Emerg Flashcards
Criteria for consideration of termination of resuscitation
All of the following present:
1) Arrest not witnessed
2) No bystander CPR
3) No ROSC before transport
4) No shock delivered before transport
Epinephrine dose in asystole/PEA
1 mg IV/IO every 3-5 min
Epinephrine dose in anaphylaxis
1:1000 epinephrine
0.01 mg/kg, max 0.5mg
Every 5-15 min as needed
Autoinjector doses for various weights
<10kg –> 0.1 mg dose (Auvi-Q)
10-25 kg –> 0.15 EpiPen Jr
25+ –> 0.3 mg EpiPen
After 3 shocks for VF/pVT, consider what meds?
Amiodarone 300 mg IV/IO followed by 150 mg
Lidocaine 1-1.5 mg/kg IV/IO followed by 0.5-0.75
Ddx mnemonic for symptomatic/unstable bradycardia
Don’t led bradycardia patients DIE
Drugs
Ischemia
Electrolytes
(also many others)
Crystalloid fluid bolus quantity in critically ill patient (w/out fluid overload condition like CHF or advanced renal failure)
30 ml/kg (2-4 L in adults)
Initial management of patient with suspected sepsis (11)
2 large bore IVs
Lactic acid
Initial fluid bolus of 30 mL/kg over first 3 hours
CBC
CMP
2 sets blood cultures
CXR, EKG
Continuous sat monitoring/supplemental O2
Urinalysis w/ culture + pregnancy test in WOCBA
(LP if meningitis suspected)
Empiric ABs (ideally after blood cultures obtained)
(Pressors if continued high lactate or hypotension after fluid bolus)
Example of antibiotic approach to sepsis with source unclear?
Pip/tazo (broad spectrum GN, covers pseudomonas, tazo is B-lactamase inhib)
Vancomycin (GP/MRSA, quite narrow-spec)
Amikacin (aminoglycoside)
Diagnostic criteria for ARDS
1) Acute onset
2) Bilateral infiltrates on CXR consistent w/ pulmonary edema
3) Pulmonary artery wedge pressure <18 mmHg or clinical absence of left atrial hypertension - i.e. resp failure not accounted for by heart failure/fluid overload
4) Hypoxemia with PaO2/FiO2 <300 (ALI) or <200 (ARDS)
What test should be done post-cardiac arrest? If pt can’t follow commands what should be done?
EKG (cardiac ischemia may be cause of Vfib)
Comatose –> targeted temperature management (hypothermia 32-34C for 24-28hrs), EEG
Trauma resuscitation principle that reduces bleeding and improves outcomes (regarding vitals)
Permissive hypotension
SBP goal is 85-90 mmHg (preserves perfusion to brain + vital organs)
- note: permissive hypotension shouldn’t be applied to hypotensive trauma pts w/ mod-severe TBI bc low BP can increase secondary brain injury
Target MAP in septic shock management
Target urine output
Target CVP
MAP 65+
>0.5 mL/kg/hr
CVP 8-12 mmHg (normal range)
MAP formula
=2DBP + SBP / 3
If pt remains in shock after fluid resus, what pressors are given?
Norepinephrine (Levophed) drip
2nd line: vasopressin (improves cellular response to catecholamines)
If STILL doesn’t work –> corticosteroids
Initial issue that should be immediately managed in DKA?
Fluid deficits (can be up to 10L!)
2L saline bolus in adults
10-20 mL/kg saline in children
DKA: rehydration + insulin will lower serum glucose faster than clear ketones. Insulin infusion should be continued until when?
Until anion gap returned to normal
Add dextrose to IV infusion when glucose falls to ~15 to prevent hypoglycemia
What type of insulin do you give during DKA?
Short-acting (Regular)
___ replacement is often necessary before hypokalemia can be reversed
Mg (deficiency increases ROMK K+ secretion)
___, ____ ,and ____ confirm the diagnosis of DKA and are enough reason to start ____. Some providers prefer to wait for a ____ level before starting ____
Hyperglycemia, ketosis, and acidosis
Start fluids
Wait for K+ levels before starting insulin
DKA patients are almost always ___- and have significant ___ and ___ deficits regardless fo specific lab values
Dehydrated
Sodium/potassium
Antidote to beta-blocker overdose
Glucagon (increases HR/contractility bypassing beta-AR site)
True anaphylaxis is a ____ hypersensitivity reaction occurring after a previous sensitizing exposure
vs anaphylactoid?
Type 1
IgE-mediated activation of basophils/mast cells –> PG + leukotriene + histamine release
Anaphylactoid has release of these compounds through non-immune-mediated pathways so doesn’t require prior sensitization
Diagnosis of anaphylaxis
Any 1 of the following 3 criteria:
1) Acute onset w/ reaction of skin or mucosal tissue PLUS resp Sx or hypotension
2) Acute onset of 2+ of the following after exposure to a likely antigen (skin-mucosal tissue, resp, hypotension, GI)
3) Acute hypotension after exposure to known allergen (faintness, AMS)
No response to 3 epipens in anaphylaxis –>
IV epinephrine (2-10 ug/min for adults) *Can cause MI in pts w/ CAD
Give an example of a SAMA and a LAMA
SAMA: ipratropium bromide
LAMA: tiotropium bromide
Role of H1 and H2 antihistamines (and examples) in anaphylaxis
H1 antagonists such as cetirizine or diphenhydramine can be given for cutaneous symptoms (no affect on resp/CV/GI)
H2 (ranitidine) in combo with H1 for better cutaneous treatment
Diphenhydramine for vomiting
Big diff between first gen and 2nd gen H1 antihistamines?
First gen have central effect (sedating)
2nd gen used more as antiallergic
H2 antihistamines are indicated primarily for…
gastric reflux (block H2 receptors in parietal cells of gastric mucosa)
Cetirizine (Reactin), fexofenadine (Allegra) and loratadine (Claritin) are what type of antihistamine
2nd gen H1
Risk factors for severe anaphylaxis (4)
Hx of poorly-controlled asthma or COPD
Advanced age
Pregnancy
B-blocker or ACEi use
STEMI is a ___ infarct, NSTEMI/UA are ___ infarct/ischemia
Transmural
Subendocardial
STEMI is diagnosed when ST elevation is found in __ continuous ECG leads
2+
ACS management mnemonic
MONA greet chest pain at the door (immediate) Morphine Oxygen Nitroglycerine Aspirin 162 mg!!!
BASH later Beta-blockers ACEi/ARB Statins Heparin (e.g. enoxaparin = LMWH)
BOERHAAVE SYNDROME:
Barotrauma induced rupture of the esophagus, usually caused by vomiting.
Initial treatment of Boerhaave syndrome (if perforation is contained)
NPO status NGT placement w/ suction Broad-spectrum IV antibiotics Parenteral nutrition Analgesics + antiemetics urgent surgical consultation!
Treatment of uncomplicated pericarditis
Analgesics
NSAIDS
Colchicine
Define Mallory Weiss tear
Complications? (3)
Tear in mucosal layer @ esophageal-gastric junction
GI hemorrhage, intramural esophageal hematoma, perforation
1/3 of afibers are “lone Afibers” (no clear cause)
The most common causes are what?
PIRATES PE Ischemia (MI) Resp disease (e.g. COPD) Atrial enlargement/myxoma (atrial tumor) hyperThyroid Ethanol Sepsis/Sleep apnea
Also, systemic idsease (obesity/metabolic syndrome, diabetes)
CV diseases: CAD, Htn, valvular diseases, cardiomyopathy
Tenets of treating afib (4)
1) Address overall clinical status/instability
2) Determine/treat cause
3) Control rate and/or rhythm
4) Prevent thromboembolism
In the ED, ___ is generally the first priority in treating AFib
Ventricular rate control
Afib patients with valvular Afib, risk factors for stroke, or duration > ___ get what anticoag?
Duration > 48hrs
Therapeutic OAC 3+ weeks before cardioversion OR TEE to exclude LA thrombus (+enoxaparin)
+ anticoagulation 4 weeks post-cardioversion (long-term based on CHADS-65)
2 best drugs for rate control of Afib in the ED? 2 other options and why they aren’t as ideal?
CCBs & BBs are best (if pt already on something start by trying that)
Digoxin (slow onset, work via vagal mech, not as effective if high SNS tone, won’t control rate during exercise etc; may be combined w/ CCB or BB)
Amiodarone or Dronedarone (antiarrhythmics w/ some BB activity, less effective but could be 2-in-1)
Which CCB/BB has the lowest risk of hypotension and why?
Diltiazem, least negative inotropic effect
Consideration in pt w/ WPW & Afib?
Pharmacological/electrical cardioversion
NOT AV-block agent because can increase accessory pathway conduction –> Vfib
Why is thromboembolism very common post-conversion of AFib?
“Atrial stunning” (delayed onset of atrial contractility after cardioversion, lasts several week)
Or dislodging of old clot
3 exceptions to the 48 hour rule in afib?
Past stroke, mitral valve disease, severe LV dysfunction
Name 2 common drugs used for rhythm control in Afib
Propafenone (Class Ic Na-channel blocker, contraindicated in CAD)
Amiodarone (Class 3 K-channel blocker, preferred if any structural heart disease)
In pts w/ Afib, anticoagulation therapy traditionally consists of ___ with an INR goal of ____. Now what is preferred?
Warfarin
INR 2-3
Now DOACs preferred
Most common precipitant of acute HF exacerbations
Ischemia/infarction or noncompliance with meds/dialysis/diet
Name 1 specific cause of acute left HF and 1 specific cause of acute right HF
Left: sympathetic crisis w/ hypertension (increased afterload)
Right: pulmonary embolism
Name 3 causes of high-output HF
Thyrotoxicosis, anemia, AV fistulas (decreased PVR)
Name 2 causes of peripheral edema other than CHF
DVT
Hypoproteinemia (liver failure, nephrotic syndrome, renal failure)
Things that may be seen on CXR in heart failure in order of increasing L atrial pressure
Upper zone vascular redistribution (“cephalization”)
Kerley B lines (near costophrenic angles; =interstitial edema)
Perihilar “batwing” appearance (alveolar pulmonary edema)
Patient with CHF presenting with hypotension and poor perfusion (i.e. ____) may require what 3 therapies?
Cardiogenic shock
1) Inotropes (dobutamine or milrinone to enhance myocardial contracility)
2) Vasopressors (NE for coronary diastolic perfusion by increasing DBP)
3) Small fluid bolus (increase preload)
Patient with CHF exacerbation involving resp distress and very high blood pressure likely has…
Cardiogenic pulmonary edema secondary to catecholamine surge (hypertensive emergency)
What is the goal & treatment for Cardiogenic pulmonary edema secondary to catecholamine surge (hypertensive emergency)
Redistribution of fluid from pulmonary circulation to rest of body
1) Oxygenation
2) Reduce preload & afterload
3) Diuresis (only after adequate afterload reduction if pt clinically volume overloaded)
2 ways to reduce preload/afterload in cardiogenic pulmonary edema?
BiPAP (preload/afterload)
Nitroglycerine (preload/afterload)
ACEi (afterload)
____ is no longer recommended as standard therapy for CHF
Morphine
Approach to hypertensive encephalopathy
1) NCHCT to rule out mass lesion/stroke
2) IV antihypertensives to lower MAP by 10-15% in first hour, no more than 20-25% by end of first day (not to normal range!) - e.g. nicardipine (DCCB) or labetalol
General approach to hypertensive urgency
Reduce BP over days to weeks
Discharge from ED, f/u outpatient in 24-48 hrs
Examples of evidence of acute end-organ damage in hypertensive emergency
REtinal hemorrhages
Cerebral infarction/hemorrhage, encephalopathy (altered AMS)
MI, aortic dissection, acute LV failure (chest pain, dyspnea)
Acute pulmonary edema (e.g. dyspnea)
Acute renal failure (e.g. anuria)
Microangiopathic hemolytic anemia
Preeclampsia/eclampsia
According to traditional teaching, what drug is contraindicated in cocaine/sympathomimetic intox?
Beta-blockers (unopposed alpha stimulation –>vasospasm)
**newer research indicates may not be true in humans
Gold standard imaging to diagnose/rule out aortic dissection?
CTA
What is Cerebral Perfusion Pressure? (CPP) Significance of this in management of hypertensive emergency in a chronically hypertensive patient?
Proxy for Cerebral Blood Flow used for monitoring (can’t measure CBF directly)
CPP = MAP-ICP
CBF is being maintained at a higher CPP, so if you reduce MAP too fast –> cerebral hypoperfusion
Preferred antihypertensive for preeclampsia/eclampsia
Hydralazine
Acute cerebral infarction in the context of hypertensive crisis - general approach to BP management?
Acutely elevated BP often necessary to perfuse watershed areas, so generally don’t lower acutely
(cautious lowering if >220/120 may be ok)
EXCEPTION is if candidate for thrombolysis, then lower below 180/105
In ACS should beta blockers be administered immediately?
Better to wait until hemodynamically stable bc can exacerbate LV failure
What is the only hypertensive emergency where rapid, aggressive BP reduction is indicated? Why? BP & HR target?
Aortic dissection - need to reduce shear forces of LV ejection (prevent extension of dissection)
SBP 100-110
HR <60
First line medication for aortic dissection hypertensive emergency? 2nd line if BBs contraindicated?
Beta-blockers (simultaneously lower HR & BP)
CCB is 2nd line if can’t use BB
Delayed phase of asthma is more ____ and can be targeted with ____
Inflammatory
Corticosteroids
5 main classes of agents for acute asthma
1) Oxygen
2) Adrenergic agents (preferable inhaled salbutamol; epi or terbutaline if can’t inhale)
3) Anticholinergic (ipratropium bromide = SAMA)
4) Corticosteroids
5) Magnesium sulfate
Induction agent of choice for IPPV (or sedation during PPV if can’t tolerate fully awake)
Ketamine (catecholamine release, bronchodilation)
An asthmatic patient who is intubated should be set to promote the goal of…
Pemrissive hypercapnia (high risk for hyperinflation/auto-PEEP, so use low RR/TV, limit plateau pressures)
Asthmatics who are discharged from the ED should receive…
Salbutamol
MDI spacer device
3-10 day course oral steroids (stop based on Sx resolution & self-monitored peak flow)
Best way to assess asthma severity in the ED is history + physical &…
Peak expiratory flow
What is the role of ECG/CXR/ABG in PE diagnosis
Mostly to rule out other etiologies of Sx!
Utility of V/Q scans in PE diagnosis
Many patients with PE have normal V/Q scan (need to factor in clinical suspicion/other tests)
Most beneficial in pts w/ renal failure who can’t have CT contrast (or contrast allergies)
General gold standard for diagnosing/confirming PE? Caveat?
Computed tomography pulmonary angiography (CTPA)
*can lead to false-positives
First line test for DVT?
Venous duplex ultrasonography (esp good for iliac, femoral, popliteal veins)
In what location should DVT be anticoagulated?
Definitely if popliteal or above
Isolated calf DVTs may be anticoagulated (recommended if Hx or RFs) or repeat U/S in 1 week
____ is the preferred anticoagulant for initial treatment of DVT
Enoxaparin (LMWH), self-administered subQ injection patients can do at home
PE has a notoriously vague/variable presentation. What is the most “classic” triad of Sx?
Dyspnea
Pleuritic chest pain
Tachycardia
What is a lung phenomenon that can occur 24-72 hrs after a PE?
Loss of surfactant –> atelectasis, focal infiltrate
The classic but uncommon EKG change in PE?
S1Q3T3
(deep S wave in lead I, Q wave in III, inverted T wave in III (20%). This “classic” finding is neither sensitive nor specific for PE)
What is the PERC criteria. Age component
Pulmonary Embolism Rule out Criteria
In pts w/ LOW risk of PE (Well’s score), if all 8 are absent, then no further workup needed :)
Age cutoff is 50! So anyone 50+ automatically loses on PERC
When is D-dimer useful? What predictive value is this?
NEGATIVE predicted value
i.e. if normal, excludes PE in patients w/ low pretest probability who don’t meet PERC criteria
Imaging for PE diagnosis in pts hemodynamically unstable (definitive imaging unsafe)
Bedside echo (look for signs of RH strain –> presumptive PE diagnosis so you can start treatment)
Can you prescribe BBs and CCBs at the same time?
NO! Both block AV node –> can lead to high degree blockade and significant BP drop
How might the elderly present with pneumonia?
Minimal Sx; AMS, decline in baseline function Often afebrile (may even by hypothermic), tachypnea may be most sensitive sign
Lobar consolidation is typical of what bacteria?
Streptococcus pneumoniae
Klebsiella
Most common causes of CAP
Streptococcus pneumoniae
Mycoplasma pneumonia
Chlamydia pneumoniae
Resp viruses
HAP and HCAP are most commonly caused by?
Gram-negative bacilli: Pseudomonas aeruginosa, E coli, Klebsiella pneumnoia, Acinetobacter
Healthy patients with presumed CAP and no AB use in the past 3 months should be treated with what AB?
A macrolide (azithromycin)
Antibiotic for patients w/ CAP and comorbid disease, AB use in past 3 months, or high risk of macrolide-resistant Streptococcus pneumoniae
Fluoroquinolone (levofloxacin)
or beta lactam (cefpodoxime = 3rd gen cephalosporin) + macrolide
Pts with concern for HAP/HCAP should receive what AB therapy and why?
Concern for multi-drug resistant pathogens. 3 drug combo therapy
1) Antipseudomonal cephalosporin (cefepime or ceftazidime), antipseudomonal carbapenem, or pip-tazo
2) Antipseudomonal fluoroquinolone (e.g. levofloxacin)
3) Anti-MRSA coverage (linezolid or vancomycin)
Good antibiotic for a presumed anaerobic infection (or multibacteria) in pt w/ pneumonia. What kind of patient would be likely to need a drug with a spectrum covering anaerobes?
Clindamycin
Aspiration pneumonia, e.g. alcoholic pt
Foregut, midgut, hindgut structures
foregut = oropharynx - mid-duodenum + liver, biliary tract, pancreas, spleen Midgut = distal duodenum to mid-transverse colon Hindgut = distal-transverse colon to rectum
Where is pain perceived from the foregut, midgut, and hindgut?
Foregut: epigastrum
Midgut: periumbilical
Hindgut: hypogastrium
6 categories of surgical abdo pain
I O HIPI
1) Infectious
2) Obstructive
3) Hemorrhagic
4) Ischemic
5) Perforating (may overlap with hemorrhagic)
6) Inflammatory
Mnemonic for pertinent headache history questions
SNOOP MEETS PREGNANCY Systemic Sx Neurological Sx (focal, AMS, seizures) Old age Onset (sudden) Pattern changes Mornings worse Exertion/posture/sexual activity Exposures (drugs/toxins) Trauma Secondary risk factors (HIV, cancer...) Pregnancy
What is a population that has a very high rate of serious disease (but also high rate of misdiagnosis) when they present with abdo pain? Name 3 common diagnoses in this population
Elderly folks (up to 1/3 may require surgery!) Biliary tract disease, diverticular disease, bowel obstruction
Mortality of mild and severe acute pancreatitis
5% mild
25% severe
Focus in early management of severe acute pancreatitis?
Recognition & prevention of organ dysfunction (e.g. repleting intravascular volume to prevent renal dysfunction)
**AP causes severe inflammation, capillary leakage, 3rd space loss shock
Utility of CT abdo for acute pancreatitis. Safety consideration re contrast?
Not necessary, can be useful if diagnosis uncertain
Can show degree of necrosis/disease severity
**don’t use contrast until volume depletions corrected
Is upper or lower GI bleeding more likely to deteriorate into rapid/large volume hemorrhage? What is the implication of this for most important test in pt w/ GI bleed of unknown source?
Upper more likely to deteriorate –> upper endoscopy the most important test!
What is an important distinction to make rapidly in patients with upper GI bleeds? Why?
Variceal vs non-variceal
Bc if variceal want to give octreotide (somatostatin analogue, causes splanchnic vasoconstriction)
Name 5 differentials for upper GI bleeding
Peptic ulcer disease Varices (gastric/esophageal) Mallory-Weiss tear Esophagitis Gastritis
Name 7 ddx for lower GI bleeding
1) Upper GI bleeding ;)
2) Hemorrhoids
3) Diverticulosis
4) Angiodysplasia
5) Malignancy
6) Inflammatory bowel disease
7) Infectious conditions
Name 4 common ddx for GI bleeding in children
1) Intussusception
2) Volvulus
3) Meckel diverticulum (congenital outpouching of ileum)
4) Polyps
Where is abdominal pain felt in most patients with GI bleeding?
Trick question! Most patients w/ GI bleeds don’t exhibit abdo pain (though important to do abdo exam for peritoneal signs)
As a general rule, a ____ should be given to patients w/ upper GI bleeds to decrease rebleeding rates
PPI
Transfusion of PRBCs should be considered in what patients w/ GI bleeding
1) Hemodynamically unstable after crystalloid infusion
2) Ongoing blood loss
3) Hb <70 (this restrictive transfusion threshold shown to be superior)
Why is vasopressin no longer favoured for treating variceal bleeding? What should be used instead?
Vasopressin has side effects, end-organ ischemia Somatostatin analogue (octreotide) preferred
Temporary control of massive variceal bleeding can be achieved using
Balloon tamponade
Risks of button battery ingestion? Management?
High risk for mucosal burns/esophageal perf if lodged in esophagus
Confirm location with x-ray; if past esophagus/asymptomatic –> expectant management
In esophagus or symptomatic –> surg
Repeat CXRs until cleared
After clearing an esophageal food impaction, what test should you do?
Barium swallow to confirm clearance and r/o esophageal pathology
Most common location of ingested FB in children?
In adults?
Cricopharyngeal narrowing (upper esophageal sphincter, pharyngoesophageal segment) in children In adults, usually lower esophageal sphincter
In patients with FB ingestion, fever, subcutaneous air, or peritoneal signs suggest…
Perforation –> immediate surg conseult!
In general, once an ingested foreign body passes the ____ , it will continue through GI tract and be expelled without incident
Pylorus
If plain films don’t reveal ingested FB, what are 3 other options?
Esophagogram (barium swallow, if perf not suspected), CT, endoscopy (latter can also remove it at the same time)
Treatment for injested sharp object
If in duodenum or proximal –> endoscopic removal (risk of intestinal perf)
If past duodenum, surgical consult and/or serial radiographs
Treatment for foreign body ingestion of “body packing” (illicit drugs)
Rupture may be fatal, do NOT to endoscopy bc may rupture packet
May use whole bowel irrigation w/ peg to hasten packets through GI tract, otherwise surgery to remove packets
Crampy abdo pain and high-pitched bowel sounds are features of what type of bowel obstruction?
Mechanical (not functional)
What type of bowel obstruction does NOT allow decompression? 2 examples? What type of intervention is usually required?
Closed-loop obstruction (blockage proximal & distal, e.g. volvulus, complete large bowel obstruction + competent ileocecal valve)
Usually require surgery
Small and large bowel obstructions: which is more likely to have distention? Which more likely to have vomiting>
Small bowel –> vomiting
Large bowel –> distention
(though both can have either; large less likely to have vomiting bc of ileocecal valve competence in closed-loop obstruction)
3 most common causes of small bowel obstruction?
Adhesions (70-75%)
Malignancy (8-10%)
Hernia (8-10%)
3 most common causes of large bowel obstruction?
Carcinoma (65%)
Volvulus (15%)
Why might a patient temporarily appear to improve clinically as a mechanical bowel obstruction progresses?
At first there is an increase in peristalsis, then activity diminishes –> dilated/atonic bowel proximal to obstruction (less cramps)
Blood flow also increases then decreases –> mucosal breakdown + ischemia
So baiscally spastic pain first, then ischemic/peritoneal pain
What is the significance of localized vs diffuse tenderness in bowel obstruction?
Diffuse due to distention of bowel wall, visceral pain can be resolved by NG decompression/emesis if open-loop
Localized is a BAD sign, usually means closed-loop, necrosis, perforation –> urgent CT
3 main management strategies for uncomplicated small or large bowel obstruction if identified early?
NPO
IV hydration
NG tube decompression
What defines an “uncomplicated” bowel obstruction. What imaging modality can differentiate?
No compromise to intestinal blood flow
May be partial or complete
CT scan
What imaging modality can differentiate mechanical vs functional large bowel obstructions in most patients?
CT scan (if still unclear, can do contrast enema)
Common clinical sign of colonic perforation in LBO?
Severe volume contraction due to inflammation, failure to improve with aggressive fluid management
May or may not have frank peritonitis
Most likely cause of SBO in pt w/out previous abdominal operations?
Hernia
Most acute diarrhea is ___
Viral
Most common cause of traveller’s diarrhea
Enterotoxigenic E Coli
Which type of bacterial diarrhea should NOT be prescribed antibiotics and why?
Enterohemorrhagic E Coli (shiga toxin) –> hemylotic uremic syndrome
Class of drugs commonly used to treat infectous diarrhea?
Fluoroquinolones:
Ciprofloxacin, levofloxacin, norfloxacin
What is a pathogen that can cause watery profuse diarrhea within 4-12 hours of ingestion
S aureus
Name 5 pathogens that commonly cause noninflammatory diarrhea
Enterotoxigenic E coli Staph aureus Rotavirus Norovirus Vibrio cholerae
Name 5 pathogens that commonly cause inflammatory diarrhea (fever, blood, tenesmus)
Salmonella Shigella Campylobacter Enterohemorrhagic E coli, Enteroinvasive E coli C diff
Kidney stone are most common in which sex?
Men (M:W 3:1)
Positional differences bw patients w/ acute abdomen and nephrolithiasis (comfort)
Acute abdo –> supine, still, knees to chest
Nephrolithiasis –> move around, can’t get comfy
Is pain w/ nephrolithiasis constant or colicky?
Can be either
ureteric usually colicky (stretching ureter); renal pelvis/bladder usually asymptomatic but if pain usually constant
Are neophrolithiasis stones radioopaque?
Usually (90%), most stones are Ca-based
Triad of Sx that indicate a medical emergency in nephrolithiasis
Fever, pyuria, severe CVA angle tenderness
pyelonephritis caused by obstruction –> sepsis
2 best imaging modalities for renal colic (older and newer methods of choice_
Traditionally: IV pyelogram
Newer: Helical CT imaging w/out contrast (more sensitive/specific and assesses surrounding structures, although doesn’t show degree of compromised excretion in the kidney like IVP does)
3 main goals of working up nephrolithiasis
1) Pain control
2) Determine degree of obstruction
3) Detect infection
In nephrolithiasis, definitive therapy is determined how?
Based on the types of stones being formed (strain all urine to recover stones)
Indications for urgent urologic consultation in nephrolithiasis
1) Inadequate oral pain control
2) Persistent nausea & vomiting
3) Associated pyelonephritis
4) Large stone (>7mm)
5) Solitary kidney
6) Complete obstruction
Most small stones (<6mm nephrolithiasis) can be managed via…
Conservative management: analgesics, hydration, ABs if necessary
Most patients can go home w. instructions to increase fluid intake & strain urine
When is surgery indicated for nephrolithiasis?
Stone >8mm
Persistent pain
Failure to pass despite conservative management
Name 2 meds that can help pass a stone
Alpha-blocker (Tamsulosin)
Corticosteroids (reduce edema)
Stones in the lower UT can be removed via ____, upper UT stones treated by _____
Ureteroscope
Extracorporeal Shock Wave Lithotropsy
Does degree of hematuria correspond to degree of obstruction (nephrolithiasis)
No! e.g. a complete obstruction could involve 0 hematuria
Testicular torsion can occur at any age but is most common at what ages?
<1yo
Puberty (hormones)
What is a congenital deformity that increases the probability of testicular torsion?
Bell Clapper Deformity
Horizontal lie of testis in scrotum, epididymis & testicle hang freely and can rotate in scrotum rather than being firmly attached
What are some characteristics of the presentations of epididymitis/orchitis that help differentiate them from testicular torsion?
Gradual onset of scrotal pain
Lower UTI Sx (including fever)
Normal anatomical position of testis (but swollen/tender), intact ipsilateral cremasteric reflex
What scrotal pathology involves INCREASED blood flow on color doppler?
Epididymitis
What reliefs pain in epididymitis
Elevating the testicle (Prehn sign)
Is pain on epididymitis or orchitis more sudden
Orchitis more sudden, epididymitis more gradual
Tender nodule/”blue dot sign” on scrotum are characteristic of
Appendageal torsion
Salvage time after onset of pain for testicular torsion
4-6 hours
“Classic” presentation of testicular torsion
Sudden onset severe pain in lower abdomen, inguinal area, or scrotum
Often preceded by physical activity/trauma (though can occur during sleep)
Nausea/vomiting
Horizontal lie of testicle and loss of cremasteric reflex
If uncertain whether there is testicular torsion, what study?
Ultrasound with color Doppler
Treatment for testicular torsion
1) Emergent manual detorsion (try medial to lateral “opening a book” first)
2) Surgical intervention - emergent if manual failed, elective if it worked temporarily
Does pyuria/bacteruria rule out other testicular pathologies?
No! e.g. 50% of patients w/ epididymitis have it, could also still be a torsion
Name 2 med classes that increases risk of hyperkalemia
ACE inhibitor (potassium retention) Potassium-sparing diuretics: aldosterone antagonists (e.g. spironolactones), ENaC blockers (e.g. amiloride)
Meds for hyperkalemia
a) Cardioprotection: Ca
b) Shift K+ into cells: insulin, beta-adrenergics, NaHCO3
c) Remove K+ from body: loop diuretics, sodium polystyrene sulfonate (SPSS)
Normal serum K+
3.5-5
What is a condition that predisposes someone to hyperkalemia?
CKD
Name 6 clinical features of hyperkalemia
Fatigue Weakness Paresthesias Paralysis Palpitations Anorexia/nausea/vomiting
Serum level for severe hyperkalemia –> requires immediate aggressive threatment
7.0+
What can happen if blood sample is hemolysed prior to K+ measurement?
Pseudohyperkalemia (false positive)
*most labs will report this when detected
EKG change in hyperkalemia
"Peaked" T wave (too pointy to sit on!) Wide QRS Long PR/QT ST changes (can mimic MI) Wide/absent P waves Blocks/arrhythmias **HONESTLY ALMOST ANYTHING
What is the best test to guide initial hyperK treatment? Caveat?
EKG findings
BUT correlation b/w changes and severity is poor!! Can change suddenly
All dialysis pts in cardiac arrest should receive…
Calcium (hyperK is commonly contributing)
___toxicity can cause hyperkalemia
Digoxin (Na-K ATPase is a target)
Type of Calcium and duration of action in hyperkalemia
Only lasts minutes, not long-term treatment
Ca Chloride for arrests
Ca gluconate in less-acute cases (less elemental Ca but safer)
How is insulin administered for hyperkalemia
5-10 units of regular insulin IV (lower K by 0.5 for 1-2 hours)
give w/ 25-50g of D50 to avoid hypoglycemia
Note: some docs just give D50 and let pt’s own insulin do their thing but many pts have diabetes, and high osmolar load may transiently INCREASE K
Diuresis after crystalloid repletion isn’t effective for hyperkalemia in what pts? Good in which patients?
End-stage kidney disease
good in dehydration, med effects, rhabomyolysis
Ideal treatment for pts w/ hyperkalemia & renal failure
Dialysis
Advantages of salbutamol for hyperK
Dose? Duration?
Aerosol 10-20mg, lowers K+ by 0.5 for 1-3 hours (add to insulin!)
Advantages: reduces hypoglycemia from insulin, no IV access required
Note: dose MUCH higher than for asthma (~2.5 mg)
Sodium polystyrene sulfonate (SPSS, e.g. Kayexalate) is what? Administered how for hyperK?
In what context is this most effective?
Ion-exchange resin administered orally (enema less effective)
Best for maintenance therapy bc takes several hours to start working, can last days
Mnemonic for blood transfusion reactions
Fever HALO Febrile nonhemolytic transfusion reaction Hemolysis Anaphylaxis Lung (TRALI) Overload (TACO)
Urine dipsticks for UTI measure…
Leukocyte esterase
Nitrate
What groups of patients require imaging for UTI-type complaints
Men or children <4 w/ first UTI
Suspected obstruction
Negative urinalysis
Complicated UTI
Common AB regimes for lower uncomplicated UTI (4)
TMP-SMX DS 1 tab bid for 3-5 days Ciprofloxacin 250 mg bid for 3-5 days Nitrofurantoin sustained-release 100mg bid for 3-5 days Amox/clavulanate 875/125 for 3-5 days (**amox can't be monotherapy for UTI!)
Common AB regimes for upper uncomplicated or lower complicated UTI (3)
Ciprofloxacin 500mg bid for 7-14 days
Nitrofurantoin 100mg bid 7-14 days
Amox/clavulanate 875-125mg bid for 7-14 days
Drug that can be used for UTI SYMPTOM relief
Phenazopyridine (Pyridium), up to 3 days
symptom-masking
Admission criteria for pyelonephritis
Sepsis/shock (ICU) Can't tolerate oral AB Obstruction of urogenital tract Pregnant Extremes of age Failed outpatient management Immunocompromised host Inadequate follow up/poor social circumstances
Antibiotics for UTIs during pregnancy
Keflex (Cephalexin)
Erythromycin
Amox-clavulanate
Nitrofurantoin (avoid during 1st TM if possible)
5 critical diagnoses in patients with delirium
Hypoxia/diffuse cerebral ischemia (resp failure, CHF, MI) Hypoglycemia CNS infection Hypertensive encephalopathy High ICP
Symptomatic hyponatremia causing seizure should be treated with…
Hypertonic (3%) saline
Initial treatment for hypo/hypercalcemia
Hypocalcemia –> Ca
Hypercalcemia –> IV fluids
Pt w/ delirium who has asterixis/seizures likely has what? Treatment
Uremic encephalopathy (from renal failure) IV hydration, possible hemodialysis
Empiric treatment for suspected meningitis
Vancomycin + ceftriaxone
steroids given before or with ABs
3 differentials for endocrine causes of AMS
Pancreatic abnormalities –> hypoglycemia
Hypothyroid/hyperthyroid (thyrotoxicosis, thyroid storm)
Adrenal crisis
Treatment of thyroid storm
1) Beta blocker to decrease sympathetic activity (e.g. propranolol)
2) Thioamide: Methimazole or Propylthiouracil (PTU) - block TPO, reducing TH synthesis
3) Give iodine (inhibit production/release of stored T4)
4) Steroids to treat underlying immune process if present (e.g. Grave’s)
Treatment for adrenal crisis
Hydrocortisone (replacement)
IV fluids/vasopressors as needed for BP support
Correct underlying problem
When do myoclonic jerks occur in syncope vs seizure? Eye deviation?
Seizure: BEFORE LOC, horizontal deviation
Syncope: AFTER LOC, vertical deviation
What is something important to keep in mind when suspecting a pt has a psychiatric cause of syncope (due to a prev psych history)
Many neuroleptic agents cause QT prolongation which can beget dysrhythmia!
Is vasovagal or situational syncope commonly diagnosed in elderly folks in the ED?
No, can’t safely rely on this diagnosis in most cases –> admit for monitoring (in young/healthy people more often can)
high-yield labs in pts w/ syncope (if indicated by Hx/physical)
CBC (anemia)
BMP (electrolytes, glucose)
Urinalysis (hydration, ketones, glucose, infection)
Urine pregnancy test (ectopic pregnancy)
After ensuring ABCs, what is the most important test for pt presenting w/ syncope?
EKG (abnormal usually –> admission!)
9 red flags for suspected facial nerve palsy
CN involvement other than 7 Weakness/numbness of arms or legs Bilateral facial weakness Headache, visual deficits, nausea/vomiting Hx of time in woods/tick bite Recurrent unilateral facial paralysis Slow progression of Sx Ulceration/blisters near ear (Ramsay Hunt syndrome = herpes zoster oticus, shingles affecting facial nerve)
How does Bell’s palsy typically present?
Ipsilaterally facial palsy along cranial nerve 7
Can’t close eye fully (eye rolls up when you try = Bell phenomenon)
Droop of mouth (orbicularis oris)
Tearing of eye (paralysis of orbicularis oculi prevents closure and causes lacrimal duct to sag away from conjunctiva)
Can’t wrinkle forehead (frontalis)
___ is the most common cause of facial paralysis but is a diagnosis of ____
Bell’s palsy
Diagnosis of EXCLUSION (don’t anchor!!)
What does it mean if a patient has drooping of mouth but can wrinkle forehead normally
Probably an INTRACRANIAL process (supranuclear rather than peripheral)
- innervation of upper facial muscles is bilateral, lower is contralateral
- LMN lesion like Bell’s Palsy impacts the full half of the face
Describe the onset of Bell’s palsy?
Fairly abrupt, can progress from weakness –> paralysis over 1 week
>50% of pts recall a preceding viral prodrome
May have ipsilateral loss of taste, tearing changes, hyperacusis (all impacted by facial nerve)
May say face feels numb but no actual sensory loss
80% of Bell’s palsy patients recover within…
Weeks to a few months
Treatment for Bell’s palsy
Medical (ASAP!): prednisone 1mg/kg/day for 7-10 days (reduce facial nerve edema)
Antiviral use controversial
Surgical decompression of facial nerve may be useful if steroids don’t help
Supportive: eye patch at night, eye drops hourly during day
80% of strokes are ___ and occur in people of what age?
What type more common in younger patients?
80% ischemic, usually >50yo
Hemorrhagic typically seen in younger pts
Is hypertension cause or effect in intracranial bleed?
Both! Re effect, it’s partly bc of overcoming increased ICP (?protective but also harmful)
Thrombolytics (alteplase) can only be given within how long of Sx onset in an ischemic stroke? Within how long from arrival at hospital is the stroke algorithm?
4.5 hours!
rtPA within 60 minutes of ED arrival (eval within 10 min, neuro notification within 15, CT within 25 min, read within 45)
“Golden hour” of stroke care
TIA symptoms typically resolve within…
24 hrs
Is the NIH Stroke Scale used to diagnose stroke?
No! But should do it to assess severity and track changes
In a suspected stroke pt, what are some important diagnostic tests to RULE OUT other differentials?
O2 satus
EKG
Capillary blood glucose
CBC (platelets >100 to administer thrombolytics), coagulation studies (intracranial bleed risks w/ tPA), cardiac markers
Usual diagnostic imaging for stroke pt
Non-contrast head CT (vital to rule out intracerebral bleed!)
Early finding in ischemic stroke = loss of gray-white differentiation (increased water in ischemic tissues)
Best imaging modality for subacute/chronic intracranial hemorrhage
MRI
BP control in ischemic stroke
Permissive hypertension to maintain cerebral perfusion pressure
But treat SBP >220 or DBP >120 w/ IV labetalol or nitrates (titratable)
Do not lower by more than 25% of map
BP should be <185/110 for rtPA admin
Fundamentals of treating hemorrhagic stroke
BP control (nimodipine = CCB that prevents vasospasm in SAH)
Possible reversal of anticoag (cryoprecip or platelets)
Neurovascular imaging
Surg/heme consults
What is the interesting paradox with non-contrast CT imaging in stroke
Takes 6 hours after stroke onset for it to be visible on non-contrast CT (longer that the tPA window!)
You do it to RULE OUT bleeding, masses, etc. Not to diagnose but to ensure no contraindications to empiric tPA treatment!
What is bright on T2 MRI?
WWII: Water white on T2!
Grey matter is hyperintense compared to white on T2
Stroke with visual symptoms = ___artery
Numbness & weakness more of contr. arm/face>leg =
Weakness of contr. leg>arm w/ mild sensory deficits=
Posterior cerebral artery
Middle cerebral artery
Anterior cerebral artery
Recurrent “thunderclap” headaches could be…
Reversible cerebral vasoconstriction syndrome
Does a normal CT rule out SAH?
No, but it’s important to do to rule out intracranial mass before performing LP
Gold standard diagnostic for SAH?
LP revealing xanthochromic CSF (may take up to 12 hrs to develop so bloody CSF also concerning)
Temporal arteritis almost always occurs in patients of what age range?
> 50yo
Temporal arteritis diagnostic criteria= 3 of the following 5 characteristics:
>50yo New-onset localized headache Decreased pulse or tenderness over temporal artery ESR >50 Abnormal TA biopsy
2 abortive treatments for cluster headaches
High-flow O2
Sumatriptan
Metoclopromide (e.g. for acute migraine treatment in ED) can cause what side effect? What can be done to mitigate this?
Akathisia (restlessness, distress, non-purposful limb movement)
Diphenhydramine co-administration (only if 20mg IV metoclopromide given, not required for 10 mg)
Labs to order in first-time seizure
Glucose, lytes, renal function tests, drug/tox screen
Pregnancy test
Head CT should be performed in first-time seizure patients that meet what criterisa?
Recent head trauma Persistent AMS/headache Fever Malignancy Immunocompromised Anticoagulation New focal deficits Partial-onset seizure >40yo
(overall: if no clear etiology identified or acute intracranial process suspected)
___ is one of the most frequent causes of drug-induced seizures
Cocaine
Pts w/ TCA overdose who are seizing should be treated w/ standard seizure therapy + what?
Sodium bicarb to alkalize pH –> 7.5 (decreases drug’s free form and activity)
Isoniazid-induced seizures should be treated with what?
IV pyridoxine (vitamin B6) bc INH binds/depletes it and it’s necessary for GABA function
Is CT head useful in alcohol-related seizures? What else should be done?
Yes! High diagnostic yield due to high incidence of intracranial lesions (subdural hematomas/hemorrhages)
Test electrolytes, IV fluid hydration w/ glucose + thiamine + Mg + K + multivitamins
“Red flags” for low back pain
TUNA FISH Trauma Unexplained weight loss Neurological deficits Age <18 or >50, Anticoagulants/coagulopathy, Abnormal vital signs Fever/systemic Sx IV drug use/Immunocompromise/recent Infection Steroid use/osteoporosis History of cancer
Name the landmarks of the back
Bony prominence at base of neck = C7
Spine of scapula = T3
Angle of scapula = T7
Iliac crests = L3/L4
Conus medullaris and cauda equina are at what spinal levels?
CM = T12-L2 CE = L3-S5
Most patients w/ acute low back pain have resolution within…
4-6 weeks
Most common location of herniated disk of lumbar spine? Presentation?
L4-L5 insterspace
–> low back pain radiated down posterior aspect of leg (if weakness or bowel/bladder symptoms –> emergency!)
Out of conus medullaris and cauda equina syndromes, match to unilateral/bilateral and sudden/gradual onset
CM = sudden, bilateral
CE = gradual, unilateral
(usually)
Rule to treat hypoglycemia (e.g. in seizures)
“Rule of 50”
Neonate (up to 6 mo): D10 x 5 ml/kg
Infant - preschool: D25 x 2 ml/kg
Child-adult: D50 x 1 mg/kg (or 1 “amp” = 25g glucose in 50 mL syringe, 50%)
Benzos doses for seizure in adults
10 mg IV/IM midazolam
4 mg IV/PR lorazepam
(Can repeat lorazepam x1)
Name 4 drugs that can be used for status epilepticus refractor to benzos
IV: fosphenytoin, valproic acid, levetiracetam, phenobarbital
Name 3 drugs for status epilepticus refractory to benzos AND anticonvulsants
Thiopental (barbiturate)
Propofol
Phenobarbital (barbiturate)
Concern with using succinylcholine in patient who has been seizing for a long time?
Hyperkalemia
Temp in infants must be measured how?
Rectal thermometer (>38 = fever)
The Rochester, Boston, and Philadephlia criteria are CDRs used for what? What do they agree on?
Identification of febrile infants low-risk for SBI
All support use of CBC, blood cultures, urinalysis/urine cultures
Do all febrile infants need CXR and/or stool sample?
No, only if resp Sx or GI Sx respectively
All ill-appearing infants <3 mo should be treated how?
Empiric ABs (ceftriaxone!) prior to lab results + admit to hospitals (45% will have SBI)
If LP is NOT performed on febrile infant, should you give empiric ABs?
No! could mask Sx of bacterial meningitis on f/u
What is a discharge condition of low-risk well-appearing infant with FWS?
Follow-up within 24 hours (adequate social situation)
Most common cause of SBI in infants w/ FWS!
UTI
does negative urine dipstick/urinalysis exclude UTI in infants?
No, pyuria absent on initial urinalysis in 20% of infants w/ pyelo! Need a culture
Demographics most commonly presenting with septic arthritis, and most common joint?
Hip joint
Children <3 years old
Males > females (2:1)
3% of children who present to the ED for ___ have septic arthritis
Limp
Most common 3 organisms in septic arthritis? Another in neonates/sexually active adolescents?
Most common = Staphylococcus aureus, then Group A Strep (S. pyrogenes) and Strep pneumoniae
Neisseria gonorrhea in neonates/teens
Appropriates tests in child presenting w/ limp w/ no preceding trauma
CBC, ESR/CRP, blood cultures
Plain radiographs (r/o ddx)
Bedside U/S (check for effusion)
Good physical exam test to see if limping child’s pathology is localized tothe hip
Log roll test (straight leg, rotate foot in/out to rotate hip joint)
Ideal imaging test for osteomyelitis?
MRI (plain films may not show changes until 10-20 days after Sx onset)
Most common cause of acute hip pain in children 3-10yo? What commonly precedes it? What test may be required to differentiate from septic arthritis?
Transient synovitis, commonly after URTI
Synovial fluid analysis
What is Legg-Calve-Perthes disease? Demographic?
Avascular necrosis of the femoral head, commonly found in boys 4-10yo
What is Slipped Capital Femoral Epiphysis?
Posterior displacement of capital femoral epiphysis from the femoral neck through the growth plate, most common in obese or rapidly-growing boys 11-15 yo. 30-60% eventually bilaterally
Salter Harris Type 1
actually a misnomer, the epiphysis stays in the acetabulum, the diaphysis/metaphysis move forward
What does SCFE look like on CXR?
Ice cream fallen off cone
Toddler who presents with unwillingness to weight bear but no known trauma likely has…
Toddler’s fracture (nondisplaced hairline spiral fracture of tibia) - immobilize w/ boot
Always do what tests on a child w/ fever who refuses to move a joint
Ultrasound
Arthrocentesis
Criteria for a SIMPLE febrile seizure
6mo-5yo
Fever 38C+
Generalized tonic-clonic convulsions
Spontaneous cessation of convulsions within 15 min
No recurrence within 24 hours
Return to alert mental status after convulsions
No neuro abnormalities on exam
What children w/ simple febrile seizure should get an LP?
Current AB use (can mask meningitis sx)
Unimmunized children 6-12mo
When should AOM be treated w/ ABs? AB of choice?
If child <2yo
For >2yo, can give prescrip but say only fill if no improvement after a few days (“watchful waiting”)
Amoxicillin = drug of choice
How do you prevent a simple febrile seizure?
You can’t prevent it with antipyretics or antiepileptics!
Define PID
Pelvic Inflammatory Disease
Ascending infection from vagina or cervix –> upper genital tract (endometrium, fallopian tubes, ovaries)
Diagnostic workup of suspected PID
Transvaginal U/S (r/o tubo-ovarian abscess)
Chlamydia/Gonorrhea assays, STI screen, HIV test
CBC
If uncertain diagnosis, laparoscopy = gold standard
What is “chandelier sign”?
Cervical motion tenderness (bimanual exam)
Pt “hits the chandelier” they jump off bed so high out of pain
PID may also be termed
Salpingitis
some sources say synonymous, others say salpingitis is a subset of PID
Tubo-ovarian abscess is an important complication of…
Disposition? AB consideration?
PID
Requires inpatient therapy (note: can rupture –> hypotension/shock = surgical emergency)
Note, need to use ABs that are effective against anaerobes (clindamycin, metronidazole)
Most resolve w/ ABs, ~1/3 need surgery
Is PID only caused by STIs?
No! Only ~50% of cases caused by gonorrhea/chlamydia, many causes from endogenous vaginal bacteria!
Usually polymicrobial
Treatment of PID
Broad-spectrum ABs (usually parenteral), initiated as soon as presumptive diagnosis (prevent long-term sequelae: infertility, chronic pain)
Disposition of pt w/ PID and an IUD
Hospitalization
3 Known complications of PID
Infertility
Adhesions –> chronic pelvic pain
Chronic PID
Classic triad of Sx in PID
Lower abdo tenderness
Adnexal tenderness
Cervical motion tenderness
(only 1 + clinical suspicion required)
In someone presenting w/ asymmetric polyarthritis, tenosynovitis, & pustular skin lesions, ___ should be considered in the ddx
Disseminated gonococcal infection
Quantitative hCG threshold where if you don’t see an IUP it’s probably an ectopic pregnancy
1500 IU/L
97% of ectopic pregnancies occur where?
Fallopian tube (ampullary region, the long middle party)
In a reliable & asymptomatic patient whose hCG <1500 (query ectopic pregnancy), what can you test?
Repeat hCG in 48 hours - should increase by 66%+ if a normal pregnancy
Lack of normal rise indicates probably ectopic OR miscarriage
Does an IUP visualized on ultrasound r/o ectopoic?
Not in IVF pregnancies! (can have “heterotopic” pregnancies, where one is intrauterine and other is ectopic)
Pharmacological treatment for ectopic pregnancy = ?
Requirements?
Methotrexate hCG <5000 No fetal cardiac activity No clinical contraindications Reliable pt follow-up (and patient preference for medical management)
STI prophylaxis after sexual assault
Ceftriaxone (gonorrhea) + azithromycin or doxycycline (chlamydia)
Metronidazole (Trichomoniasis)
HBIG + vaccine (if non-immune to Heb B)
Consider HIV PEP
Meds used for N&V in pregnancy
In order of severity:
Pyridoxine (vitamin B6) + doxylamine (antihistamine)
Diphenhydramine
Prochlorperazine or metocloparmide
Ondansetron (Zofran) IV or PO (for hyperemesis)
Measure for asthma severity used in place of FEV1 (since FEV1 requires spirometry)
Peak Expiratory Flow Rate (PEFR)
Treatment of asthmatics during pregnancy
Same thing, i.e. SABAs during attacks, ICS
How do ABG findings shift during pregnancy (qualitatively)
Implication?
Resp alkalosis (increased minute ventilation) w/ partial metabolic compensation i.e. high pH, high PO2, low PCO2, low HCO3
So respiratory acidosis and high PCO2 means IMPENDING RESP FAILURE
With hyperemesis gravidarum, the presence of what in urine is associated w/ significant volume depletion?
Ketones
99-100% of patients w/ bacterial meningitis have what symptom(s)
Headache + 1 of the classic triad: fever, nuchal rigidity, AMS (only 50% of pts have the full triad)
Meningitis caused by Neisseria meningitidis may case what 2 extra-CNS manifestations?
Palpable purpura
Septic arthritis
Indications for head CT prior to LP
Altered LOC/AMS
Focal neuro deficit
Immunocompromised
Hx of CNS disease (lesions, strokes, infection, surg)
New-onset seizure (<1 week before presentation)
Papilledema
Head trauma
WBCs and proteins and glucose in meningitis. Also which WBCs are dominant. Compare viral/bacterial for all of above
WBCs increased (more in bacterial; bacterial has PMN dominance, viral has lymphocyte dominance) Proteins increased (more in bacterial) Glucose decreased (more in bacterial)
2 most common bacteria that cause bacterial meningitis in adults
N. meningitidis
S. pneumonia
Antibiotics for meningitis in adults
Ceftriaxone or cefotaxime (3rd gen cephalo)
Vancomycin
If >50, immunocompromised or alcoholic –> add ampicillin
What should be co-administered with or before antibiotics in meningitis?
Dexamethasone
attenuate inflamm response to antibiotics
Prophylaxis for household/daycare of people with meningitis caused by what organism? What AB?
N meningiditis
Rifampin or fluoroquinolones (ciprofloxacin) or ceftriaxone
Clinical evaluation of SSTIs always begins with what?
Search for a pus pocket! Presence of pus/abscess vastly changes management. May need to use U/S
What are furuncles? What is usually the causative pathogen? What might patients call these?
Spontaneous superficial skin abscesses
Usually caused by Staph aureus, >50% MRSA
“Spider bite”
In SSTI eval, once abscess is r/o, what is the main diagnostic question?
NSTI (necrotizing soft tissue infection) vs cellulitis
Nonpurulent cellulitis is typically caused by what pathogen?
Group A beta-hemolytic streptococci (Strep pyogenes)
What is a superficial, sharply demarcated nonpurulent cellulitis that often occurs on face/lower extremities and causes fever & leukocytosis? Most common causative pathogen?
Erysipelas (usually caused by S pyogenes)
RFs for necrotizing fasciitis
Injection drug use
Neglected diabetic foot ulcer
Infection of scrotum/perineum
Combo of findings on bloodwork that suggests NSTI
Extreme leukocytosis
Hyponatremia
When NSTI is suspected what is the best diagnostic approach?
Prompt SURGICAL exploration!!
Antibiotics for NSTI
Clindamycin (anaerobes, staph, strep)
Vancomycin (MRSA)
Pip-Tazo (anaerobes, Strep)
NSTI infections are usually polymicrobial and often involve what species?
Clostridium perfringens
Nonpurulent cellulitis typically treated w/
Cephalexin (Keflex) or cefazolin (ancef, IV) = 1st gen cephalosporins
(Good for SSTIs, preventing surgical site infections esp Staph & Strep)
Do all drained abscesses need AB treatment?
No, 5cm or less with minimal to mod cellulitis usually doesn’t need AB, just draining and loop drainage or packing (pt can remove packing themself)
Define exanthem
widespread rash that is usually accompanied by systemic symptoms such as fever, malaise and headache. It is usually caused by an infectious condition such as a virus, and represents either a reaction to a toxin produced by the organism, damage to the skin by the organism, or an immune response
Red flags for serious rash
Immunocompromise Fever Toxic appearance Hypotension Petechiae/purpura (non-blanching!) Diffuse erythema Severe or localized pain Mucosal lesions
How long do sutures stay in?
Face: 5 days
Body: 7-10d
What can be added to local anesthetics to increase their duration of action? What else does it do?
Epinephrine (local vasoconstriction decreases systemic absorption)
Also augments hemostasis
In wound care does irrigation come before or after anethesia?
Before! So that if there’s a foreign body etc the pt can feel it
In patients with trauma to the ear region you should always examine for signs of…
Basilar skull fracture
Tympanic membrane rupture
3 signs of basilar skull fracture
1) Periorbital ecchymosis (raccoon eyes)
2) Mastoid ecchymosis (Battle’s sign)
3) Hemotympanum
Consequence of unaddressed auricular hematoma
Abnormal cartilage production –> “Cauliflower ear”
Treatment of buccal (intraoral) wounds
No sutures if <2cm (if >2cm prone to food getting stuck) Prophylactic ABs (penicillin, amoxicillin, cephalexin, or clindamycin)
Flagyl = what antibiotic? Used for what?
Metronidazole, for anaerobes & protozoa
Dose of adacel
0.5 mL
When should TDaP be administered
Clean, minor wound: unknown, <3, or 3+ but >10 years since last vax
Other wounds: unknown, <3, or 3+ but >5 years since last vax
When should TIG be administered for wounds:
Clean, minor wound: never
Other wounds: if unknown of <3 vax history
If someone can scrunch their eyes against resistance but has ptosis what is the likely nerve/muscle injury and what ISN’T
Likely injury to levator palpebrae superioris or CNIII (occulomotor nerve) which innervates it
Unlikely to be the facial nerve CN VII which innervates the orbicularis oculi for scrunching eyes against resistance
What is chromic gut?
Absorbable suture
Vicryl is a ____ sutuer
Absorbable
What area of the body needs to be PRECISELY approximated for cosmesis if lacerated?
Vermillion border
PEP for rabies? When is it indicated?
Rabies Ig (passive) + human diploid cell vaccine (HDCV, active)
After bites from uncaught wild animals and animals the start behaving abnormally
(esp bats!!)
Wound irrigation should be performed with…
Saline
Test to be performed after animal bite
Radiograph (look for foreign bodies/teeth, fractures)
What type of bite injury to hand may require admission for IV Abx/Sx?
“Fight bite” (clenched-fist injury) because commonly bacteria embedded in joint spaces/tendon sheaths of hand
Bites >12 hrs old should generally…
What other types of wounds also?
Be left open due to infection risk
Also puncture wounds, bites of hands/feet, infections
Mainstay of treatment for cocaine intoxication
Supportive care
Benzos (lorazepam/diazepam) - don’t use haloperidol bc can lower seizure threhold and worsen hyperthermia/arrhythmia
Physiologic impacts of cocaine
Release of NE, E, serotonin, dopamine –> sympathomimetic
Na channel blockade –> anesthesia, arrhythmias
Tests in cocaine intox with
1) Hyperthermia or agitation
2) AMS/Seizures
1) BMP & CK (assess for renal failure, metabolic acidosis, rhabdomyolysis)
2) Head CT to assess for intracerebral hemorrhage
Meds for arrhythmia in cocaine intox
Benzos
CCBs
NaHCO3 for wide complex tachy, or lidocaine if refractory
Severe hypertension in cocaine intox should be treated with…
Phentolamine (alpha-antagonist)
Not BBs (controversial)
IV nitroglycerine or nitroprusside may also be used
Seizures in cocaine intox treated w…
Benzos!
“Antidote” used to decrease absorption of a toxin within 1-2 hrs after ingestion
Activated charcoal (very high surface area, adsorbs)
What is the Rumack Matthew Nomogram?
Chart showing serum acetaminophen concentration vs time since injection, showing when hepatic toxicity is likely vs unlikely
Starts 4 hrs post-ingestion
Antidote for acetaminophen overdose
N-acetylcysteine (NAC)
What is the most common vessel infarcted in stroke? Presentation?
Middle cerebral artery
Contralateral hemiparesis & hemisensory loss
Contralateral central facial nerve palsy (can move eyebrows)
If dominant hemisphere (usually L) affected —> Broca or Wernicke aphasia
If nondominant hemisphere (usually R hemisphere) affected –> hemineglect
Toxidrome for antimuscarinics Vitals: Pupils: Skin: Bowels: Antidote:
Vitals: increased Pupils: dilated Skin: dry Bowels: reduced Antidote: physostigmine (acetylcholinesterase inhibitor; not for cyclic antidepressants); also benzos
Toxidrome for cholinergics Vitals: Pupils: Skin: Bowels: Antidote:
Vitals: decreased Pupils: small Skin: diaphoretic Bowels: increased Antidote: atropine, pralidozime (2-PAM) for organophosphates
Toxidrome for opioids Vitals: Pupils: Skin: Bowels: Antidote:
Vitals: decreased (esp resp) Pupils: constricted Skin: dry Bowels: reduced Antidote: naloxone
Toxidrome for sedatives/hypnotics Vitals: Pupils: Skin: Bowels: Antidote:
Vitals: decreased
Pupils: unchanged (difference from opioids!)
Skin: dry
Bowels: decreased
Antidote: supportive care; flumazenil (rarely, can cause seizures in chronic benzo users)
Toxidrome for sympathomimetics Vitals: Pupils: Skin: Bowels: Antidote:
Vitals: increased Pupils: dilated Skin: diaphoretic Bowels: increased Antidote: benzos
Antimuscarinic toxidrome mnemonic
Red as a beet (vasodilation/skin flushing)
Blind as a bat (myadrisis)
Hot as a hare
Mad as a hatter (hallucinations, incomprehensible)
Dry as a bone
Full as a flask (urinary retention, can cause agitation)
Stuffed as a pepper (constipation)
What’s the difference between the agitation on sympathomimetics and the “mad as a hatter” in an anticholinergic overdose?
On sympathomimetics usually you can understand what they’re saying, they can be cursing at you etc
Anticholinergic often incomprehensible gibberish
Although clinical evidence of hepatotoxicity may be delayed for _____, with maximum liver injury after _____, NAC most effective if started within ____ hours of ingestion
24-72, maximum 72-96
8 hours of ingestion
What happens in the liver in acetaminophen overdose?
Glutathione depleted (usually combined w/ NAPQI, a toxic intermediate) –> NAPQI accumulation
Glucagon can be used as antidote for..
CCB
BB
Antidote to warfarin
Vitamin K1 (phytonadione)
Antidote to UFH
protamine sulfate
Antidote for hypermagnesia
Calcium gluconate
In general, ____ and ____should be tested on any patient w/ overdose history even when denied
Acetaminophen & salicylate levels
Malnourish patients with alcohol abuse should receive what supplements?
Thiamine and folate
2 concerns w/ activated charcoal
Charcoal pneumonitis (if aspirated) Can make subsequent endoscopy challenging
What compounds aren’t adsorbed well by activated charcoal? (4 categories)
Alcohols: ethanol, methanol, isopropyl alcohol, ethylene glycol
Hydrocarbons
Caustics (acids & bases)
Lithium & other salts
The first dose of activated charcoal may be given with..
Sorbital
3 substances that can be dialyzed in case of overdose. Common property?
Lithium
Methanol
Aspirin (also tylenol but usually just use NAC)
*key is they need a low volume of distribution, i.e. water soluble, stays in serum, less distributed into tissues
What is an elimination method for aspirin & phenobarbital toxicities?
Urinary alkalization: give NaHCO3 –> urine with pH > 7.5, alkaline urine traps ions
What might you see in overdose with TCAs, diphenhydramine, and other various antidepressants/antipsychotics? Treatment and precaution?
Prolonged QRS due to Na blockade
Treat w/ NaHCO3
**note can worsen long QT by pushing K into cells so check that QT is ok first
How does the anti-muscarinic toxidrome differ from symopathomimetic?
Antimuscarinic had dry skin
Sypathomimetic has diaphoresis
What can cause cholinergic toxidrome?
Insecticides (e.g. organophosphates)
ACh inhibitors e.g. physostigmine
Mnemonic for cholinergic toxidrome
DUMBBELLS Defecation Urination Miosis Bradycardia Bronchorrhea/Bronchospasm Emesis Lacrimation Lethargy Salivation
Poor prognostic indicator in overdose
Fever
If you have a seizing patient who isn’t responding to benzos, consider ___ as the cause
Hyponatremia
Treatment for acute hyponatremia of not seizing/altered/obtunded (usually just generally “weak”)
DO NOTHING
Just water restrict, do NOT hydrate even with normal saline bc correcting too rapidly can lead to central pontine myelinolysis –> neuronal damage/death
If pt w/ hyponatremia is seizing/altered/obtunded what is the treatment? How much do you raise Na by?
Hypertonic saline (3%): 3ml/kg x 3% saline pushed over 9 minutes (rule of 3s) Increase by 6 points for severe symptoms (or until Sx cease) no more than this in 24 hrs
Pnemonic for hyperkalemia treatment
C BIG K DIE Calcium Beta agonists/Bicarb Insulin Glucose Kayexylate (polystyrene sulfonate) Die -diuretics (Lasix), dialysis
What are papilla?
Polygonal/cobblestone shapes on tarsal plate (eyelids)
Represent an acute innate inflamm process (bilateral often allergies, unilateral often bacteria)
Bacterial conjunctivitis: what organism is bad in both neonates and adults, can puncture cornea, and is severely purulent
Gonococci (Neisseria gonorrhea)
*pseudomonas can also puncture cornea
Treatment of bacterial conjunctivitis
Broad spectrum antibiotics
No steroids
EMERGENCY if not improved in 2 days
What do you see on exam in bacterial conjunctivitis?
Normal visual acuity
Papilla
No corneal abrasion w/ fluorescein staining
Blepharitis: definition Sx O/E Rx
Inflammation of sebaceous glands
Sx: gritty, tearing, crusting
O/E: red eyelin margins, debris in lashes, conjunctival hyperemia
Rx: warm washcloth
clinical entity characterized by coarse, raised intraepithelial lesions surrounded by focal inflammatory cells, with punctate staining as well as areas of negative staining on fluorescein.
Punctate epithelial keratitis
can be seen with various corneal pathogens, sometimes dry eye
What are follicles (eye)
Round nodules on tarsal plate, upper & lower fornix
Lymphocytic (adaptive) immune response
DDx of follicular conjunctivitis that is acute, <30d, pre-auricular lymph notes
Viral
Chlamydia
DDx of Chronic (>30d) follicular conjunctivitis
Molluscum contagiosum
Chronic eye drop usage
What is the most common cause of red eye
Viral conjunctivitis (adenovirus)
Prognosis of viral conjunctivitis
Spontaneous resolution in 1-2 weeks, contagious for that time Symptomatic relief (no steroids!)
What eye issue commonly present w/ swollen lids, clear discharge, crusting, blurry vision, proceeding URTI, photophobia
preauricular nodes, follicles
Viral conjunctivitis
Define keratitis
Inflammation of cornea
What eye infection is characterized by keratitis, stromal edema, keratic precipitates, dendritic ulcers, and decreased corneal sensation over ulcer?
Herpes conjunctivitis (usually self-limited to 14d)
What is stromal edema
Fluid in stroma of the cornea
What eye injection presents with conjunctival hyperemia, follicles, mucoid discharge, enlarged lymph nodes, STI sx
Chlamydia conjunctivitis
Treatment for chlamydia conjunctivitis
Peds: EMERGENCY referral!!
Adults: azithromycin, doxycycline/erythromycin
Prophylaxis for parents/partners
Refer adults within 72 hrs if no improvement (culture)
What is the area direclty around the iris called? What is it termed when it’s red?
Limbus Ciliary flush (dilated blood vessels)
What are anterior chamber cells and how are they diagnosed?
Inflammation in anterior segment of eye –> breakdown of blood-aqueous barrier –> more cells/protein in aqueous humor
Requires slit-lamp exam
DDx of ciliary flush
Anterior uveitis/iritis
Acute angle closure, glaucoma
DDx of anterior chamber cells
Anterior uveitis/iritis Acute angle closure, glaucoma Endophthalmitis Corneal Ulcer Trauma
What is hypopyon
WBCs in anter`ior chamber of eye
Internal eye infection usually seen post-surgery (cataracts) that is characterized by pain, decreased VA, conjunctival edema, anterior chamber cells, hypopyon
Endophthalmitis
EMERGENCY referral required!
Iritis is caused by what?
90% idiopathic, may be assoc w/ collagen vascular diseases
What is episcleritis? How do you differentiate it from scleritis? Rx?
Dilation of radial vessels of episclera
Attempt to move vessels (freeze conjunctiva), if they move –> episcleritis; they don’t move –> scleritis (patterns indistinguishable looking at them)
If redness improves with phenyl it’s episcleritis and vice versa
Rx: Ibuprofin
inflammation of ___ requires testing for an underlying disorder. Treatment?
Sclera (scleritis)
Ibuprofen , may require steroids
Intraocular pressure (normal)
10-21 mmHg
DDx of raised IOP
Angle closure glaucoma Open angle glaucoma Trauma Anterior uveitis Hemorrhage-hyphema Chemical burns
What is hyphema?
Blood in front of eye between cornea and iris
What eye problem present w/ pain, halos, blurred vision, headache, malaise, nausea/vomiting/epigastric pain, unreactive mid-dilated pupil, etc.
Acute angle closure glaucoma
Rx for acute angle closure glaucoma
EMERGENT REFERRAL
Stabilize IOP ASAP
Start Diamox (acetazolamide)
Laser iridotomy
What is going on in acute angle closure glaucoma?
Iris blocks trabecular meshwork –> Aqueous humor builds up –> vascular compromise, ischemia
Using fluorescein dye and blue light on ophthalmoscope, what do the following findings indicate:
1) Multiple pinpoint uptakes
2) Single larger stained area
3) Dendriform staining
1) Punctate epithelial erosions, suggesting dry eye or exposure
2) Corneal abrasion or ulcer (ulcers white vs abrasions green??; abrasions have well-defined borders when stained)
3) Herpetic disease
What is the diagnosis where pt present with glaucoma Sx but normal IOP?
???
Sx of glaucoma (open angle)
Usually asymptomatic. Later in disease, get visual field deficits from nasal –> central (e.g. arcuate scotoma)
Finding on exam of optic disc in glaucoma; cutoff value?
Increased “cup to disc” radio due to neuron damage (>0.5= suspicious for glaucoma)
Treatment of corneal abrasion
Abx, eye patch
NO steroids
Treatment of corneal ulcer
EMERGENCY referral + Abx
____ needs to be performed before fluorescein staining and slit lamp exam
Visual acuity
Dilated pupil exam should not be performed until ____ is ruled out
Globe injury
Test performed to determine if someone has chlamydia causing eye infection
Corneal scrapings –> culture
take scraping before starting empiric ABs
ADE of topical steroids for eye
Increased IOP (can lead to acute angle closure glaucoma)
Purpose of fluorescein staining?
Visualize abnormalities of cornea
Keratic precipitates are common with ___ infections
Herpes virus infections (less so with Chlamydia, Adenovirus)
Way to tell follicles vs papilla
Papilla = red (vascular) Follicles = white (inflamm cells)
Diagnosis of mesenteric ischemia
Noncontrast CT abdo
oral contrast can obscure mesenteric vessels & bowel wall enhancement
Resus mnemonic
MOVIE M= Monitors: 3 lead cardiac monitors Pulse oximetry Blood pressure cuff
O=Oxygen
Nasal prongs 02 at 15L
Titrate to Spo2 > 95%
V= Vitals:
Repeat VITALS Always. They came in normotensive and may now be hypotensive and tachycardic
IV= IVs and bloodwork
2 large bore IVs.
IF CANT get IV access with two experienced operators, establish an IO.
E= Everything else
2 general categories of PEA
Narrow complex –> usually mechanical (tamponade, tension pneumo, PE, hyperinflation)
Wide complex –> usually metabolic, toxicologic, or MI (or obstructive w/ abberancy) - hyperK, Na channel blockers, MI
Empiric treatment of wide complex PEA (other than CPR)
Calcium chloride and sodium bicarbonate
Noncontrast CT is sensitive for SAH within __ hrs of Sx onset, after that if it’s negative you need ____
6 hrs
LP for xanthochromia
At what class of hemorrhagic shock (and what volume of blood loss) do you get tachy? Hypotension?
Tachy = class II = 750-1500 mL lost Hypotension = class III = 1500-2000 mL lost
Triad of death
Coagulopathy, acidosis, hypothermia
What do the FAST and eFAST exams look at?
FAST: Pericardial, perihepatic (RUQ), perisplenic (LUQ), pelvis
e-FAST adds pleural spaces
Doses for Propofol, ketamine, etomidate, succinylcholine, and rocuronium (all mg/kg IV)
Propofol = 1 Ketamine = 1.5 Etomidate = 0.3 Succs = 1.5 Roc = 1 (variable depending on source)
Kawasaki disease: definition + diagnostic criteria
Self-limiting medium vessel vasculitis predominantly affecting Asian male children 1-5 yo
"WARM CREAM" Warm = 5 days of fever or more Plus 4 of the following 5: - Conjuncitivitis - Rash (nonvesicular, generalized) - Extremity changes - erythema/edema of hands and feet followed by desquamation Adenopathy (cervical) Mucous membrane changes (cracked red lips, "strawberry" tongue)
Treatment for Kawasaki disease
IVIG + ASA to prevent cardiovascular complications
BREATHE mnemonic for urgent differential of SOB?
Bacteria (pneumonia, endocarditis) Reactive airway disease (asthma, COPD, anaphylaxis) Embolism (PE) ACS Tension pneumo, Tamponade Heart failure Electrical excitation (arrhythmia)
Score for diagnostic probability of Strep throat?
M-CENTOR M - Must be older than 3 years C - Cough absent (+1) E - exudate or swelling of tonsils (+1) N - cervical lymph Nodes (+1) T - Temp >38C (+1) O - Often Young <15yo (+1) R - Rarely Old >45yo (-1)
2-3 rapid, ABs based on culture if rapid negative
4+ –> high likelihood, consider empiric therapy
Bacterium that causes strep throat
Group A beta-hemolytic strep
= Streptococcus pyogenes
Best Abx for strep throat?
Penicillin
J wave AKA ___ is a finding in what clinical condition?
Osborn wave
Hypothermia
4 stages of hypothermia: temps & treatments
1 (32-35C, shivering) - passive rewarming
2 (28-32C, not shivering) - active external, make sure any fluids given are warm
3 (24-28, unconscious) - active internal (+external)
4 (<24, VSA) - above + CPR, ECMO
Common active external rewarming device used in hospital
Bear hugger (forced air)
