Exam Flashcards
Diabetic Ketoacidosis
Profound deficiency of insulin results in hyperglycemia
Plenty of glucose…but can’t get it into the cells
Lack of insulin leads to breakdown of triglycerides/fatty acids for energy with production of ketones
**Often the initial clinical presentation of a patient with DM I
Diabetic Ketoacidosis
Anion Gap
Anion Gap = Serum NA+ – (Serum Cl- + HCO3-)
Cause of increased anion gap metabolic acidosis:
“MUDPILERS”
(Methanol, Uremia, Diabetic/alcoholic/starvation ketosis, Paraldehyde, Isoniazid/Iron, Lactic acidosis, Ethylene Glycol, Rhabdo, Salicylates)
Tx of DKA
- Fluid: normal saline
- Insulin: 1hr post IVF
- Electrolytes: K+ replacement
- Once the blood glucose is ~200-250 mg/dL, start D5 (5% dextrose) in 1/2NS.
- Slow IVF rate to 250cc/hr when dehydration is improved
- Keep blood glucose between 150-250
- Give SQ Insulin at least 1/2 hour before stopping the insulin drip
if pH <6.9, consider giving bicarb
When do you give Insulin in Tx of DKA?
1hr post IVF
correct orthostatic hypotension from fluid loss first
What happens when you don’t gradually correct blood sugar and correct it too rapidly?*
Keep blood glucose between 150-250**
Too rapid of a correction can lead to sequelae such as cerebral edema**
Most common cause of HHNK*
Infection
look for infection in pts w/known DMII
Which population of pts more affected by DKA v HHS?
DKA: type I DM, usu <40yo
HHNK: type II DM, usu >60yo
but not exclusive!
HHS is characterized by
Severely elevated glucose levels often >600mg/dl**
Commonly >800 mg/dl
Adequate insulin activity, but ↓ cell response
Hence, absence of lipolysis and ketogenesis
significant dehydration*
Causes of HHS
Precipitating Event:
Infection – most common*
MI, CVA, trauma, drug effects (steroids) or interactions
What respiration is NOT present in HHS*
Usually Kussmaul Respirations are NOT present
Why do you need to be more judicious in treating pts with HHS than DKA?
HHS patients often have underlying CVD making rehydration more complicated…
admit to ICU
Pts in myxedema coma are very sensitive to
very sensitive to opiates and may die from average doses.
Right heart strain on EKG and what is it classically associated with
S1Q3T3 (presence of an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III)
PE
Exertional chest pain is what until proven otherwise
Exertional chest pain is angina (CAD) until proven otherwise!!!
exercise stress test unless unstable
if high probability of CAD, get cardiac cath
most common cause of non-cardiac chest pain
GERD
Redflags of HAs
Fixed neurological deficits
Extremely abrupt onset
Papilledema
New onset headache especially in patients over < 5 or >50 y/o
Signs of infection (constitutional symptoms, nuchal rigidity)
Altered level of consciousness
New HA in a cancer patient or immunocompromised patient
Test most helpful in identifying CNS infection
Lumbar puncture
Test most helpful in identifying intracranial lesion or bleed
CT no contrast (do before LP) or MRI
Migraines are NOT treated with
narcotics (percocet, dilaudid, demerol)
Very poor indicators of respiratory failure in pediatrics
bradypnea
bradycardia
(both late signs)
Difference between O2 consumption in adults v children
Adults: oxygen consumption= 4mL/kg/min
Children: O2 consumption= 8mL/kg/min (so develop hypoxia and hypoxemia more rapidly)
MOST COMMON cause of shock in children worldwide*
Hypovolemic shock (from diarrhea, hemorrhage)
most common distributive shock in children
septic shock
difference between vein and artery when palpating
arteries have bounding pulse and veins don’t
What is the smallest gauge needle you should use when putting in an IV? (adults)
20 gauge (18 even better)
Disadvantage of peripheral IV access
can only be in 72hrs (3 days)!* then have to change to different site
potential for phlebitis
What medications can’t you give through peripheral IV?*
Can not give TPN - total parenteral nutrition via peripheral IV) chemotherapy Hypertonic solutions Potassium Amiodarone Vasopressors (Epinephrine, dopamine)
When can you draw labs with peripheral IVs?
only during initial insertion!
subsequent labs not reliable from medications given
contraindication for peripheral IVs
If the medication can be given orally Cellulitis Injury to the Extremity Previous IV infiltration Surgical Procedures: Compromised Lymphatic: Lymph node dissection (breast cancer /radical mastectomy), Lymphedema Burns AV fistula
Extravasation
severe version of infiltration of fluid from IV into surrounding tissue; severe local tissue damage (tissue necrosis, disfigurement, loss of function)
avoid by not administering contraindicated medications(Chemotherapy, potassium, vancomycin, cefotaxime, Hypertonic solution, amiodarone, calcium chloride)
central venous catheters can be used to asses
assess right ventricular function and systemic fluid status.
goes right in SVC through subclavian vein
contraindications to central venous catheters
trauma
hemodialysis, pacemaker
mod to severe coagulopathy
PICC(Peripheral Inserted Central Catheter)
Inserted into cephalic, basilic, brachial vein into the distal Superior Vena Cava
Ultrasound guided, placed by an IV nurse, confirmation placement via CXR (can take over 1hr total for placement!)
15-30 days
can draw blood from it
Order of preference of veins for PICC
Basilic
Brachial
Cephalic
Median cubital vein
difference between PICC and central line
PICC typically few days to months, administer IV antibx. Central line CVP/PCWP monitoring, TPN, chemo, more long term treatment.
majority of central line associated bloodstream infections are from
Non-tunnel central venous cath (e.g Quinton)
short term use
(tunneled has cuff that prevents bacteria)
Locations to insert central venous catheter
internal jugular
subclavian: most preferred
femoral
What do you not give during spinal trauma?
steroids, no evidence
Nexus criteria for imaging
imaging isnotnecessary if patientsyounger than 60 yearssatisfyallfiveof the following low-risk criteria:
Absence of posterior midline cervical tenderness
Normal level of alertness
Altered mental status:
Glasgow Coma Scale (GCS) score below 15
Disorientation to person, place, time, or events
Inability to remember three objects at five minutes
Delayed or inappropriate response to external stimuli
No evidence of intoxication
No abnormal neurologic findings
No painful distracting injuries
Most injuries to the middle column are
unstable
composed of PLL, post vertebral body, post annulus fibrosis
Corticobulbar/Corticospinal tracts
Motor impulse originates in cerebral cortex
Crosses over at the medulla
Signal travels down the contralateral side via the corticospinal and corticobulbar tracts to target muscle
Corticobulbar/Corticospinal tracts
Motor impulse originates in cerebral cortex
Crosses over at the medulla
Signal travels down the contralateral side via the corticospinal and corticobulbar tracts to target muscle
Corticobulbar tract: connection to brainstem nuclei of cranial nerves
Corticospinal tract: connection to spinal nerves
Upper motor neuron lesions cause:
Spasticity Increased tone Positive Babinski sign Clonus Possibly mild muscle atrophy Hemiparesis/weakness
Lower motor neuron lesions cause:
Fibrillation’s (single fiber - invisible)
Fasciculation’s (motor unit - visible)
Paralysis/hypotonic
Flacid muscles with atrophy
Flexion contracture of tendons cause skeletal deformity
Spinothalamic Tract
Pain and temperature; crude touch
Crosses over shortly after sensory input enters spinal cord
Travels spinothalamic tract on the contralateral side to thalamus and then into cerebral cortex
Posterior (Dorsal) Column
Position and vibration; Fine touch
Travels up ipsilateral side of spine where signal entered
Crosses over at medulla then to thalamus and cerebrum
Which nerves supply the diaphragm?
C3-C5 Nerve roots innervate the phrenic nerve which supplies diaphragm
C5 injury or higher – intubation
Watch for Respiratory Failure
Hypotension is from what in trauma until proven otherwise?*
Hypotension is from blood loss UNTIL proven otherwise in the trauma setting!
SEARCH for the CAUSE
spinal cord injury causes loss of what in neurogenic shock?*
SCI causes loss of alpha adrenergic tone –> dilation of arteries/veins* to the areas that the cord innervates such as T1-4 (heart) –> Bradycardia**
The sudden loss of sympathetic nervous system signals to the smooth muscle in the vessel walls results in uncontrolled vasodilation**
Spinal Shock
Immediate transient loss of spinal cord function below level of injury
Areflexia- no reflexes
Hypotension
Flaccid Paralysis
Goal of mean arterial pressure
85-90 mmHg
Primary Assessment
Airway Breathing Circulation Disability Exposure
Secondary Assessment - spine trauma
Neuro Exam: Mental Status Exam Sensory Exam (dermatomes) Motor (myotomes) Sweating and skin vasomotor tone are absent below the level of spinal cord lesion. DTRs
spinal compressions are common in
osteoporosis
can be treated w/balloon kyphoplasty if severe
Flexion Distraction vFlexion Dislocation
flexion distraction (n seat belt injuries) affect posterior and middle columns, intact anterior prevents dislocation flexion dislocation affects all 3 columns, most damaging
Jefferson fracture
Fracture of anterior and posterior arches of C1
“burst fracture of C1”
40% have associated Axis fractures (C2)
50% associated with vertebral artery injury
How to best see Jefferson Fractures
open-mouth odontoid view: shows overhang of Cl on C2 (THESE STILL ARE GOING TO GET CTs!!)
How to manage jefferson fractures
Most will be managed with skeletal traction/immobilization (halo) - 6-12 weeks
Unstable: Will need ORIF
Hangman’s fracture
Traumatic spondylolisthesis
Bilateral fracture of pars interarticularis
Anterior displacement of vertebra in relation to vertebrae below
Usually the result of hyperextension + axial compression.
Flexion Teardrop Fracture
Considered MOST UNSTABLE and dangerous C-spine injury: force great enough to displace anterior-inferior edge of vertebral body usually causes comminution of vertebral body and displacement of fragments into spinal cord.
lateral C spine to Dx
usu causes acute anterior cervical cord syndrome
usu C5-6 (greatest flexion/extension points)
Clay Shoveler’s
Usually an avulsion of spinous process of C7 or T1, due to heavy lifting (or shoveling clay) or direct trauma
stable - flexion force of neck
Tx: soft collar, activity modification
where does the spinal cord end?
L1
where in thoracic and lumbar spine most at risk of injury
T11-L2 transition zone between fixed T spine and mobile L spine most at risk for traumatic injury due to stress during motion
What should you image with calcaneal fractures?*
T/L Spine!
Central Cord Syndrome
Most common Cord syndrome 9%
Injury to corticospinal tract
Greater loss of motor (more weakness) UE>LE
Corticospinal tract for UE more centrally located
Hyperextension injury with cervical stenosis
Vascular compromise of anterior spinal artery
can have permanent hand disability
loss of bladder control
anterior spinal cord syndrome
Injury to ventral 2/3s of cord, sparing posterior column
Paraplegia (loss of motor function - corticospinal tract) + disassociated sensory loss with loss of pain/temperature (Spinothalamic tract)
Dorsal intact: Position sense, vibration, deep pressure
Infarction of the cord in the territory of anterior spinal artery
Poorest prognosis
Brown-Sequard Syndrome
Hemi-dissection of the cord typical with penetrating trauma
Rare 1-4%
Ipsilateral motor loss (pyramidal deficit) + ipsilateral loss of position, tactile discrimination, and vibratory sensation (Dorsal column) + contralateral loss of pain and temperature (Spinothalamic tract) 1-2 levels (dermatomes) below injury
Some recovery seen
Conus Medullaris
transition of spinal cord from CNS to PNS
Located between T12 and L2
LE weakness- symmetrical motor impairment
Absent lower-limb reflexes
Saddle anesthesia
Areflexic bowel and bladder
Cauda Equina Syndrome
Lumbar, Sacral, Coccygeal nerve roots (vertebral column injury distal to L2)
Peripheral Nerve injury rather than SCI
Lower motor neuron only (absent DTR, permanent areflexic bladder, absent bulbocavernosus reflex)
Motor/Sensory Loss in LE (Asymmetrical motor impairment)
Sciatica
Bowel/Bladder Dysfunction
Saddle Anesthesia
Lethal Six
airway obstruction tension pneumothorax open pneumothorax massive hemothorax flail chest Cardiac tamponade (burns too)
Hidden Six
thoracic aortic disruption tracheobronchial disruption myocardial contusion traumatic diaphragmatic tear esophageal disruption pulmonary contusion Rib Fractures ****
Becks Triad
JVD
Muffled Heart Tones
Hypotension
cardiac tamponade
what should prompt concern for an intraperitoneal injury
Any wound from the nipple line to the groin anteriorly or scapular tip to the infragluteal fold posteriorly
Tx of neurogenic shock
Hypotension + Bradycardia (IVF)
Consider Dopamine, Phenylephrine, Levophed if not responding
MAP goal
Tx of hypovolemia
Hypotension + Tachycardia (give the, what they need –> 1:1:1)
Consider Dopamine, Phenylephrine, Levophed if not responding
MAP goal
What should you do ASAP in spinal trauma?
CLEAR CERVICAL COLLAR AND OFF BACK BOARD ASAP
Bulbocavernosus reflex
squeeze the penis to determine if the anal sphincter simultaneously contracts Indicative of S2-S4
Cremasteric reflex
running a pin or blunt instrument up medial aspect of thigh– if scrotum rises SPINAL Cord is intact
Rectal tone indicates in spinal trauma
Cauda equina syndrome, cord transection
Priapism indicates in spinal trauma
complete spinal cord injury
SIRS Criteria***
Temp > 38 or <36 HR > 90 RR > 20 or PaCO2 < 32 WBC > 12,000 < 4,000 > 10% immature forms (bands)
Sepsis tx
Goal directed therapy: Central venous O2 saturation >= 70 CVP >= 8 to 12 MAP >= 65 Urine output >= 0.5 cc/kg/hr
Sepsis immediate measures within 1st hour
Blood cultures
Administer broad spectrum antibiotics:
Piperacillin/tazobactam, unasyn (amp/sulbactam), if PCN allergy 3rd gen cephalosporin and add metronidazole/Flagyl (to cover anaerobes)
Perforated appendicitis: use cipro and Flagyl for anaerobes, treat like diverticulitis
Measure lactic acid Administer crystalloids (30 cc/kg)
Sepsis Tx within 6hrs
Repeat lactic acid
Assess for perfusion improvement
Initiate pressors as indicated
What is neurogenic shock secondary to?**
cord issue, NOT HEAD TRAUMA
Neurogenicshock Treatment
Trendelenburg position
IV fluids: Increase intravascular volume
Pressors: It’s a vasodilation problem due to loss of tone so tone them up sympathetically! Pressors!
Must balance fluids and pressors
primary goal in Tx of head trauma
prevent secondary brain injury
MOST COMMON INJURED MENINGEAL Vessel
middle meningeal artery, can cause epidural hematoma
pterion injury
Which meninges are vascular and which ar avascular
dura is vascular
arachnoid is avascular
subarachnoid space contains
CSF and veins/arteries
Normal intracranial pressure
10mmHg = normal >20mmHg = abnormal >40mmHg = severe
Interventricular measurement of ICP can
Ability to measure ICP AND DRAIN CSF**
CPP (Cerebral Perfusion Pressure)
difference between your mean arterial pressure and intracranial pressure (MAP-ICP)
net pressure gradient that drives oxygen delivery to brain tissue, but NOT actually CEREBRAL BLOOD FLOW
normally 50-150mmHg
Systolic shouldn’t go below what*
90mmHg
Primary survey of head traumas
Mechanism– Direct/Indirect/Penetrating. This is your brief history.
ABCDE’s
Immobilize C-spine: suspect until proven otherwise\
IV access/labs at the end
What should you get before intubating a head trauma?
get Glasgow coma scale - get baseline neuro
“less than 8 intubate” (Referring to GCS) - Loss of gag/inability to clear secretions
Cushings Reflex
Bradycardia, Respiratory depression—INCREASED ICP
intracranial bleeds do not cause
hypotension
Crystalloid of choice in hypotension
normal saline
H’s of secondary brain injury
Hypotension Hypoxia Hypoglycemia Hyperthermia Hypocapnia - dec cerebral blood flow
Disability survey in ABCDEs
glasgow coma scale: doc before meds
pupillary response
rule out other causes
what vaccine should you inquire about in secondary survey?
tetanus status
What labs should you draw during head trauma
CBC CMP Type/Cross ABG Tox Screen/ETOH Coags*** Lactate esp if bleeding/ongoing Hypotension Pregnancy
Where should the head of bed be with TBIs?
30degrees
Most common vessel affected in epidural hematoma*
middle meningeal arteries (arterial bleed)
Sx of epidural hematoma
Initial, brief LOC—lucid interval—rapid neuro deterioration
Fixed dilated pupil on the unilateral side as herniation (swelling impinges CNIII)
Subdural Hematoma
30% of TBIs, more common than epidural Shearing force on venous bridging veins between dura and arachnoid expands more slowly more severe bc damage parenchyma may be relatively non-Sx - nonfocal***
what type of hematoma is subdural?*
concave hematoma, follow contour of cortex
who are most commonly affected by subdural hematoma?
elderly and alcoholics
If isolated Subarachnoid hemorrhage– Consider*
aneurysm
subarachnoid hemorrhage
non-space occupying
venous bleed
may inc ICP if blocks CSF outflow
if asymp and stable serial CT and normal exam can discharge
Most common type of skull fracture!
linear skull fractures
usu minimal clinical signif, unless affect middle meningeal artery and vein
If the skin is violated (open fracture) in a depressed skull fracture, DON’T
DON’T probe wound
Basilar Skull Fractures
Petrous portion of temporal bone 75%
+/- CSF LEAK
Increased risk of developing meningitis
Sx: Hemotympanum, CSF otorrhea/rhinorrhea, Raccoon Eyes, Battle Sign (bruising over mastoid process)
Penetrating Brain Injury (PBI) need early
IV antibiotics
What is a pertinent Hx question in brain/spinal trauma?*
anticoagulants!
Heat exhaustion*
INTACT MENTAL STATUS*
Early identification critical to prevent progression to heat stroke
Heat stroke*
LIFE THREATENING CONDITION
High core body temperature causes proteins to denature which leads to multi-system organ damage
Body can’t regulate core temp
Forms of heat stroke
Exertional heat stroke – young people w/ who engage in prolonged strenuous physical activity, more rapid onset
Classic non-exertional heat stroke – think elderly, debilitated patients –> gradual environmental exposure
human bite with highest risk of infection
clenched-fist wound
Human oral flora*
Eikenella, group A Strep
Human skin flora*
staphylococci and streptococci
Most significant oral animal flora bacteria*
Pasteurella spp. – 50% dogs wounds, 75% cat wounds
organism in cat scratch fever
Bartonella henselae
infections are more common with what animal bite?*
cat bites
Superficial signs of infection*
tenderness, erythema, swelling, warmth, purulence, lymphangitis, fluctuance (abscess)
Deep signs of infection*
above PLUS persistent pain, pain with passive ROM, pain out of proportion, crepitus, joint swelling, systemic illness (fever, hemodynamic instability), persistent signs of infections despite intervention
Most bite wounds should be left to heal by *
secondary intention (a.k.a. left open) due to high risk of infection (exception may be made for facial wounds)
Schedule for rabies post-exposure prophylaxis***
Vaccine: 1 mL IM (deltoid) given on days 0, 3, 7, 14, 28*
*add day 28 If immunosuppressed
Anti-venoms*
FabAV (CroFab) or Fab2AV (Anavip)
Reserved for those with bites to face or neck, or those with progressing symptoms (mod-severe)
Coral Snake Bites
“Red on yellow kill a fellow, red on black venom lack”
What is important to do first w/inset bites?*
Remove stinger right away! Longer sitting in there, longer they deposit venom
Insect Sting anaphylaxis tx
ABCs!
IM Epinephrine into anterolateral thigh
pathognomonic rash for fire ant bites
sterile pustules
Clinical manifestation of black widow spider bites*
neurologic overstimulation (e.g. muscles aches, spasm, rigidity) tx w/diazepam and ca gluconate
Clinical manifestation of brown recluse spider*
infarct of skin –> rapid blood coagulation within vessels
Single grey “sinking” macule, eroded in center, halo of hemorrhage; dec in 5-10 days
most concerning spider bite
debridement not proven beneficial
when glucose is 30-50mg/dL
Catecholamine release:
Irritability, hunger (“hangry”), trembling
Diaphoresis
Tachycardia
when glucose is <30mg/dL
Neuroglycopenic effects:
Focal neurologic deficits, headaches, dizziness
Confusion, bizarre behavior, visual disturbances
Hypothermia
Seizure or seizure-like activity
Most common life-threatening complication of diabetes
diabetic ketoacidosis
more common in type 1
Kussmaul respiration
Deep, rapid, sighing; aka air hunger
Tx of alcoholic ketoacidosis
Administration of IV fluids containing dextrose can correct the acidosis
Thiamine 100mg IV or IM: malnutrition
Thiamine deficiency can lead to
Wernicke’s syndrome (ataxia, muscle paralysis, confusion) or Korsakoff’s syndrome (memory)
lactic acidosis - serum lactate level
Serum lactate is at least 4-5 mmol/L but may be as high as 10-30 mmol/L
Reference range ~1-2 mmol/L
Clinical features of myxedema coma
Hypothermia
Hypoventilation leading to hypoxia and hypercapnia
Hyponatremia
Hypotension
Seizures and abnormal CNS signs may occur including altered mental status.
how is Dx of adrenal insufficiency confirmed?*
confirmed by the synthetic ACTH (cosyntropin) stimulation test
Tx of Adrenal insufficiency
Acute: Hydrocortisone 100mg IV q8h or Dexamethasone 0.1mg/kg q8h. Saline infusion. Thereafter, continue hydrocortisone 50-100 mg q 6-8 hours
Convalescent: Hydrocortisone (AM 10-20 mg; PM 5-10 mg) and Fludrocortisone acetate (.05-.2 mg); both glucocorticoid and mineralocorticoid
Chvostek sign
sign of hypocalcemia
Tap over the facial nerve about 2 cm anterior to the tragus of the ear. Depending on the calcium level, a graded response will occur: twitching first at the angle of the mouth, then by the nose, the eye, and the facial muscles
Trousseau sign
sign of hypocalcemia
Inflation of a blood pressure cuff above the systolic pressure causes localized ulnar and median nerve ischemia, resulting in carpal spasm
Dx of hypercalcemia
Calcium >12 mg/dl
EKG – Prolonged PR interval, shortened QT interval & flattened T waves
Dx of hypocalcemia
Calcium <2 mg/dl
ABG
Respiratory or metabolic alkalosis
Hypercapnia secondary to severe hypocalcemia
EKG – prolongation of the QT interval
Dx of adrenal insufficiency
Low cortisol level
Eosinophil count is high
Electrolyte abnormalities
Blood, urine or sputum culture may be positive if bacterial infection is the cause of the crisis
How do you differentiate between sympathomimetic and anticholinergic toxidromes*
sweating
Antidote for Acetaminophen
N-acetylcysteine***
Antidote for Anticholinergic agents*
Physostigmine*
Antidote for Benzodiazepines*
Flumazenil*
Antidote for Cocaine (or other sympathomimetics)
Benzodiazepine
Antidote for Ethylene glycol
Fomepizole, ethanol, hemodialysis
Antidote for Hydrofluoric acid
Calcium gluconate
Used in carpet cleaners, consumes Ca like nothing and continue through body and bone, life threatening
most common cause of cardiac tamponade
pericarditis
RF for aortic dissection
Marfan syndrome or hypertension
Imaging for aortic dissection
Ct w/contrast or transesophageal echo
up to 30% of PE can have elevation of what
elevated troponin
What is test is 90% sensitive to PE?
D Dimer
difference between STEMI and NSTEMI physiologically
STEMI: Full wall thickness infarction
NSTEMI: Subendocardial damage so no ST elevation
MC cause of pericarditis
viral
Dressler’s syndrome
pericarditis - post MI/tissue death immune response
what position are Sx of pericarditis aggravated by
supine
better sitting up
What should you rule out w/HA
Meningitis and Subdural Bleed
classic triad of meningitis
Fever – 95% of patients
Nuchal Rigidity – 88% present with it, may last 7 days
Altered Mental Status – 78% confused or lethargic, 22% only responsive to pain, 6 percent unresponsive to all stimuli
meningitis can be
bacteria (can kill you) or viral (wish it can kill you; Sx tx)
Diagnostic testing for subarachnoid hemorrhage
CT no contrast
mandatory LP
LP findings in subarachnoid hemorrhage
elevated opening pressure and an elevated red blood cell count that does not diminish from CSF tube one to tube four
gold standard test for intracranial aneurysms after Dx of SAH made
digital subtraction angiography (images are produced using a contrast, and then a pre-contrast images is ”subtracted”)
Subdural Hematoma is usu caused by
from tearing of the bridging veins, most commonly from head trauma*
(Arterial rupture accounts for 20-20% of cases)
50% of subarachnoid hemorrhage presents as
coma
(up to 38 percent of patients have a transient “lucid interval” that is followed by a progressive neurologic decline to coma)
Migraine cocktail
Reglan + Toradol +Benadryl + IV fluids
What medication reduce the risk of early recurrence of headache
single dose of Dexamethasone, 10-25 mg
In contrast to adults, cardiac arrest in infants and children in usually NOT from*
not from a cardiac cause
usually the result of Progressive respiratory failure Or SHOCK or both
Respiratory Distress
increased respiratory rate and effort. Adequate ventilation is still maintained
still maintain adequate gas exchange
how does respiratory failure develop from respiratory distress
As the child tires and/or function deteriorates
Respiratory Failure
inadequate oxygenation, ventilation or both
REQUIRES intervention to prevent respiratory arrest-cardiac arrest
confirmation through ABG
Head position during infant ventilation
Keep infants head in neutral position during breaths, because extending the head can block the airway.
Quick Systolic Blood Pressure formula for children 1 year and older
Median: 90mmHg + (2 X age in years)
Minimum: 70mmHg + (2 X age in years)
what voltage of defibrillator should you not exceed in infants/children
10J/kg
use 2-4J/kg, then 4 J/kg
child pads
Choking-INFANTS
Alternating Back slaps (5) and Chest thrusts (5)
Repeat until the object is removed or the infant becomes unresponsive (then CPR, but looking for the object every time you open the airway. If you can see it, grab it!)
choking pregnant women or people obese
perform chest thrusts instead of abdominal thrusts.
Choking in children>1 and adults
Stand or kneel behind victim
Make a fist with one hand
Place thumb side against the victim’s abdomen, in midline, slightly above the navel and below the breastbone
Press fist into the abdomen with a quick forceful upward thrust
Repeat thrusts until the object is expelled or the victim becomes unresponsive (Again, if unresponsive, start CPR looking for the object)
Secondary Assessment history
S: signs and symptoms A: allergies M: medications P: PMH L: last meal E: Events leading to current illness
Most common cause of bronchiolitis in children
RSV
Disordered Control of Breathing are mostly what causes
neurologic: Seizures, CNS infections, head injury, brain tumor, hydrocephalus, neuromuscular disease
oropharyngeal airway (OPA) or a nasopharyngeal airway (NPA) is contraindicated in
OPAs are contraindicated in responsive patients with a gag reflex because of the risk of vomiting and aspiration
NPAs are contraindicated in
patients with basilar skull fractures because of the concern about the airway device entering the cranial vault through a thin disrupted cribriform plate.
BAG MASK VENTILATION contraindication
severe facial trauma
Good indicators of circulatory volume (indicating moderate dehydration) when used together
Capillary refill time > 2 seconds, decreased urine output, absent tears, dry mucous membranes, generally ill appearance.
septic shock
Abnormal reduction in systemic vascular resistance, vasodilation, venodilation=pooling of blood in venous capacitance system and relative hypovolemia
Anaphylactic Shock
Venodilation, systemic vasodilation and increased capillary permeability
Neurogenic Shock
head injury, spinal injury, generalized loss of vascular tone.
presentation of distributive shock in children
warm or cold shock
HYPOTENSION with a wide pulse pressure (warm shock) or a narrow pulse pressure (cold shock)
Bounding peripheral pulses
Brisk or delayed capillary refill
Warm flushed skin (extremities) or pale skin with vasoconstriction
Tachypnea
Tachycardia
Changes in mental status
Oliguria
Petechial or purpuric rash (septic shock)
Signs of congestive heart failure
JVD, hepatomegaly, pulmonary edema
can result in increased respiratory effort
cardiogenic shock
Obstructive Shock
Cardiac tamponade
Tension pneumothorax
PE
congenital heart lesions
fluid resuscitation in shock*
isotonic crystalloid-NS or LR- in a 20mL/kg bolus over 5-20 minutes repeated to restore BP
possible causes of delirium
Hypoglycemia (or hyper) Wernicke’s Encephalopathy (thiamine deficiency) Hypertensive Encephalopathy Delirium Tremens or other withdrawal states Sepsis or Shock Hypoxia or Hypercapnia Hypothyroidism or Hyperthyroidism Hypercalcemia (as in metastatic breast cancer) Uremia Severe hyponatremia NCS (non- convulsive status epilepticus) Simple UTI in Nursing Home Patients
201 psychiatric admission
Voluntary
Adult or emancipated minor
Understands legal aspects and signs form
302 psychiatric admission
Involuntary Commitment
Requires a petitioner and a physician, and involvement of County Crisis Team
Must offer voluntary option
In PA, lose right to buy a gun
Medical psychiatric clearance minimum testing
Electrolytes, BUN, Creatinine CBC LFT’s O2 Sat. by pulse oximeter or ABG’s if COPD EKG over 40 CT if recent head trauma
If there is decreased breath sounds and hypotension, you should suspect
ptx
crystalloids in traumas have what kind of outcome
bad outcomes (NS/LR) best is blood transfusion for hypotension/hypovolemia
heat rash
Skin irritation due blocked sweat ducts trapping sweat beneath the skin
Typically found on the neck, chest, groin, in skin folds
Rash may be papular, pustular or vesicular
May sting or be pruritic
Typically self-limiting
SxS of heat stroke
Elevated core temp (typically >40.5°C)
Hot, dry skin (although some patients are diaphoretic)
Vague prodrome – HA, N/V, weakness
CNS symptoms – confusion, slurred speech, hallucinations, ataxia, seizures, syncope, delirium, coma
Hyperdynamic CV response – high CVP, low SVR, tachycardia
Elevated hepatic transaminases
Coagulopathy
Rhabdomyolysis and renal failure
Heat Stroke – Work-up
CT head – r/o cerebral edema
CXR – heat stroke can be complicated by ARDS
Labs – CBC, CMP, VBG, PT/PTT, CPK
EKG – may develop myocardial ischemia
Urinalysis – look for myoglobinuria (seen w/ rhabdo)
Rapid cooling measures in heat stroke
Evaporative cooling – fans, misting
Ice water immersion (most effective) – avoid prolonged cooling once to target temperature
Cool saline bags to neck, groin and axilla
Antipyretics are ineffective and may be harmful!
ADMIT pts
Complications of heat stroke
Disseminated Intravascular Coagulation (DIC)
Acute Kidney Injury
Rhabdomyolysis
Adult Respiratory Distress Syndrome (ARDS)
GI bleed
Hepatocellular Necrosis (Shock Liver) - iver susceptible to heat illness
Mortality <10% if treated appropriately but can have permanent neurologic injury in up to 20% of cases
frostnip
Mildest form of peripheral cold injury
Superficial nonfreezing cold injury secondary to vasoconstriction
Pale skin +/- associated numbness and paresthesia
Skin is still pliable (different than frostbite)
Chilblains (Perniones)
More severe than frostnip
Caused by exposure to nonfreezing temps and damp air
Onset within 1-5 hrs of cold exposure
Develops over hrs to days but subsides slowly over weeks
Develop red to violet raised lesions (papules or nodules)
Inflammatory lesions that may itch, burn or be painful
See on unprotected extremities – hands, feet
May progress to blisters, erosions or ulcers
Seen more in young and middle-aged women
Frostbite pathophysiology
Decreasing temperature results in decreased tissue perfusion – eventually temp low enough to form intra and extracellular water crystals that disrupt cell membranes and protein structures
Ultimately leads to cell death w/ tissue ischemia and necrosis
Frostbite – Four Degrees of Severity
First degree – hyperemia and edema
Second degree – hyperemia and edema AND large clear blisters
Third degree – hyperemia and edema and vesicles w/ hemorrhagic fluid (typically smaller than second degree)
Hemorrhagic fluid indicates deeper tissue injury
Fourth degree – most severe, complete necrosis with gangrene (typically dry)
Simpler classification (preferred by many clinicians) – superficial (1st & 2nd degree) vs deep (3rd & 4th degree)
What sign is concerning in frostbites
loss of pain
Frostbite Tx
Initial treatment of choice = rapid rewarming in a water bath at a temperature of 39-42°C (102.2-107.6°F)
Continue until extremity has a flushed appearance (typically 30-45 min)
Monitor temperature of water bath closely
Process is painful!!
tetanus prophylaxis if hemorrhagic blisters (deeper)
Hunter’s Response
Initial vasoconstriction followed by a paradoxical and cyclical vasodilatation in response to cold that often occurs in the fingers, toes, and face.
cold induced vasodilation
Temp of mild v moderrate hypothermia
Mild hypothermia (32-35°C) – vigorous shivering, hyperventilation, tachypnea, tachycardia, and cold diuresis as renal concentrating ability is compromised.
Moderate hypothermia (28-32°C) – further CNS depression, hypoventilation, hyporeflexia, decreased renal flow, and paradoxical undressing may be noted. Higher risk of arrhythmias, presence of J-wave on EKG Pupils become dilated and minimally responsive
severe hypothermia
Severe hypothermia (<28°C) – marked susceptibility to v-fib, pulmonary edema, oliguria, coma, hypotension, rigidity, apnea, pulselessness, areflexia, unresponsiveness, fixed pupils, and decreased or absent activity on EEG Metabolic acidosis, rhabdomyolysis “They’re not dead till they’re warm and dead.”
Who gets antibiotic prophylaxis in bites?
pretty much everyone!
if no infection, 3-5days; if infection, 5-14days
Incubation time for rabies
2wks to 40-45days
exception to tetanus prophylaxis in bites
insects
Coma cocktail
for patient with altered consciousness
Dextrose to treat hypoglycemia: If rapid bedside glucose monitoring (1st) is not available or reveals low/near-low levels
Thiamine to prevent Wernicke’s encephalopathy
Nalaxone for suspected opioid intoxication
common anticholinergic agents
Antihistamines: Diphenhydramine (Benadryl, common people take for sleeping), hydroxyzine, meclizine (motion sickness) Antispasmotics:Dicyclomine, oxybutynin Atropine TCA’s: Amitriptyline Sleep aids (RX and OTC) Jimson Weed
cholinergics produce the same effects as what system
parasympathetic system
Heparin antidote
protamine sulfate
CO toxicity presents as
cherry red face
fomepizole and ethanol MOA as antidotes for toxic alcohols
fomepizole inhibits alcohol dehydrogenase which metabolizes the toxic alcohols
ethanol is competitive inhibitor of ADH
