Common Problems in Acute Care Flashcards
Amphetamines (e.g. MDMA): presentation
euphoria, elation
dilated pupils
agitation, anxiety, insomnia
tachycardia, hypertension
vomiting
decreased appetite
tremors, muscle twitching, bruxism
perspiration, chills, pallor
resolves 24-48 hours after ingestion
pneumocystis jirovecii: CXR
bilateral interstitial infiltrates
pneumocystis jirovecii: treatment
TMX-SMZ
malignant hyperthermia
Genetic disorder that causes a fast rise in body temperature and severe muscle contractions when someone receives general anesthesia with one or more of the following drugs: (DISH-Succ)
- desflurane
- isoflurane
- sevoflurane
- halothane
- succinylcholine
malignant hyperthermia: Dx
caffeine halothane contracture test
Usually based on clinical signs and symptoms
malignant hyperthermia: signs
Earliest indication: increased end-tidal CO2 that is resistant to increases in minute ventilation
Late sign: hyperthermia
tachyarrhythmias
tachypnea
acidosis
malignant hyperthermia: treatment
dantrolene - interferes with muscle contraction by inhibiting calcium ion release from the sarcoplasmic reticulum
malignant hyperthermia: ABG
respiratory acidosis
malignant hyperthermia: SVO2
decreased d/t significantly increased O2 consumption
organophosphate (insecticide, pesticide) poisoning: S/Sx
AMS, slurred speech, coma
Headache
Miosis, blurred vision
Lacrimation
Excessive salivation
Bradycardia
Diffuse wheezing
diaphoresis
N/V/D, cramping
Urination
organophosphate (insecticide, pesticide) poisoning: management
atropine
sodium nitrite
Wash skin thoroughly
If insecticide was ingested, give activated charcoal
cutaneous anthrax: S/Sx, presentation
begins 1-7 days after exposure to infected livestock or livestock products
Painless pruritic papule appears and rapidly develops into an ulcer within 24 hours
Over the next 72 hours, the ulcer becomes dry and dark with surrounding edema (“black eschar”)
May cause bacteremia
cutaneous anthrax: Dx
BC negative unless bacteremia
Tissue biopsy with gram stain, culture, and immunohistochemical stain to confirm Dx
arsenic poinsoning: S/Sx
diarrhea with negative workup
Leukonychia (white lines on nails)
Major causes of anion gap metabolic acidosis
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Iron, Isoniazid
Lactate
Ethanol, Ethylene glycol
Salicylates
Normal anion gap
8-12
How to calculate anion gap
Na - (Cl + HCO3)
necrotizing fasciitis: S/Sx
Early: flu-like symptoms
Later:
-rapidly spreading erythema
-pain extending beyond borders of erythema
-palpable crepitus
-Swelling of affected tissues
-Blisters filled with bloody or yellowish fluid
-Tissue death (necrosis)
-hypotension, sepsis
necrotizing fasciitis: labs/Dx
CT
necrotizing fasciitis
Infection of the fascia
Systemic toxicity
testicular torsion: presentation
acute onset of unilateral testicular pain after exercising
high riding testes
“bell-clapper deformity”
absent cremasteric reflex
testicular torsion: management
immediate surgical exploration
intraoperative detorsion with fixation of the testes
delay in correction of testicular torsion results in…
necrosis of testicular tissue d/t ischemia
If surgery is unavailable within two hours, manual detorsion can be attempted
WHO Ladder of Pain Management: Step 1
Non-opioid +/- adjuvant (not traditionally used as 1st line for pain, e.g. nortriptylline)
WHO Ladder of Pain Management: Step 2
Choice from Step 1 [non-opioid +/- adjuvant] PLUS
Codeine
Dihydrocodeine
Oxycodone
Hydrocodone
Tramadol (not with ASA/APAP)
+/- adjuvants
WHO Ladder of Pain Management: Step 3
Choice from Step 1 [non-opioid +/- adjuvant] PLUS
Morphine
Hydromorphone
Methadone
Levorphanol
Fentanyl
Oxycodone
+/- Nonopioid analgesics
+/- adjuvants (e.g. surgery for terminal cancer)
What is recommended for breakthrough cancer pain?
fentanyl patches for sustained release
Metastatic bone pain: management
bisphosphonates – inhibit bone resorption and prevent the development of cancer-induced bone lesions
Stage 1 Pressure Injury
Intact skin with erythema that does not blanch
Does not include purple or maroon discoloration
Stage 2 Pressure Injury
Partial-thickness loss of skin with exposed dermis
Wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister
Adipose and deeper tissues are not visible
Should not be used to describe moisture associated skin damage including incontinence associated dermatitis, intertriginous dermatitis, medical adhesive related skin injury, or traumatic wounds (skin tears, burns, abrasions)
Stage 3 Pressure Injury
Full-thickness skin loss
Adipose is visible and granulation tissue and epibole (rolled wound edges) are often present
Slough and eschar may be visible but do not obscure the extent of tissue loss
Stage 4 Pressure Injury
Full-thickness skin and tissue loss
Exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone
Slough and/or eschar may be visible but do not obscure the extent of tissue loss
Epibole (rolled wound edges), undermining, and/or tunneling often occur
Unstageable Pressure Injury
Obscured full-thickness skin and tissue loss
Extent of tissue damage cannot be confirmed because it is obscured by slough or eschar
Stable eschar on the heel or ischemic limb should not be softened or removed
Deep Tissue Pressure Injury
Intact or non-intact skin with localized areas of persistent non-blanch able deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister
Do not use to describe vascular, traumatic, neuropathic, or dermatologic conditions
Pressure injury management considerations
hypoalbuminemia – reliable factor for pressure ulcer development (normal: 3.5-5)
wound care specialist consult
dressings
- weeping: hydrocolloid dressing
Initial treatment of post-op fever
In the absence of any indication of infection, the first response should include hydration and measures to expand lung function
Causes of non-infectious post-op fever
post-op atelectasis
increased basal metabolic rate
dehydration
drug reactions
-amphotericin B
-bactrim
-beta-lactam antibiotics
-procainamide
-isoniazid
-alpha-methyldopa
-quinidine
treatment of infectious post-op fever
supportive fluid and acetaminophpen
treat the apparent underlying source
gram stain, C&S all invasive lines or catheters as indicated
hypoalbuminemia
Increased risk for drug toxicity and interactions
Indicates protein malnutrition
Indications for duodenal tube
Able to use GI tract safely
Does not need tube feeds for >6 weeks
Risk for aspiration
Indications for NG tube
Able to use GI tract safely
Does not need tube feeds for >6 weeks
Not at risk for aspiration
Indications for PEG
Able to use GI tract safely
Needs tube feeds for >6 weeks
Indications for PPN
Unable to use GI tract safely
Does not need nutritional support for >2 weeks
Can administer via PIV
Indications for TPN
Unable to use GI tract safely
Needs nutritional support for >2 weeks
Administer via central line
Complications of enteral nutritional support
Involve the solution itself
Aspiration
Diarrhea (Is formula too concentrated? Switch bolus to continuous feeds? Slow down the rate?)
Emesis
GI bleeding
Mechanical obstruction of the tube
Hypernatremia
Dehydration
Refeeding syndrome
Refeeeding syndrome: labs
Hypophosphatemia
hypokalemia
hypomagnesemia
hypocalcemia
thiamine deficiency
Complications of parenteral nutritional support
Involve the mode of delivery
Pneumothorax
Hemothorax
Arterial laceration
Air emboli
Catheter thrombosis
Catheter sepsis
Hyperglycemia
HHNK
First and most important step in managing poisoning/drug toxicities
Obtain a detailed history
Poisoning/drug toxicities: GI decontamination
Gastric lavage
Activated charcoal – most beneficial within the first hour of ingestion
Cathartics – not routinely indicated with activated charcoal
-exception: Sorbitol often used with first dose of activated charcoal
Whole bowel irrigation – using polyethylene glycol to treat enteric-coated or sustained-release overdoses
Antidotes
Acetaminophen intoxication: S/Sx
Usually asymptomatic in the early phase
Around 24-48 hours:
-N/V
-RUQ pain
-Signs of hepatotoxicity: jaundice, elevated LFTs, prolonged PT, -AMS, delirium
Acetaminophen intoxication: management
1st line: emesis or gastric lavage
Activated charcoal
N-Acetylcysteine (Mucomyst) with a loading dose of 140 mg/kg orally, as needed
Acetaminophen intoxication: examples
Acetaminophen
Anacin-3
Panadol
Salicylate intoxication: examples
aspirin
Salicylate intoxication: S/Sx
Delayed
HA, dizziness, tinnitus
apnea, cyanosis
dehydration
N/V
hyperthermia
metabolic acidosis
elevated LFTs
salicylate intoxication: management
activated charcoal
sodium bicarbonate IV to correct severe acidosis (pH <7.1)
treat S/Sx
gastric lavage
organophosphate (insecticide, pesticide) poisoning: examples
malathion
parathion
antidepressant toxicity: S/Sx
Confusion, hallucinations, blurred vision
Seizures
Hypotension, tachycardia, dysrhythmias
Hypothermia
Urinary retention
antidepressant toxicity: management
ICU if CNS or cardiac toxicity evident
Activated charcoal
Dysrhythmias, acidosis/maintain pH: Sodium bicarbonate IV
Seizures: Benzodiazepines
Serotonin syndrome: dantrolene (Dantrium)
Rigors: clonazepam (Klonopin)
Temperature: cooling blankets
Opioid toxicity: S/Sx
drowsiness
hypothermia
respiratory depression, shallow respirations
miosis
coma
opioid toxicity: management
activated charcoal
naloxone (Narcan)
emetics are contraindicated
benzodiazepine toxicity: S/Sx
drowsiness, confusion
slurred speech
hyporeflexia
respiratory depression
benzodiazepine toxicity: management
respiratory and BP support
Flumazenil (Romazicon) IV
activated charcoal if recent ingestion
beta blocker overdose: S/Sx
delirium
hypotension
sinus bradycardia
bronchospasm
coma
beta blocker overdose: management
Charcoal if recent ingestion
glucagon
atropine as needed
stabilization of airway
ethylene glycol (antifreeze) overdose: S/Sx
First stage (30 min-12 hrs)
- loss of coordination
- headache
- slurred speech
- N/V
Second stage (12-24 hrs)
- irregular heartbeat
- shallow breathing
- Changes in BP
Third stage (24-72 hrs)
- kidney failure
TCA toxicity: treatment
sodium bicarbonate
ethylene glycol (antifreeze) overdose: management
Fomepizole (Antizole)
Ethanol (if fomepizole not available)
Compartment syndrome
Increased interstitial pressure within a closed fascial compartment (skin, fascia, muscle, bone)
May result from hemorrhage, edema, sustained external pressure on a limb or constrictive casts, dressings, etc.
Should be suspected in any unconscious patient with a swollen limb
Compartment syndrome: S/Sx
severe ischemic pain
parasthesias
tensely swollen
skin perfusion, arterial pulses normal
passive stretch of muscle is painful
progressive loss of sensory/motor function
repeated examinations are required to check for developing compartment syndrome
Compartment syndrome: Diagnostics
Often using a Stryker tonometer; Normal compartment pressure: 0-8 mm Hg
>30 mmHg: Indicates compartment syndrome and a need for fasciotomy
- Within 10-30 mmHg of DBP: Indicates inadequate perfusion and relative ischemia of the involved extremity
Delta pressure: perfusion pressure of a compartment
= (diastolic BP) - (intracompartmental pressure)
<30 mmHg: indicates need for fasciotomy
compartment syndrome: management
release constricting appliances
fasciotomy: effective only if performed within a few hours
Dog, cat, human bites: management
Timely, copious, high-pressure irrigation with NS to reduce infection rates
Animal bites: ascertain rabies status
Wounds of the hand or lower extremities should be left open
- >6 hours: leave open to heal by secondary intention
Human and animal bites: ppx ABx to cover staphylococci and anaerobes (e.g. Augmentin) x3-7 days
X-rays as needed
Plastic surgery consultation as appropriate
staphylococcus: class
gram positive
streptococci: class
gram positive
enterococci: class
gram positive
bacilli: class
gram positive
corynebacterium: class
gram positive
serrate marcescens: class
gram negative
escherichia coli: class
gram negative
klebsiella: class
gram negative
pseudomonas: class
gram negative
proteus mirabilis: class
gram negative
Moraxella catarrhalis: class
gram negative
acinetobacter: class
gram negative
enterobacter: class
gram negative
acute otitis media: most likely pathogen and empiric therapy
S. pneumoniae
Empiric therapy:
-amoxicillin
-augmentin
-cefuroxime
-bactrim
sinusitis: most likely pathogen and empiric therapy
S. pneumoniae
Empiric therapy:
-amoxicillin
-augmentin
-cefuroxime
-bactrim
acute endocarditis: most likely pathogen and empiric therapy
staphylococcus aureus
vancomycin + ceftriaxone
subacute endocarditis: most likely pathogen and empiric therapy
viridian streptococci, enterococci
penicillin + gentamicin
peritonitis d/t ruptured viscus: most likely pathogen and empiric therapy
coliforms
bacteroides fragilis
empiric therapy: metronidazole +
-cephalosporin 3rd generation (ceftriaxone, ceftazidime)
-pip/tazo
intra abdominal infection: most likely pathogen and empiric therapy
E. coli
Klebsiella
Enterococci
empiric therapy: metronidazole +
-cefuroxime
-ceftriaxone
-ciprofloxacin
-levofloxacin
cellulitis: most likely pathogens and empiric therapy
staphylococcus aureus
Group A streptococcus
1st generation cephalosporin (cefazolin)
vancomycin
clindamycin
daptomycin
linezolid
s. pneumoniae is the #1 pathogen causing…
otitis media
sinusitis
bronchitis
meningitis
CAP
colorectal, non-perforated appendectomy: ABx prophylaxis for staphylococci, streptococci, enteric gram-negative rods
cefazolin
colorectal, non-perforated appendectomy: ABx prophylaxis for MRSA+
vancomycin
colorectal, non-perforated appendectomy: ABx prophylaxis for enteric gram-negative rods, anaerobes
metronidazole plus:
-cefoxitin
-cefotetan
-cefazolin
sepsis: most likely pathogens and empiric therapy
staphylococcus aureus
empiric therapy:
- 1st generation cephalosporins (cefazolin, cephalexin)
- 5th generation cephalosporins (ceftaroline)
vancomycin
linezolid
osteomyelitis: most likely pathogens and empiric therapy
staphylococcus aureus
empiric therapy:
- 1st generation cephalosporins (cefazolin, cephalexin)
- 5th generation cephalosporins (ceftaroline)
vancomycin
linezolid
CAP: most likely pathogens and empiric therapy
streptococcus pneumoniae
amoxicillin + macrolide (azithromycin)
MRSA: empiric therapy
1st line treatment: vancomycin
Alternative:
-daptomycin
-linezolid
-doxycycline
-ceftaroline
-clindamycin
-bactrim
pharyngitis: most likely pathogen and empiric therapy
streptococcus pyogenes
Empiric therapy: vancomycin
impetigo: most likely pathogen and empiric therapy
streptococcus pyogenes
Empiric therapy: vancomycin
meningitis: most likely pathogen and empiric therapy
staphylococcus pneumoniae
empiric therapy: penicillin G
Cephalosporins: best Gram+ coverage
1st generation: cefazolin, cephalexin
Cephalosporins: best Gram- coverage
5th generation: ceftaroline
Acute rejection of an organ: presentation
Immediate failure of that organ
Flu-like symptoms
Acute rejection of an organ: labs/Dx
immediate biopsy of the transplanted organ
Acute rejection of an organ: management
- corticosteroid:
- methylprednisolone
- prednisone - antimetabolite:
- azathioprine (Imuran)
- mycophenolate mofetil (CellCept)
- mycophoneolate sodium (Myfortic)
- cyclophosphamide (Cytoxan) - calcineurin inhibitor or mammalian target of rapamycin inhibitor:
- calcineurin inhibitors: tacrolimus, cyclosporine
- mTOR inhibitors: sirolimus, temsirolimus, everolimus
Shingles: S/Sx
Pain along a dermatomal distribution, usually on the trunk or chest
Grouped vesicle eruption of erythema and exudate along the dermatomal pathway
Regional lymphadenopathy may be present
Shingles: management
Treatment:
-acyclovir
-famciclovir
-valacyclovir
If suspected ocular involvement, immediate referral to ophthalmologist
Post-herpetic neuralgia: gabapentin, pregabalin
Shingles vaccine
Indicated for all adults >50, regardless of previous vaccine
- two dose regimen with 2nd dose given 2-6 months after 1st dose
actinic keratoses
Premalignant
Asymptomatic, small rough flesh colored/pink/hyperpigmented patches
actinic keratoses: treatment
liquid nitrogen to freeze off
squamous cell carcinoma
arise out of actinic keratoses
Firm, irregular papule or nodule
squamous cell carcinoma: management
biopsy and surgical excision (Mohs)
seborrheic keratoses
benign, not painful lesions
beige, brown, or black plaques
“stuck on” appearance
seborrheic keratoses: treatment
none or liquid nitrogen
basal cell carcinoma
Most common skin cancer
Slow growing lesion
Waxy pearly appearance, may be shiny red
Central depression or rolled edge
May have telangiectatic vessels
basal cell carcinoma: treatment
shave/punch biopsy and surgical excision
malignant melanoma: criteria
highest mortality rate of all skin cancers
Median age at diagnosis: 40
Yes to 2+ = 97% sensitive to malignant melanoma:
- Assymetry
- Border irregularity
- Color variation
- Diameter >6 mm
- Elevation, Enlargement
malignant melanoma: treatment
biopsy and surgical excision
brain death criteria
coma
absence of brain stem reflexes
apnea
most important feature of headaches to assess in order to determine the type of headache
chronology
Components of headache evaluation
Chronology – most important
Location, duration, quality
Associated activity: exertion, sleep, tension, relaxation
Timing of the menstrual cycle
Presence of associated symptoms
Presence of “triggers”
most common type of headache
tension headache
tension headache: S/Sx
vise-like or tight in quality
usually generalized
may be most intense around the neck or back of the head
no associated focal neurological symptoms
usually last for several hours
migraine headaches: causes
Related to dilation and excessive pulsation of branches of the external carotid artery
Onset usually in adolescence or early adult years
Often family history
Females > males
Nitrate containing foods
Changes in weather
migraine triggers
emotional or physical stress
lack or excess sleep
missed meals
specific foods, esp nitrate containing foods
alcohol
menstruation
OCPs
changes in weather
migraines: S/Sx
Unilateral, lateralized throbbing headache that occurs episodically
May be dull or throbbing
Build gradually and last typically for 2-72 hours
Focal neurologic disturbances may precede or accompany migraines (may present like TIA)
Follow the trigeminal nerve pathway
Visual disturbances: field deficits, luminous visual hallucinations
Aphasia, numbness, tingling, clumsiness, or weakness
Nausea, vomiting
Photophobia, phonophobia
Concerns with new migraines
rule out tumor
migraines: labs/Dx
BMP, CBC
VDRL to rule out tertiary syphillis
ESR
head CT to rule out tumor
migraines: prophylaxis
Avoidance of trigger foods
Relaxation/stress management
Prophylactic daily therapy if >2-3 acute attacks/month
migraines: prophylactic daily therapy
Anticonvulsants: topiramate, valproic acid
Beta-blockers: atenolol, metoprolol, propranolol, timolol
Botox: around face and scalp Q3 months; indicated if >15 headaches/month
CCBs: diltiazem, verapamil
TCAs: amitriptyline, nortriptyline
Calcitonin gene-related peptide (CGRP) inhibitors: eptinezumab, erenumab, fremanezumab, galcanezumab
NSAIDs and certain triptans: naproxen; can be helpful in treating women with migraines that are associated with menstrual cycle
migraines: management of an acute attack
Rest in a quiet, dark room
Simple analgesic (ASA) right away
Sumatriptan (Imitrex) 6mg SQ at onset, repeat in 1 hour TID PRN
Sumatriptan (Imitrex) 25mg PO at onset of headache
Cluster headaches: incidence
mostly affecting middle aged women
Cluster headaches: causes
Often no family history of headache or migraine
May be precipitated by alcohol
Cluster headaches: S/Sx
Severe, unilateral, periorbital pain occurring daily for several weeks
Usually occur at night, awakening the person from sleep
Usually lasts less than 2 hours
Pain free months or weeks between attacks
Ipsilateral nasal congestion, rhinorrhea, and eye redness may occur
Cluster headaches: management
Treatment of individual attacks with oral drugs is usually unsatisfactory
100% O2
Sumatriptan (Imitrex) 6mg SQ
Ergotamine tartrate aerosol inhalation (Ergostat)
most common electrolyte abnormality
hyponatremia
hyponatremia: first step in treating
determine the cause
hyponatremia: evaluation to determine the cause
Urine sodium
Serum osmolality
Clinical status
normal urine sodium
10-20 mEq/L
normal urine osmolality
50-1200 mOsm/kg
normal serum osmolality
275-295
isotonic hyponatremia: labs
serum osmolality 284-295 mOsm/kg
isotonic hyponatremia
A laboratory artifact
Occurs with extreme hyperlipidemia or hyperproteinemia
Asymptomatic
isotonic hyponatremia: treatment
cut down fat
no fluid restriction
hypotonic hyponatremia: labs
serum osmolality <280 mOsm/kg
hypotonic hyponatremia
State of body water excess diluting all body fluids
hypotonic hyponatremia: first step in management
Assess if the patient is hypovolemic or hypervolemic
If hypovolemic, determine if hyponatremia is due to extrarenal salt losses or renal salt wasting by measuring urine sodium
urine sodium >20 mEq/L
suggests renal salt wasting (a problem with the kidneys)
urine sodium <10 mEq/L
suggests renal retention of sodium to compensate for extrarenal fluid losses (a problem other than the kidneys)
hypovolemic hyponatremia w/urine Na+ <10 mEq/L: causes
dehydration
diarrhea
vomiting
hypovolemic hyponatremia w/urine Na+ >20 mEq/L: causes
diuretics
ACE inhibitors
mineralocorticoid deficiency
hypervolvemic, hypotonic hyponatremia: causes
edematous states
CHF
liver disease
advanced renal failure
hypervolvemic hypotonic hyponatremia: treatment
restrict water
hypertonic hyponatremia: serum osmolality
> 290 mOsm/kg
hypertonic hyponatremia: cause
hyperglycemia – most common cause
rapid correction of hyponatremia can result in…
osmotic demyelination syndrome
hypovolemic hyponatremia: management
mild (Na >120): NS
severe (Na <120): 3%
hyponatremia w/urine Na+ >20 mEq/L: management
treat the cause (diuretics, ACEIs, mineralocorticoid deficiency)
Symptomatic hyponatremia: management
NS with loop diuretic
If CNS symptoms are present, consider 3% saline with loop diuretics
- raise Na+ slowly. Too fast can cause cerebral edema
Hypernatremia: causes
Usually due to excess water loss
Always indicates hyperosmolality
Excessive sodium intake is rare
normal sodium
135-145 mEq/L
hypernatremia: management
Depends on cause
Severe hypernatremia with hypovolemia: NS (isotonic to increase BP) followed by 1/2 NS (when normotensive)
Hypernatremia with euvolemia: free water (D5W)
Hypernatremia with hypervolemia: free water and loop diuretics; may need dialysis
Normal potassium
3.5-5.2 mEq/L
hypokalemia: causes
Diuretics
GI loss
Excess renal loss
Alkalosis
Trauma patients: elevated serum epinephrine
hypokalemia: S/Sx
muscle weakness, fatigue, cramps
constipation or ileus d/t smooth muscle involvement
Severe (<2.5): flaccid paralysis, tetany, hyporeflexia, rhabdomylosis
hypokalemia: EKG changes
decreased amplitude
broad T waves
prominent U waves
PVCs, VT, VF
hypokalemia: management
If K >2.5 mEq and no EKG abnormalities: oral replacement
If K <2.5 mEq or severe signs/symptoms: 40 mEq/L/hr IV
-check Q3h
-continuous telemetry
Mg+ deficiency frequently impairs K+ correction
hyperkalemia: causes
Excess intake
Renal failure
Drugs (e.g. NSAIDs)
Hypoaldosteronism
Cell death
Acidosis
hyperkalemia: S/Sx
weak, flaccid paralysis
Abdominal distention
Diarrhea
hyperkalemia: EKG changes
tall, peaked T waves
hyperkalemia: management
Exchange resins (e.g. Kayexalate)
If >6.5 or cardiac toxicity or muscle paralysis is present:
- insulin 10 U with one amp D50
- calcium gluconate
normal total calcium
2.2-2.6 mmol/L
8.5-10.5 mg/dL
normal ionized calcium
1.1-1.4 mmol/L
4.5-5.5 mg/dL
ionized calcium
Does not vary with the albumin level
-Useful to measure when serum albumin is not within normal range
Increases with acidemia, decreases with alkalemia
What does a normal calcium level in the presence of low albumin suggest?
hypercalcemia
hypocalcemia: causes
hypoparathyroidism
hypomagnesemia
pancreatitis
renal failure
severe trauma
multiple blood transfusions
hypocalcemia: S/Sx
increased DTRs
muscle/abdominal cramps
convulsions
Chvostek’s sign
Trousseau’s sign (captopedal spasm)
prolonged QT
Chvostek’s sign
twitching of ipsilateral facial muscles on percussion d/t irritability of facial nerve
sign of hypocalcemia
hypocalcemia: management
check blood pH for alkalosis
acute: IV calcium gluconate
chronic: oral supplements, vitamin D, aluminum hydroxide
hypercalcemia: causes
hyperparathyroidism
hyperthryroidism
vitamin D intoxication
prolonged immobilization
rarely, thiazide diuretics
hypercalcemia: S/Sx
fatiguability
muscle weakness
depression
anorexia
N/V
constipation
severe hypercalcemia can cause coma and death
hypercalcemia: management
calcitonin if impaired cardiovascular or renal function
NS with loop diuretics
severe: dialysis
respiratory acidosis: labs
pH <7.35
pCO2 >45
respiratory acidosis: cause
decreased alveolar ventilation
respiratory acidosis: S/Sx
somnolence
confusion
coma
myoclonus with asterixis
normal pH
7.34-7.45
normal pCO2
35-45
normal HCO3-
22-26
normal PaO2
75-100
respiratory acidosis: management
narcan for all patients with no obvious cause
improve ventilation, intubate if necessary
increase rate on ventilator
respiratory alkalosis: cause
hyperventilation
respiratory alkalosis: labs
pH >7.45
pCO2 <35
serum HCO3 low if chronic
respiratory alkalosis: S/Sx
light-headedness
anxiety
parasthesias
stocking/glove tingling
tetany if very severe
respiratory alkalosis: management
manage underlying cause
If an acute hyperventilation syndrome is present, have the patient breathe into a paper bag
Decrease rate on ventilator as needed
Sedation if needed
Rapid correction of chronic alkalosis may result in metabolic acidosis
metabolic acidosis: labs
pH <7.35
HCO3 <22
anion gap formula
Na - (HCO3 + Cl)
normal anion gap
5-15
metabolic acidosis with increased anion gap: causes
DKA
alcaholic ketoacidosis
lactic acidosis
metabolic acidosis with normal anion gap: causes
diarrhea
ileostomy
renal tubular acidosis
recovery from DKA
metabolic acidosis: management
treat underlying cause
fluid resuscitation
metabolic alkalosis: labs
pH >7.45
HCO3- >26
pCO2 >55 compensatory
metabolic alkalosis: causes
post-hypercapnia alkalosis
NG suction
vomiting
diuretics
metabolic alkalosis: management
correct volume deficit with NaCl and KCl
-if volume replacement is contraindicated: acetazolamide 250-500mg IV Q4-6 hours
discontinue diuretics
H2 blockers if GI loss
1st degree burn
dry, red, no blisters
involves epidermis only
2nd degree burn
partial thickness
moist, blisters
extends beyond epidermis
3rd degree burn
full thickness
dry, leathery, black, pearly, waxy
extends from epidermis to dermis to underlying tissues, fat, muscle and/or bone
Adult Rule of Nines
Each arm = 9%
Each leg = 18%
Thorax: front = 18%, back = 18%
Head = 9%
Perineum/genitals = 1%
Parkland formula
4 ml/kg x TBSA % burned = fluid in 24 hours
Fluid resuscitation in burns
1/2 of all fluid requirements during the first 24 hours administered within 8 hours of injury
Remaining 1/2 of fluid to be given over the next 16 hours
burns: monitoring
metabolic acidosis expected in the early resuscitation phase
hyperkalemia during the first 24-48 hours; hypokalemia following fluid resuscitation/diuresis around 2 days post burn
burns: indications for prophylactic intubation
burns to the face
singed nares or eyebrows
dark soot/mucous from nares and/or mouth
tar burn injury: management
use a petroleum-based product to remove the burning tar
diabetic retinopathy: S/Sx
microaneurysms are the earliest detectable sign
-ruptured microaneurysms results in retinal hemorrhages either superficially (flamed-shaped hemorrhages) or in deeper layers of the retina (blot and dot hemorrhages)
cotton-wool spots
AV nicking
sign of chronic hypertension
Arcus sinilis
a cloudy appearance of the cornea with a gray/white arc or circle around the limbus d/t deposition of lipid material
no effect on vision
cause: hyperlipidemia
chemical conjunctivitis: management
self-limiting
flush with normal saline
bacterial conjunctivitis: management
self-limiting
antibiotic drops (e.g. levofloxacin, ofloxacin, ciprofloxacin, tobramycin, gentamycin ophthalmic solution)
gonococcal conjunctivitis: management
opthalmic emergency
ceftriaxone 250mg IM + azithromycin
chlamydial conjunctivitis: management
ceftriaxone 250mg IM + azithromycin
allergic conjunctivitis: management
oral antihistamines
-refer to allergist/ophthalmologist if no response
steroids are not ordered in primary care because of possible increased intraocular pressure and activation of HSV
viral conjunctivitis: management
symptomatic care
-mild: saline drops, artificial tears
-moderate: decongestants, antihistamines, mast cell stabilizers, NSAIDs
Sulfacetamide 10% ophthalmic solution for bacterial (secondary) prophylaxis
herpetic conjunctivitis: management
refer to ophthalmologist
What type of conjunctivitis has purulent discharge?
bacterial
copious: gonococcal
What type of conjunctivitis has stringy discharge and increased tearing?
allergic
What type of conjunctivitis has watery discharge?
viral
What type of conjunctivitis makes the conjunctiva bright red and irritated?
herpetic
glaucoma: pathology
increased intraocular pressure
closed angle: acute
open angle: chronic
closed angle glaucoma: S/Sx
closed angle: acute
-extreme pain
-blurred vision
-halos around lights
-pupil dilated or fixed
open angle glaucoma: S/Sx
Open angle: chronic
-asymptomatic
-elevated IOP
-cupping of the disc (earliest sign)
-constriction of visual fields
glaucoma: screening
tonometry: screening recommended by age 40
open angle glaucoma: management
Open angle: chronic
-prostaglandin analogs (latanoprost, bimatoprost, tafluprost, travoprost, latanoprostene bunod)
-alpha 2-adrenergic agonists (brimonide, alphagan)
-beta-adrenergic blockers (timolol)
-miotic agents (pilocarpine)
closed angle glaucoma: management
closed angle: acute
-carbonic anhydrase inhibitors (acetazolamide)
-osmotic diuretics (mannitol)
-surgery
cataract: pathology
clouding and opacification of the normally clear lens of the eye
highest cause of treatable blindness
cataract: causes
Aging – biggest risk factor
heredity
trauma
toxins, drugs, tobacco, alcohol
congenital
diabetes
UV sunlight exposure
cataracts: S/Sx
painless
clouded, blurred, or dim vision
difficulty with vision at night
sensitivity to light and glare
fading/yellowing of colors
diplopia in a single eye
halos around lights
the need for brighter light for reading
no red reflex
opacity of the lens
cataracts: management
refer to opthalmologist for surgery
sodium phosphate enemas: adverse effects
Significant electrolyte abnormalities in patients with renal insufficiency, heart failure, cirrhosis, or elderly frail individuals
cutaneous anthrax: management
post-exposure prophylaxis and treatment: 60 days of ciprofloxacin and doxycycline regardless of vaccination status
Penicillin is no longer recommended due to increased resistance
inhalation anthrax: treatment
raxibacumab
rifampin
Opioid withdrawal: S/Sx
Depressed mood
Insomnia
Mydriasis, lacrimation
Runny nose
Yawning
N/V/D
myalgias
diaphoresis
fever
Haemophilus influenzae: class
Gram negative
HAP: most likely pathogens and empiric therapy
S. aureus
S. pneumoniae
H. influenzae
empiric therapy:
-pip/tazo
-cefepime
-levofloxacin
-imipenem or meropenem
If MRSA suspected: + vancomycin or linezolid
If high risk of mortality or IV ABx within previous 90 days:
-two of above ABx + vancomycin or linezolid
VAP: most likely pathogens and empiric therapy
MRSA
- vancomycin or linezolid
pseudomonas aeruginosa
-pip/tazo
-cefepime or ceftazidime
-imipenem or meropenem
-aztreonam
-levofloxacin or ciprocloxacin
-amikacin or gentamicin or tobramycin
-colistin or polymyxin B
necrotizing fasciitis: pathogen and treatment
Group A streptococcus
Treatment: ampicillin, penicillin, and clindamycin
Surgery
beta lactam antibiotics: examples
penicillins
cephalosporins
carbapenems
monobactams (aztreonam)
beta lactamase inhibitors (clavulanic acid, sulbactam, and tazobactam)
placenta previa
Condition in which the placenta is implanted in the lower uterus, adjacent to or over the os
-Risk factors: multiple pregnancies, multiple surgeries
placenta previa: S/Sx
soft, nontender uterus
painless right red vaginal bleeding in the third trimester
abruptio placenta
premature separation of the placenta from the uterine wall
-risk factors: diabetes, renal disease, HTN, eclampsia, abdominal trauma
-DIC can occur
abruptio placenta: S/Sx
painful dark red bleeding
abdominal pain
methanol toxicity: S/Sx, labs
optic disc changes including hyperemia of the optic disc (engorged vessels)
anemia
leukocytosis
high osmolar gap
methanol toxicity: management
ethanol
hemodialysis
paronychia
infection of the lateral and proximal nail fold
Risk factors:
-nail biting
-diabetes
-sucking
-frequent immersion of hands in water
SJS/TEN involves __% of BSA
10-30%
Stevens-Johnson Syndrome: presentation
Erythematous, purpuric rash with scattered bullae that are often painful
Mucosal involvement: eyes, mouth, genitals
Involves <10% of BSA
Stevens-Johnson syndrome is most often associated with which drug
bactrim
treatment for delirium
1st line: antipsychotics
precedex
Avoid opioids, benzos
Kehr’s sign
Pain in the tip of the shoulder caused by irritation of the diaphragm due to the presence of blood in the peritoneal cavity
-characteristically occurs in the left shoulder in patients with a severe splenic injury
Obtain CT A/P
Who is at risk for infections caused by cryptococcal meningoencephalitis?
opportunistic infection seen in patients with untreated AIDS
Who is at risk for listeria monocytogenes?
neonates
immunosuppressed
pregnant
elderly
CAP d/t Legionella spp.: treatment
macrolides (azithromycin)
Main sign that a patient will likely need amputation of a limb
necrosis of the digits
cytomegalovirus: S/Sx
profound diarrhea with little to no other abdominal or infectious symptoms
cytomegalovirus: treatment
ganciclovir (Cytovene)
abdominal compartment syndrome
Third spacing of fluids into the abdominal cavity –> distended, tense abdomen, which causes:
-increased pressure on the inferior vena cava, impeding blood return to the heart and causing a prerenal state of shock
-increased thoracic pressure
Massive transfusions and large amounts of IV fluid administration are risks for…
abdominal compartment syndrome
erythema multiforme
rash most commonly caused by HSV infection
Target lesions demonstrating 3 zones of color change
Can a patient’s decision to be an organ donor be overridden by family or HCP?
No
Call the local organ procurement agency
acute graft vs host disease: presentation
Within the first 100 days after bone marrow transplant
Involves skin, liver, GI system
Often febrile
Early stages can present with morbilliform rash
Sunburn-like rash with blistering is concerning for severe disease
Recommended carbohydrate intake
55-60% of diet
Increases with illness and trauma
