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.
