace
Pain control- non-opioid and opioid if needed
No antibiotics unless concern for infected necrosis
Re: NPO- Evidence for early EN (within 48-72h) to prevent gut translocation of bacteria
What is Electromechanical dissociation
Pulseless electrical activity
PARDS severity cutoffs
Mild: OI 4-8
Moderate: 8-16
Severe: OI > 16 (high morbidity)
Differences between ARDS and PARDS
- PF ratio in adults instead of OI in peds
- Adults require bilateral opacities (kids can have unilateral opacity on imaging)
remember: ARDS is a disease of decreased lung compliance
Lung protective ventilation for PARDS
*Low tidal volume (4-6ml/kg)
*P-plat <28 or PIP <32
*Permissive hypercapnia pH >/= 7.25
*Permissive hypoxemia SpO2 88-92%
*Open-lung ventilation strategy (PEEP optimization)
*Early chemical paralysis to meet above goals
*Strict avoidance of fluid overload
Adjunct treatments for ARDS
Lung protective ventilation for everyone
Paralysis
Prone
Nitric oxide
Non-conventional ventilation (ex. HFO)
Restrict fluids
Steroids (controversial – likely not the right answer)
ECMO (not great evidence but if they are going to die, can choose ECMO)
Most likely causes of PARDS
Pulmonary: pneumonia
Non-pulmonary: sepsis
Risk factors for fatal asthma
o Previous attack with rapid/severe deterioration
o Prior picu admission +/- mechanical ventilation
o Syncope or seizure during previous attack
o >1 hospitalization or ED visit in past year
o >/= 1 cannister per month rescue
o Poor knowledge/compliance of disease management
o Social issues
o Comorbid illness (including obesity, chronic lung disease, food allergy)
How does heliox work in asthma
reduces airway resistance to improve air flow
Improves laminar airflow
helium is less dense than air (increases velocity of flow)
Persistent lactic acidosis in burn patient
carbon monoxide or cyanide poisoning until proven otherwise
inhalational injury + altered LOC
carbon monoxide or cyanide poisoning until proven otherwise
Which paralytic is contraindicated in burn patients
succinylcholine
3 causes lactic acidosis from house fire
- Carbon monoxide poisoning
- Cyanide poisoning (everything synthetic burning)
- Tissue damage, decreased CO, hypovolemic shock, necrosis
Septic Shock
sepsis + severe cardiovascular dysfunction (hypotension, need for pressors, high lactate > 2xULN, CRT > 5 s)
SIRS Criteria
Require 2 of the following 4 (of which 1 MUST BE either Temp or WBC):
- T>38.5 or <36
- HR > 2SD above normal for age w/o other stimuli
- Bradycardia for infants <1year w/ HR <10% for age
- RR > 2 SD above normal for age
- WBC<5 or >15 or >10%bands
Warm shock pressor choice
norepinephrine
PALS starting dose 0.1-2 mcg/kg/min
Cold shock pressor choice
epinephrine
PALS
starting dose 0.1-1 mcg/kg/min
Cold shock features
- low cardiac output
- high SVR
Use epinephrine to:
- increase CO
- increase SVR
works through Beta 1 and Beta 2 agonism
at high dose also increases alpha
Dosing: 0.01-0.05 mcg/kg/min
High dose: 0.06-0.1 mcg/kg/min
Warm shock features
++ increased cardiac output
decreased SVR
increased SVO2
Use norepi
- increases SVR
- increases CO
- increases HR
Works on
- low dose alpha 1
- high dose Beta 1 and Beta 2
Dosing
Low 0.01-0.05 mcg/kg/min
High 0.06-0.1 mcg/kg/min
PALS:
starting dose 0.1-2
Milrinone function
increases cardiac output
decreases SVR
acts as PDE inhibitor
Bruising red flags for NAT (CPS statement)
- Bruises in babies who are not yet cruising / babies (<4mo)
- Bruises on the ears, neck, feet, buttocks or torso (torso includes chest, back, abdomen, genitalia)
- Bruises not on the front of the body and/or overlying bone
- Bruises that are unusually large or numerous/extensive
- Bruises that are clustered or patterned (patterns may include handprints, loop or belt marks, bite marks)
- Bruises that do not fit with the causal mechanism described
Medical investigations for bruises concerning for NAT (CPS statement)
- Complete blood count (CBC) (including platelets)
- Peripheral blood smear
- INR and PTT
- Fibrinogen
- Von Willebrand studies
- Blood group (for interpretation of vW levels)
- Factor VIII level
- Factor IX level
- Liver function tests (for secondary platelet dysfunction)
- Renal function tests (for secondary platelet dysfunction)
Systemic illnesses causing increased predisposition to bruising
- hematologic problems (ex. ITP, von willebrand disease, hemophilia, platelet disorders, Glanzmann’s thromboasthenia)
- Systemic infections (ex. Meningococcemia)
- Malignancy (ex. Leukemia, neuroblastoma)
- Nutritional deficiencies (ex. Vitamin K or C)
- DIC
- Connective tissue disorders (Ehlers-Danlos, Osteogenesis imperfecta)
- Autoimmune/inflammatory (ITP, HSP, Gardner-Diamond)
ingestion causing mixed respiratory alkalosis and metabolic acidosis
salicylate toxicity (ASA)
Treat with sodium bicarb infusion (alkalinization of urine to help with excretion)
TCA ingestion pearls
looks like anticholinergic but high mortality risk
GET AN ECG - its TCA if QRS >100 (wide complex tachycardia)
don’t use physostigmine
often present sedated and hypotensive (fluid refractory) and seizures
ex amitriptyline
give sodium bicarb!
ABCs of tox
ABC
D - decontamination
E - elimination
F - find the antidote
sympathomimetic vs anticholinergic
both have mydriasis but non-reactive in antichol vs. reactive in sympathom
dry in antichol, sweaty in sympatho
antihypertensive drug to avoid in sympathomimetic overdise
beta blockers
antidote for cholinergic toxidrome
atropine (use q 5 mins until secretions stop)
atrovent
pralidoxime also used for cholinergic intoxication but only helps nicotinic effects (weakness, fasciculations)
drugs that don’t work with activated charcoal
Alcohols
Caustics: alkalis and acids
Cyanide
Heavy metals (e.g., lead)
Hydrocarbons
Iron
Lithium
toxic dose of tylenol ingestion
> 200 mg/kg in children and >7.5-10 g in adolescents and adults.
Repeated administration of APAP at supratherapeutic doses (>90 mg/kg/day for consecutive days) can lead to hepatic injury or failure in some children,
Kings Criteria for Liver Failure Transplant
These criteria include acidemia (serum pH <7.3) after adequate fluid resuscitation, coagulopathy (INR >6), renal dysfunction (creatinine >3.4 mg/dL), and grade III or IV hepatic encephalopathy
Toxic causes of hot and altered
Sympathomimetic toxidrome
Anticholinergic toxidrome
Neuroleptic Malignant Syndrome
Serotonin Syndrome
Malignant Hyperthermia
Substance Withdrawal
ASA
Toxic rigidity syndromes
NMS
- triggered by antipsychotics
- d/t too little domamine
- lead pipe rigidity, slower onset over days
- antidote: bromocriptine or amantadine
Serotonin syndrome
- too much serotonin usually d/t SSRI OD
- hyper-reflexic, lower>upper extremitiies
- antidote: cyproheptadine
Malignant hyperthermia
- triggered by anesthetics with genetic predisposition, usually inhaled gasses or succinylcholine
- antidote: dantrolene
Toxins causing mydriasis (big pupils)
- anticholinergic
- sympathomimetic
- withdrawal
Toxins causing miosis (small pupils)
- opioids
- cholinergics
- sedative-hypnotics
- phenothiazine (old antipsychotic)
physostigmine vs pralidoxime
pralidoxime - for cholinergics (atropine is 1st line, pralidoxime only treats nicotinic effects ie weakness)
physostigmine - for anticholinergics (NOT in TCA)
radio opaque drugs in OD
COINS
-chloral hydrate
-pioid packets
-iron and other heavy metals
-neuroleptics (if early)
-sustained release taboets/salicylates (early)
ketosis without acidosis
isopropyl alcohol
hypothermia associations
hypoglycemia
hypocalcemia
hypokalemia
metabolic acidosis
metabolic acidosis following house fire
cyanide toxicity
treat with cyanocobalamin
Rotary nystagmus is pathognemonic for what toxidrome?
PCP
