2017
Internal Medicine
Residency Program
Boot Camp 2017
Introduction Welcome to Boot Camp 2017! Copyright laws prohibit us from copying articles and “re-
publishing” them in a Boot Camp book. Therefore, what you will find in this book are the cases
and occasional summaries of the topics provided by some of our residents. At the end of each
section there is a list of references that will be covered. Some topics have multiple references
and, in general, the first and/or second references are to be considered the “primary”
references. All articles with Internet addresses are accessible utilizing the KUMC web server. If
the article is not available electronically, the article may be obtained from the library. We have
made every attempt to ensure that all primary references are available electronically.
To obtain a reference you must either be on campus, logged in through KU Remote Access (dial-
up Internet) or be using the KUMC proxy server (if you have a high-speed connection). Once
you have located the appropriate Internet site, you will need to locate the article by using the
listed reference. Searching by citation is usually the quickest and easiest method. If you have
trouble locating the appropriate Internet site, go to the Dykes Library Online Journals site for a
link. (Web address below)
http://mt8fd2he2v.search.serialssolutions.com/
You need to be logged on through KU to maximize the links through the library site.
All cases and direct links to the articles are published on the KU Internal Medicine Intranet site.
https://share.kumc.edu/SOM/wichita/IM/default.aspx
We look forward to a new and exciting year of Morning Teaching Conference beginning with
Boot Camp. If you have suggestions or find any errors, please contact the Internal Medicine
Chief residents so that changes can be incorporated for next year.
Table of Contents
Topic Date Page
Introduction: High Yield Basics Wed 7/5 5
Acute Coronary Syndromes I & II Thu 7/6 10
Acute Respiratory Distress Syndrome Tu 7/11 23
Sepsis Overview Wed 7/12 27
Heart Failure Thu 7/13 34
Pancreatitis Tu 7/18 38
Neutropenic Fever Wed 7/19 44
Atrial Fibrillation Thu 7/20 48
GI Bleeding Tu 7/25 56
Acute Kidney Injury We 7/26 63
Hypertensive Emergencies Thu 7/27 68
Status Epilepticus Tu 8/1 76
Chronic Obstructive Pulmonary Disease + Asthma Wed 8/2 81
Aortic Dissection Thu 8/3 87
Acid-Base Analysis Tu 8/8 93
Pleural Effusions + Pulmonary Embolism Wed 8/9 102
Topic Date Page
Syncope Thu 8/10 116
Stroke Tu 8/15 124
Community Acquired Pneumonia Wed 8/16 132
Acute Infective Endocarditis Thu 8/17 137
Hyponatremia + Hypernatremia Tu 8/22 142
Meningitis Wed 8/23 153
Hyperkalemia Thu 8/24 159
Delirium Tu 8/29 164
Diabetic Ketoacidosis Wed 8/30 170
Alcohol Withdrawal Thu 8/31 175
Pain Management + Leaving Against Medical Advice Tu 9/5 181
Morning Teaching Conference Tutorial Wed 9/6
Introduction/High Yields “Survival Guide”
Admissions:
1. Work with your senior resident. You may evaluate patient alone or together with the senior.
2. Typically, beginning of the year, the senior will do the orders and the intern will write the
H & P. As the intern becomes more comfortable with cases, will transition to doing
admission orders and writing the H & P.
3. Notes don’t get things done for patients, orders do. Orders come first, especially for
critically ill.(i.e. antibiotics, IV fluid boluses, pressors)
4. Consults:
a. Consult earlier as early in day as possible (Attending approval if needed, some have
different thresholds)
b. Typical life-saving consults needed STAT:
i. Urgent dialysis - call nephrology
ii. Acute abdomen (peritoneal signs, lactic acidosis) - call surgery
iii. STEMI, NSTEMI – call cardiology
iv. Unstable GI Bleed
v. Compartment syndrome/Nec Fasc - Ortho or wound surgery
Daily Activities on Inpatient 1. Round on all patients prior to MTC
2. Inform senior of any unstable/critical overnight changes
3. Essential early morning orders (replace lytes, fluids, drips, etc)
4. Initiate progress notes and complete as much as possible to expedite post-rounds duties
5. PROGRESS NOTES:
a. EMRs make it extremely tempting to copy/paste everything. While good for
efficiency please be aware of the dangers
b. In addition to being crucial to patient care - YOUR NOTE IS A LEGAL &
BILLING DOCUMENT and you are responsible for the content
i. Update your physical exam EVERY DAY
ii. Update your assessment and plan EVERY DAY
iii. Document acuity and resolution of problems as hospitalization progresses
1. Move resolved problems to bottom of list
iv. Use dates rather than words like ‘tomorrow/today’ ie. “CT on 5/19”
v. Keep your note clean and easy to follow. Providers/consultants need a
quick synopsis of the patient
Discharges:
1. Do medicine reconciliation (Med Rec) first
a. Print scripts, sign, place into chart or electronically send to patient’s pharmacy
b. Discuss important changes w/ patient - Write them a list of changes if needed
c. Poor med-recs cause readmissions!
2. Pt's w/o insurance/income may need scripts in-hand at discharge
a. Coordinate with social worker early in hospitalization to anticipate which meds are
critical on discharge
i. Can get samples through Dispensary of Hope, etc…
2. Confirm outpatient follow-up is scheduled, preferably within 7 days of discharge
a. Discuss with social worker any foreseeable barriers to transition
b. If no PCP:
i. If pt has insurance and is a good patient → f/u w/ KU Residency Clinic
ii. If no insurance → f/u w/ GraceMed, Hunter Health
b. Weekends:
i. For KU patients: use "ScheduleMe" site at: wichita.kumc.edu/scheduleme.html
ii. Others: Patient to make own f/u. Document this well
b. For complex patients, do not be afraid to call PCP to ensure smooth transition
2. Sign the DC order and instructions; nurse will print off the "instructions" and give to
patient which includes a new Med-Rec list and will provide the patients their new/changed
scripts you placed into their charts
3. **DC Summaries - IMPORTANT. Means of communication to the next doctor to best help
in transitioning the patient safely to out-patient setting
a. Best if done within 24h of discharge, but definitely < 3 days.
b. Use DC sum templates at various hospitals but...
c. Most important items are:
i. Primary and secondary diagnoses (for billing) - Highest acuity dx first
ii. Meds on DC (please note specific changes in home meds, stopped meds, added
meds, and try to mention why)
iii. Follow-up recommendations/instructions for patient and follow up physician;
"high-risk" points of transition
1. Please put these in bulleted form on DC SUM
b. DC sums are NOT simply the progress note on the day of discharge
Replacing electrolytes
Potassium
o Goal 3.5 unless cardiac patient’s goal 4.0
o For K 3.0 - 3.5: every 0.1 in serum K+ = 10meq KCl
o For K < 3.0: every 0.1 in serum K+ = ~30meq KCl
o If tolerating PO, then use PO: give up to 40meq PO KCl q4h
▪ Consider crushing and putting in orange juice or powder forms
▪ Don't give too much without rechecking serum K+!
▪ If very low, can give oral + IV
o If not tolerating PO, then give IV: give up to 10meq IV KCl / hour
Magnesium
o Goal 1.8 unless cardiac patient’s goal 2.0
o If tolerating PO, can give Mag-Oxide 400mg tidwm (not known correlation with
[serum])
o For IV: give Mag-Sulfate
● The slower you run it, the better - best to run 1g over 3h
● 1g Mag-Sulfate = 0.1 in serum Mg2+
o Correct for albumin if low: every drop in albumin by 1 below 4, add 0.08 to measured
serum Mg2+
Phosphorus
o If mildly low, ~2.0 - 2.5: use skim milk + PO 1-2 Neutra-phos vs K-Phos powder
(or tabs) tidwm
o If <2.0: suggest IV
● IV K-Phos or IV Na-Phos: usually in 15, 20, 30, or 40mmol options
● Use Na-Phos if hyperkalemic (15mmol K-phos has ~22meq K+)
Calcium
o 1st thing: correct for albumin! For every 1 albumin below 4, add 0.8 to serum Ca2+
o PO Tums (Calcium carbonate) 500mg tidwm
o IV 1g CaCl2, IV 1g CaGluconate:
● Used only for symptomatic hypocalcemia <7.7 mg/dL, hyperkalemia, and codes
o There is usually an underlying cause
Fluids:
● Usually give Normal Saline (NS) or Lactated Ringers (LR)
o LR best for pancreatitis
o Do NOT give LR if liver failure (liver metabolizes lactate --> bicarb), or lactic
acidosis
o LR contains physiologic 4meq/L K+, 28meq/L HCO3-, and 3meq/L Ca2+
● Fluid bolus 500mL - 30mL/kg for volume resuscitation, sepsis, hypotension
● Maintenance
o Only do if patient is not tolerating PO or NPO
o 4, 2, 1 rule = hourly rate of IVFs
● 4 mL/kg/hr for first 10kg + 2 mL/kg/hr for 2nd 10kg + 1 mL/kg/hr for
remaining kg weight
● ie. 60ml/hr + 1 ml/kg/hr for every 1 kg after 20kg
● Special circumstances
o Hypernatremia - can give 1/2NS or D5W
o Severe hyperkalemia +/- severe renal failure - sterile water + 3amps bicarb @
150mL/h
o Overcorrection of hyponatremia - D5W
o Symptomatic hyponatremia - 3% hypertonic saline (measure Na q2h)
Common Complaints and reasons for Pages:
Nausea/Vomiting
o Options:
● Ondansetron (Zofran) 4mg PO/IV/IM q4h prn (5-HT3 blocker)
● Metoclopramide (Reglan) 5-10mg PO/IM/IV q6h prn (D2-blocker)
● Prochlorperazine (Compazine) 5-10mg q6h prn (D2-blocker)
● Haloperidol (Haldol) 1mg q4 prn (D2-blocker)
● Promethazine (Phenergan) 25mg q6h prn (anticholinergic/antihistamine)
● Diphenhydramine (Benadryl) 25-50mg q8h prn (anticholinergic/antihistamine)
● Scopalamine patch q3d prn (anticholinergic)
o For severe N/V, use combos with different pharmacologic mechanisms (receptors)
o Caution QT prolongation
Pain
o Tylenol (Acetaminophen) - up to 650mg q6h
● Avoid or minimize in liver failure, HCV, alcoholics
o NSAIDs
● Options
▪ PO Ibuprofen - start 400-600mg q8h, titrate up to 800mg q8h
▪ PO Naproxen - 250mg q 12h, titrate up to 500mg q12
▪ IV/IM Ketorolac - 15-30mg q 12h; maximum of 5 days
▪ Diclofenac (Voltaren) Gel - 2-4g apply to localization of pain [best for
local pain/swelling/joints]
▪ PO Meloxicam - up to 15mg qd (COX-2) (avoid if have CV risks)
▪ PO Celecoxib - 100mg q12h (COX-2) (avoid if have CV risks)
● Avoid NSAIDs in renal failure patients, GI bleeds (peptic ulcers, gastritis, etc)
● Minimize NSAIDs in cardiac patients
o Neuropathic pains:
● Gabapentin - start 300 daily → 300 bid → 300 tid → 600 tid
● Pregabalin (Lyrica) - 75mg bid → 150mg bid
● Duloxetine (Cymbalta) - 30mg qd → 60mg qd
▪ Diabetic neuropathy, fibromyalgia, lower back pain w/ osteoarthritis +/-
depression
o Opioids (non-comprehensive)
● If taking PO:
▪ Percocet 5-10/325 q4-6h prn
▪ Norco 5-10/325 q4-6h prn
▪ Oxycodone 5-15mg q6h prn (no acetaminophen)
● IV Opioids
▪ Use for breakthrough pain or not taking PO
▪ Dilaudid 0.5mg q4h → titrate up to 1mg q2h
▪ Morphine 2mg q2-4h prn
● Be aware of opioid conversions
● Caution initiating opioids in chronic non-cancer pain
o Non-Pharmacologic
● Lidocaine patch - for local pain
● Heat pack/Ice pack
Insomina/"Can't Sleep" ● Educate nurse to keep pt awake during day (open blinds), ambulate if possible, remove
nightly stimulating factors
● Pharmacologic options
o Trazadone 25-50mg PO qhs
o Seroquel 25mg PO qhs
o Benadryl 25-50mg qhs (for non-geriatric patients)
● If absolutely needed, consider less desired meds:
o Ambien 5-10mg PO qhs
o Ativan 0.5-2mg PO qhs
Agitation/Combativeness/Delirium
● Frequent reorientation, familiar environment, open blinds, frequent family checkups,
sleep protocol without interventions at night
● Pharmacologic (caution QT)
o Haldol IM 0.5 – 5mg IM q3-6h
o Ziprasidone 10mg IM q2h prn
o Seroquel 50mg qhs for if recurrent/high risk
● Avoid benzodiazepines (makes worse)! Unless EtOH w/d or seizures
● Soft wrist restraints if harm to self or nursing staff
● Call security for combative
Coughing
● Tessalon Perles w/ Benzonate
● Dextromethorphan - 30mg q8h prn
● Breathing tx if bronchospasm
Constipation
● Best go to: Miralax (polyethylene glycol) 17g PO q12h prn
o Can give up to q2-4h until has BM!
● Lactulose
● Bulk laxatives: metamucil powder PO bid prn
● Stool Softener: docusate 50-200 bid
● Osmotics: Milk of Mag qd prn
● Stimulants: Senokot-S 2-4 tabs qd, Dulcolax 5-15mg qd
Itching/Pruritis
● Systemic
o Hydroxyzine 25mg PO/IM q6h prn
o Benadryl 25-50mg PO/IV/IM q6h
● Local
o Benadryl Itch Cream
o Topical Capsaicin
o Hydrocortisone (avoid if fungal)
o Triamcinolone (avoid if fungal)
Fungal Itching (Cutaneous candida)
● Topical Miconazole 2% cream bid
● Topical Clotrimazole 1% cream/solution bid
● Topical Ketoconazole 2% cream q daily, foam, shampoo
● Topical Nystatin cream/powder bid-tid
Acute Coronary Syndromes Part I: ST Elevation Myocardial Infarction
CC: Chest Pain/Pressure
HPI: 73 yo white male presents to the ED with two hours of severe, pressure-like discomfort in
the center of his chest associated with nausea, vomiting, and diaphoresis. The discomfort does
not radiate. The pressure is rated at 8 on a 1-10 point scale but decreased to a 4 when given
sublingual nitroglycerin by EMS. The patient complains of SOA that started with the chest
discomfort
PMH: Benign prostatic hyperplasia, Hypertension
PSH: TURP
Meds: HCTZ 25mg qd, tamsulosin 0.4mg qd
Allergies: NKDA
FMH: Mother – HTN, Father – deceased MVA, age 50, Sister 78 with “heart problems”
SOC: Smoked 1 ppd for 30 years. Quit 13 years ago. Denies alcohol or drug use. Married with
four children.
ROS: No weight change, recent decreased exercise tolerance. No SOA until acute episode. No
prior cardiac events.
PE
Vitals: T 98.8 RR 30 P 110 BP 150/90
GEN: Well-developed, well-nourished, in moderate distress secondary to pain and SOA.
NECK: JVD to 15cm
CV: normal S1, S2. S3 is present. No murmur; pulses equal bilaterally
Lungs: Bilateral crackles over the lower lobes
Abd: benign
Ext: No edema
Labs
CBC: WBC 10.5, Hgb 15.2, Plts 226
BMP: Na 135, K 4.2, Cl 113, Bicarb 23, BUN 13, Cr 0.8, Glu 157
Cardiac: Troponin = 2.0
CXR bilateral congestion
EKG see attached
Objectives 1. Risk factors for myocardial infarction
2. Diagnosis of ST elevation MI
3. Treatment of ST elevation MI
Differential Diagnosis of chest pain
- Cardiac: ACS, pericarditis, myocarditis
- Vascular: Aortic dissection, pulmonary embolism
- Pulmonary: Pneumonia, tension pneumothorax, pleuritis
- Chest wall: Costochondritis, sternoclavicular arthritis, zoster, muscle strain, rib
fracture or contusion, neuropathic pain…
- GI: esophagitis, esophageal spasm, PUD, gastritis, biliary pain, pancreatitis
- Psych: Anxiety, somatiform disorders
Differential Diagnosis of ST segment elevation
o Myocardial ischemia/infarction
o Acute pericarditis
o Early repolarization (normal variant)
o LVH or LBBB
o Trauma, tumor, myocarditis, hyperkalemia, hypothermia, Brugada syndrome
DEFINITIONS
Acute coronary syndrome (ACS) — Applied to patients where myocardial ischemia is
suspected. Classified into three types:
1. ST Elevation myocardial infarction (STEMI)
2. non-ST elevation myocardial infarction (NSTEMI)
3. Unstable angina
The first two (the infarctions) are characterized by a typical rise in markers of myocyte injury
(i.e. cardiac enzymes). These biomarkers do not rise in unstable angina.
Myocardial Infarction (MI) - Joint Task Force of the European Society of Cardiology,
American College of Cardiology Foundation, the American Heart Association, and the World
Health Federation (ESC/ACCF/AHA/WHF) defined acute MI as:
-clinical (or pathologic) event caused by myocardial ischemia in which there is evidence
of myocardial injury or necrosis
Generally, change in cardiac biomarker values (preferably troponin) with at least one of
the following are needed to meet criteria for an MI:
● Symptoms of ischemia
● Development of pathologic Q waves in the ECG
● New or presumed new significant ST-segment-T wave (ST-T) changes or new left
bundle branch block (LBBB)
● Identification of an intracoronary thrombus by angiography or autopsy
● Imaging evidence of new loss of viable myocardium or a new regional wall motion
abnormality.
Clinical Classification of MI:
o Type 1: Pathologic process in the wall of the coronary artery (eg: plaque rupture)
o Type 2: Increased oxygen demand or decreased oxygen supply (eg: coronary artery
spasm, anemia, arrhythmias, hypotension/sepsis)
o Does not require anticoagulation or discharge meds - Please document Type 2
MI to not initiate ACS Quality Measures
o Type 3: Sudden unexpected cardiac death before blood samples could be taken
o Type 4a: Associated with PCI (i.e. after PCI)
o Type 4b: Stent Thrombosis
o Type 5: Associated with CABG (i.e. after CABG)
Localizing Area of Ischemia on EKG (Figure from ACP Smart Medicine)
Risk Factors:
o Non-modifiable
Family history - (only first degree relatives, male< 55, female <65)
Estrogen (male or post-menopausal female)
Age (male>40, female>50)
Race (Black>Caucasian)
o Modifiable
HTN/CAD
Obesity/Sedentary lifestyle
Tobacco
Diabetes mellitus
Hyperlipidemia
o Past Procedures
Previous heart catheterization/CABG
Initial evaluation and interventions of patients presenting with possible ACS: ● Remember, women, the elderly, and diabetics may have atypical presentations
● within 10 minutes: triage for rapid care and start MONA-Morphine, oxygen,
nitroglycerin and aspirin
● IV access, focused H&P, continuous cardiac monitor, and initial ECG (first ECG
should ideally be done by EMS)
● Basic labs (CBC, INR, aPTT, BMP, magnesium, lipids, cardiac markers)
● Repeat ECG at 5-10 min intervals if initial ECG is non-diagnostic
● Aspirin chewed (160 to 325 mg)
● Supplemental oxygen
● Nitroglycerin (0.4 mg sublingually q5 min x 3) – Unless phosphodiesterase-5
inhibitor used in last 24 hours or suspect inferior MI
● Morphine (2-4 mg IV q 5 min for chest pain uncontrolled with nitro)
● Beta blocker (Metoprolol 25mg) PO unless heart failure, low output state, bradycardia,
heart block or reactive airway disease. Continue indefinitely in absence of
contraindications
● IV beta blocker (metoprolol 5 IV) only if hypertensive or ongoing ischemia and
no risk of cardiogenic shock.
● High intensity statin therapy should be continued or initiation (even before PCI if
possible)
● PROVE IT-TIMI 22 trial showed benefit in 30d
● Note on cardiac biomarkers:
-cardiac troponin is the most useful biomarker. CKMB and CPK are usually unnecessary
in the evaluation of acute coronary syndromes
- troponin usually starts to rise 2-3 hours after the onset of acute MI. Within 2-3 hours of
presentation, up to 80% of patients with acute MI will have elevated troponin. However,
up to 12 hours may be required to detect elevations in all patients.
- Troponin typically remains detectable in the blood for up to 10 days
Therapy for STEMI: ● IV nitroglycerin for persistent chest pain or hypertension if no contraindication
● Anticoagulation: unfractionated heparin (most common), enoxaparin, or fondaparinux
● Plavix load with 600 mg if going for primary PCI and 300mg if thrombolysis or no
reperfusion and <75 yo. Can alternatively use prasugrel or ticagrelor. (Note: while
adding a second antiplatelet agent on top of aspirin is recommended in the guidelines,
for practical purposes, it is usually best to contact the cardiologist first and ask
before giving clopidogrel, as it can delay CABG for patients who need it. Patients can be
loaded with clopidogrel in the cath lab if it is determined that the patient will not require
CABG).
● GP IIbIIIa inhibitor (cardiologist will usually decide whether or not to use) during PCI
● Primary PCI is the preferred reperfusion strategy. First medical contact (FMC) to device
time should be 90 min or less (this has replaced the old "door to balloon time")
● Thrombolysis should have door to needle time of 30 min or less. (Should ideally be
within 12 hrs of symptom onset and no contraindications).
● Initiated only if in a non-PCI hospital and that FMC to device (PCI) estimated
time will be more than 120 minutes.
Additional Therapy ● Facilitated PCI (tPA immediately before PCI) not recommended unless ongoing ischemic
sx, severe heart failure or hemodynamic compromise
● ACE-I/ARB: 2013 guidelines gave weak recommendation for ACE-I to all STEMI
patients. They gave a strong recommendation for ACE-I for patients with STEMI and
anterior location, heart failure, or EF </= 40%
● Aldosterone antagonist (i.e. eplerenone) if: pt on beta blocker and therapeutic dose of
ACE/ARB with EF</= 40% AND has symptomatic heart failure or DM
● NSAIDs and COX-2 inhibitors should not be initiated and should be discontinued in
those taking them prior to admission
● Long-Term Risk Factor Modification (smoking, glycemic control, hypertension, diet,
exercise)
● Aspirin for life (75-100 mg is the recommended dose, higher doses of maintenance
aspirin offer no added benefit)
● Dual Antiplatelets (usually ASA 81mg daily and clopidogrel 75 mg daily) should be given for at
least 1 year to all patients with STEMI who receive a stent (bare-metal or drug-eluting)
during primary PCI and even for those that did not receive PCI. Consider continuing P2Y12
inhibitor beyond one year for those who received DES. This is the current recommendation from
the 2013 ACC/AHA guidelines.
● Note: Effient (prasugrel) should not be given to patients with a prior history of
TIA or stroke
● LVEF should be measured in all patients with STEMI (usually measured during heart cath or
with TTE at hospital day 2-3
Discharge planning for patients with STEMI:
1. Need to facilitate transition to coordinated and effective outpatient follow up with goal of
preventing hospital readmission
2. Exercise-based cardiac rehab/secondary prevention programs recommended
3. All STEMI patients need a clear, detailed, and evidence-based plan of care that promotes
medication adherence, timely follow-up, appropriate dietary and physical activities, and
compliance with interventions for secondary prevention
4. Encouragement and advice for smoking cessation and avoidance of secondhand smoke
should be provided to all STEMI patients.
References: 1. Institute for Clinical Systems Improvement Health Care Guideline: Treatment of acute
myocardial infarction.
http://www.icsi.org/display_file.asp?FileId=183
1. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction:
Executive Summary. Circulation.2013; 127: 529-555
http://circ.ahajournals.org/content/127/4/529.full
1. The Joint European Society of Cardiology/American College of Cardiology
Committee. Myocardial infarction redefined – a consensus document of The Joint European
Society of Cardiology/American College of Cardiology Committee for the redefinition of
myocardial infarction. JACC 2000;36:959-969.
http://www.acc.org/clinical/consensus/mi_redefined/redefined.pdf
1. Initial Evaluation and Management of Suspected Acute Coronary Syndrom in the
Emergency Department – uptodate.com
1. Overview of the acute management of ST elevation myocardial infarction – uptodate.com
Objectives Definition and diagnosis of Non-ST elevation MI (Non-
STEMI) vs. unstable angina
Treatment of Non-STEMI and unstable angina
Prevention of myocardial infarction
Acute Coronary Syndromes Part II:
Unstable Angina/NSTEMI
Unstable Angina/NSTEMI
HPI: 69 yo WM presents to the ED with complaints of increasing chest discomfort over the last
week. He has a known history of coronary artery disease and underwent PTCA about 5 years
ago. Since then, he has had angina approximately 2-3 times per month, which occur mostly with
prolonged exertion. In the past his discomfort had always resolved with rest and one or two
sublingual nitroglycerin. Recently he has begun to have chest discomfort with minimal exertion
and also at night. As a result, he has had to significantly limit his activity. He finds that although
his discomfort diminished with some nitroglycerin, it does not resolve completely. Today, while
doing the dishes, he began to have severe chest discomfort that did not resolve after three
sublingual nitroglycerin.
PMH:
CAD, S/P Anterior MI; PTCA LAD 1993 S/P Bilateral Aorto-Femoral bypass
HTN x 20 years S/P Cholecystectomy
Hyperlipidemia
Meds:
Metoprolol 25mg bid
ASA 81mg daily
Lisinopril 20 mg po daily
Atorvastatin 20mg qHS
NTG SL PRN
SOC: Lives with wife, retired truck driver. Smokes 4-6 cig/day. Drinks 6-10 beers/day
PE:
Vitals: T 98.8 P74 R16 BP 164/85
Gen: slightly obese WM, active chest pain
HEENT: unremarkable
Neck: no JVD or bruits
Lungs: diminished breath sounds throughout, no crackles or wheezes
CV: Normal S1, S2 with S4
Abdomen: benign
Ext: diminished peripheral pulses, no clubbing or edema
Neuro: intact
Labs:
Initial Troponin-WNL
EKG (with active chest pain): shown
NSTEMI/Unstable Angina (UA): Continuum of same disease
For angina to be considered unstable, it needs to present in one of the following ways:
▪ Angina at rest, usually lasting for at least 20 minutes
▪ New onset anginal chest pain that significantly limits physical activity
▪ Increasing angina that occurs more frequently, lasts longer, or occurs with a smaller
amount of exertion than previous angina
NSTEMI is distinguished from UA by the presence of elevated serum biomarkers.
NSTEMI and UA may be indistinguishable at presentation as cardiac biomarkers can take
several hours for them to become detectable in the bloodstream
Prehospital care:
● Administer ASA 162-325 mg (chewed) unless contraindicated. Or already taken.
● If suspected ACS, 1 dose of sublingual nitro only, before calling EMS
● If chronic stable angina, pt may take nitro q 5 min x 3 prior to calling
In Hospital care: Initial Evaluation (similar to STEMI)
● EKG within 10 min
● Repeat EKG within 15 min if 1st is non diagnostic, the patient remains symptomatic and
there is a high clinical suspicion for ACS
● Consider checking posterior leads V7, V8, and V9 if there is evidence of posterior wall
ischemia, i.e. prominent R waves and ST depressions in leads V1 and V2
● Measure cardiac biomarkers. Troponin is preferred. In all patients who present with
symptoms consistent with ACS, troponin should be obtained at presentation and at 3-6
hours after symptom onset. Additional troponin levels should be obtained beyond 6
hours in patients with normal troponin levels on serial examination when changes on
EKG and/or clinical presentation confers an intermediate or high suspicion for ACS
(Class I, Level of Evidence A per 2014 Guidelines
● Continuous monitoring
● Risk stratification models (TIMI, GRACE, or PURSUIT), to help with decision regarding
aggressiveness of management (early [within 24 hrs] vs delayed cath)
● TIMI score (1 pt each):
● Age >65,
● At least 3 risk factors for CAD (HTN, DM, smoking, DL, early family
history),
● Prior coronary stenosis,
● ST deviation on EKG,
● 2 anginal events in prior 24 hrs,
● Use of ASA in last 7 days,
● Elevated biomarkers
TIMI score:
0-1 4.7 % all cause mortality
2 8.3%
3 13.2%
4 19.9%
5 26.2%
6-7 40.9%
Early Hospital Care (similar to STEMI except no immediate need for emergent reperfusion):
● Bed rest or chair rest
● O2 to maintain sat of 90% for hypoxic patients. No benefit from O2 if sat >90%
● Ongoing chest pain may need IV NTG for persistent ischemia, HF, or HTN unless
contraindicated (RV infarct, severe AS, use of 5PDE inhibitor within 24 hrs)
● Oral beta blocker within 24 hrs if no: signs of HF, low output state, increased risk of
cardiogenic shock, other contraindications (heart block, active asthma)
● If stable HFrEF continue BB therapy with either metoprolol succinate, carvedilol, or
bisoprolol (only three beta blockers proven to reduce mortality in patients with HF)
● ACE-I: evidence less strong for use in NSTEMI and UA compared to STEMI,
but should be started in patients with diabetes, heart failure, LVEF <40
percent, and hypertension. May be beneficial in all patients after any MI.
● NSAIDs (except ASA) should be discontinued due to high risk of adverse cardiovascular
events
● Morphine for uncontrolled ischemic chest pain
● No nitrates if sbp < 90 or pulse < 50
● No nitrates for pts receiving 5PDE inhibitor for ED within 24 hrs
● Aspirin 81-325mg once daily for life
● Plavix or similar antiplatelet (P2Y12 inhibitor) in addition to aspirin is
recommended in all pts with UA/NSTEMI for one year, irrespective of whether
patients were managed with invasive or conservative strategies. As above, for practical
purposes, usually best to check with cardiologist first.
● Statin (atorvastatin 40-80mg) should be started prior to hospital discharge if no
contraindication
Management Strategy Invasive vs. Conservative (refer to algorithms in ACC/AHA guidelines for
NSTEMI/UA) http://circ.ahajournals.org/content/116/7/e148.full.pdf
● Invasive approach:
o Recurrent angina at rest or low level activity despite max medical therapy,
Elevated biomarkers, New ST depression, Signs/sx of HF or worsened MR, High
risk findings on noninvasive testing, Hemodynamic instability, Sustained V. tach,
PCI within 6 mo, Prior CABG, High risk score (TIMI, GRACE), Decreased
LVEF < 40%
● Conservative approach:
o Low risk score, Absence of high risk features
Early Invasive Strategy
● UFH or enoxaparin or fondaparinux or bivalirudin (only use with early invasive strategy)
● Clopidogrel (or another P2Y12 receptor blocker such is ticagrelor or prasugrel) or GP
IIb/IIIa inhibitor (or both if delay to angio, high risk features, early recurrent pain).
Discuss with cardiologist first.
● Proceed with coronary angiography--> stenting vs. CABG
● Continue plavix (or ticagrelor) in addition to ASA for up to one year (Ia)
o IIb to continue beyond 1 year
Early Conservative strategy
● UFH or enoxaparin or fondaparinux
● Plavix (or ticagrelor or prasugrel)
● Consider IV GP IIB/IIIA inhibitor-eptifibatide or tirofiban (cardiologist dependent)
● May choose to proceed directly with stress test or first evaluate LVEF, if < 40 % go to
cath. If > 40%, proceed to stress test for further risk stratification
o Noninvasive stress testing is recommended in low and intermediate risk patients
who have been free of ischemia at rest for 12-24 hrs
o Treadmill exercise testing is useful if patients are able to exercise and EKG is free
of resting ST changes
o Stress testing with imaging modality should be used if patient is able to exercise
but has ST changes on resting EKG
o Pharmacological stress testing with imaging is recommended when physical
limitations preclude adequate exercise stress
● Continue plavix (or ticagrelor) in addition to ASA for up to one year (Ia)
o IIb to continue beyond 1 year
Note, in patients with UA and NSTEMI, IV fibrinolysis therapy should not be used (no benefit
for mortality or MI)
All eligible patients should be referred to a comprehensive cardiovascular rehabilitation program
and receive education on risk factor modification
References 1. ACC/AHA 2007 Guidelines for the Management of Patients With Non-ST-Elevation
Acute Coronary Syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228
2. Overview of the Acute Management of Unstable Angina and Non-ST Elevation
Myocardial Infarction – Uptodate.com
Acute Respiratory Distress Syndrome Objectives
1. Definition of ARDS
2. Pathology of ARDS
3. Management of ARDS
CC: "I can't breathe"
HPI: 62 yo male called 911 complaining of extreme dyspnea with no further detail given
secondary to dyspnea. Pt found by EMS at home in chair in severe respiratory distress,
diaphoretic and cyanotic. History obtained per family members.
PMH: Ischemic stroke ’96 with residual left hemiparesis
HTN
DM non-insulin requiring
CHF: ECHO 5 mo PTA EF=45%
Diabetic Nephropathy
Non-adherence with meds
All: NKDA
Meds: clopidogrel 75 mg po qd
acetaminophen PRN
metoprolol 25 mg po qd
isosorbide dinitrate 30 mg po qd
fosinopril 25 mg po qd
glyburide 10 mg po qd
Soc: Positive tobacco for years; unable to quanitate further. Positive ETOH
FMH: CAD in father, DM non-insulin dependent in brother
PE: T 98.6 BP 210/120 P 130 RR=26
General: obese male in severe distress, unable to speak more than one word at a time
HEENT: PERRL, EOMI, Fundi-pt unable to cooperate with exam
NECK: Supple, no adenopathy, no bruit, no JVD
Lungs: Diffuse crackles, no wheeze, ronchi; accessory muscles used
CV: S1, S2, gallop, tachycardic
Abd: Obese, no obvious organomegaly, soft, doughy, no spiders, no caput medusa
Ext: 3-4+ pitting edema to mid-tibia bilaterally
Labs:
ABG: pH 7.07, pCO2 62, pO2 46 on a 100% Non rebreather mask
CBC: WBC 20, Hgb 13 Plts 341
BMP Na 141, K 4.5, Cl 98, HCO3 23, BUN 30, Cr 2.7, CPK=89, LDH=194
EKG: sinus tachycardia, no ST-T changes
CXR: bilateral alveolar infiltrates without cardiomegaly or effusion.
Patient intubated secondary to respiratory failure.
Repeat ABG post-intubation: 7.35/42/60 on 80% with 8cm H20 PEEP.
Patient diuresed 1,500cc fluid without improvement in oxygen requirements.
Acute Respiratory Distress Syndrome
I. Definition
Adult respiratory distress syndrome (ARDS) refers to a diffuse parenchymal
inflammation with noncardiogenic pulmonary edema, resulting in severe respiratory
distress and hypoxemic respiratory failure.
The pathologic hallmark is diffuse alveolar damage, but lung tissue rarely is available
for a pathologic diagnosis. ARDS is a diagnosis of exclusion and requires all of the
following Berlin criteria to be met:
➔ Respiratory symptoms beginning within 1 week of clinical insult
➔ Bilateral opacities consistent with pulmonary edema
➔ Respiratory failure must not be fully explained by cardiac
failure/fluid overload
➔ Moderate-severe impairment in oxygenation (based on PaO2/FiO2)
a. 200 - 300 = Mild
b. 100 - 200 = Moderate
c. < 100 = Severe
II. Epidemiology – 10-15 % of ICU patients and 20% of mechanically ventilated patients
meet criteria for ARDS.
III. Pathophysiology
a) Alveolar injury leads to impaired gas exchange, decreased lung compliance and in
up to 25% of patients pulmonary hypertension
b) Stages:
1) Exudative stage: Diffuse alveolar injury –>increased neutrophils -> toxic
mediators -> alveolar damage and capillary endothelial damage -> increased leak
of protein rich material -> pulmonary edema and hyaline membrane formation
2) Proliferative stage – 7-10 days later, resolution of edema, proliferation of type
II alveolar cells and interstitial inflammation
3) Fibrotic stage – some progress to this stage- obliteration of normal lung
architecture, diffuse fibrosis, cyst formation
c) Important to remember:
Epithelial cells (pneumocytes)
i. Type I – 90% - barrier
ii. Type II – 10% - make surfactant, ion transport, replenish type I
iii. Dysfunction of type II cells can occur in ARDS resulting in:
1. Increased permeability and alveolar flooding
2. Decreased ion transport and impairment of edema removal
3. Decreased production of surfactant with alveolar collapse
4. Loss of barrier and increased risk of septic shock
5. Reorganization of epithelial cells can lead to fibrosis (scar)
IV. Risk factors
Direct Lung Injury Indirect Lung Injury
Common
Pneumonia Sepsis
Aspiration Severe trauma with shock
Less Common
Pulmonary contusion Cardiopulmonary bypass
Fat emboli Drug overdose
Near-drowning Acute Pancreatitis
Inhalation injury Blood product transfusion
Reperfusion after lung
transplant
V. Outcomes
a. Mortality of 26-58%%
b. Increased mortality: increased age, failure of oxygenation to improve, sepsis,
chronic liver disease, non-pulmonary organ dysfunction
c. Failure to improve in first week is poor prognostic indicator
VI. Treatment
a. Treat the cause – pneumonia, sepsis
b. Decrease oxygen consumption: treat fever, pain, and anxiety which can all
increase O2 consumption with antipyretics/sedation/analgesia
c. Nutrition/Fluids
i. Enteral preferred over parenteral if possible – Increased risk of nosocomial
infections when using parenteral nutrition
ii. Conservative fluid management- aim to minimize or eliminate positive
fluid balance
d. Prevention
i. GI prophylaxis
ii. DVT prophylaxis
e. Mechanical Ventilation-
i. Goal is to maintain adequate gas exchange until inflammation subsides
w/o causing ventilator—induced lung injury
ii. Reduced tidal volume (TV) ventilation-> helps prevent alveolar
overdistension and improves mortality – 6-8 mL/kg IBW
iii. PLATEAU pressure goal ≤ 30 cmH2O, if >30 then gradually
decrease the TV and can even go down to 4ml/kg for TV
iv. Permissive hypercapnia (as a result of low TV)
1. Maintain oxygenation even if CO2 rises
2. Maintain physiologic pH 7.2-7.5, can increase RR to compensate
while trying to keep TV low
v. PEEP
1. Used to maintain oxygenation because keeps alveoli open
2. May have very high levels 10-20 cm H2O
3. Refer to table for correlation of PEEP to FiO2
vi. Oxygen
1. Try to titrate to <60% if possible
2. Remember hypoxia kills
f. Surfactant
i. Normal increases surface tension of alveoli and maintains patency
ii. Exogenous replacement not yet shown effective in adults
g. Nitrous oxide
i. May improve oxygenation but has not shown decrease in mortality
h. Glucocorticoids
i. Should not be initiated 14 days or longer after onset of ARDS and impact
of earlier therapy is still uncertain but may be helpful
References:
1. Ware LB, Matthay MA. The acute respiratory distress syndrome. NEJM 2000;342:1334-
1349.
o http://content.nejm.org/cgi/reprint/342/18/1334.pdf
2. Tobin MJ. Advances in mechanical ventilation. NEJM 2001;344:1986-1996.
o http://content.nejm.org/cgi/reprint/344/26/1986.pdf
3. Piantadosi, CA, Schwartz, DA. The Acute Respiratory Distress Syndrome. Ann Intern Med
2004;141:460-470.
4. www.ardsnet.org
5. Hansen-Flaschen, J. Acute respiratory distress syndrome: clinical features and diagnosis in
adults. UptoDate 2014.
6. Siegel, M. Acute respiratory distress syndrome: epidemiology, pathophysiology, pathology,
and etiology in adults. Supportive care and oxygenation. UpToDate 2014.
Sepsis
CC: Respiratory Failure
HPI: 68 yo female from Ponca City with a history of demyelinating polyneuropathy
who was brought to the hospital by EMS with respiratory failure. She was
intubated in the ED secondary to altered mental status. She had a SBP of 90/43
in Trendelenburg position and was started on a dopamine drip at 10
mcg/kg/min. According to her family she had been treated for pneumonia as
an outpatient with a Z-pack.
PMH: Demyelinating neuropathy with unknown etiology
Osteoarthritis
Depression
COPD, mild
Cholecystectomy
Hysterectomy
Streptococcal Pneumonia 9/2004
All: NKDA
Meds: Combivent MDI
Paxil 100mg daily
Lortab prn pain
Neurontin 900mg TID
Soc: Lives alone, Divorced nonsmoker, nondrinker.
FMH: unobtainable
PE: Vitals: T 102 BP 90/43 P 109 RR 17
General: Intubated, responds to painful stimuli, pale obese female
HEENT: NC/AT, PERRLA 3 mm bilat. Sclerae anicteric, conj. Normal, ETT and
NGT in place
NECK: Supple, no adenopathy, no JVD, Right IJ central line C/D/I
Lungs: Coarse breath sounds bilaterally
CV: S1, S2, tachycardic RR
Abd: Obese, TTP diffusely, nondistended. Soft bowel sounds
Ext: Cyanosis in fingers/toes. Cool, mottled extremities with significant pitting
edema from ankles to mid-shin
NEURO: Responds to deep pain only, moves left lower extremity only with pain.
No spontaneous movements.
Labs:
ABG: pH 7.42, pCO2 23, pO2 80 on a 100% FiO2
CBC: WBC 64.2, Hgb 12 Plts 184 diff: 1 Meta, 6 Bands, 91 Segs, 1 Lymph,1 mono
BMP Na 149, K 6.1, Cl 115, HCO3 18.5, BUN 155, Cr 2.2, T. Prot 4.2, Alb 1.1,
T. Bili 0.9, AST 537, ALT 360, A.P. 222
EKG: sinus tachycardia, no ST-T changes
CXR: bilateral alveolar infiltrates without cardiomegaly or effusion.
Sepsis Overview
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection.
Septic shock is a subset of sepsis with circulatory and cellular/metabolic dysfunction associated
with a higher risk of mortality
Definitions - SIRS vs QSofa vs SOFA In the presence of suspected infection
See Sepsis 3 Guidelines
**Controversy over best way to diagnose and prognosticate sepsis. Unfortunately, payment
systems move slower than research and we need to be aware of clinical vs financial “quality-
measure” based decisions and documentation
-We still need to document SIRS pathway for medicare payment and hospital based quality
measure guidelines. Use qsofa/sofa when making clinical decisions.
● SIRS (Used for diagnosis)
▪ Temp >100.4˚F or <96.8˚F
▪ Heart rate >90 bpm
▪ Resp. rate >20 bpm or PaCO2 <32 mmHg
▪ WBC > 12,000 cells/mm3, <4,000 or with >10% bands
o Document highest severity of sepsis as problem - correlate with
infection/organism as much as possible (ie. Severe sepsis due to S. Pneumo CAP)
▪ Sepsis = SIRS + Infection
▪ Severe sepsis = sepsis + organ dysfunction
▪ Septic Shock = severe sepsis + hypotension not responsive to IVF and/or
requirement of pressors
● Qsofa (Early Identification, Prognostic)
o For floor and ED patients - Need ⅔
▪ RR > 22
▪ Altered Mental Status
▪ Systolic BP < 100 mmHg
● SOFA (Prognostic, Not diagnostic)
o http://clincalc.com/IcuMortality/SOFA.aspx
o SOFA > 2 = organ dysfunction => ~10% mortality
o SOFA score ≥2 + pressor requirement + lactate >2 mmol/L
=> 40% Mortality
Epidemiology
● >650,000 cases annually with >100,000 deaths.
● Mortality
o SIRS-7%
o Sepsis- 16%
o Severe Sepsis 20%
o Septic Shock 46%
Risk Factors
● Positive blood cultures
● Middle-aged and elderly
● Cancer
● Pre-existing Renal Failure
● Pre-existing Hepatic Failure
● AIDS
● Community acquired pneumonia
Natural History
● Sepsis is a continuum and will progress in not treated promptly
o 48% pts with SIRS progressed to a form of sepsis
o Incidence of positive blood cultures increased along the continuum
o Increasing mortality from SIRS → Septic shock
o Complications include severe organ dysfunction manifested as ARDS, ARF, DIC
Factors associated with Poor Prognosis
● Afebrile or hypothermia
● Leukopenia
● Age >40
● Comorbid condition- AIDS, Cirrhosis, Hematologic Malignancy, Mets Cancer,
Immunosuppression
● Malnutrition
● Nursing home/care home resident
● Indwelling catheters/central line
● GI or Lung source of infection
● Nosocomial infection
Management:
A. Initial Resuscitation
● Within 60 minutes: Cultures and Abx
o Shock: Broad spectrum, narrow later
o Not hypotensive, may target suspected source
● Within 3 hrs: 30ml/kg crystalloid for sepsis induced hypoperfusion:
o Use dynamic markers of fluid responsiveness (Passive leg raise)
o Weak recommendation to target normal lactate
● Procalcitonin can be used as adjunct to clinical picture to shorten duration, or discontinue
abx (weak recommendation
B. Find the Infection
o Blood cultures x 2 (aerobe/anaerobe) prior to abx
o Urine
o Skin exam
o Abdominal exam +/- Imaging
o Consider sputum
o Consider viral panel
o Consider stool studies/C Diff
o LP for meningeal signs
o Can use galactomannan if suspect invasive candidiasis
C. Antimicrobial Therapy
o Neutropenic: Combination not required for sepsis w/o organ dysfunction/shock
o Empiric should not be administered for more than 3–5 days.
▪ De-escalation to the most appropriate single therapy ASAP (grade 2B).
o Duration typically 7–10 days
▪ longer if slow clinical response, undrainable foci of infection, bacteremia
with S. aureus; some fungal and viral infections or immunologic
deficiencies, including neutropenia (grade 2C).
o Antiviral therapy if indicated
o Antimicrobial agents should not be used in patients with severe inflammatory
states determined to be of noninfectious cause (ie. pancreatitis, burns)
D. Source Control (ie abscess, cholecystitis...)
o Within 12 hours if possible (grade 1C).
o Pancreatic necrosis: Delay intervention until adequate demarcation of viable and
nonviable tissues has occurred (grade 2B).
o When source control in a severely septic patient is required, the effective
intervention associated with the least physiologic insult should be used (eg,
percutaneous rather than surgical drainage of an abscess) (UG).
o Remove pre-existing indwelling lines
E. Infection Prevention
● Oral care in intubated patietns
F. Fluid Therapy of Severe Sepsis
o Crystalloids
o Consider albumin if substantial amounts of crystalloid required (2C)
o Fluid challenge technique be applied wherein fluid administration is continued as
long as there is hemodynamic improvement either based on dynamic (eg, change
in pulse pressure, stroke volume variation) or static (eg, arterial pressure, heart
rate) variables (UG).
▪ Stroke volume variation (SVV) measured using arterial line:
● If greater than or equal to 13% then need to give more IVF’s
● If <13%, check cardiac output
▪ Cardiac output (CO):
● If CO increases with leg elevation, give more IVF’s
● If CO stays the same with leg elevation, can be less aggressive
with IVF’s
G. Vasopressors
o Vasopressor therapy initially to target a MAP of 65 mm Hg (grade 1C).
o Norepi as the first choice vasopressor (grade 1B) => Add Epi next (2B)
o Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of
either raising MAP or decreasing NE dosage (UG)
o Low dose vasopressin is not recommended as the single initial choice. Reserve
higher doses for non-response to primary agents
o Dopamine only in highly selected patients (eg, low risk of tachyarrhythmias and
absolute or relative bradycardia) (2C).
o Phenylephrine is not recommended in the treatment of septic shock except in
circumstances where
▪ norepinephrine is associated with serious arrhythmias,
▪ CO is known to be high and blood pressure persistently low
▪ salvage (grade 1C).
o Low-dose dopamine should not be used for renal protection (grade 1A).
o All patients requiring vasopressors should have A Line as soon as able
H. Inotropic Therapy
● Trial dobutamine up to 20 micrograms/kg/min if:
o myocardial dysfunction as suggested by elevated cardiac filling pressures
and low cardiac output
o Salvage (grade 1C).
I. Corticosteroids
o Consider hydrocortisone if refractory to fluids and pressors, not before
o Taper when no longer needed
J. Blood Product Administration
o Target Hb 7 except MI, ongoing hemorrhage(1B).
o No EPO just for sepsis (grade 1B).
o No FFP in absence of bleeding or planned invasive procedure (2D)
o No antithrombin
o Platelets only when < 10k in absence of bleeding. < 20k if high risk bleed. <50k
w/ active bleed
K. Immunoglobulins
o No IVIG (2B)
L. Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
o Minimize sedation, target specific endpoint (RASS)(1B)
o Avoid Neuromuscular blocking agents (NMBAs) if possible. Consider in ARDS
M. Glucose Control
o Target < 180 (1A)
o Interpret POC glucose with caution, as such measurements may not accurately
estimate arterial blood or plasma glucose values (UG)
o Use drip if needed
N. Renal Replacement Therapy
o If indications for dialysis call nephrology, consider CRRT though early
implementation not beneficial (2B).
O. Sodium Bicarbonate Therapy
● Only if pH < 7.15 (2B)
P. Deep Vein Thrombosis Prophylaxis
o Use chemoppx (1B) unless contraindication (thrombocytopenia, severe
coagulopathy, active bleeding, recent intracerebral hemorrhage)
o Use ICDs whenever possible ( 2C)
Q. Stress Ulcer Prophylaxis
o H2 blocker or PPI w/ severe sepsis/septic shock who have bleeding risk factors
(grade 1B).
o Patients without risk factors do not receive prophylaxis (grade 2B).
R. Nutrition
o Oral or enteral within 48 hrs (2C).
o Avoid mandatory full caloric feeding in the first week but rather suggest low dose
feeding (eg, up to 500 calories per day), advancing only as tolerated (grade 2B).
o Use intravenous glucose and enteral nutrition rather than total parenteral nutrition
(TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first
7 days after a diagnosis of severe sepsis/septic shock (grade 2B).
o Use nutrition with no specific immunomodulating supplementation rather than
nutrition providing specific immunomodulating supplementation in patients with
severe sepsis (grade 2C).
S. Setting Goals of Care
o Discuss goals of care and prognosis with patients and families (grade 1B).
o Incorporate goals of care into treatment and end-of-life care planning, utilizing
palliative care principles where appropriate (grade 1B).
o Address goals of care as early as feasible, but no later than within 72 hours of
ICU admission (grade 2C).
Reference:
Sepsis 3 Guidelines: (Definitions of Sepsis)
http://jamanetwork.com/journals/jama/fullarticle/2492881
Surviving Sepsis Campaign 2016 Update (Management)
http://journals.lww.com/ccmjournal/Fulltext/2017/03000/Surviving_Sepsis_Campaign___Interna
tional.15.aspx
Congestive Heart Failure
Objectives:
1. Diagnosis and treatment of acute pulmonary edema
2. Etiology of acute decompensation of chronic CHF
3. Treatment of chronic heart failure
CC: Difficulty breathing
HPI: GF is a 67 y/o WM who presents with increasing SOA over the last 4 days. Normally he
is able to walk 4-5 blocks before becoming breathless. Recently he has begun to feel
SOA with minimal activity, like getting up to go to the bathroom. His worst time is at
night, and he must prop himself up with three pillows in order to breathe while sleeping.
He has noticed a 15 pound weight gain in the last 7-10 days, but is not sure how this has
happened; money has been so tight he has just been living on crackers and soup for the
last week.
PMH: CAD; s/p inferior MI 1988
Obesity
Hyperlipidemia
Moderate LV dysfunction; EF 35%
Gout
HTN x 25 years
DM x 23 years; insulin dependent x 8 years
All: NKDA
Meds: digoxin 0.125 mg daily
lisinopril 10 mg po daily
ASA 325 mg daily
NTG 0.4 mg SL prn chest pain
atorvastatin 10 mg qHS
furosemide 40mg qday
insulin 70/30 - 14 units qam; 10 units qpm
SOC: Lives with wife and son. No ETOH or tobacco
ROS: Denies fever, chills, sweats, cough or sputum production. He admits to have occasional
heart palpitations and recent increased lower extremity swelling. He has stable angina 2-3
times per month, with moderate exertion, always relieved by nitroglycerin.
PE: Vitals: T 99.0 P 123 (irreg) R 26 BP 179/93 02 sat 84% on RA
Gen: WD obese WM, with moderate respiratory distress
HEENT: negative
Neck: +JVD to angle of jaw
Lungs: bibasilar crackles
Heart: irregularly irregular
Abd: benign
Ext: 3+ pitting edema to mid-tibia bilaterally
Neuro: intact
Lab:
CBC: WNL
BMP: WNL
EKG: See below
CXR: Cardiomegaly, bilateral pulmonary congestion, mild left pleural effusion
Congestive Heart Failure
Definition:
Heart failure is a clinical syndrome that is usually secondary to a structural or functional heart
disorder that reduces the ability of the ventricle to fill with or eject blood. It is characterized by a
specific set of symptoms and signs such as shortness of breath, fatigue, dyspnea, and fluid
overload. Heart failure is mainly a clinical diagnosis that is based upon a careful history and
physical examination. It is classified into two broad categories, heart failure with reduced
ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).
Signs/Symptoms:
o SOA/dyspnea, functional decline, fatigue
o cough--dry or occasional white frothy
o lower extremity swelling, weight gain
o orthopnea, PND
Classifications: (NYHA)
o Class I – symptoms of HF only at levels that would limit normal individuals
o Class II – symptoms of HF with ordinary exertion
o Class III – symptoms of HF with less than ordinary exertion
o Class IV – symptoms of HF at rest
Etiology for Acute Decompensation:
o CAD/MI
o Atrial fibrillation
o Volume/salt overload: dietary vs salt substitute
o Infection/fever
o Renal failure
o Ethanol, cocaine, other illicit drugs
o Uncontrolled hypertension
o Cardiomyopathy
o Non-compliance
Diagnosis/Evaluation:
o History and physical (history of MI, S3 on exam, gallop, crackles, JVD, edema)
o Basic labs, ECG and CXR
o BNP: significant if >500, indeterminate if 200-500, likely insignificant if <200; Elevated
in certain conditions such as renal failure, do not order serial BNPs, do not order if
patient is on nesiritide. BNP should help you rule out HF, it is sensitive but not specific.
o 2D Echo: EF <40% indicates systolic HF (HFrEF); EF 40-49%
borderline, EF ≥ 50% indicates diastolic heart failure (HFpEF)
indicators of diastolic dysfunction on echo include poor
ventricular relaxation, reversed E/A ratio
o CAD should be ruled out by first non-invasive testing and then heart catheterization if
necessary
Therapy:
o Acute:
● Assess for etiology: rule out MI, non-compliance with therapy/diet/fluid
restriction
● Initiate salt/H20 restriction
● IV/oral diuretics
● Lasix 40mg PO = Bumex 1 mg PO = Torsemide 20mg PO
● Lasiv 40mg PO = Lasix 20mg IV
● Bumex and torsemide are 1:1 IV:PO conversion
● Supplemental oxygen, NIPPV can help w/ pulmonary edema
● NTG
● BP control or support if indicated
● PCI if indicated
● Initiate ACE-I (with systolic dysfunction, but may hold on initiation until patient
hemodynamically stable. start with low doses and titrate up)
● Treat arrhythmias
● Beta-blockers: for patients on chronic beta-blocker therapy- if acute CHF is mild
continue beta-blocker, if moderate or severe CHF then decrease dose or withhold
beta-blocker. In patients not previously on beta-blocker therapy do not start in
acute stage, but may be started when patient is stable/euvolumic (even just prior
to discharge). Usually start ACE-I first and titrate up before starting beta blockers.
o Chronic:
● Salt/H20 restriction
● Loop diuretics
● ACE-I (mortality benefit)
● Beta blocker (the only beta blockers with a proven mortality benefit in heart
failure are carvedilol, metoprolol succinate (extended release), and bisoprolol).
Start with low doses and double dose every 2 weeks until target dose reached.
● Aldosterone Antagonists: if indicated (for NYHA Class II-IV heart failure with
EF </= 35%). Also recommended to reduce morbidity and mortality following
acute MI in pts who have EF 40% or less who develop symptoms of HF or have a
history of DM
● Hydralazine plus nitrates: recommended in African-American with persistent
NYHA class III to IV HF and LVEF <40 percent despite optimal therapy. Can
also be used in place of ACE-I/ARB in all patients who are unable to tolerate
them due to hyperkalemia, worsening renal insufficiency, etc.
● Digoxin (decreases hospitalizations and symptoms only, no mortality benefit)
● Exercise training (cardiac rehab for pts with class II-III HF without
contraindications). Reduces symptoms, improves quality of life, reduces
hospitalization, and increases survival in patients with chronic HF
o Devices:
ICD for primary prevention of sudden cardiac death:
1. Cardiomayopathy (ischemic or non-ischemic) + LVEF of 35% or less + NYHA class II
or III symptoms
2. At least 40 days post-MI with LVEF of 30% or less.
Cardiac Resynchronization Therapy (CRT) in patients in sinus rhythm
with LVEF ≤35 percent:
•NYHA II-IV on good Rx w/ LBBB & QRS duration ≥150 ms
-Consider in NYHA III-IV w non-LBBB and QRS > 150ms
● Discharge planning:
Comprehensive discharge support including close follow-up in the immediate
postdischarge period is extremely important and may reduce the risk of readmission
**Do good Med Rec!
References:
1. Hunt et al. Evaluation & Management of Heart Failure
http://www.acc.org/clinical/guidelines/failure/hf_index.htm
Jessup M, Brozena S. Medical Progress: Heart failure. NEJM 2003;348:2007-2048.
http://content.nejm.org/cgi/reprint/348/20/2007.pdf
2. 2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary
Circulation. 2013 Oct 15;128(16):1810-52
http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8807.full.pdf
Acute Pancreatitis
Objectives:
1. Causes of acute pancreatitis
2. Diagnosis
3. Ranson criteria
4. Treatment
CC: Abdominal pain
HPI: A.P. is a 64-year-old male who presented with a one day history of
abdominal pain, described to be in the upper abdomen, sharp and stabbing,
radiating to his back. It was continuous and increasing in severity. Pain was
associated with nausea and vomiting. Patient was unable to keep fluids down.
Patient denies recent trauma or recent alcoholic binge.
PMH: Hypertension
All: NKDA
Meds: HCTZ
Soc: Smoker x 45 years, social drinker
FMH: Hyperlipidemia in father
ROS: Felt feverish, no chills, no weight loss. RUQ pain after large meals. No other
changes in bowel habits.
PE: Vitals: T 100.4 P 125 BP 110/80 R 22
HEENT: Dry mucus membranes
Neck: Supple
CV: Tachycardia
Lungs: Decreased breath sounds over LLL, otherwise clear
Abd: Positive guarding, positive direct and rebound tenderness in epigastric area,
decreased BS
Rectal: Heme positive stools
Ext: No c/c/e
Labs:
CBC: WBC 17.0 HCT 42
BMP: Na 135 K 3.3 Cl 98 CO2 22 BUN 23 Cr 1.3 Ca 9.0 Glu 180
LFT: AST 350, ALT 430 AP 540 BiliT 3.2 Direct 2.1
Other: Amylase 4200, Lipase 6230
CXR: Left pleural effusion, no free air
KUB: No Air-fluid levels
Acute Pancreatitis (AP) Classification: According to the Atlanta classification, AP can be divided into two broad categories:
● Interstitial edematous
● Necrotizing
According to the severity, AP is divided into the following:
● Mild AP: Absence of organ failure and local or systemic complications
● Moderately severe AP: No organ failure or transient organ failure (<48 hours) and/or
local complications
● Severe AP: Persistent organ failure (>48 hours) that may involve one or multiple organs
Etiology:
● Gallstones (40%)
● Chronic alcohol abuse (30%)
● High TGs (3%) (Usually greater than 1000)
● Post ERCP
● Medications (1%)
o Drugs with highest evidence
▪ Marijuana
▪ Codeine
▪ Dapsone
▪ Enalapril
▪ Lasix
▪ Isoniazid
▪ Flagyl
▪ Pravastatin/Simvastatin
▪ Tetracycline
▪ Valproic acid
▪ Mesalamine
● Infections/Toxins
o Viruses, Bacteria, Aspergillus, Parasites, Venom
● Trauma
● Hypercalcemia (Uncommon)
● Biliary sludge
● Idiopathic (25%)
● Anatomic (divisum)
● Malignancy or Cyst (IPMN)
Clinical Manifestations:
● Upper abdominal pain
o Almost all have upper abdominal pain at onset
o Usually in midepigastrium
o Band-like radiation to back in 1/3
o Sometimes relief when bending forward
● Nausea/vomiting (90%)
● Fever
● Tachycardia
● Shock, shallow respirations, grey-turner flank discoloration
Diagnosis
● 2 of the 3 criteria:
● Acute onset of typical pain
● Elevation in serum lipase or amylase to three times or greater than the upper limit
of normal - - -Pay attention to reference ranges!
● Characteristic findings of AP on imaging: CT,MRI or ultrasonography
● Serum amylase (Less specific)
● Serum lipase
o 85-100% sensitive
o Likely elevates earlier than amylase and lasts longer
o No utility in ordering both
▪ Does not improve accuracy
o Daily monitoring does not correlate with progress or prognosis
▪ Initial level does not correlate to level of severity
● KUB
o Mainly to rule out other causes
● CXR
o 1/3 are abnormal
o Findings
▪ Elevated hemidiaphragm
▪ Pleural effusions
▪ Basal atelectasis
▪ Pulmonary infiltrates
▪ ARDS
● Abdominal US
o Get for every patient in first episode of pancreatitis to look at GB
o Gallstone actually usually passes during acute event
● CT abdomen
o When to test
▪ Clinical pancreatitis with elevated lipase AND
▪ Do not improve with initial conservative therapy OR
▪ Those suspected of having complications OR
▪ Those suspected of having other diagnosis
● MRI/MRCP
o Being increasingly used but time consuming and expensive
o Advantages over CT
▪ Lower risk of nephrotoxicity
▪ Can better categorize fluid collections: Necrosis, abscess, hemorrhage,
pseudocyst, fluid
▪ Greater sensitivity for mild pancreatitis
Severity assessment:
● 15-25% are severe
● Severe has 17% mortality; Mild has 3% mortality
● CRP can be considered (UTD recommends testing, especially at 48 hours)
● American GI Association recommends APACHE II
o APACHE II
▪ >8 is severe
▪ Criteria
● Age, Chronic disease
● Temp, BP, HR, RR, PO2
● Na, K, Bicarb, Creat
● WBC, HCT
● Glasgow
● Ransons
o Metanalysis showed poor predictor of severity
o Score <3 0-3% mortality
o Score ≥3 11-15% mortality
o Score ≥6 40% mortality
o Criteria at 0 hours & 48 hours
● SIRS criteria
o This is the quickest & maybe best method
▪ Really compares pretty well to other methods
o Criteria (2 or more)
▪ Temp >38.5
▪ HR >90
▪ RR >20
▪ WBC >12 or 10% bands
o Prognosis
▪ 0% mortality if never meets SIRS
▪ 25% mortality if persistent SIRS at 48hrs
▪ 8% mortality if SIRS on admission but resolves
● BUN is the single best indicator of severity
o Some use hematocrit
o BUN at the time of admission and the change in BUN during the first 24 hours of
hospitalization predict mortality
Treatment:
● Summary of care
o Fluids
o Pain relief
o Nausea relief
o Maintain awareness for compartment syndrome
o Electrolyte replacement
o Majority recover with this and eat within 3-5 days
o Maintain awareness for longer term complications
● Fluids
o All patients: 5 to 10 mL/kg /hr of LR unless cardiovascular, renal, or other related
comorbid factors preclude aggressive fluid replacement.
o LR preferred likely due to less NAGMA compared to high volume NS
o Severe volume depletion:
▪ 20-30 mL/kg of IVF given over 30 minutes
▪ 3 mL/kg/hour for 8 to 12 hours.
o AP due to hypercalcemia: LR is contraindicated because it contains 3mEq/L
calcium. If malignant hypercalcemia, tx accordingly
o Fluid requirements reassessment: Frequent intervals in the first 6hrs of admission
and for the next 24 to 48 hours.
o Rate of fluid resuscitation should be adjusted based on clinical assessment,
hematocrit and BUN values.
o Adequate Improvement in vital signs (goal heart rate <120 beats/minute, mean
arterial pressure between 65 to 85 mmHg), urine output (>0.5 to 1 cc/kg/hour) and
reduction in hematocrit (goal 35 to 44 percent) and BUN over 24 hours.
o Initial fluid replacement: Reduction in M&M.
o Continued aggressive fluid resuscitation after 48 hours may not be advisable:
Increased need for intubation and increased risk of abdominal compartment
syndrome.
● Pain relief
o Recommend hydromorphone or fentanyl
▪ Decent starting point is dilaudid 1-2mg q2 hours
▪ Fentanyl: Better safety profile, especially in renal impairment
o Other options are meperidine & morphine
▪ Morphine theoretically can cause spasm of sphincter of Oddi
● Nausea/vomiting
o Ex: Zofran 4mg IV q6
● Nutrition
o NPO Initially if severe
▪ Sips & chips ok
o If absence of ileus, severe N/V, diet can be initiated as soon as patient wants
o Low fat diet may help o Enteral feeds
▪ Duodenal = Jejunal feeds in terms of outcomes. Gastric may be
suboptimal
▪ Use high protein, low fat, semi-elemental feeding formulas (eg, Peptamen
AF) because of a reduction in pancreatic digestive enzymes.
▪ Advance slowly
o TPN only if contraindication to enteral (Outlet obstruction, persistent SBO)
● Antibiotics
o No need for prophylactic abx
o 1/3 of patients with necrosis will get infection
o Consider carbapenem after 7 d if no improvement
● Electrolytes
o Monitor and replace as needed: Hypocalcemia, Hypomagnesemia, Hypoglycemia
● Long Term Complications
o Pseudocyst vs WOPN
▪ Allow to mature prior to considering intervention
▪ Drainage only for symptomatic patients
▪ Endoscopic drainage preferable to open surgery
o Chronic Pancreatitis & Pancreatic Insufficiency
▪ Treat pain
▪ Mealtime enzyme replacement (Pancrealipase)
▪ Monitor for fat-soluble vitamin deficiency
o Splanchnic Vein Thrombosis
o Splenic Artery Pseduoaneurysm
o Abscess
Treat the underlying condition
▪ Gallstone
o Best to try and remove stone with ERCP within 48-72 of presentation
o Need acute ERCP if acute cholangitis or persistent biliary obstruction
o Lap chole prior to discharge
▪ If not, then 30% have reccurrence within 2-4 months
▪ High TGs
o Plasma exchange
▪ Want TG below 500
▪ Initiate as soon as possible
o Insulin, Only if:
▪ Can’t tolerate plasma exchange OR
▪ Glucose >500
o Insulin will enhance lipoprotein lipase activity, causing decrease TG
o Start gemfibrozil 600mg BID
References: 1. www.utdol.com Treatment of acute pancreatitis. Clinical manifestations and diagnosis of acute
pancreatitis. Predicting the severity of acute pancreatitis
2. Forsmark CE, Baillie J, AGA Institute Clinical Practice and Economics Committee,
AGAInstitute Governing Board. AGA Institute technical review on acute
pancreatitis.Gastroenterology 2007; 132:2022.
3. Clinical manifestations and diagnosis of acute pancreatitis. Predicting the severity of acute
pancreatitis
Neutropenic Fever
Objectives
1. Evaluate a neutropenic patient with fever.
2. Explain initial empiric therapy and modifications of the initial regimen.
3. Understand strategies to enhance host defense
HPI: A 41 yo white male presents with a fever of 1 day duration. He states he had chills and feels
fatigued. He has Hodgkin's lymphoma and is status-post recent cycle of chemotherapy. He denies
any respiratory symptoms. He reports no GI or GU complaints. He denies having a headache.
PMH: Hodgkin's lymphoma x 2 yrs
All: NKDA
Meds: None
Soc: Married - Two children in good health. No history of smoking or EtOH abuse.
ROS: Negative for respiratory, GI or GU complaints. No skin lesions were noted.
PE: Vitals: P 110 R 20 BP 130/85 T 102.2
Gen: WD in no apparent distress.
Skin: Intact
HEENT: PERRL, EOMI; TMs: normal, MMM
Neck: Supple; no lymphadenopathy
Lungs: CTA bilaterally
CV: Tachycardic, S1S2, no murmur
Abd: Soft, non-tender. No hepatosplenomegaly
Ext: No C/C/E; Good pulses symmetrically all over
Neuro: A, Ox3, CN II-XII - intact
Rectal: DRE not done but perianal area inspected and normal
Labs: CBC: WBC 0.0, ANC 100, Hgb 8.0, Plts 25
BMP: Glucose 80, BUN 15, Cr 0.9
U/A: negative for infection
CXR: no acute process
Neutropenic Fever Overview Definition:
•Single temperature >38.3ºC (101ºF), or a sustained temperature >38ºC (100.4ºF) for more than one
hour
•Absolute neutrophil count (ANC) <500 cells/microL, or <1000 cells/microL with a predicted nadir
of <500 cells/microL. Profound neutropenia is defined as an ANC ≤100
cells/microL. The ANC = WBC * (%Neutrophils + %Bands)
Most common organisms
• Gram positive cocci, Gram negative rods
• Always need coverage for Pseudomonas aeruginosa
• Cannot rely on negative blood cultures as only a few organisms can cause fever
• Consider the possibility of fungal and viral pathogens
Initial management:
-Full physical exam including perianal area, CBCD, CMP, U/A, Blood cultures x2, CXR, swab cultures
of wounds
-Determine if patient is high risk or low risk
-High risk: anticipated prolonged neutropenia of > 7 days, profound neutropenia, and or medical
comorbidities (hypotension/pneumonia/neuro changes/etc) -> IV treatment and admit to hospital
-Low risk: anticipated brief neutropenia of < 7 daysor no/few comorbidities -> oral treatment
-Antibiotics should be given within 60 minutes of presentation.
If outpatient, low risk:
Fluoroquinolone like cipro 750 mg BID plus beta-lactam like amoxicillin-clavulanic acid (500/125 mg
TID).
If inpatient, high risk:
• Cefepime or ceftazidime (meropenem, imipenem, piperacillin-tazobactam can also be used)
• Additional antibiotics (fluoroquinolones, vancomycin, azithromycin) may be used if specific
infections more likely
• Addition of antifungal therapy recommended after 4-7 days of continued fevers, in patients who are
expected to have neutropenia >7 days, or in patients becoming more clinically unstable with
ermpiric antibiotic therapy
Vancomycin criteria:
• pneumonia
● skin/soft tissue infections
● severe mucositis in patients who were receiving prophylaxis with fluroquinolone
● hemodynamic instability/severe sepsis
● positive blood cultures for gram positive bacteria
● suspected central line infection
● history of resistant organisms like MRSA
Stop vancomycin after 48 hours if negative blood cultures
At 48 hours if fever persists:
• D/C cefepime or ceftazidime
• Start imipenem/cilastatin or meropenem to cover for anaerobes
At 96 hours (after 4 days) if fever persists:
• Add amphotericin B, caspofungin, or voriconazole for Candidemia/Aspergillosis
At 7 days if fever persists:
• CT scan of sinuses:
• Look for any sign of sinusitis, especially fungal sinusitis.
• Aspergillus will require 1 – 1.5 mg/kg of amphotericin B for treatment
Hematopoietic Colony-Stimulating Factors – ASCO Guidelines
• Primary Prophylaxis (before Febrile Neutropenia)
● Not Recommended routinely
● May use if expected incidence of neutropenic fever >20% or if <20% then could consider if
pre-existing neutropenia, advanced cancer, age >65, poor performance status
• Secondary Prophylaxis (to avoid febrile neutropenia from occurring in next cycle)
● Not recommended routinely and usually recommend to just decrease dose of next cycle of
chemo
● Should use it however if dose-reduction not recommended especially for potentially
curable malignancies (i.e. germ cell tumor)
● Adjunctive Therapy for Febrile Neutropenic Patients: not routinely used but in patients that remain
neutropenic and febrile after initiation of antibiotics. Also, consider for those with poor prognostic
factors (ANC < 100/ul, age >65, uncontrolled primary disease, pneumonia, hypotension, multi-
organ dysfunction of invasive fungal infection)
Duration of therapy:
-In patient with documented infection secondary to specific organism then duration is dictated by the
organism but should be continued at least until ANC greater than or equal to 500
-If unidentified source of fever, then continue empiric therapy until marrow recovers, ie ANC is greater
than or equal to 500
References:
1. Freifeld, A, et al. Clinical practice guideline for the use of antimicrobial agents in neutropenic patients
with cancer: 2010 update by the IDSA. www.idsasociety.org 2014.
2. Hughes WT, Armstrong D, Bodey GP, Bow EJ, Brown AE, Calandra T, et al. 2002 Guidelines for the
use of antimicrobial agents in neutropenic patients with cancer. Clin Inf Dis 2002;34:730-51.
3. http://www.journals.uchicago.edu/CID/journal/home.html
4. Up to Date 2014, “Fever in the Neutropenic Adult Patient with Cancer”
Atrial Fibrillation
Objectives 1. Recognize atrial fibrillation (AF)
2. Understand the common causes for new onset AF
3. Understand the approach to the patient with AF
4. Review the indications for anticoagulation in patients with AF
CC: Burning sensation in chest
HPI: 67 y/o male who has a sudden onset of a burning sensation in his chest. He was doing
well until the morning of admission. Shortly after taking his medications, he began to
develop a burning sensation in his chest that radiated to his neck and left jaw. He reports
having similar discomfort three years ago at which time he underwent coronary
angiography with percutaneous transluminal angioplasty and stent placement. He denies
ever having suffered an acute myocardial infarction. He denies any dyspnea, nausea or
vomiting. He denies any palpitations.
PMH: DM – II, non-insulin requiring
HTN
CAD
Hypercholesterolemia
PSH: PTCA/Stent placement in RCA three years ago
PTCA RCA two years ago
Meds: Metoprolol 25 mg twice daily
Simvastatin m40g daily
Omeprazole 20 mg daily
Multivitamin
All: NKDA
FMH: Brother with CAD/CABG at age 54. Several first degree relatives with diabetes and HTN
SOC: Remote tobacco use with estimated 20 pack year history. Occasional alcohol use which
is quantified as 1 – 2 drinks per week.
ROS: Unremarkable
PE
Vitals: T: 98.6, BP: 136/82, P: 110, RR: 24
GEN: WD/WN in moderate distress secondary to discomfort and dyspnea.
HEENT: PERRLA, EOMI
CV: Normal S1, S2. No audible murmur. No JVD. Distal pulses 2/4. Rhythm is
irregularly irregular
Lungs: Minimal bilateral crackles lower lobes
Abd: Benign
Ext: No edema
Labs
CBC: WBC: 6.8, Hg: 11.6, Plt: 185
BMP: Na: 135, K: 4.2, Cl: 109, Bicarb: 23, BUN: 13, Cr: 0.8, Glu: 157
EKG: shown
Atrial Fibrillation
• Most common cardiac arrhyhmia
• Identified by irregularly irregular rhythm on ECG with absence of distinct p waves
Risk factors
o hypertension and ischemic heart disease
o age, rheumatic heart disease, CHF, congenital heart disease, sick sinus syndrome, WPW
o pericarditis, PE, COPD, thyrotoxicosis, post-operatively, DM, ethanol, sympathomimetic
drugs
o caffeine, hypoxia, hypokalemia, hypoglycemia, systemic infection
Consequences
o Thromboembolism / stroke
o CHF / Cardiomyopathy
Classification
o Paroxysmal AF —recurrent AF (≥2 episodes) that terminates
spontaneously in ≤ 7 days, usually < 24 hours. o Persistent AF — AF that fails to self-terminate within seven days. Usually need
pharmacologic or electrical cardioversion to revert to sinus rhythm. progression to
persistent and permanent AF occurs in >50 % of patients despite therapy
o Long-standing persistent AF--persistent AF that lasts for ≥ 1
year
o Permanent AF — patients with persistent AF where a decision has been made to no
longer pursue a rhythm control strategy
Signs/Symptoms
o Often asymptomatic
o When symptomatic, symptoms can include palpitations, tachycardia, fatigue, weakness,
dizziness, lightheadedness, reduced exercise capacity, increased urination, or mild
dyspnea. More severe symptoms include dyspnea at rest, angina, presyncope, or
infrequently, syncope
Diagnosis
o EKG, thyroid, electrolytes, 2D Echo (ventricular function, atrial size, valve disease)
o Eval for CAD in pt with risk factors
Therapy:
***If hemodynamically unstable, perform immediate Synchronized Direct Current
Cardioversion 100-200J
Acute treatment: A-Fib with RVR (rapid ventricular response)
• Rate control
o Goal < 110 bpm
o Can try bolus prior to continuous infusion
o 1st line: beta blockers, calcium channel blockers
▪ Diltiazem, verapamil, metoprolol, esmolol
o 2nd
line: digoxin
▪ Can be preferred agent in CHF or hypotension
• Rhythm control
o Can use electrical cardioversion or chemical cardioversion
o Anticoagulation needed first if symptoms >48 hts
▪ 3 weeks prior and 4 weeks after cardioversion
▪ Other option is TEE and proceed with cardioversion if no thrombus
Chronic treatment
o RATE VS. RHYTHM CONTROL--AFFIRM TRIAL
1. Showed no mortality benefit in rhythm vs. rate control in long term management,
but trend toward better survival with rate control arm of study
2. No decrease seen in CVA’s in rhythm control; therefore continued
anticoagulation needed after A.fib converted to NSR (eg pt probably still going in
and out of A.fib after conversion)
o Rate Control
1. Meds: Beta blocker, Ca channel blocker, Digoxin
o Rhythm Control: most effective if a.fib duration short
1. Amiodarone, Procainamide, Propafenone (contraindication in CAD), Sotalol
2. Efficacy rate approx 50-70% in maintaining NSR at 6 months
3. Proarrhythmia risk
o Other treatment options
1. Ablation
o Consider if on meds and still symptomatic
o Higher success rate in atrial flutter
Stroke prevention
o DOAC Preferred for non-valvular
● Factor Xa Inh
▪ Rivaroxaban (Xarelto) 20mg daily, 15mg daily if eGFR 30-50.
▪ Apixiban (Eliquis) 5mg BID, 2.5mg BID if > 80, <60kg, Creat > 1.5
● Least renal clearance
▪ Edoxaban (Savaysa) 60mg daily
● Direct Thrombin Inhibitor
▪ Dabigatran (Pradaxa) 150mg BID
o Warfarin
● Valvular heart disease, especially mitral valve
o CHADS2 score:
● 0 → aspirin alone
● 1 → aspirin or anticoagulation
● ≥ 2 → anticoagulation
Use CHA2DS2-VASc score if CHADS2 equivocal
HAS-BLED score used to estimate risk of bleeding:
References: 1. Fuster et al., ACC/AHA/ESC guidelines for the management of patients with atrial
fibrillation J Am Coll Cardiol 2001;38:1266i-1xx
2. Cheng and Kumar. Overview of atrial fibrillation. UpToDate, Waltham, MA, 2013
3. www.utdol.com
4. MKSAP 16
5. UptoDate.com https://www.uptodate.com/contents/anticoagulation-in-older-
adults?source=machineLearning&search=hasbled&selectedTitle=1~18§ionRank
=1&anchor=H10#H10
GI Bleeding
Objectives
1. Identify causes of GI bleeds.
2. Identify the best way to make a diagnosis and treat a patient.
HPI: A 58 yo white female visiting from Texas woke up around 1 am feeling nauseated and
began vomiting. She said that she vomited dark blood. She denies having syncope or abdominal
pains. The patient called 911 and was brought to the hospital. The patient is a recovering
alcoholic. She was still drinking approximately eight months ago.
PMH: liver cirrhosis with ascites, breast cancer
PSH: Bilateral mastectomies 20 years ago with partial reconstruction of the breasts for
cancer. She did not have radiation or chemotherapy.
All: No known drug allergies
Meds: Furosemide
Spironolactone
PE:
Vitals: P 120 BP 124/68 (lying), 108/52 (sitting), 86/46 (standing)
Gen: 58 yo female who looks older than her stated age; no acute distress
HEENT: Icteric sclerae. NG tube present with suctioned coffee-ground material
Chest: Spider angiomas over anterior chest
CV: Regular rate and rhythm with tachycardia
Lungs: Clear bilaterally. Decreased at the bases
Abd: Non-distended. Slightly tender in the epigastric area. Bowel sounds positive though
decreased. No rebound.
Rectal: Normal sphincter tone. Black tarry stool, heme positive
Ext: Revealed no clubbing, cyanosis, or edema.
Vasc: Pulses slightly decreased, but symmetrical in the lower extremities.
Skin: Pale with a yellow tinge.
Neuro: There were no neurological deficits. Cranial nerves were grossly intact.
Lab:
CBC: Admission WBC 15.5 Hgb 7.5 Hct 26.7 MCV 105 Plts 96
Coags: PT 16.5 PTT 46.3INR 1.6
BMP: Na 132 K 4.7 Cl 99 CO2 27 BUN 39 Cr 0.9 Glucose 168
LFT: ALT 27 AST 71 AP89 Albumin = 2.8 BiliT 5.8Direct 1.7 Indirect 4.1
GI Bleeding
Upper GI bleeding
Bleeding that occurs from mouth to upper part of small intestine (ligament of treitz)
Lower GI bleeding
Bleeding that occurs distal to the ligament of treitz (small intestine, colon, rectum)
Both can range from microscopic to massive and life-threatening
Etiologies:
Upper bleeds:
• Peptic ulcer disease (H. pylori, NSAIDs, stress, gastric acid) — 55%
• Esophageal/gastric varices — 14%
• Arteriovenous malformations (AVMs) (angiodysplasia, vascular ectasia) — 6%
• Mallory-Weiss tears — 5%
• Tumors and erosions — 4% each
• Other (include GAVE [gastric antral vascular ectasia], portal hypertensive gastropathy,
aortoenteric fistula, Dieulafoy’s lesion, plus others) — 11 %
Lower Bleeds:
• Diverticular — 5 to 42%
• Ischemia — 6 to 18%
• Anorectal (hemorrhoids, anal fissures, rectal ulcers) — 6 to 16%
• Neoplasia (polyps and cancers) —3 to 11%
• Angiodysplasia (AVM) — 0 to 3%
• Postpolypectomy — 0 to 13%
• Inflammatory bowel disease — 2 to 4%
• Radiation colitis — 1 to 3%
• Other colitis (infectious, antibiotic associated, colitis of unclear etiology) — 3 to 29%
• Small bowel/massive upper GI bleed — 3 to 13%
• Other causes — 1 to 9%
• Unknown cause — 6 to 23%
History of melena, melena on rectal exam, blood or coffee grounds seen during nasogastric
lavage, and BUN/Cr ratio > 30 predictive of upper GI bleed
Presence of blood clots in stool or BRBPR predictive of lower GI bleed
Hematochezia resulting from an upper GI source requires loss of around 1000 ml of blood.
Initial Evaluation and Management (any GI bleed - upper or lower)
• Stabilize.
• ICU admission
• ABC’s
• IV (2 large bore)
• Targeted history (NSAIDS, antiplatelets, anticoagulants, steroids, smoking, ETOH, wt
loss, prior hx of gi bleeding, liver disease, history of AAA or aortic graft)
• Exam (vital signs, petechiae, spider angiomas, abdominal tenderness, organomegaly,
rectal exam)
• Labs: CBC, CMP, coagulation panel, type and crossmatch, Serial blood testing H/H.
• Admitting H/H is not necessarily indicative of current circulating volume. Vital signs are
more accurate (ORTHOSTATIC VITALS IMPORTANT)
• Volume resuscitation (isotonic fluids)
Estimating fluid status using vital signs:
• Resting tachycardia = mild to moderate hypovolemia
• Orthostatic hypotension = blood volume loss of at least 15%
• Supine hypotension = blood volume loss of at least 40%
Transfusions:
▪ Transfuse for:
o Hemodynamic instability despite crystalloid resuscitation
o Hemoglobin <9 g/DL (90 g/L) in high risk patients (eg elderly, coronary artery
disease)
o Hemoglobin <7 g/dL (70 g/L) in low-risk patients
o Avoid over-transfusion with possible variceal bleeding (Don’t transfuse >10)
o FFP for coagulopathy(INR>1.5); plts for (platelets <50,000)or platelet
dysfunction (chronic aspirin therapy)
▪ NG lavage: controversial. Studies have not shown a benefit with regard to outcomes.
Can be used to confirm UGI bleeding if red blood or coffee grounds present in aspirate,
however, negative NG lavage does not r/o UGI bleeding. NG lavage can be used to
remove particulate matter, fresh blood, and clots from the stomach to facilitate
endoscopy.
Meds:
● Hold NSAIDS, anticoagulants, antiplatelets
● NPO
● Treatment with bolus IV PPI 80 mg once then IV PPI (pantoprazole, esomeprazole, or
omeprazole) 40mg BID or continuous infusion: Pantoprazole 80 mg IV bolus then
continuous infusion at 8 mg/hr)
● 2014 Meta-analyses of randomized trials have failed to show superior outcomes with
high-dose continuous IV PPI administration compared with intermittent dosing and
giving the PPI intermittently rather than as a continuous infusion could decrease resource
utilization and cost,and lower risk of rebleeding noted.
● If suspected cirrhosis/portal hypertension: Octreotide; 50µg IV bolus then 50µg/hr
continuous infusion for 5 days
● If known cirrhosis, and UGI bleeding, give abx for infection prophylaxis (mainly SBP),
ceftriaxone 1 g/24hr or IV/PO quinolone for 7 days shown to decrease rebleeding and
mortality.
Endoscopy:
● Consult GI for EGD and/or colonoscopy--several endoscopic therapeutic modalities
available to help stop active bleeding (Epinephrine injection, Endoscopic hemoclips,
Variceal banding, Heat probes, Argon plasma coagulation (APC) )
● EGD is recommended within 24 hours of an upper GI bleeding episode.
● In acute variceal bleeding, EGD recommended within 12 hours of presentation.
● Endoscopic predictors of recurrent ulcer hemorrhage: 60-75% of rebleed occurs within
first 72 hours.
Forrest classification Endoscopic finding prevalence risk of rebleeding
Ia Active arterial bleeding 10% 90%
Ib Oozing without visible vessel 10% 10 -20%
IIa Non-bleeding visible vessel 25% 50%
IIb Adherent clot 10% 25-30%
IIc Flat spot 10% 7-10%
III Clean ulcer base 35% 3-5%
● Management: Ia, Ib, IIa: dual endoscopic therapy + IV PPI for 72 h
IIb: Expose the underlying and treat endoscopically + IV PPI 72h
IIc, III: No endoscopic therapy, PO PPI once or twice daily
● Ulcer bleed: Test for H pylori and stop NSAIDs
● Gastric stress ulcers: occur in the setting of multi-organ failure in critically ill patients
due to gastric mucosal hypoperfusion.
● Treatment: supportive, blood transfusion, IV PPI
● Prophylaxis: IV H2 blockers or IV PPI: most studies have showed that IV H2 blockers
are equally effective compared to IV PPI. A meta-analysis showed that PPIs are superior
to IV H2 blockers. However, the magnitude and cost-effectiveness of this effect is
unclear. In most cases, IV H2 blockers are sufficient and effective in preventing stress
ulcers.
Lower GI bleed:
Obscure GI bleeding (OGIB)
• Defined as bleeding from the GI tract without an obvious source after EGD and
colonoscopy.
• OGIB is classified as overt (visible bleeding with hematochezia or melena) or obscure
(IDA due to GI blood loss with or without hemoccult positive stool).
• If recurrent and suspicion of UGI source, it is reasonable to repeat an upper endoscopy.
• Yield of repeat colonoscopy is low unless the colonoscopy was incomplete or the prep
was inadequate.
• If still negative, or if bleeding is occult, need to consider small bowel bleed
– Wireless video capsule endoscopy (test of choice)
– Push enteroscopy (therapeutic intervention in proximal small bowel)
– Double/single balloon enteroscopy or spiral enteroscopy (therapeutic intervention
throughout small bowel)
– Radionuclide scan: scans for overt OGIB, if positive follow by angiography for
further localization and treatment.
– Angiography: indicated in acute massive GI bleed, however capsule endoscopy
has a higher diagnostic yield in patients with acute overt OGIB.
– CT enterography
– Intraoperative enteroscopy (patients with continued overt OGIB in which other
techniques are unsuccessful).
References
1. Saltzman, JR. Approach to acute upper gastrointestinal bleeding in adults. In: UpToDate,
Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
2. Rockey, DC. Major causes of upper gastrointestinal bleeding in adults. . In: UpToDate,
Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
3. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding.
N Engl J Med. 2013 Jan;368(1):11-21.
Acute Kidney Injury
Objectives:
1. Describe the three general types of renal failure and the differential of each type
2. Initial diagnostic tests
3. Calculation of fractional excretion of sodium (FENa)
4. Indications for dialysis
CC: Nausea and vomiting
HPI: RF is a 55 yo male who presents with a several week history of nausea and vomiting.
Nausea is present most of the time with occasional emesis. Nausea is unrelieved by
emesis. No hematemesis. Pt reports decreased energy levels for “months.” Pt has noticed
a 20 pound weight gain despite decreased intake. No chills, sweats or fevers.
PMH: hypertension
“high blood sugars”
arthritis
All: NKDA
Meds: Atenolol 25mg daily
HCTZ 25mg daily
Lisinopril 10mg daily
Ibuprofen 400mg PRN
Soc: He has smoked 1-2 ppd since age 16 for a 50+ pack year history. He denies any alcohol or
illicit drug use, is divorced and a retired CIA agent.
FMH: CAD in his father and insulin-dependant diabetes (adult onset) in his mother; both are
living.
ROS: Urinates 4-6 times per night, no dysuria, no diarrhea, no chest pain, no dyspnea, no rashes,
no confusion, no HA—otherwise as per HPI.
PE: Vitals: T 98.5 BP 152/88 P 72 R 16
Gen: WD, WN male in NAD
HEENT: PERRL at 5 mm, EOMI
Fundoscopic: Positive venous nicking, no hemorrhages noted
Neck: No bruit or JVD, no LAD
CV: RRR, S1S2, no murmur, pulses 2/4 in all extremities, no edema
Lungs: No crackles or wheezes
Abd: soft, no masses, no organomegaly, no abdominal bruits
Rectal: Enlarged prostate, firm, no nodules, normal tone
Skin: No rashes, ecchymosis, excoriations or lesions noted
Labs:
BMP: Na 138, K 4.9, Cl 101, CO2 18, BUN 92, Cr 6.1
CBC: WNL
UA: No blood, no casts, leukocyte negative
Spot Urine Na 55, Cr 50
Acute Kidney Injury
Definition:
Sudden impairment of kidney function resulting in the retention of nitrogenous and other waste
products normally cleared by the kidneys. Abrupt elevation in the SCr or a decrease in UO.
AKI definition (KDIGO 2012 Criteria):
- ↑ in SCr ≥ 0.3 mg/dL within 48h or
- ↑ in SCr ≥ 50% within 7 days or
- Urine output < 0.5 mL/kg/hr for > 6h
1. Prerenal
o Etiology: primarily result from decreased effective arterial volume with poor renal
perfusion; most common type of AKI
o Hypovolemia: dehydration, over-diuresis, poor PO intake (nausea, vomiting),
diarrhea, burns, hemorrhaging
o Heart failure (poor cardiac output = poor effective arterial volume despite
picture of “fluid overload.”)
o NSAIDs – block PGE2 and PGF2 = renal arteriole vasocontriction
o ACE-Is/ARBS – efferent vasodilation = reduced pressure gradient across
glomerulus needed for filtration
o Hypotension: sepsis, over medicated with anti-hypertensives, hypovolemia
o Renal arterial obstruction, cirrhosis with hepatorenal syndrome (HRS)
o Large Vessel Disease: renal artery stenosis (RAS) (suspect if large ↑ in SCr
after placing on ACE-I/ARB), venous thromboembolism, renal artery
dissection, vasculitis, abdominal compartment syndrome
o Contrast nephropathy, cyclosporine, calcineurin inhibitors
o Labs, UA, Sediment, Indices
o Bland, transparent hyaline casts
o FENA < 1%, except if from diuretics – if suspected, check for FEUREA
o BUN/Cr > 20, UNA < 20, UOSM > 500
2. Intrinsic (Renal)
o Acute Tubular Necrosis (ATN)
o Think of ATN in part as a continuum with severe pre-renal AKI (ischemia),
and then also from direct tubular toxins
o Ischemia: same for pre-renal:
▪ shock (all causes), hemorrhaging, sepsis, heart failure, DIC
o Toxins:
▪ Drugs: aminoglycosides, amphotericin (“amphoterrible for kidneys”),
cisplatin
▪ Hgb, myoglobin, Ig light chains (kappa, lambda)
▪ Crystals: uric acid, acyclovir, methotrexate, indinavir, oral Na3PO4
o Contrast-induced (CIN) - ↓ in renal blood flow and also a toxin
▪ CIN usually detected by ↑ in SCr 48-72h after contrast given
o Increased risk if CKD, DM, HF, Age, Hypotension
o Injury proportional to volume of contrast used
o Prevention: give fluids 3 mL/kg/h x 1h before contrast, then 1 mL/kg/h
x 6h after
o Gadolinium (for MRIs): can cause AKI if stage IV CKD, potential for
nephrogenic systemic fibrosis 2-4 weeks after exposure if moderate-
severe CKD
o Labs, UA, Sediment, Indices
▪ Pigmented granular muddy brown casts (~75%)
● May not be seen in CIN (‘pre-renal picture’)
▪ ± RBCs & protein from tubular damage
▪ FENA > 2%, BUN/Cr < 20, UNA > 20 (except for Hgb, myoglobin, and
CIN-induced), UOSM <350
o Glomerulonephritis (Nephritic ± Nephrotic Syndromes)
o ANCA Small Vessel Vasculitis (Pauci-Immune)
▪ Granulomatosis with Polyangiitis (Wegener’s): C-ANCA (anti-
proteinase 3/-PR3), granulomas
▪ Eosinophilic Granulomatosis with Polyangiitis (Churg Strauss): P-
ANCA (anti-MPO), asthma, eosinophilia
▪ Microscopic Polyangitis: P-ANCA (anti-MPO)
o Anti-Glomerular Basement Membrane
▪ Anti-GBM disease, Goodpastures (+ pulmonary hemorrhaging)
o Immune Complex Disease (Granular Immunofluorescence)
▪ Normal C3
● IgA Nephropathy (~1-3 days shortly after URI or GI infection
w/ gross hematuria)
● Fibrillary GN
▪ Normal C4 + ↓C3
● Post-streptococcal GN (~1-2 weeks after infection strep, staph)
● Membranoproliferative GN (chronic indolent infections or
rheumatologic: HCV & cryoglobulinemia, HBV, syphilis,
subacute BE, osteo, lupus, sjogrens, malignancies
● C3 glomerulonephropathy
▪ ↓C4 + ↓C3
● Lupus nephritis (anti-dsDNA, +ANA, 6 classes)
● Cryoglobulinemia (HCV, HIV, multiple myeloma)
o Labs, UA, Sediment, Indices
▪ Dysmophric RBCs, RBC casts, protein
o Acute Interstitial Nephritis (AIN)
o Allergic: Abx! PCNs, Cephs, sulfa; NSAIDs, PPIs
o Infectious: pyelonephritis, legionella, TB, leptospirosis
o Infiltrative: sarcoidosis, lymphoma, leukemia
o Autoimmune: Sjogren’s, SLE
o Labs, UA, Sediment, Indices
▪ WBCs, WBC casts but with negative UCx! ± RBCs
▪ Urine eosinophils if abx; urine lymphocytes if NSAIDs
o Small-Medium Vessel Disease
o HUS/TTP, DIC, preeclampsia, polyarteritis nodosum (PAN - a/w HBV),
malignant HTN, scleroderma renal crisis, cholesterol emboli
o Labs, UA, Sediment, Indices
▪ ± RBCs, urine eosinophils in cholesterol emboli
3. Postrenal (urinary tract obstruction)
o Etiology: think obstruction anywhere along the renal/urothelial tract
o Bladder neck: BPH, prostate cancer, neurogenic bladder (hx spinal cord injury,
anticholinergic meds, etc)
o Ureteral bilaterally: malignancy, retroperitoneal fibrosis, nephrolithiasis
o Labs, UA, Sediment, Indices
o Bland, variable FENA, ± non-dysmorphic RBCs
Approach to the patient:
Compare current SCr to old Cr baseline if available. Does pt have AKI, CKD, or AKI on CKD?
o Old labs/imaging suggestive of pre-existing CKD: Small/shrunken kidneys on U/S,
renal osteodystrophy, normocytic anemia, hyperparathyroidism w/
hyperphosphatemia and hypocalcemia
History:
o Nausea, vomiting, diarrhea, orthostasis, decreased urine volume, dark urine, frothy
urine, recent illness, decreased urine output, recent heart cath or imaging with
contrast, recent procedures
o Is there a history of heart failure, liver disease, diabetes, known kidney disease, recent
abdominal surgery, BPH, pelvic malignancy, renal stones, difficulty passing urine,
recent contrast studies?
o Thorough medication review: NSAIDs, ACE-I/ARBs, Abx, cisplatin, acyclovir,
MTX
Physical exam: Assess for Volume Status:
● vital signs (tachycardia, hypotension, febrile); orthostatic hypotension
● mucous membranes (dry vs moist)
● neck veins/JVD/hepatojugular reflex (HF, fluid overload)
● S3 on cardiac exam (HF)
● crackles in lungs (fluid overload, pulm edema)
● spider angiomata, jaundice, ascites, abdominal fullness (stigmata of liver disease)
● prostate enlargement (post-obstructive)
● purpura, petechiae, joint swelling, skin rash (GN)
● neuro changes
Workup: Labs/Imaging
1. Rule out post-obstructive! Bladder scan and/or insert foley catheter, renal U/S
2. Urine electrolytes: UNA, UCr, UUREA, preferably obtained at same time as serum
a. FENA: (UNA/PNA)/(UCR/PCR); UOSM
b. FEUREA: use if pt on diuretics: < 35% suggestive of pre-renal
3. Urinalysis (UA)
4. Renal U/S – r/o obstruction; evaluate kidney size/chronicity of disease
5. Monitor strict urine output
Treatment: foundation of management depends on correcting the underlying cause:
o Optimize hemodynamics (maintain MAP and CO)
o If hypovolemic – fluid resuscitation with isotonic fluids: preferably NS or LR
o If hypervolemic – diuresis in HF to shift along starling curve to lower cardiac
filling pressures
o Avoid nephrotoxic agents! (NSAIDs, ACE-I/ARBs, contrast, caution w/ Abx)
o Adjust medication doses based on renal clearance – pharmacy can help
o Foley catheter if indicated
o If severe anemia – transfuse if indicated
o Correct acid/base disturbances
o Call nephrology if suspect need for HD! (see below)
Indications for acute dialysis:
A = acidosis (severe metabolic acidosis resistant to tx). pH<7.1 or bicarb is contraindicated.
E = electrolytes, specifically hyperkalemia resistant to medical treatment
I = ingestions (lithium, salicylates, methanol, ethylene glycol, theophylline, amanita mushrooms,
gabapentin, topiramate)
O = overload (fluid, resistant to diuresis)
U = uremia (nausea/vomiting/mental status changes not attributable to other causes, seizures,
pericarditis)
Addendum
Hypertensive Emergencies
Objectives:
1. Hypertensive emergency vs. hypertensive urgencies; how to distinguish
2. Identification of signs/symptoms of end organ damage in patients with elevated blood
pressure
3. Autoregulation
4. Etiology of hypertensive crisis
5. Treatment options for various types of hypertensive crises
6. Use of sublingual nifedipine; adverse effects
CC: Confusion
HPI: JB is a 43 year-old black male brought to the ED by friends. They say JB has not been feeling
well for the last 36 hours. He had a large party a couple of nights ago and drank a significant
amount of alcohol. The following morning he complained of headache and nausea. He vomited
several times. He also complained of blurred vision. Thinking it was just a hangover, JB did not
seek medical attention. Today his friends noticed that he has been sleeping a lot. When they tried
to wake him, he seemed very disoriented and confused.
PMH: HTN, never treated Polysubstance abuse Pancreatitis
Back pain
All: NKDA
Meds: Lortab 7.5/500 mg prn
Soc: Divorced. Disabled secondary to back pain. Tobacco 2-ppd x 30 years. Drinks EtOH daily and to
intoxication 2x/week. Uses marijuana weekly, denies any other drug use.
PE: Vitals: T 99.6 P 116 R 18 BP 264/156 Gen: Thin BM, confused, disoriented HEENT: PERRL, EOMI, Fundi: bilateral exudative retinopathy Lungs: CTA bilaterally Heart: Tachy, +S4 Abd: Benign Ext: No c/c/e Neuro: Disoriented to person, place and time; cannot follow commands. Moves all 4 ext; DTRs
- 2/4 bilaterally; plantar reflexes downgoing bilaterally
Lab: CMP: Na 141, K 5.5, Cl 119, CO2 22, BUN 12, Cr 1.6, Glucose 143, Alb 2.9,
GGT 887, AST 436, ALT 291, INR 1.2
CBC: WBC 12.1, Hgb 14.7, Platelets 89 UDS: + cannabis, + cocaine
EKG: LVH, no acute changes
Definitions:
Hypertensive emergency is present when severe hypertension is associated with acute end-
organ damage.
Hypertensive urgency (or severe hypertension) is defined as significantly
elevated blood pressure (SBP ≥ 180 or DBP ≥ 120) and no
signs/symptoms of end organ damage.
End Organ Damage:
● Neurological
o Hypertensive encephalopathy
o Acute CVA/Cerebral ischemia
o Subarachnoid/intracranial hemorrhage
o Seizure
● Cardiovascular
o Myocardial ischemia/infarction
o Acute left ventricular dysfunction
o Acute pulmonary edema
o Aortic dissection
● Other
o Acute renal failure (elevated creatinine, proteinuria)
o Retinopathy/Retinal hemorrhage – papilledema
o Eclampsia
o Microangiopathic hemolytic anemia
o Hyperadrenergic crisis (cocaine, pheochromocytoma, amphetamines)
o Post-operative hypertension
Etiologies:
1. Discontinuation of anti-hypertensive meds
2. ETOH/Drugs (cocaine, amphetamines)
3. Renal artery stenosis (possible acute occlusion)
4. Dysregulation of renin-aldosterone-angiotensin axis
5. Severe arteriosclerosis
6. Aortic dissection
7. MAOI and tyramine containing foods
8. Pheochromocytoma
9. Scleroderma crisis
Evaluation of patients with severely elevated blood pressure:
First decide if there is evidence of acute end organ damage that would warrant emergency
treatment. The following should be included in the initial workup:
--Neurologic Examination (including CT head if confusion or positive findings on exam)
--CV exam (including ECG, cardiac enzymes, CXR, bilateral BP measurements)
--Direct ophthalmoscopy
--Urinalysis and UDS, Urine preg if indicated
--Serum creatinine (metabolic panel), CBC, TSH, cardiac enzymes
Treatment:
General Overview:
Once the diagnosis of a true hypertensive emergency is established and end-organ damage
confirmed, for most hypertensive emergencies, MAP should be reduced gradually by about 10-
20% in the first hour and by a further 5-15% over the next 23 hours. More rapid reduction in BP
should be avoided since it may worsen end-organ function. These BP goals are best achieved by
a continuous infusion of a short-acting, titratable, parenteral antihypertensive agent along
with constant, intensive patient monitoring.
Please note there are exceptions to this general rule, most important ones are:
o Acute ischemic stroke: BP should not be decreased unless BP >220/120 or if BP
>185/110 and getting/given tPA
o Aortic dissection: SBP should be rapidly lowered to 100-120mmHg within 20
minutes.
Specific treatment guidelines for each type of hypertensive emergency is detailed below:
Neurological emergencies:
Hypertensive encephalopathy
● Preferred medications
● Labetalol
● Nicardipine
● Esmolol
● Medications to avoid
● Nitroprusside
● Hydralazine
● Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours.
Acute ischemic stroke
● Preferred medications
● Labetalol
● Nicardipine
● Treatment guidelines: Withhold antihypertensive medications unless the systolic
blood pressure (SBP) is >220 mm Hg or the diastolic blood pressure (DBP) is
>120 mm Hg UNLESS patient is receiving IV or IA fibrinolysis, then goal BP:
SBP <185 mmHg and DBP <110 mmHg. After treatment with fibrinolysis, the
SBP should be maintained <180 mm Hg and DBP <105 mmHg for 24 hours.
Acute intracerebral hemorrhage
● Preferred medications
● Labetalol
● Nicardipine
● Esmolol
● Medications to avoid
● Nitroprusside
● Hydralazine
● Treatment guidelines: Treatment based on clinical/radiographic evidence of
increased intracranial pressure (ICP). If signs of increased ICP, maintain Cerebral
Perfusion Pressure (CPP) in the range of 61 to 80 mmHg. Patients without
increased ICP, maintain MAP <110 mmHg (or SBP <160 mmHg) for first 24
hours after symptom onset.
Subarachnoid hemorrhage
● Preferred medications
● Nicardipine
● Labetalol
● Esmolol
● Medications to avoid
● Nitroprusside
● Hydralazine
● Treatment guidelines: Maintain SBP <160 mmHg until the aneurysm is treated or
cerebral vasospasm occurs. Oral nimodipine is used to prevent delayed ischemic
neurological deficits, but it is NOT indicated for treating acute hypertension.
Cardiovascular emergencies:
Aortic dissection
● Preferred medications
● Labetalol
● Nicardipine
● Nitroprusside – given with beta-blocker
● Esmolol
● Morphine sulfate
● Medications to avoid
● Avoid beta-blockers if there is aortic valvular regurgitation or suspected
cardiac tamponade.
• Treatment guidelines: Maintain SBP <120 mmHg, as tolerated. Preferred
treatment includes a combination of narcotic analgesics (morphine sulfate), beta-
blockers (labetalol, esmolol), and vasodilators (nicardipine, nitroprusside).
Calcium channel blockers (verapamil, diltiazem) are an alternative to beta-
blockers. BP should be decreased very quickly within 20 minutes to <120.
Acute coronary syndrome
● Preferred medications
● Beta-blockers
● Nitroglycerin
● Treatment guidelines: Treat if SBP >160 mm Hg and/or DBP >100 mm Hg.
Reduce BP by 20-30% of baseline. Thrombolytics are contraindicated if BP is
>185/100 mm Hg.
Acute heart failure
● Preferred medications
● Nitroglycerin
● Enalaprilat
● Medications to avoid
● Hydralazine
● Beta-blockers
● Treatment guidelines: Treatment with vasodilators (in addition
to diuretics) for SBP ≥140 mm Hg. IV or sublingual
nitroglycerin is the preferred agent.
Other disorders:
Cocaine toxicity/pheochromocytoma
● Preferred medications
● Diazepam
● Phentolamine
● Nitroglycerin/nitroprusside
● Medications to avoid
● Beta-adrenergic antagonists prior to phentolamine administration
● Treatment guidelines: Hypertension and tachycardia from cocaine toxicity rarely
require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the
preferred agents for cocaine-associated acute coronary syndromes.
Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity.
Beta-blockers can be added for BP control only after alpha-blockade.
Preeclampsia/eclampsia
● Preferred medications
● Hydralazine
● Labetalol
● Methyldopa
● Nicardipine
● Medications to avoid
● Nitroprusside
● Angiotensin-converting enzyme inhibitors
● Esmolol
● Treatment guidelines: In women with eclampsia or preeclampsia, SBP should be
<160 mm Hg and DBP <110 mmHg in the prepartum and intrapartum periods. If
the platelet count is <100,000 cells/mm3 BP should be maintained below 150/100
mmHg. Patients with eclampsia or preeclampsia should also be treated with IV
magnesium sulfate to avoid seizures.
Perioperative hypertension
● Preferred medications
● Nitroprusside
● Nitroglycerin
● Esmolol
• Treatment guidelines: Target perioperative BP to within 20% of the patient’s
baseline BP, except if there is the potential for life-threatening arterial bleeding.
Perioperative beta-blockers are first choice in patients undergoing vascular
procedures or in patients with an intermediate or high risk of cardiac
complications.
Dosing of medications:
o Nitroprusside — a rapidly acting arteriolar and venous dilator, given as an intravenous
infusion. Initial dose: 0.25 to 0.5 µg/kg per min; maximum dose: 8 to 10 µg/kg per min
which should be continued for no more than 10 minutes. Cyanide toxicity.
o Nitroglycerin — a rapidly acting venous and, to a lesser degree, arteriolar dilator, given
as an intravenous infusion. Initial dose: 5 µg/min; maximum dose: 100 µg/min.
o Labetalol — an alpha- and ß-adrenergic blocker, given as an intravenous bolus or
infusion. Bolus: 20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose
of 300 mg. Infusion: 0.5 to 2 mg/min.
o Nicardipine — a calcium channel blocker, given as an intravenous infusion. Initial dose:
5 mg/h; maximum dose: 15 mg/h.
o Clevidipine — a calcium channel blocker. Initial dose: 1 mg/hour; maximum dose: 16
mg/hour.
o Fenoldopam — a peripheral dopamine-1 receptor agonist, given as an intravenous
infusion. Initial dose: 0.1 µg/kg per min; the dose is titrated at 15 min intervals,
depending upon the blood pressure response.
o Hydralazine — an arteriolar dilator, given as an intravenous bolus. Initial dose: 10 mg
given every 20 to 30 minutes; maximum dose: 20 mg.
o Propranolol — a ß-adrenergic blocker, given as an intravenous infusion and then
followed by oral therapy. Dose: 1 to 10 mg load, followed by 3 mg/h.
o Phentolamine — an alpha-adrenergic blocker, given as an intravenous bolus. Dose: 5
to 10 mg every 5 to 15 minutes.
o Enalaprilat — an angiotensin converting enzyme inhibitor, given as an intravenous
bolus. Dose: 1.25 mg every six hours.
Hypertension Management (JNC 8 Guidelines)
o Set blood pressure goal based on Age, DM, CKD
o Age >/= 60 withOUT DM or CKD: Goal BP <150/90
▪ Nonblack: thiazide diuretic/ACEI/ARB/CCB (alone or in combination)
▪ Black: thiazide diuretic or CCB (alone or in combination)
o Age < 60 withOUT DM or CKD: Goal BP <140/90
▪ Nonblack: thiazide diuretic/ACEI/ARB/CCB (alone or in combination)
▪ Black: thiazide diuretic or CCB (alone or in combination)
o All ages with DM and no CKD: Goal BP <140/90
▪ Nonblack: thiazide diuretic/ACEI/ARB/CCB (alone or in combination)
Black: thiazide diuretic or CCB (alone or in combination)
o All ages with CKD +/- DM: Goal BP <140/90
▪ All races: ACEI or ARB (alone or in combination with other drugs, do not
use both ACEI and ARB at together)
Evidence-Based Dosing for HTN
o Thiazide diuretics
o Chlorthalidone
▪ Initial daily dosing: 12.5mg qday
▪ Target dose: 12.5mg - 25mg
o HCTZ
▪ Initial daily dosing: 12.5 - 25mg qday or BID
▪ Target dose: 25mg - 50mg
o Indapamide
▪ Initial daily dosing: 1.25mg q day; Target dose: 1.25mg - 2.5mg
▪ ACE Inhibitors
o Captopril
▪ Initial daily dosing: 12.5mg TID or 25mg BID
▪ Target dose: 100mg BID
Enalapril
▪ Initial daily dosing: 5mg qday or BID
▪ Target dose: 20mg
o Lisinopril
▪ Initial daily dosing: 10mg qday
▪ Target dose: 40mg
o Angiotensin Receptor Blockers
o Candesartan
▪ Initial daily dosing: 4mg qday
▪ Target dose: 12mg - 32mg
o Eprosartan
▪ Initial daily dosing: 400mg qday or BID
▪ Target dose: 600mg - 800mg
o Irbesartan
▪ Initial daily dosing: 75mg q day
▪ Target dose: 300mg
o Losartan
▪ Initial daily dosing: 50mg qday or BID
▪ Target dose: 100mg
o Valsartan
▪ Initial daily dosing: 40mg - 80mg qday
▪ Target dose: 160mg - 320mg
o Calcium Channel Blockers
o Amlodipine
▪ Initial daily dosing: 2.5mg qday
▪ Target dose: 10mg
Diltiazem extended release
▪ Initial daily dosing: 120mg - 180mg qday
▪ Target dose: 360mg
o Beta Blockers
o Atenolol
▪ Initial daily dosing: 25-50mg q day
▪ Target dose: 100mg
Metoprolol
▪ Initial daily dosing: 50mg q day or BID
▪ Target dose: 100mg - 200mg
References:
1- 2014 evidence-based guideline for the management of high blood pressure in adults:
report from the panel members appointed to the Eighth Joint National Committee (JNC
8). James PA, Oparil S, Carter BL, et al. JAMA. 2014 Feb 5; 311(5): 507-20.
2- Evaluation and treatment of hypertensive emergencies. Elliot and Varon. UpToDate. June
04, 2014.
Status Epilepticus
Definition:
● Single unremitting seizure with duration longer than 5 minutes (some definitions use
30 minutes), or frequent seizures without an interictal return to baseline.
Etiology:
1. Subtherapeutic AED levels
2. Withdrawal
a. ETOH, benzos, barbiturates,
3. Hypoxia
4. Metabolic abnormalities
a. Hypoglycemia, hyperglycemia, hepatic encephalopathy, uremia,
hyponatremia, hypomagnesemia, hypocalcemia
5. Acute cerebral injury
a. Stroke, trauma, SAH, meningitis, encephalitis, abscess
6. Chronic cerebral injury
a. Tumor, mets, prior head injury or surgery, cerebral palsy, AV malformations
7. Meds that lower seizure threshold
a. i.e. quinolones, TCAs, metronidazole, bupropion, lithium, beta-lactams,
tramadol, clozapine)
8. Chronic epilepsy
Acute complications
● Rhabdomyolysis
● Hypoxia
● Metabolic/lactic acidosis
● Cognitive defects & future seizures
Mortality:
● 1st episode: 20%
● Due to hypoxia: >70% mortality
Clinical Evaluation:
● Pt usually w/o recollection – need to talk to a witness
o Unusual behavior before seizure (aura)
o Obtain the type and pattern of the movements, head turning, eye deviation (gaze
preference away from seizure focus)
o Loss of responsiveness
● HPI: recent illnesses/fevers, head trauma, sleep deprivation, medication compliance
PMHx: prior seizures, FHx, meningitis, stroke, head trauma
Meds, alcohol, illicit drugs
Diagnostic Studies:
● Accucheck glucose, CMP, CBC, Mg, Phos, UDS
● EEG
● Initial work up:
o Treat the status epilepticus first
o O2, cardiac monitor, IV Access x 2, frequent vital signs, respiratory monitoring
o Consider thiamine + glucose
Classification of Seizures:
1. Simple partial
a. Continuous or repeated focal motor seizures, focal sensory sx, or cognitive
symptoms without impaired consciousness
2. Complex partial:
a. Continuous or repeated episodes of focal, motor, sensory, or cognitive sx with
impaired consciousness
3. Generalized tonic-clonic
a. Always associated with impaired consciousness
4. Absence
a. Altered awareness, but not necessarily unconsciousness. Usually confused or
stuporous, may be associated myoclonus
5. Myoclonic
a. Frequent myoclonic jerks usually in setting of altered mental status
6. Psychogenic
a. Bilateral motor movements with preserved consciousness. May need EEG to
help.
Nonconvulsive Status Epilepticus:
● Must keep this in differential of unresponsive patient!
● Definition: Alteration of awareness - ranging from confusion to coma, but lacks motor
manifestations of a seizure
● Diagnosed with EEG
** Prolactin levels drawn shortly after onset of a seizure can help differentiate epileptic and
non-epileptic events, prolactin levels normalize during prolonged seizures and are not helpful in
the diagnosis of status epilepticus**
Treatment: GCSE is an emergency and must be treated immediately: Consult neurology
1. 1st line treatment is benzo + AED
2. Benzodiazepines
a. Most commonly IV lorazepam
b. Dosing:
i. Lorazepam 0.02-0.03mg/kg (i.e. 2mg for 70kg) x1
ii. Reassess for additional dosing every 1 minute
iii. Max dose 0.1mg/kg
3. Antiepileptic
a. Most commonly fosphenytoin
i. Can be administered more quickly than phenytoin
ii. Less risk of thrombophlebitis or skin necrosis
iii. Dosing equivalents are equal to phenytoin
b. Dosing:
i. Fosphenytoin/Phenytoin: Infusion of 20mg/kg. Can repeat 10mg/kg if
status persists
ii. Keppra: 500-1000mg IV push will be used at times, less well studied
4. Refractory status
a. Consider intubation
b. Start continuous EEG
c. Barbiturates:
i. Phenobarbital
ii. Pentobarbital
d. Propofol
e. Versed
i. May be best choice if hemodynamically unstable, as others will
decrease BP
References:
1. www.utdol.com
2. MKSAP 16
3. Pocket Medicine 4th
Edition
Chronic Obstructive Pulmonary Disease
CC: SOA
HPI: TE is a 69 yo white male who presents to the ED with complaints of increasing shortness
of air for the past 36 hours. He notes increased cough with yellow-green productive sputum for
the last 2-3 days. He denies, fever, chills, sweats, chest pain, orthopnea, PND or lower extremity
edema. He has a history of COPD for which he takes albuterol and ipratropium, but he ran out of
his inhalers a week ago and hasn't had the money to refill them. He uses home oxygen at 2L/NC,
but currently feels so short of breath he has increased it to 5L/NC without relief.
PMH: COPD dx in 1987, O2 dependent since 1995; FEV1/FVC = 62%, FEV1=0.94 L
CAD s/p MI 1992 - Moderate LV dysfunction, EF-35%
HTN x 25 years
GERD
BPH
Allergies: NKDA
Meds: Albuterol MDI 2-4 puffs qid/prn
Ipratropium bromide 2 puffs bid
Digoxin 0.25 mg daily
Lisinopril 20 mg daily mg qhs
Terazosin 2mg qhs
Lansoprazole 30mg qhs
SH: Divorced, lives with son. Smokes 1 1/2 ppd (70 pack/year history), drinks 10 beers daily
PE: Vitals: T 98.0 P 116 R 36 BP 145/91
Gen: WD WM, in moderate respiratory distress
HEENT: Unremarkable
Neck: Negative
Chest: Diminished breath sounds bilaterally, mild expiratory wheezing
Heart: Tachy without murmur
Abd: Benign
Ext: no C/C/E
Lab: CBC: WBC 6.4, Hgb 16.8, Hct 48.4, Platelets 440K, normal diff
ABG: 7.32/74/42 on 2L/NC
CXR: flattened diaphragms, increased retrosternal airspace, no acute infiltrate
Objectives Risk factors for the
development of COPD
Pathophysiology of COPD
Diagnosis of COPD
Maintenance therapy for
COPD
Treatment of exacerbation of
COPD
COPD
Airflow limitation that is not fully reversible
Chronic bronchitis
Productive cough for 3 months in each of 2 successive years in a patient in whom other
causes of sputum production have been ruled out.
Emphysema
Presence of permanent enlargement of airspaces distal to the terminal bronchioles with
destruction of their walls without obvious fibrosis.
Risk factors:
Tobacco smoke, occupational dust, chemical agents, air pollution, low birth weight,
childhood illness, alpha 1 antitrypsin deficiency
Smoking is major cause: 90% of the risk
Bronchial gland hypertrophy and goblet cell metaplasia, and inflammatory cell infiltrate.
Airway squamous epithelial metaplasia, ciliary loss and dysfunction and proliferation of
smooth muscle and connective tissue.
Diagnosis:
Assess presence of cough, sputum, dyspnea, exercise tolerance and energy.
Spirometry:
FEV1/FVC ratio < 0.7 confirms the presence of airflow limitation.
SEVERITY CLASSIFICATION OF COPD
SEVERITY/STAGE FEV1/FVC FEV1 (% PREDICTED)
Mild <0.70 ≥80
Moderate <0.70 50 to 80
Severe <0.70 30 to 50
Very Severe <0.70 <30
Patient Evaluation
1. H/P
2. Clinical criteria: Increased dyspnea, increased volume of sputum, increased thickness
of sputum or increased purulence of sputum.
3. CXR: relatively high rate of abnormalities
4. PFT: unreliable in acute setting
5. Peak flow: unreliable in acute setting
6. ABG to assess need for NPPV
Admission Criteria
1. Marked increase in intensity of symptoms and/or new symptoms
(cyanosis, peripheral edema)
2. Frequent exacerbations
3. Failure to respond to initial medical management
4. Comorbidities (pneumonia, pneumothorax)
5. Arrhythmia (new onset)
6. Signs of respiratory failure (respiratory acidosis)
7. Poor home support
8. ICU admission: need for NPPV, vent management, severe dyspnea, tachypnea or
tachycardia, confusion, hypoxemia or worsening respiratory acidosis
Treatment :
1. Acute exacerbations: short acting beta agonist (Albuterol/Xopenex) + anticholinergics
(Ipratropium) added if no response to beta agonist
a. Administer ASAP for acute exacerbations
2. Maintenance therapy: long acting anticholinergics (Tiotropium), and long acting
beta agonists in combination with inhaled corticosteroids
3. Methylxanthines (Theophylline): optional. High toxicity
4. Systemic steroids: meta-analysis showed fewer treatment failures when adding
systemic steroids, rapid improvement in FEV1 and no difference in mortality.
5. Antibiotics: beneficial for treatment of infectious exacerbation of COPD. Need
coverage against S. pneumo, M. cattarrhalis, H. flu
6. Oxygen. Goal saturation: SA02 90%, PO2 60.
a. Hypoxemia should not be allowed to persist because of the fear of
hypercapnia narcosis and acidosis. Monitor with ABG measurement
(pulse ox alone not enough)
7. NPPV
a. Increased PCO2> 45, decreased pH < 7.35 or RR>25
b. Hypoxemia easily correctable
c. Respiratory distress (tachypnea, accessory muscle use)
d. Expected need for support < 2-3 days
e. Good protection of airway
f. Hemodynamically stable
g. Patient alert and cooperative
8. Intubation
a. Respiratory arrest
b. Impaired mental status
c. Failure on NPPV
d. Sustained respiratory rate >35
e. Severe dyspnea
f. Hypoxemia (PaO2 <40 or PaO2/FIO2 < 200)
g. Severe acidosis pH< 7.25 and hypercapnia PCO2 >60
h. Hemodynamic instability
i. Other : metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, etc
Asthma
Objectives
1. Pathophysiology of asthma
2. Identification of triggers and inducers
3. Diagnosis and management of severe asthma exacerbation – NIH guidelines for
asthma management
4. Outpatient management of asthma
CC: SOA
HPI: KL is a 22 year-old white female who presents to the ER with a 12 hour history of
shortness of air and wheezing. She has a long history of asthma exacerbation since early
childhood and has had multiple hospitalizations for in the past. On three previous
occasions she has been intubated and mechanically ventilated for respiratory failure. Her
boyfriend states that she began complaining of breathlessness late yesterday evening. She
tried multiple treatments with her albuterol nebulizer without relief. She was unable to
sleep all night because of cough and wheezing. No history of fever, chills, night sweats,
nausea, vomiting, diarrhea or other symptoms.
PMH: Asthma, dx at age 5
Seasonal allergies
All: Milk, peanuts, strawberries, NKDA
Meds: Albuterol nebulizer prn
SH: College student at WSU, lives with boyfriend, smokes 1/2 ppd, drinks ETOH socially.
Recently took in a longhair stray cat and her five babies.
FMH: Mother and 3 siblings with moderate to severe asthma, otherwise unremarkable
PE: Vitals: T 96.8 P 112 R 40 BP 98/45 Pulsus paradoxicus = 18
Gen: thin WF, diaphoretic, breathless, unable to speak in complete sentences
HEENT: Unremarkable
Neck: Negative
Chest: Quite, minimal air movement and wheezing
Heart: Tachy, no murmur
Abd: Paradoxical abdominal movements, otherwise benign
Ext: no C/C/E
Labs:
Peak flow: 80 L/min
CXR: mild hyperinflation, otherwise negative
CBC: WBC 26.4, 12% bands, 73% segs, otherwise normal
ABG:
7.34/46/60 on RA
Asthma
Pathophysiology:
o airway inflammation leading to bronchospasm, mucous plugs, airway remodeling
o denudation of airway epithelium, collagen deposition below basement membrane, edema
o mast cell activation, inflammatory cell infiltration (esp. neutrophils)
Triggers/Inducers:
o seasonal allergies/sinusitis, pollen/dander
o air pollution
o food allergies, sulfites
o smoking
o exercise-induced
o GERD
o viral infection
o meds: ASA, Beta blockers
Diagnosis:
o Clinical signs & symptoms and H&P
o CXR: not routine unless symptoms of pneumonia in addition to asthma symptoms
o ABG
o Peak flow: FEV1
SEVERITY CLASSIFICATION OF ASTHMA
CLASSIFICATIO
N
SYMPTOMS NOCTURNAL
SYMPTOMS
INTERFERENCE
WITH NORMAL
ACTIVITY
SABA USE
Intermittent <2days/week <2x/month None <2days/week
Mild Persistent >2days/week 3-4x/month Minor limitation >2days/week
Moderate Persistent Daily >1x/week Some limitation Daily
Severe Persistent Continuous Frequent Extreme limitation Throughout day
Treatment:
o Maintenance Therapy (Stepwise Approach)
● Step 1: SABA PRN
● Step 2: Low dose ICS
● Step 3: Medium dose ICS or low dose ICS+LABA/LTRA/Theophylline
● Step 4: Medium dose ICS + LABA
● Step 5: High dose ICS + LABA
● Step 6: High dose ICS + LABA + systemic corticosteroids (SABA: short acting beta agonist, ICS: inhaled corticosteroids, LABA: long acting beta agonist, LTRA: leukotriene receptor antagonist)
o Severe Acute Exacerbation Therapy
1- Clinical signs suggestive of worsening respiratory distress
● Use of accessory muscles of respiration
● Brief, fragmented speech
● Inability to lie supine
● Profound diaphoresis
● Agitation
● Resolution of respiratory alkalosis or developing respiratory acidosis
● Inability to maintain respiratory effort
● Cyanosis
● Depressed mental status
2 - Assessment
● PEFR <40 percent predicted (or <200 L/minute in most adults) indicates
severe obstruction; PEFR unable to be performed if severe distress
● Severe hypoxemia (SpO2 ≤95 percent despite high flow
O2 treatment by nonrebreather mask)
● ABG results can aid assessment if intubation is not an immediate concern
National Heart, Blood, and Lung Institute. Guidelines for the Diagnosis and Management of Asthma. 2007
● Hypercapnia usually does not occur unless a PEFR <25% of normal
(generally <100 to 150 L/min) is present
● CXR only if complications suspected (eg, pneumonia, pneumothorax),
diagnosis is in doubt, or patient is high-risk (eg, IV drug abuser,
immunosuppressed, chronic pulmonary disease, CHF)
3- Treatment
● Inhaled beta agonist:
o Albuterol 2.5 mg every 20 minutes for three doses by nebulization,
o 4 to 8 puffs every 20 minutes for up to four hours, by MDI with
spacer.
o Or 10 to 15 mg can be administered by continuous nebulization over
one hour.
● Oxygen: SaO2 ≥92 % ● Ipratropium bromide:
o 500 mcg by nebulization every 20 minutes for 3 doses,
o 8 puffs by MDI with spacer every 20 minutes as needed for up to 3
hours
● Magnesium sulfate: give 2 g IV over 20 minutes for severe exacerbations
● Corticosteroids:
o Methylprednisolone 60-125 mg IV or prednisone 40-60 mg po;
o Dexamethasone 6-10 mg IV or hydrocortisone 150-200 mg IV
4- Endotracheal intubation and ventilation
● The goal of mechanical ventilation is to maintain adequate oxygenation and
ventilation while minimizing elevated airway pressures.
o high inspiratory flow rates (80-100 L/min),
o low tidal volumes (6-8 mL/kg),
o low respiratory rates (10-14/minute).
o elevated PaCO2 must be tolerated to avoid barotrauma (ie,
permissive hypercapnia).
● Based on clinical situation:
o slowing of respiratory rate
o depressed mental status
o inability to maintain respiratory effort
o hypoxemia
References:
7. Rodrigo, GJ, Rodrigo, C, Hall, JB. Acute asthma in adults: a review. Chest 2004; 125:1081.
8. http://www.chestjournal.org/cgi/reprint/125/3/1081
9. Institute for Clinical Systems Improvement Health Care Guideline: Asthma.
10. http://www.icsi.org/display_file.asp?FileId=151
11. National Heart Lung and Blood Institute. Guidelines for the diagnosis and management of
asthma. 1997. www.nhlbi.nih.gov/guidelines/asthma/
12. Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. Journal of
Allergy and Clinical Immunology 2007. http://www.jacionline.org/article/S0091-
6749%2807%2901823-4
Objectives Pathogenesis of aortic dissection
Risk factors for aortic dissection
DeBakey and Stanford classification systems for aortic dissection
and how they affect management and treatment
Physical exam findings in patients with dissection
How to estimate the location of the dissection based on exam
findings (proximal vs. distal)
Diagnostic workup of acute aortic dissection: which test to use
Management of aortic dissection: surgical vs. medical
Aortic Dissection
CC: Chest discomfort
HPI: A 70 years WM presents to the ER after the abrupt onset of severe retrosternal chest
discomfort while straining to have a bowel movement this evening. He describes the sensation as
“tearing” that started in the front of his chest and radiates to his back. The patient does feel SOA
and slightly nauseated, but has not had any emesis.
PMH: HTN x 30 years
CAD S/P CABG x 3 1994
Hyperlipidemia
GERD
Depression
Constipation
All: NKDA
Meds: aspirin 325 mg daily
isosorbide dinitrate 20 mg tid
opemrazole 20 mg qhs
amlodipine 5mg daily
fluoxetine 20mg daily
docusate sodium
senna daily
SOC: Denies ETOH, occ smokes cigars. Widower x 1 year. Retired farmer.
PE:
Vitals: T96.8 P 94 R 26 BP 174/84 02 Sat 87% on RA
Gen: WD WN WM, obvious distress secondary to pain
HEENT: Fundi: grade II hypertensive changes, otherwise negative
Neck: Supple, no JVD, no thyromegaly, no bruits
Lungs: Faint bibasilar crackles, otherwise clear
Heart: RRR with 2/6 decrescendo diastolic murmur over left sternal border
Abd: Benign
Ext: No C, C, E. Radial pulses 2/4; Femoral ¼; DP, PT absent to palpation
Aortic Dissection
Primary event: Tear in aortic intima. Degeneration of the aortic media or (cystic medial
necrosis) is needed for development of nontraumatic aortic dissection. False lumen is created.
Propagation occurs proximal or distal to initial tear. Can involve branch vessels and aortic valve,
or enter pericardial sac.
Epidemiology:
2.6-3.5 cases per 100,000 person-yrs.
60-80 year-old men
Risk factors:
● Male to female ratio 2-5:1
● Age peak 60-80
● HTN (most common)
● Aortic disease: aneurysm, bicuspid valve, coarctation
● Connective tissue disease (Marfan Syn., Ehlers-Danlos Syn)
● Genetic: Marfan Syndrome-cause of most dissections less than age 40, familial forms
of thoracic aneurysm and dissection
● Drugs: cocaine
● Pregnancy
● Post CABG
● Prior AV replacement
● Trauma
● High intensity weight lifting
Classification:
Daily/Stanford classification
Type A dissection involving the ascending aorta, regardless of site of primary tear
Type B dissection of descending aorta
DeBakey classification
Type 1 dissection of ascending and descending thoracic aorta
Type 2 dissection of the ascending aorta
Type 3 dissection of the descending aorta
Classification of aortic dissections. Stanford classification: Type A dissections (top panels)
involve the ascending aorta independent of site of tear and distal extension; type B dissections
(bottom panels) involve transverse and/or descending aorta without involvement of the
ascending aorta. DeBakey classification: Type I dissection involves ascending to descending
aorta (top left); type II dissection is limited to ascending or transverse aorta, without descending
aorta (top center + top right); type III dissection involves descending aorta only (bottom
left).(From Harrison’s principles of Internal Medicine 18th
edition)
Patient presentation:
● Abrupt, severe, sharp, “tearing” posterior chest or back pain, or anterior chest pain.
● Syncope
● Stroke or altered mental status
o Dissection involves carotid arteries
● Myocardial infarction
● Heart failure
● Hypotension/shock
● Hypertension
● Pulse deficit
96% of dissections in one study could be identified based on some combination of these 3
clinical features:
● Abrupt onset of thoracic or abdominal pain with a sharp, tearing and or ripping character
● Mediastinal and or aortic widening on CXR
● Variation in pulse (absence of a proximal extremity or carotid pulse) and or blood
pressure difference between right and left arm > 20 mm/Hg
Differential diagnosis:
AMI (STEMI or NSTEMI), pericarditis, PE, Aortic regurg without dissection, aortic
aneurysm without dissection, M/S pain, mediastinal tumors, pleuritis, cholecystitis, PUD,
pancreatitis, Atherosclerotic embolism.
Diagnosis:
● D-dimer: Useful to rule out PE if <500
● EKG:
● Help differentiate from MI
● However, 15% of dissections showed ischemic changes on EKG
● TEE if clinically unstable. Can be done in OR while waiting anesthesia induction, if
surgery is pending.
● MRI preferred for pt with chronic chest pain and hemodynamically stable, or follow-up
for chronic dissection.
● CT with contrast, most common initial screening study
● Aortography if noninvasive testing unavailable
Management:
● Ascending aortic dissections are surgical emergencies.
● ICU admission
● Pain control with morphine
● Systolic blood pressure control to 100-120 or lowest level tolerated (beta blocker)
● Heart rate goal < 60 beats/min (beta blocker)
o Propranolol 1-10 mg load and 3 mg/hr
o Labetalol 20 mg initially, followed by 20-80 mg q 10 min for total dose of 300
mg. or infusion of 0.5-2 mg/min
o Esmolol can be used with asthma or heart failure
o Verapamil or diltiazem are alternatives to pt that cannot tolerate beta blockers
o Switch to oral when HR goal is achieved
● If blood pressure cannot be controlled with above meds:
o Sodium nitroprusside 0.25-0.5mcg/kg/min. Not to be used alone d/t activation of
SNS and increased aortic stress
o ACE inhibitors or CCB’s can be used also
● Hypotensive pts:
o Evaluate for blood loss, hemopericardium with tamponade, or cardiac failure prior
to fluid resuscitation.
**AVOID INOTROPIC AGENTS. INCREASES AORTIC SHEAR STRESS
Definitive Treatment:
● Medical therapy: is choice for uncomplicated dissections (Stanford type B or DeBakey
type 3)
● Oral beta blocker with bp goal < 120/80. Combo therapy usually needed.
● Avoid strenuous activity to minimize aortic shear
● Serial imaging: baseline thoracic MR scan prior to discharge and at 3, 6, and 12 months
if asymptomatic, then every 1-2 yrs thereafter.
● Surgery: reserved for patients with complicated course.
o Occlusion of major aortic branch, continued aortic expansion or extension of the
dissection, aortic rupture
o Type A dissections should be treated as a surgical emergency d/t to high
complication risk such as AR, cardiac tamponade, or MI. Mortality rate is 1-2%
per hour early after symptom onset
REFERENCES
● Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and
management: Part I: from etiology to diagnostic strategies. Circulation. 2003 Aug
5;108(5):628-35. http://circ.ahajournals.org/cgi/content/full/108/5/628
● Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and
management: Part II: therapeutic management and follow-up. Circulation. 2003 Aug
12;108(6):772-8. http://circ.ahajournals.org/cgi/content/full/108/6/772
● Harrison’s principles of Internal Medicine, 18th
edition.
● www.utdol.com
● MKSAP 16
Acid Base Analysis – Part I
CC: Vomiting
HPI: UC is a 50 yo white female that presents to the ED with a history of severe vomiting. Her
husband states she began to feel ill four days ago after attending a birthday party for her 3 yo
niece. He says that she has vomited approximately 6-8 times per day and has had little success in
keeping any fluids down. Earlier today she began to act confused and lethargic.
PMH: Unremarkable
All: NKDA
Meds: None
Soc: Non-smoker, non-drinker. Works as a secretary.
ROS: No fever, chills, sweats, diarrhea, or abdominal pain
PE:
Vitals: T98.4 P121 BP 81/50 R20
HEENT: Dry mucous membranes, PERRL, EOMI, fundi normal
Neck: No JVD, no adenopathy
Lungs: CTA bilaterally
CV: Tachycardic without murmur
Abd: Soft, NT, ND, positive BS
Ext: No c/c/e
Neuro: Patient is unresponsive, except to deep pain. No focal motor or sensory deficits.
Labs:
BMP: Na 140, K 3.3, Cl 85, CO2 25
ABG: 7.40/41/75 on RA
Systematic approach to the acid-base problem solving involves answering five questions:
1. Is the patient acidemic or alkalemic?
2. Is the acid-base disorder primarily metabolic or respiratory?
3. What is the anion gap?
4. If a metabolic acidosis exists, is there appropriate respiratory compensation?
5. If an anion-gap academia is present, is there a complicating metabolic disturbance?
Acidosis or Alkalosis?
A pH above 7.4 indicates alkalosis, while a pH below 7.4 is consistent with acidosis.
It is important to note that both the CO2 and the HCO3 may be abnormal, but the ratio of the two
may be normal and therefore you have a normal pH.
Metabolic or Respiratory?
● Metabolic disorders are processes primarily affecting changes in the HCO3.
● Respiratory disorders are processes primarily affecting changes in pCO2.
● If the patient is acidotic, a low HCO3 level would indicate a primary metabolic acidosis,
whereas a high pCO2 would indicate a primary respiratory acidosis.
● If the patient is alkalemic, a high HCO3 level would indicate a primary metabolic
alkalosis, whereas a low pCO2 would indicate a primary respiratory acidosis.
Anion Gap
Understanding of the anion gap is based on the principle of electroneutrality. The number of net
positive charges (cations) equals the number of net negative charges (anions). A high anion gap
occurs from an increase in the unmeasured anions or decrease in unmeasured cations.
Anion Gap = [Na] – ([Cl] + [HCO3])
Na+ + K+ + Ca+++ Mg++= HCO3- + Cl- + PO4-- + SO4-- + proteins- + organic acids-
Na+ + unmeasured cations = HCO3- + Cl- + unmeasured anions
Na+ - (HCO3- + Cl-) = unmeasured anions - unmeasured cations
Normal anion gap = 12 ± 2
The presence of low albumin (anion) or an unmeasured cationic light chain (multiple myeloma)
results in a low anion gap. The correction for albumin is 2.5 x (4 – measured albumin)
Complicating Metabolic Disturbance? Delta Gap
General Rule: The change in anion gap should equal the change in bicarbonate. This is true in
simple high anion gap acidosis. If the anion gap increases by 1 mmol/L then the HCO3 level
should decrease by 1 as well. Deviation from this rule implies a mixed disorder.
Delta AG = Measured AG – 12 (normal AG)
Calculating the corrected HCO3: (implies what the bicarbonate concentration would be if the
anion gap acidosis were not present)
Corrected HCO3 = [measured HCO3] + [delta AG]
● If the corrected HCO3 is <24 ± 2, a co-existing non-anion gap metabolic acidosis is
present.
● If the corrected HCO3 is >24 ± 2, a co-existing metabolic alkalosis is present.
Osmolal Gap
An osmolal gap is present when the measured plasma osmolality exceeds the calculated plasma
osmolality by >10 mOsm/kg.
Osmolal Gap = Measured Osm – Calculated Osm
Calculate Osm = (2 x [Na]) + ([glucose]/18) + ([BUN]/2.8)
● Ethylene glycol poisoning causes an anion-gap acidosis and acute renal failure, presence
of calcium oxalate crystals in urine.
● Methanol poisoning also causes an AG acidosis and osmolal gap and optic nerve toxicity.
● Isopropyl alcohol poisoning causes an osmolal gap but no acid-base disturbance.
Compensation of a primary disorder
The compensatory response to a primary disturbance is predictable and brings the pH toward
normal. Compensation may be appropriate even if the pH is abnormal. Assessment of
compensation helps detect mixed respiratory and metabolic acid-base disturbances.
Metabolic Acidosis
Every 1mml/L decrease in HCO3- = 1mmHg decrease in PCO2
Expected PCO2= (1.5xHCO3-) +8 +/-2
Metabolic Alkalosis
Every 1mmol/L increase in HCO3- = 0.7mmHg increase in PCO2
Respiratory Acidosis
ACUTE: 10mmHg increase in PCO2 = 1 mmol/L increase in HCO3-
CHRONIC: 10mmHg increase in PCO2 = 4 mmol/L increase in HCO3-
Respiratory Alkalosis
ACUTE: 10mmHg decrease in PCO2 = 2mmol/L decrease in HCO3-
CHRONIC: 10mmHg decrease in PCO2 = 4 mmol/L decrease in HCO3-
HIGH ANION GAP METABOLIC ACIDOSIS
A high anion gap metabolic acidosis develops with the addition of an acid to the blood. The
additional acid is caused by retention of hydrogen ions bound to unmeasured anions.
Causes
“MUDPILES”
M- Methanol
U- Uremia
D- DKA
P- Paraldehyde or Phenformin
I- Iron tabs or INH
L- Lactic acidosis (tissue hypo-perfusion, seizures, drugs- metformin, nucleoside therapy)
E- Ethanol or Ethylene glycol
S- Salicylates or Starvation ketosis
“KULOST”
K: Ketones (DKA, starvation, alcoholic)
U: Uremia
L: Lactic acidosis (several types)
O: Osmolar (Ethylene glycol, methanol)
S: Salicylates
T: Tylenol toxicity (rare), Toluene (very rare, glue sniffing)
Labs to consider ordering in high AG metabolic acidosis (patient specific):
● serum creatinine/BUN,
● urinalysis
● serum ketones
● serum lactate
● serum osmolarity
● blood alcohol level, salicylate level
The key to treatment of anion gap metabolic acidosis is reversing the condition that led to the
excess acid production. Treatment with bicarbonate is unnecessary, except in extreme cases of
acidosis when the pH is <7.1 - 7.2, a level at which dysrhythmia becomes more likely and
cardiac contractility and responsiveness to catecholamines are impaired.
NON-ANION GAP METABOLIC ACIDOSIS
A non-anion gap metabolic acidosis is a hyperchloremic metabolic acidosis that is due to either
loss of fluids containing sodium bicarbonate or addition of hydrogen chloride to the extracellular
fluid.
Causes
Diarrhea- loss of bicarb (intestinal fluid below the stomach is relatively alkaline)
Type II RTA- reduced capacity of kidney to reabsorb bicarb
Type I RTA- inability of renal tubules to generate or maintain a normal pH
Type IV RTA- hypoaldosteronism or inadequate renal tubular response to aldosterone
Urinary Anion gap
Calculation of the urinary anion gap is helpful in determining the etiology of a non-anion gap
(hyperchloremic) metabolic acidosis. The premise is this: an increase in the NH4+ excretion is an
important feature of an appropriate renal response to acid loading, be it endogenous or
exogenous. In patients with GI loss of bicarbonate but a normal capability for renal acidification,
NH4+ excretion should increase as a normal response of metabolic acidosis. This mechanism is
compromised in patients with a renal cause of hyperchloremic metabolic acidosis.
Urine Anion Gap= [Na+] +[K+]-[Cl-]
measured anions + unmeasured anions = measured cations + unmeasured cations
Cl- + UA = Na+ + K+ + UC
UA-UC = Na+ + K+ - Cl-
Since NH4+ is an unmeasured cation and its excretion is accompanied by Cl, the urine anion gap
becomes progressively negative as NH4+ increases. Thus a negative urinary anion gap suggests
that distal urinary acidification is intact and therefore the loss of bicarbonate is of GI in origin. A
positive urinary anion gap suggests altered distal urinary acidification because NH4+ excretion is
inappropriately low for the acidosis.
Treatment
Bicarbonate therapy is generally indicated in non-anion gap acidosis, whereas correction of the
underlying cause is the primary concern in high anion gap acidosis. Oral bicarbonate therapy is
the preferred agent for chronic therapy for non-anion gap acidosis. For acute presentation,
especially in patients with concomitant impaired respiratory function, intravenous bicarbonate
therapy is indicated.
RESPIRATORY ACIDOSIS
Respiratory acidosis is due to a primary increase in arterial PaCO2 which accumulates when
ventilation is inadequate. Hypoventilation can result from:
● neurological disorders (stroke)
● medications (narcotics) that affect the CNS respiratory center
● respiratory muscle weakness (myasthenia gravis, Guillain-Barre syndrome)
● chest wall deformity (severe kyphoscoliosis)
● obstruction of airways (chronic obstructive pulmonary disease)
● ventilation-perfusion mismatch (venous thromboembolism)
Treatment of respiratory acidosis should focus on treating the underlying disorder. In patients
with acute respiratory acidosis and hypoxemia, supplemental oxygen may be administered.
References:
4. www.utdol.com Approach to the adult with metabolic acidosis simple and mixed acid-base disorders
5. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. NEJM 1998;338:26-34 and 107-111.
6. Abelow B. Understanding acid-base. New York: Lippincott Williams & Wilkins; 1998
7. Alguire P. Acid Base Disorders. Internal Medicine Essential for Clerkship Students II; 2009.
8. ACID/BASE© chart done by Jon Pankow, MD
Acid Base Analysis – Part II
CC: nausea/vomiting
HPI: B.C. is a 36yo female who presents with 1 week history of nausea/vomiting. She states
that she’s had 6-8 episodes of emesis per day and has had difficulty keeping anything down. She
also complains of mild abdominal cramping. She denies fevers/chills.
PMH: HTN
Medications: HCTZ 25mg daily
Allergies: PCN
SH: Married, 2 kids. Runs an in-home daycare. Denies Tob/EtOH/Drug use.
FMH: Father with CAD and HTN. Mother has DM.
ROS: No fevers/chills, no chest pain. Mild SOA. Abdominal cramping but no diarrhea.
Nausea/vomiting per HPI.
P.E.: T 99.1 BP- 98/50 HR- 115 R- 24 O2- 93% RA
HEENT: Dry mucous membranes, PERRL, EOMI,
Neck: No JVD, no adenopathy
Lungs: CTA bilaterally
CV: Tachycardic without murmur
Abd: Soft, mild diffuse TTP, no guarding/rebound, BS hyperactive
Ext: No edema
Neuro: No focal deficits
Labs:
BMP: Na 130, K 3.0, Cl 85, CO2 36, BUN 40, Cr 1.9, Gluc 116
ABG: pH 7.58, paCO2 42, PaO2 74
Urine: Na 50 meq/L, K 30 meq/L, Cl 2 meq/L
METABOLIC ALKALOSIS
A primary increase in HCO3 concentration can result from loss of hydrogen chloride or less
commonly, addition of bicarbonate. Once generated, the metabolic alkalosis is corrected through
urinary excretion of the excess bicarbonate. Alkalosis is maintained only when renal bicarbonate
excretion is limited owing to a reduction in renal function or stimulation of renal tubule
bicarbonate reabsorption. Increased reabsorption is caused by extracellular fluid volume
contraction, chloride depletion, hypokalemia, or elevated mineralocorticoid activity.
Chloride Responsive Metabolic Alkalosis (Urinary Cl < 20)
● NG losses
● Vomiting
● Diarrhea
● Villous adenoma
● Diuretics
● Cystic fibrosis
● Rapid correction of chronic hypercapnia
Administration of sodium chloride fluid reverses the alkalosis by expanding the intravascular
volume and reducing the activity of the renin-angiotensin-aldosterone axis.
Chloride Resistant Metabolic Alkalosis (Urinary Cl > 20)
● Hyperaldosteronism
● Cushing’s syndrome
● Bartter’s syndrome
● Licorice
● Milk-alkali syndrome
● Blood transfusions
● Hypokalemia
● Drugs
Less commonly, metabolic alkalosis is maintained in the absence of volume depletion. This
condition is recognized by a high urinary chloride level related to elevated mineralocorticoid
effect and does not correct with sodium chloride volume replacement.
Respiratory Alkalosis
Hyperventilation reduces the arterial PaCO2, which increases the pH, causing respiratory
alkalosis. Common causes of respiratory alkalosis can be sorted by condition involving:
● pulmonary vasculature (pulmonary HTN, venous thromboembolism)
● pulmonary parenchyma (pulmonary fibrosis, heart failure, pneumonia)
● pulmonary airways (asthma)
● ventilatory control (anxiety, aspirin toxicity, sepsis, hypoxia, pregnancy)
The underlying cause for respiratory alkalosis should always be pursued.
References:
1. www.utdol.com Approach to the adult with metabolic acidosis simple and mixed acid-base
disorders
2. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. NEJM
1998;338:26-34 and 107-111.
3. Abelow B. Understanding acid-base. New York: Lippincott Williams & Wilkins; 1998
4. Alguire P. Acid Base Disorders. Internal Medicine Essential for Clerkship Students II; 2009.
Pleural Effusions
Pathophysiology
Transudative effusions
● systemic factors create increased pulmonary capillary wedge pressure (PCWP) or
reduced oncotic pressure (low albumin)
Exudative effusions
● local factors create an increase in pleural surface permeability
Causes of Transudates
1. Heart Failure (40%)
a. 80% is bilateral; can be exudative after aggressive diuresis or chronic HF
2. Constrictive Pericarditis
3. Cirrhosis – “hepatic hydrothorax” from a diaphragmatic defect w/ passage of ascites
a. Usually right-sided, and can be a massive transudate
4. Nephrotic Syndrome
5. PE (but usually exudative)
6. Malignancy (from lymphatic obstruction)
7. Myxedema
Causes of Exudates
1. Lung parenchymal infection (25%)
a. Parapneumonic bacterial effusion
i. Spectrum from sterile exudative to infected fibropurulent to an organized
fibrotic rigid pleural peel
ii. Uncomplicated: normal pH, normal glucose, negative cultures
iii. Complicated: pH < 7.2, glucose < 60, but negative cultures
iv. Empyema: pH < 7.2, glucose < 60, +cultures & organisms on gram stain
v. Organisms: Strep pneumo, Staph aureus, Strep milleri, Klebsiella,
Pseudomonas, Haemophilus, Bacteroides, Peptostreptococcus, mixed
flora if from aspiration PNA
b. Mycobacterial: > 50% lymphocytes, ADA > 40
c. Fungal, viral, parasitic
2. Malignancy (15%)
a. Primary lung cancer – most common; metastases – breast, lymphoma;
Mesothelioma
3. Pulmonary embolism (10%) – 75% are exudates, 25% are transudates, ± hemorrhagic
4. Autoimmune – RA (larger effusion), SLE (smaller effusion)
5. GI – pancreatitis, esophageal rupture, abdominal abscess
6. Hemothorax – Hcteff/Hctblood > 50%
a. Trauma, PE, malignancy, coagulopathy, leaking aortic aneurysm, aortic
dissection, pulmonary AVM
7. Chylothorax – triglycerides > 110
a. Thoracic duct damage from trauma, malignancy
8. Post-CABG – left sided, clears after a few weeks
9. Dressler’s Syndrome – pericarditis and pleuritic after an MI
10. Asbestos exposure - eosinophils
11. Drug-induced – nitrofurantoin, amiodarone, bromocriptine
12. Uremia
13. Post-XRT
14. Sarcoidosis
15. Meigs’ Syndrome
Symptoms
● Cough (nonproductive or productive w/ sputum production), dyspnea, pleuritic chest
pain, fevers, chills
Diagnosis:
● History and physical exam
● CXR
o Upright CXR will show blunting of costophrenic angle if 500ml effusion
o Lateral decub will show even 2ml effusion
▪ 1cm effusion = 250ml = enough to sample with thoracentesis
● CT chest w/ IV contrast: can better assess type of effusion vs. empyema vs. abscess
vs. mass
● Ultrasound: can better assess free flowing vs. loculated vs. mass
● EKG: useful to exclude pericardial disease or right ventricular strain
● Thoracentesis (Dx and therapeutic) with pleural studies and Light’s criteria (see
below)
● Pleural Fluid Studies
o Routine:
▪ total protein, LDH (needed for Light’s criteria), glucose, cell count w/
diff, gram stain and culture, pH
o Others
▪ Cell count w/ diff: lymphocytes >50% suggest cancer, TB,
rheumatologic; eosinophils > 10% suggest blood, air, drug rxn,
asbestos, Churg-Strauss, or PE
▪ RBC & Hct: Hcteff 1-20% suggests cancer, PE, trauma; Hcteff > 50% =
hemothorax
▪ Adenosine deaminase (ADA): granulomas, TB if > 70, excludes TB if
< 40
▪ Cytology
▪ Glucose: < 60 mg/dL suggests infection, RA, or malignancy
▪ NT-proBNP ≥ 1500 pg/mL: 91% Se, 93% Sp for CHF
▪ Amylase: esophageal rupture, pancreatic disease
▪ Triglycerides: >110 suggests chylothorax
▪ Cholesterol: >60 seen in chronic effusions from HF, RA, or old TB
▪ Creatinine: Creff/Crserum > 1 suggests urinothorax
● Light’s criteria: At least 1 of 3 = exudate
1. Pleural fluid to serum total protein ratio > 0.5
2. Pleural fluid to serum LDH ratio > 0.6
3. Pleural fluid LDH value > 2/3 of the upper limit of normal for serum LDH
❖ Can have falsely positive “exudates” that are actually transudate
Treatment Options
● Thoracentesis
o Indications
▪ All effusions > 1cm on lateral decubitus view
● If likely from HF, attempt diuresis first (80% response)
▪ Presence of asymmetry, fever, chest pain, failure to resolve
▪ Quickly tap parapneumonic effusions ASAP
▪ Symptomatic relief: effusion with dyspnea and or respiratory
compromise
o CXR after the thoracentesis!
● Tube thoracostomy: complicated or loculated parapneumonic effusion, empyema
● Video-assisted thorascopic surgery (VATS): loculated effusion
● Intrapleural t-PA + DNase (α-dornase) bid x 3 days: for loculated effusions,
“liquefies” the contents for easier drainage and ↓ need for surgical intervention
● Pleurodesis
Treatments by Disease Process
● Parapneumonic Effusions
o Uncomplicated: antibiotics for PNA
▪ Empiric anaerobic (clindamycin, ampicillin-sulbactam, pip-tazo,
meropenem) and gram (-) coverage (ceftriaxone, FQs)
o Complicated or empyema or ½ hemothorax: tube thoracostomy
o Loculated:
▪ tube thoracostomy
▪ video-assisted thorascopic surgery (VATS)
▪ intrapleural t-PA + DNase (α-dornase)
● Malignant effusions
o Serial thoracentesis
o Tube thoracostomy + pleurodesis
▪ Pleurodesis agents: talc, bleomycin, doxy
o Indwelling pleural catheter
● TB effusions - usually resolve spontaneously, but treat for active TB
● Hepatic hydrothorax
o Goal to change the pressure gradient – NIPPV for short term; decrease ascitic
fluid volume
o Avoid chest tubes! May do prn thoracentesis
o Pleurodesis, TIPS, VATS closure of diaphragmatic defect if medical Rx fails
o Transplant – definitive Rx
Complications
● Pneumothorax (5-10%)
● Hemothorax (1%)
● Re-expansion pulmonary edema
o Pathophysiology: capillary leak around damaged alveoli
o Reduced risk if <1.5L removed
● Spleen, liver laceration
● Bleeding and nerve injury - needle over top on rib
References:
UpToDate
MKSAP 16
Pocket Medicine, 5th
Edition
Pulmonary Embolism
CC: SOA
HPI: PE is a 56 year-old white female you are asked to evaluate while on call. She underwent a
right total knee replacement five days ago. Her surgery was uneventful with the exception of a
postoperative hematoma, which had to be drained. The patient states she was doing fine until a
couple of hours ago when she began to feel short of breath. At first she just thought she "wore
herself out" after ambulating today for the first time since her surgery. However, her
breathlessness hasn't resolved with rest, and she is now feeling lightheaded. She denies fever,
chills, sweats, nausea, vomiting, diarrhea or chest pain. She has no cough, pleuritic chest pain or
hemoptysis.
PMH:
1. Breast cancer, dx 1996
i. S/P mastectomy 1996
ii. She just completed her sixth course of doxorubicin/cyclophosphamide five weeks ago
after new metastatic lesions were found in her liver earlier this year
2. Osteoarthritis
3. Hypothyroidism
4. Depression
5. Fibromyalgia
6. Obesity
Allergies:
Penicillin, sulfa, hydrocodone, meperidine, morphine, benadryl, alprazolam, ranitidine
Meds:
Cefazolin
APAP/oxycodone
Levothyroxine
Sertraline
Soc: No tobacco or ETOH. Married with five children. Disabled secondary to arthritis and
fibromyalgia.
PE:
Vitals: T100.8, P123, R28, BP102/63, 02sat 88% on RA
Gen: Obese, anxious appearing, diaphoretic white female
HEENT: Unremarkable
Lungs: Diminished breath sounds at the bases, otherwise negative
Heart: Tachy without murmur
Abd: Soft, obese, non-tender +BS
Ext: Right leg is braced. 1-2+ bilateral pitting edema. No lower extremity erythema, warmth or
tenderness.
Labs:CXR: Poor inspiration, no infiltrate
Pulmonary Embolism
Definitions:
Thrombosis originating in the venous system and embolizing to the pulmonary arterial
circulation
Incidence: 1 case/1000 person years; total of 250,000 cases per year
Risk Factors
● Virchow’s triad for thrombogenesis
1. Stasis: bedrest, inactivity, CHF, CVA within past 3 months, air travel > 6h
2. Injury to endothelium; trauma, surgery, prior DVT/PE, inflammation
3. Thrombophilia
▪ Acquired
● Drugs: OCPs/HRT, tamoxifen, raloxifene, warfarin 1st 5 days,
heparin (HIT)
● Pregnancy, antiphospholipid antibody syndrome (APLA),
malignancies (12% of “idiopathic DVT/PE): pancreas, GI, lung,
ovarian
● Hyperviscosity: myeloproliferative disorders (PCV, ET), sickle
cell, acute leukemia, waldenstroms
● Nephrotic syndrome: loss of protein C, protein S, and AT-III
● HIT, DIC, PNH
▪ Hereditary
● Factor V leiden, AT-III deficiency, protein C and S deficiencies,
prothrombin 20210A mutation, hyperhomocysteinemia
Clinical Manifestations:
● DVT: Calf pain and swelling, usually >3cm, venous distention, erythema, warmth,
tenderness, ± palpable cord, ± Homan’s sign (calf pain on dorsiflexion but only seen in
<5% of pts); Phlegmasia cerulean dolens (stagnant blood causes edema, cyanosis, and
pain
● 50% of patients with sxs from DVT will have an asx PE
● PE: Dyspnea (73%), pleuritic chest pain (66%), cough (37%), hemoptysis (13%),
tachypnea (>70%), crackles (51%), tachycardia (30%), syncope, fever, cyanosis, pleural
friction rub, loud P2 on auscultation
o Massive PE; syncope, hypotension, PEA, elevated JVP, R-sided S3, “Graham
Steell” murmur (pulmonary regurgitant, early diastolic, high pitched murmur at L
2nd
ICS)
Well’s Score pre-test probability for PE
1. DVT sxs; leg swelling and pain w/ palpation in deep-vein region? (3 pts)
2. PE likely or or more likely than alternative diagnosis? (3 pts)
3. Immobilization: bedrest ≥ 3 days or surgery in last 4 weeks
(1.5 pts)
4. Heart Rate >100 bpm? (1.5 pts)
5. Previous DVT/PE? (1.5 pts)
6. Hemoptysis? (1 pt)
7. Malignancy: cancer treatment currently or in last 6 months, or receiving palliative
care? (1 pt)
● 3 Tier System
o <2: low probability
o 3-6: moderate probability
o >6: high probability
● Cut-off point: ≤4 points = PE unlikely if D-dimer is negative
● Not diagnostic, but helps guide further workup (i.e. order d-dimer, CTA?)
Diagnosis
● ABG
o Hypoxemia, hypocapnia w/ respiratory alkalosis, (tachypnea), ↑A-a gradient
o 18% may have good PaO2 at room air, and 6% with a normal A-a gradient
● D-dimer
o Very sensitive (99%), but poor specificity (~25%)
o Best to order if lower pre-test probability (“unlikely”) to rule out PE
● CT angiography
o Basically today’s “gold standard” since used more than Pulm Angio or MRA
o Se ~90%, Sp ~95%; PPV & NPV >95% if imaging concordant w/ clinical
suspicion
o Beneficial b/c may provide another alternative diagnosis
● V/Q scan
o High Se ~98%, but low Sp ~10% (Sp improves to 97% for high prob VQ
o Use when pretest probability of PE is high but CT is contraindicated
● Lower extremity compression U/S
o Shows DVT in 9% of cases
o Does NOT change outcome when added to CTA
● Pulmonary angiography: previously gold standard, but not performed often now
● MR angiography
● Echocardiography
o Useful to detect right ventricular dysfunction for submassive and massive PEs
● ECG
o Most common sign is sinus tachycardia
o Signs of RV strain w/ right axis deviation (esp massive PE)
o RBBB, cor pulmonale
o SIQIIITIII & TWI V1-V4 – specific but not sensitive
● CXR
o Hampton hump - uncommon
▪ Wedge shaped, pleural based consolidation associated with pulmonary
infarction. Low Se ~11% and high Spe ~92%
o Westermark sign - uncommon
▪ Dilation of pulmonary arteries proximal to embolus and collapse of distal
vasculature creating appearance of a sharp cut off
o Atelectasis, effusion, raised hemidiaphragm
● Troponin: elevated in 30-50% w/ moderate-large PE
Approach
● If lower pretest probability or unlikely PE (Well’s Score), order D-Dimer with initial goal
to rule out PE
o If D-Dimer < 500 ng/mL, PE is excluded
o If D-Dimer ≥ 500 ng/mL, PE should be reconsidered and
consider CTA based on clinical suspicion
● If higher pretest probability or likely PE (Well’s Score), order the CTA
o If CTA is negative:
▪ PE excluded
▪ Consider additional imaging if there still remains a high slincial suspicion
and no other alternative diagnosis
Thrombophilic Workup:
● (+)FHx, consider if <50 yo
● Send panel 2 weeks after complete anticoagulation b/c thrombus, heparin and warfarin all
interfere with results
Malignancy Workup:
● 12% of patients w/ idiopathic DVT and PE will have a malignancy
● Best to follow age appropriate screening and avoid extensive w/u
Risk Stratification
● Hypotension ± tachycardia = ~30% mortality; hypoxemia
● RV/LV dimension ratio of 0.9
● ↑ Troponin, BNP = ↑ mortality
● ECHO – RV dysfunction
Treatment:
● Support if hemodynamically unstable
o Oxygen, pressors, IVFs
● Acute anticoagulation – initiate immediately if high clinical suspicion!
o LMWH: Enoxaparin (Lovenox) 1mg/kg subcutaneous bid
o IV Unfractionated Heparin (Heparin drip)
▪ if renal failure CrCl < 25
▪ consider in severely obese pts, if hemodynamically unstable or if high
bleeding risk (can stop if emergently need to)
▪ 80 U/kg bolus, then 18 U/kg/h; titrate to PTT 1.5 – 2.3 x control (follow
hospital order set protocol)
o Thrombolysis: TPA 100mg x 2 hours
▪ Indications:
● Massive PE: hemodynamically compromised
● “Submassive” PE: marked dyspnea, severe hypoxemia, ECHO
findings of RV dysfunction “D-sign”, RV enlargement on CTA.
Indicated in patients:
o <65 years old; questionable if >65 years old
o Lower bleeding risk
❖ ↓Mortality, ↓Recurrent DVTs
▪ Intracranial hemorrhage risk 1%
o Catheter-directed therapy: fibrinolytic and thrombus fragmentation/aspiration
▪ Consider if
● Massive PE w/ hemodynamic compromise
● High risk and not a candidate for systemic fibrinolytic therapy or
surgical thrombectomy
o Thrombectomy
▪ Consider if large, proximal PE + hemodynamically compromised & there
is a contraindication to thrombolysis
o IVC Filter
▪ if contraindication to anticoagulation
▪ Failure of anticoagulation or bleeding
▪ Adding a filter to anticoagulation ↓ PE by ½ but ↑ DVT by 2x, and no
mortality difference
● Chronic Anticoagulation
o Duration essentially comes down to a clinical decision weighing (1) risks of
bleeding on anticoagulation vs. (2) risk of recurrent VTE without anticoagulation
and (3) patient preferences.
▪ 1st proximal DVT or PE secondary to a reversible or time-limited risk
factor
● 3 months anticoagulation after removal of risk factor
● Consider using D-dimer to help guide duration
▪ 1st unprovoked proximal DVT or PE
● 3 months anticoagulation, then reassess clinically balancing risks
vs benefits
o If low bleeding risk: lifelong anticoagulation
o If high bleeding risk: stop and perform frequent
reassessments
❖ “Patients with unprovoked proximal DVT or PE who are stopping
anticoagulation should receive aspirin to reduce the risk for
recurrent VTE, assuming aspirin is not contraindicated” – CHEST
Guidelines January 2016
▪ 2nd
VTE: lifelong
o Agents:
▪ Warfarin
● Goal INR 2-3; start same day as heparin unless unstable or
questionable need for thrombolysis
● Bridging: optimally need 5 days overlap with
heparin & ≥ 24h of INR ≥2
▪ Novel oral anticoagulants (NOACs)
❖ “For patients without cancer who have deep vein thrombosis
(DVT) of the leg or pulmonary embolism (PE), the guidelines
suggest using dabigatran, rivaroxaban, apixaban, or edoxaban
instead of vitamin K antagonists for the first 3 months' treatment
and beyond” – CHEST Guidelines January 2016
● Rivaroxaban (Xarelto): 20mg qd
● Apixaban (Eliquis): 2.5mg PO bid
● Dabigatran (Pradaxa): 150mg PO bid
● Edoxaban (Savaysa): 60 mg PO qd
▪ LMWH – best if cancer-related
o If risk of bleeding negates benefit from anticoagulation, consider first switching to
ASA which can ↓ risk of recurrent VTE by 32%
Treatment cont…
● Patients with low-risk PE may be treated at home or receive an early discharge
Complications
● Post-thrombotic syndrome (PTS) (25%)
o Pain, swelling
o Recent evidence to support NOT using compression stockings in acute DVT to
prevent PTS
● Recurrent VTE: predictors: abnormal D-dimer 1 mo after d/c anticoagulation, (+) U/S at
3 mo of anticoagulation
● Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
o Rx: thromboendarterectomy
Prognosis
● Mortality: 10% for DVT, 10-15% for PE at 3-6 months
REFERENCES
● Dalen JE. Pulmonary embolism: what have we learned since Virchow? Natural history,
pathophysiology and diagnosis. Chest 2002;122:1440-1456.
● Dalen JE. Pulmonary embolism: what have we learned since Virchow? Treatment and
prevention. Chest 2002;122:1801-1817.
● Langan CJ, Weingart S. New diagnostic and treatment modalities for pulmonary
embolism: one path through the confusion. Mt Sinai J Med. 2006 Mar;73(2):528-41.
● www.utdol.com.
● UpToDate
● MKSAP 16
● Pocket Medicine, 5th
Edition
● CHEST guidelines January 2016
Syncope
Objective:
1. Discuss the different etiologies of syncope
2. Discuss the approach to a patient presenting with syncope
IIPI: 85 yo white male who woke up at 2 am in the morning of the admission to
urinate. He has been feeling well except for some nausea, vomiting , and
diarrhea. These symptoms have been ongoing for the last three days but had
recently stopped the day prior to the admission. At the time he started
voiding, he felt dizzy and the next thing he knew, his wife found him lying
on the bathroom floor. The patient seemed moderately alert; did not seem
confused and denied any symptoms of palpitations or dizziness prior to this
episode. EMS was called and the patient was transported to the ED for
further evaluation. The patient states that he did have a similar episode six
months earlier for which he did not seek medical attention.
PMH: Non-contributory. The patient has no known coronary disease, no known
hypertension, no history of stroke. History of nephrolithiasis approximately
30 years earlier.
Meds: PRN OTC anti-inflammatory
ALL: NKDA
Soc: The patient is retired; lives with wife. No alcohol use for greater than 30
years and no history of tobacco ingestion.
FMH: Non-contributory
ROS: Occasional headaches for which he uses over the counter anti-
inflammatories. Mild to moderate shortness of breath on exertion which
started approximately a year prior to this evaluation. Occasional chest
discomfort with severe exertion. No syncope or pre-syncopal symptoms
except one episode six months earlier. The patient does have difficulty
voiding and uses the bathroom 2-3 times a night.
PE:
Vitals: T97.2 P93 BP128/83, not orthostatic
Gen: Mild distress secondary to back discomfort
Neck: Supple, no thyromegaly. No lymphadenopathy
CV: RRR, no murmurs, rubs or gallops
Lungs: Decreased breath sounds in both bases and diffuse basilar crackles
Abd: Soft, non-tender with positive bowel sounds
Ext: No c/c/c
Neuro: A&Ox3, CNII-XII intact, strength and sensation intact, no cerebellar
signs
Labs:
BMP: Na 138, K 3.9, C1 98, CO2 17, BUN 29, Cr 0.9, Glu 89
EKG: NSR with right bundle branch block. No ST abnormalities
Lumbar L2, L3 compression fractures
Syncope Overview
Syncope: The abrupt and transient loss of consciousness associated with absence of postural
tone, followed by complete and rapid spontaneous recovery.
Distribution of causes of syncope
▪ Reflex (neutrally-mediated; this includes vasovagal) - 58%
▪ Cardiac disease (often a bradyarrhythmia or tachyarrhythmia) — 23%
▪ Neurologic or psychiatric disease — 1%
▪ Unexplained syncope — 18%
The term "syncope" should be reserved LOC secondary to transient global cerebral
hypoperfusion.
Not all LOC = syncope (i.e. seizures causes LOC, but not due to cerebral hypoperfusion,
therefore technically not syncope)
Identification of the underlying etiology for syncope can often be made from just the
history, physical examination (including orthostatic vitals), and an ECG.
Physician findings and clinical presentation
● Blood pressure: if low, consider orthostatic hypertension: if unequal in
both arms (difference >20 mmHg), consider subclavian steal or dissecting
aneurysm.
● Pulse: if tachycardia, bradycardia, or irregular rhythm, consider
arrhythmia.
● Mental status: if confused after the “syncopal episode,” consider postictal
state.
● Heart: if there are murmurs present suggestive of AS or HOCM, consider
syncope secondary to left ventricular outflow obstruction; if there are JVD
and distal heart sounds, consider cardiac tamponade.
Clues for etiology
● Vasovagal (vasodepressor) Neurally Mediated Syncope
1
.
Psychophysiologic (panic disorders, hysteria)
2
.
Visceral reflex
3
.
Carotid sinus hypersensitivity
4
.
Glossopharyngeal neuralgia
5
.
Reduction of venous return caused by Valsalva maneuver, cough,
defecation, or micturition
● Syncope due to Orthostatic hypotension
1
.
Hypovolemia
2
.
Antihypertensive drugs
3
.
Neurogenic (autonomic neuropathy)
4
.
Idiopathic
● Cardiovascular
1. Reduced cardiac output
2. Arrhythmias or asystole
a. Extreme tachycardia (>160 to 180 bpm)
b. Severe bradycardia (<30 to 40 bpm)
c. Sick sinus syndrome
d. AV block (second- or third-degree)
e. Ventricular tachycardia or fibrillation
f. Long QT syndrome
g. Pacemaker malfunction
3. Vertebrobasilar TIA, spasm, subclavian steal, Basilar migraine
Classification of Syncope
Reflex (neurally mediated) syncope
Vasovagal:
Mediated by emotional distress: fear, pain, instrumentation, blood phobia
Mediated by orthostatic stress
Situational:
Cough, sneeze
Gastrointestinal stimulation (swallow, defecation, visceral pain)
Micturition (post-micturition)
Post-exercise
Postprandial
Others (eg, laughter, brass instrument playing, weightlifting)
Carotid sinus syncope
Atypical forms (without apparent triggers and/or atypical presentation)
Syncope due to orthostatic hypotension
Primary autonomic failure:
Autonomic failure,multiple system atrophy,Parkinson with autonomic dysfunction, Lewy body
dementia
Secondary autonomic failure:
Diabetes, amyloidosis, uremia, spinal cord injuries
Drug-induced orthostatic hypotension:
Alcohol, vasodilators, diuretics, phenothiazines, antidepressants
Volume depletion:
Hemorrhage, diarrhea, vomiting, etc
Cardiac syncope (cardiovascular)
Arrhythmia as primary cause:
Bradycardia:
Sinus node dysfunction (including bradycardia/tachycardia syndrome)
Atrioventricular conduction system disease
Implanted device malfunction
Tachycardia:
Supraventricular
Ventricular (idiopathic, secondary to structural heart disease or to channelopathies)
Drug-induced bradycardia and tachyarrhythmias
Structural disease:
Cardiac: cardiac valvular disease, acute myocardial infarction/ischemia, hypertrophic
cardiomyopathy,
cardiac masses (atrial myxoma, tumors, etc), pericardial disease/tamponade, congenital
anomalies of coronary arteries,
prosthetic valves dysfunction
Others: pulmonary embolus, acute aortic dissection, pulmonary hypertension
The ECG is suggestive of an arrhythmic cause of syncope if any of the following abnormalities
is present:
▪ Bifascicular block (defined as left bundle branch block or right bundle branch block
combined with left anterior or left posterior fascicular block).
▪ Other intraventricular conduction abnormalities (QRS duration
≥0.12 sec)
▪ Mobitz I second degree atrioventricular block
▪ Asymptomatic sinus bradycardia (<50 beats/min), sinoatrial
block, or sinus pause ≥3 seconds in the absence of negatively
chronotropic medications. ▪ Pre-excited QRS complexes, suggesting Wolff-Parkinson-White syndrome
▪ Long or short QT intervals
▪ Right bundle branch block pattern with ST-elevation in leads V1-V3 (Brugada syndrome)
▪ Negative T waves in right precordial leads, epsilon waves and ventricular late potentials
suggestive of arrhythmogenic right ventricular cardiomyopathy.
▪ Q waves suggesting myocardial infarction
The 2009 ESC guidelines list the following as diagnostic of arrhythmia-related syncope:
▪ Persistent sinus bradycardia <40 beats/minute in an awake patient or repetitive sinoatrial
blocks or sinus pauses >3 seconds.
▪ Mobitz II second or third degree atrioventricular block
▪ Alternating left and right bundle branch block
▪ Ventricular tachycardia or rapid paroxysmal supraventricular tachycardia
▪ Pacemaker or implantable cardioverter-defibrillator malfunction with cardiac pauses
Risk Stratification:
▪ Short-term, high-risk criteria indicate need for intensive evaluation and/or prompt
hospitalization:
1. Evidence of significant heart disease (HF, low LVEF or previous MI).
2. Clinical or electrocardiographic (ECG) features suggesting arrhythmic syncope
3. Comorbidities: severe anemia or electrolyte disturbance
▪ If there are single or rare episodes of syncope with low-risk clinical features, no further
evaluation is indicated.
▪ If there are recurrent episodes with low-risk features, work-up should include tests for
cardiac or neurally-mediated causes, as appropriate.
Testing
Based on the results of the initial evaluation, and many times is not needed. Several tests, mostly
cardiologic, can be used in the evaluation of the patient with syncope. Neurologic testing is
usually low yield and overused, unless specifically suggested by history or physical exam
Testing can include:
▪ Carotid sinus massage in patients >40 years old.
o Diagnostic if syncope is reproduced together with asystolic longer than 3 seconds
and/or fall in systolic blood pressure (BP) >50 mmHg.
o Should be avoided in patients with history of transient ischemic attach or stroke
within the past three months and in patients with carotid bruits (except if carotid
Doppler studies excluded significant stenosis).
▪ Orthostatic challenge: when syncope is related to the standing position or there is
suspicion of a reflex mechanism
▪ Echocardiography
o When there is previously known heart disease or data suggestive of structural
heart disease or syncope secondary to cardiovascular cause (i.e. exertional
syncope, sudden onset palpitations immediately before syncope, abnormal ECG,
etc.
o Can Diagnose: Left ventricular dysfunction, hypertrophic cardiomyopathy, or
significant aortic stenosis, PE, PAH.
o Only a finding of severe aortic stenosis, obstructive tumor or thrombus (eg, atrial
myxoma), cardiac tamponade, aortic dissection, or congenital anomaly of the
coronary artery is considered diagnostic as a cause for syncope.
▪ Electrocardiographic monitoring:
o In-hospital monitoring
o Continuous 24 to 48 hour (Holter) monitoring
o External event recorder
o Implantable loop recorder
▪ Electrophysiology study (EPS):
o Patients with coronary artery disease and syncope after an ischemia evaluation
o ICD placement
▪ Exercise Testing
o Syncope patients at risk for or with a history of coronary artery disease
o Patients with syncope during or shortly after exertion
o Echocardiography is recommended prior to exercise testing
o Diagnostic when:
▪ Syncope is reproduced during or immediately after exercise in the
presence of ECG abnormalities or severe hypotension.
▪ Mobitz II second or third degree AV block develops during exercise even
without syncope
▪ Psychiatric Evaluation
▪ Neurological evaluation or blood tests
o Only when there is suspicion of non-syncopal transient loss of consciousness
High Value Cost-Conscious Care
Syncope workups in the United States have an annual cost of $2.4 billion. The average annual
cost for patients with recurrent syncope of unknown origin was $5281.
Order neurologic testing only if there is specific evidence of a neurologic event. Remember,
neurologic disease accounts for less than 1% of all syncopal episodes.
● Do not obtain brain imaging studies (CT/MRI/EEG/Carotid U/S) in patients with simple
syncope and a normal neurological exam. Only order if there is a suspected central nervous
system process.
● Perform EEG only if seizure is suspected.
References:
1. Olshansky, B. Evaluation of Syncope in Adults. Uptodate 2014.
2. Task Force for the Diagnosis and Management of Syncope, European Society of Cardiology
(ESC), European Heart Rhythm Association (EHRA), et al. Guidelines for the diagnosis and
management of syncope (version 2009). Eur Heart J 2009; 30:2631.
Stroke
HPI: 69 yo left-handed male on warfarin for atrial fibrillation had recently noticed an increase
of palpitations, fatigue, and dyspnea on exertion. A recent positive treadmill test led to
hospitalization for further evaluation. Heart catheterization on admission showed no significant
lesions. Cardioversion was unsuccessful. Pacemaker was placed in the left chest without
apparent complications (INR 2.4).
On the day of discharge, the patient noticed that his right hand was unable to operate the remote
to the TV. This progressed to right arm weakness. Within twenty minutes of the onset of
symptoms, neurologic evaluation for stroke and possible t-PA use was initiated.
PMH:
Transient ischemic attack ten years ago – blurred and double vision
Atrial fibrillation
Anticoagulation secondary to #1
Depression
Diverticulosis
PSH:
Colon resection, adenomatous polyp removed
All: NKDA
Meds:
amiodarone 200mg qd
digoxin 0.25mg qd
warfarin 1mg qday (held 5 days)
aspirin/dipyridamole 25/200 bid
triamcinolone 55mcg spray qd
lithium 300mg qd
alprazolam 0.25mg qd
FMH: Mother deceased at age 83 from stroke
Soc: Lives at home with wife. Rural postal delivery person – now retired. Recent travel to
Hawaii. Five children in good health. Quit smoking in 1974. Prior 30 pack year history. Alcohol
– 2 beers per day.
ROS: Denies any double or blurred vision or headache. Denies PND, orthopnea, or chest pain.
Mild tenderness at pacemaker sight. Denies melena, hematochezia, hematuria or dysuria. No
previous MI, hemorrhagic CVA, or seizures.
PE
Objectives
Risk factors for stroke
Lab/studies needed prior to giving t-PA and work up for
stroke
Importance of the NIH stroke scale
Time frame for t-PA to be given
Absolute and relative contraindications for t-PA
Importance of BP control and what medication/target range to
use
Vitals: T97.8 P65 BP190/90 R20
Gen: WN WD male
HEENT: PERRL, EOMI. No ocular hemorrhages or papilledema
Neck: No carotid bruits or JVD
Lungs: Lungs are clear to auscultation bilaterally
CV: RRR with occasional skipped beats
Abd: Soft, NT, ND, no abd bruits
Ext: No c/c/e. 2/4 equal pulses
Neuro: GEN/MSE: A&Ox3, Slight dysarthria, NIH stroke scale 12
CN: II-XII intact except dysarthria
Motor: RUE 0/5, RLE 4/5 progressing to 0/5; LUE 4/5, LLE 5/5
Coordination: Intact on left, unable to test right
Reflexes: DTR RUE 3/4, RLE 2/4, LUE 2/4, LLE 2/4;
Babinski upgoing on right.
Sensory: Decreased/absent on the right.
Gait: Unable to test.
Labs:
CBC: WBC 8.5, Hgb 16.7, HCT 49.6 Plt 98, no left shift
BMP: Na 135, K 4.0, Cl 104, CO2 23, BUN 12, Cr 1.2, Glc 99
Coags: INR 2.2, PTT 34.5
EKG: Afib with occasional pacer spikes
CT head: Large infarct of left posterior frontal lobe with secondary hemorrhage into the superior
portion (intraparenchymal)
Carotid Duplex: No evidence of plaque or stenosis
2D Echo: No embolic particles noted.
Stroke
Stroke classification
Ischemic (80%)
● Embolic (75%)
o Cardiac source: from left atrium or left ventricle: suspect if atrial
fibrillation/flutter, recent MI, rheumatic mitral/aortic valve, prosthetic/mechanical
valve, HF w/ EF < 30%, dilated cardiomyopathy
o Aortic source: ascending aortic atheromatous disease > 4mm
o Paradoxical, cryptogenic
● Thrombotic (25%)
o Large vessel: atherosclerosis at bifurcation of common carotid, MCA stem,
vertebral arteries
o Small vessels (lacunar strokes): lipohyalinotic occlusions related to HTN,
hyperlipidemia, and diabetes at the penetrating branches of the ACA, MCAP,
PCA, and basilar
● Other: dissection, vasculitis, vasospasm, global hypoperfusion, moyamoya, bindwanger’s
disease, primary thrombosis, cerebral mass
Intracranial Hemorrhage (ICH) (20%)
● ~½ are subarachnoid, ~½ are intracerebral
● Other: epidural hematoma, subdural hematoma
Transient ischemic attack (TIA)
● Newer definition: transient neurologic dysfunction caused by cerebral ischemia, but no
infarction seen on imaging (thus, requires MRI)
● Old definition (but still used clinically): sudden onset of a focal neurologic dysfunction
lasting less than 24 hours from reversible ischemia.
● Sxs usually last <1h
● Differential diagnosis: seizure, migraine, hypoglycemia, amyloid spells, anxiety
● ABCD2 score: assess the risk of a subsequent stroke
o Age ≥60y (1 pt)
o Blood pressure ≥ 140/90 (1 pt)
o Clinical features: unilateral weakness (2 pts) or speech impairment without
weakness (1 pt)
o Duration: ≥60min (2 pts) or 10-59min (1 pt)
o Diabetes (1 pt)
Clinical presentation:
Ischemic: embolic = sudden deficits; thrombotic = suttering course
ACA
Motor and/or sensory deficit (LEG>> face, arm)
Abulia (Akinetic Mutism), Slowness, Delay, Apathy, Intermittent Interruption, lack of spontaneity, whispering, paratonic rigidity
Contralateral Primitive Reflexes:
Grasp, Sucking reflexes
Gait apraxia - impaired gait and stance
MCA Contralateral MOTOR (FRONTAL LOBE) deficit (FACE, ARM> leg > foot) Contralateral SENSORY (PARIETAL LOBE) deficit (FACE, ARM> leg > foot) May be complete hemiplegia if internal capsule involved
Deficit Area
Expressive/Broca's Aphasia Dominant Hemisphere (Usually LEFT) - SUPERIOR Division - FRONTAL Lobe
Receptive/Wernicke's Aphasia Dominant Hemisphere (Usually LEFT)- INFERIOR Division - TEMPORAL Lobe
Hemispatial NEGLECT NON-dominant Hemisphere (Usually RIGHT) - INFERIOR Division - TEMPORAL LOBE
Eye deviation toward side of lesion
SUPERIOR Division - FRONTAL LOBE - FRONTAL EYE FIELDS
Contralateral SUPERIOR QUADRANTANOPSIA
INFERIOR Division - TEMPORAL Lobe - Meyer's Loop Optic Radiations
Contralateral INFERIOR QUADRANTANOPSIA
SUPERIOR Division - PARIETAL Lobe - Baum's Loop Optic Radiations
Contralateral HEMIANOPSIA TEMPORAL + PARIETAL Lobe Optic Radiations
PCA Homonymous Hemianopia with MACULAR SPARING
Deficit Area
Alexia without agraphia (can't read it but can write it)
Dominant hemisphere
Visual Hallucinations & Perseverations Calcarine cortex
Sensory loss Choreoathetosis Spontaneous Pain Syndrome
Thalamus
CNIII Nerve Palsy Paresis of vertical eye movement motor deficit
Cerebral Peduncle, midbrain
Penetrating Vessels 1. Pure motor hemiparesis (classic lacunar syndromes) 2. Pure sensory deficit 3. Pure sensory-motor deficit 4. Hemiparesis, homolateral ataxia 5. Dysarthria/clumsy hand
Vertebrobasilar Diplopia, Dizziness, Dysarthria, Dysphagia NAUSEA, VOMITING; Hiccups GAIT ATAXIA; Limb Ataxia, Motor deficit Cranial nerve palsies; Crossed sensory deficits Coma Bilateral signs suggest basilar artery disease
Internal Carotid Progressive or stuttering onset of MCA syndrome, occasionally ACA syndrome as well if insufficient collateral flow
Lateral Medullary Syndrome = Wallenberg's Syndrome = PICA
Deficit Area
Loss of Pain/Temp on Contralateral BODY Anterolateral System
Loss of Pain/Temp on Ipsilateral FACE Spinal Trigeminal Tract/Nucleus
DYSPHAGIA, HOARSENESS, ↓ GAG Reflex, Soft Palate Paralysis
Nucleus Ambiguus
Horner's Syndrome Ipsilateral Miosis, Ptosis, Anhidrosis, Flushing
Descending Hypothalamic Fibers
Nausea, Dipolopia, Fall to Ipsilateral Side Vestibular Nuclei
ATAXIA on Ipsilateral side Restiform Body Spinocerebellar Fibers
Lateral Pontine Syndrome - Long circumferential branches of basilar artery
Deficit Area
Loss of Pain/Temp on Contralateral BODY Anterolateral System
Loss of Pain/Temp on Ipsilateral FACE Spinal Trigeminal Tract/Nucleus
Ipsilateral FACIAL PARALYSIS Facial Motor Nucleus
Ipsilateral MASTICTORY PARALYSIS Trigeminal Motor Nucleus
Horner's Syndrome Ipsilateral Miosis, Ptosis, Anhidrosis, Flushing
Descending Hypothalamic Fibers
Nausea, Dipolopia, Fall to Ipsilateral Side Vestibular Nuclei
ATAXIA on Ipsilateral side Restiform Body Spinocerebellar Fibers
Clinical Presentation: Subarachnoid Hemorrhage
● Sudden, severe headache (97%), abrupt, “worst headache of my life” or “thunderclap”
headache, loss of consciousness, nausea, vomiting, meningismus (breakdown of blood in
the CSF), seizures (<10%; predictor of poor outcome)
● Terson’s syndrome – vitreous preretinal hemorrhages
● Sentinel headaches – hx of sudden, severe headaches that precede the major SAH by up
to 6-20 days
Risk factors
● Diabetes, hypertension, hyperlipidemia, tobacco use, family history, atrial fibrillation,
personal history of stroke or TIA, recent myocardial infarction, CHF, cocaine
Differential diagnosis
DDX Distinguishing features
Psychogenic Lack of objective cranial nerve findings, neurological findings in
a nonvascular distribution, inconsistent exam
Seizures Hx of seizures, witnessed seizure activity, postictal period
Hypoglycemia Hx of diabetes, low serum glucose, decreased LOC
Migraine with aura
(complicated migraine)
Hx of similar events, preceding aura, headache
Hypertensive
encephalopathy
Headache, delirium, significant HTN, cortical blindness, cerebral
edema, seizure
Wernicke's encephalopathy Hx of EtOH abuse, ataxia, ophthalmoplegia, confusion
CNS abscess Hx of drug abuse, endocarditis, medical device implant + fever
CNS tumor Gradual progression of sxs, other primary malignancy, seizure at
onset
Drug toxicity Lithium, phenytoin, carbamazepine
Assessment
● Rapid evaluation is essential for use of time-sensitive treatments
● Vital signs
● Blood pressure is usually elevated (preservation of ischemic penumbra)
● Fever (normal temp should be maintained)
Physical exam
● Thorough neurological exam; NIH stroke scale
● Arrhythmias, murmurs, carotid and subclavian bruits, peripheral emboli
Immediate Workup
● Assess and manage ABCs
● Stat blood glucose (hypoglycemia can mimic stroke!) – treat accordingly
● O2sat > 94%
● Stat CT scan without contrast within 25min – r/o hemorrhage
o Not good for early detection of AIS, but excellent to r/o a ICH
● Stat CT-angio head & neck (or other non-invasive vascular study) strongly recommended
if predict need for intra-arterial fibrinolysis or mechanical thrombectomy (usually
determined by neurointensivist)
● Stroke team alert and possible triage to neuro ICU
● Cardiac monitoring & 12-lead ECG
● Renal panel, Mag, CBC, PT/INR, PTT, troponin
● Determine last “known well” time
● For selected patients:
o LFTs, UDS, EtOH, Pregnancy test, ABG, CXR
o Lumbar puncture – if SAH is suspected and CT is negative for blood
o EEG – if seizures suspected
Continued Workup
● MRI brain without contrast within 24h;
o MRI best for posterior circulation and early detection of AIS within minutes
o Must be ordered in patients with suspected TIA within 24h
● Carotids and circulation:
o Carotid U/S with Doppler or
o CT-angio head and neck or
o MRA neck w/ contrast + head w/o contrast
● 2D-ECHO with agitated saline bubble study
o ECHO assess for thrombus or vegetation
o Bubble study assess for PFO or atrial septal aneurysm
● More labs: lipid panel, HbA1c, TSH, ESR/CRP, BCx is septic/meningitis
● Hypercoagulable workup if <65 yo or cryptogenic stroke
Acute Treatment
● Blood Pressure:
o If no thrombolysis – allow permissive HTN up to maximum 220/120 x first 24h
o If considering thrombolysis - lower to <185/110
o After thrombolytic given – keep <180/105 x 24h
o For ICH – goal SBP < 160
o For SAH – goal SBP < 140
o Medications:
▪ IV Labetalol 10-20mg, repeat x 1 as needed
▪ IV Nicardipine (Cardene) ggt 5mg/h and titrate 2.5mg/h q5-15min
▪ IV Hydralazine, enalaprilat
o Restart home anti-hypertensives after 24h
● Thrombolysis: IV tPA 0.9 mg/kg (max 90mg)
o 0-3h: improved neurologic outcome with improved mortality
o 0-4.5h: improved neuro outcome but no mortality benefit
o Reversal agent if hemorrhages: aminocaproic acid
Inclusion Criteria Exclusion Criteria
AIS + measurable neuro
deficit
Head trauma, prior stroke past 3 mo
Onset < 3h (must know last
known well!)
Sxs suggest SAH
Age ≥ 18 yo Arterial puncture at noncompressible site
past 7 days
Hx previous ICH
Existing IC neoplasm, AVM, aneurysm
Recent IC or intraspinal surgery
Elevated BP: >185 SBP or > 110 DBP
Active internal bleeding
Platelets <100,000
Heparin given within past 48h w/ ↑ aPTT >
ULN
Current use of anticoagulant w/ INR > 1.7 or
PT > 15s
Use of a NOAC (novel oral anticoagulant):
direct thrombin inhibitors or factor Xa
inhibitors
Blood glucose <50
CT evidence of multilobar infarction w/
hypodensity >1/3 cerebral hemisphere
Relative Exclusion Criteria
Minor or rapidly improving stroke sxs
Pregnancy
Seizure at onset w/ postictal neuro impairments
Major surgery or trauma past 14 days
Recent GI or Urologist hemorrhage past 21 days
Recent acute MI past 3 months
● Intra-arterial Fibrinolysis and Mechanical Thrombectomy
o Symptoms < 6 hours duration
o Selected pts with large strokes of the MCA who are not candidates for tPA
o Mechanical Thrombectomy - solitaire FR and Trevo stent retrievers
● Hyperthermia/pyrexia if >38: acetaminophen & cooling blankets
● Hyperglycemia: goal glucose 140 - 180
● Treat hypoglycemia if glucose < 60
● If hypotensive – use vasopressors to improve cerebral blood flow
● Aspirin 325mg first dose, then, 81mg qd thereafter
o If no thrombolysis: start within 24h
o If thrombolysis: start 24h after tPA given
● Cont statin acutely if already taking
● Swallowing:
o Bedside swallow – initial assessment before anything PO
o Speech therapy
o If fails – place NG or dobhoff for feeds
o Consider PEG if can’t swallow after 2 weeks
● DVT ppx:
o If ischemic stroke – Lovenox or UFH for immobilized pts within 24h (Grade 1A)
o If ICH – Intermittent external compression devices; no anticoagulants
o External compression devices if contraindication to anticoagulants
● Cerebral Edema
o Occurs 1-5 days after a large MCA or cerebellar stroke
o Cytotoxic edema from ischemia (contrast to vasogenic edema from tumor)
o Highest risk in young patients
o ICP monitoring
▪ If GCS <8, evidence of herniation, hydrocephalus
▪ CPP = MAP – ICP
● Normal CPP: 70-90 mmHg
● Normal ICP: 10-15 mmHg
● Normal MAP: 80-100 mmHg
● Goal CPP: >60-70 mmHg
● Goal ICP: <20-25 mmHg
o 3% hypertonic saline (per protocol); Elevated HOB > 30°
o Decompressive craniectomy in pts <60 yo + unilateral MCA infarctions +
deteriorating within 48h despite medical therapy
Secondary Stroke Measures
● Aspirin 325mg first dose, then 81mg qd thereafter
o Give immediately if ischemic stroke and no tPA given; wait 24h after if tPA given
o If “failed” aspirin therapy (must confirm pt was actually taking it!), then switch to
Clopidogrel
● Long term goal SBP: 120-139
● Atorvastatin 80mg (goal LDL < 70) or highest dose tolerable
● Physical therapy, occupational therapy, speech therapy
● Carotid Revascularization (CEA)
o Symptomatic stenosis of 70-99%
o Consider if symptomatic 50-69% stenosis
o Asymptomatic stenosis 70-90% if <79 yo
● Stop anticoagulation for large strokes x 2 weeks to prevent hemorrhagic conversion (a-fib,
valves, hypercoagulable state, DVT/PE, cardiac or paradoxical emboli).
● SSRI – depression is common after strokes!
● Optimize tx of other risk factors
References
Pocket Medicine 5th
edition
Evidence-Based Guidelines for the Management of Large Hemispheric Infarction. Neurocrit
Care (2015) 22:146–164.
Stroke chart, Jon Pankow, MD
Community Acquired Pneumonia
Objectives 1. Etiology of community acquired pneumonia (CAP)
2. Criteria for hospitalization in patients with CAP
a. Utility of Pneumonia Port Severity Index (PSI)
3. ID society guidelines
a. Initial laboratory
b. Empiric treatment
CC: Cough, fever
HPI: MM is a 66 yo white male who presents to your office with complaints of productive
cough. His symptoms began 4-5 days ago with low-grade fever and non-productive
cough. The day before presentation he developed shaking chills and his cough became
productive of yellow-green sputum. He is seeking medical attention today because his
sputum has become rust-colored and his most recent temperature was 102° F. He also
notes right-sided chest pain that is worse with cough and deep inspiration.
PMH: diabetes mellitus, insulin requiring
renal insufficiency
impotence
mild COPD
peptic ulcer disease
diverticulosis
All: NKDA
Meds: aspirin 325mg qd
albuterol MDI prn
omeprazole 20mg qhs
metformin 1000mg bid
glyburide 5 mg po qd
Soc: Non-smoker, non-drinker, works at Dillons as a sacker
PE: VS: T102.3° BP 101/55 P118 R30 SaO2 87% on RA
Gen: obese WM, moderate distress
HEENT: NCAT, anicteric sclerae, EOMI
Neck: Left carotid bruit
Chest: RLL Rhonchi
CV: S1S2, no murmur, tachycardic
Abd: S/NT/ND +BS
Ext: No c/c/e
Labs: CBC: WBC 18.6 Hgb 15.5 Plt 501
BMP: Na 132, K 4.1, Cl 108, CO2 18, BUN 28, Cr 1.7, Glu 213, Ca 8.6
ABG: 7.38/35/68 on RA
CXR: Alveolar infiltrate in RLL
COMMUNITY ACQUIRED PNEUMONIA OVERVIEW
Etiology
● Typical organisms which include:
• Streptococcus pneumoniae (the most common cause)
• Haemophilus influenzae
• Staphylococcus aureus
• Moraxella cattarhalis
• other Gram negative Bacteria
• Anaerobes
● Atypical organisms include:
o Legionella sp
o Mycoplasma pneumonia
o Chlamydia pneumonia
● Viral & fungal
Diagnosis:
● Clinical symptoms (cough, fever, pleuritic chest pain, dyspnea and sputum production)
● Lab - leukocytosis
● Imaging - Infiltrate on CXR considered the gold standard for diagnosis (when clinical
and microbiological features are supportive)
● Sputum cx, blood cx, strep & legionella antigen
o See following table
Decision to hospitalize
● CURB 65
▪ Confusion
▪ Urea (BUN) > 20mg/dl
▪ RR > 30
▪ BP <90 systolic, or < 60 diastolic
▪ Age > 65
▪ 0-1: can be treated as outpatient; 2 should be hospitalized;
≥3 ICU admission.
● Pneumonia severity index (PSI)
▪ Most validated
▪ <70, outpatient
▪ >90, inpatient
Antibiotic treatment
Duration of Therapy
● Patients with CAP should be treated for a minimum of 5 days (except azithromycin
monotherapy 3 day), should be afebrile for 48–72h, and clinically stable before
discontinuation of therapy.
Prevention
● Pneumonococcal vaccine
o Age >65
o Age <65 and risk factors
▪ Includes smokers, COPD, DM and many others
References
1. IDSA/ATS Guidelines for the Management of Community-Acquired Pneumonia in
Adults. Clinical Infectious Diseases 2010
2. UptoDate: Community acquired pneumonia in the adult:Risk stratification and the
decision to admit.
3. MKSAP 16
Acute Infective Endocarditis
Objectives:
1. Risk factors for bacterial endocarditis
2. Diagnosis of bacterial endocarditis
3. Pathognomonic physical exam findings in endocarditis
4. Treatment of native valve endocarditis
5. Treatment of prosthetic valve endocarditis
6. Surgical indications for endocarditis antibiotic prophylaxis
CC: Fever
HPI: FH is a 27 year-old WM who presents to the ER with complaints of not feeling well for
the last 4-5 days. He has had daily fevers with a Tmax 103° F. He also notes chills, night
sweats, malaise, anorexia and fatigue during this time. He thought it was simply a viral
illness but his symptoms have not improved with rest and anti-inflammatory medicine.
Today he developed a productive cough with yellow-green sputum, shortness of air and
right pleuritic chest pain.
PMH: Negative
All: NKDA
Meds: None
SOC: Works as a short-order cook. Divorced with two children. He smokes 2-ppd and drinks
ETOH socially. Had a history of polysubstance abuse in the past-cocaine, heroin, and
crank, but states he has been “clean” for the last 6 months except for occasional
marijuana use.
PE: VS T 102.8 P 116 R 22 BP 101/56
Gen: Thin, ill-appearing, multiple unique tattoos
HEENT: PERRL, EOMI, conjunctivae clear bilaterally, pharynx clear, tongue is pierced.
Neck: supple, no lymphadenopathy
Heart: Tachy without murmur
Lungs: RLL crackles, otherwise clear
Abd: Benign
Ext: No c/c/e
Skin: No petechiae or rash
Lab:
CBC: WBC 27.9, 31% bands; Hgb 11.2; platelets 416
CMP: Serum chemistry is unremarkable
UA: Negative
BC: Staphylococcus aureus in all bottles at 12 hours
UDS: Positive for heroin and cocaine
CXR: RLL infiltrate with pleural effusion, probable early left lingular infiltrate
2D ECHO: Several discrete mobile echogenic masses on the tricuspid valve
Infective Endocarditis
Epidemiology: 10,000-15,000 new cases per year
Microbiology:
Staph (aureus species overall most common organism, 2nd most common nosocomial), Strep
(viridans species 50-60% of subacute IE), Enterococci, HACEK (hemophilus, actinomycetes,
cardiobacter, Eikenella, Kingella) 5% of all IE
-Early prostethic valve endocarditis (<60 days post op): Staph aureus, Staph epidermidis
-Late prosthetic valve endocarditis (>60 days post op): Strep viridians, Staph epidermidis, Staph
aureus
Risk Factors o Age >60, male
o Lines
o Procedures--dental, endoscopies, etc.
o Prosthetic valves
o IVDU
o Previous IE (infective endocarditis)
o Underlying heart disease: e.g. valvular disease such as rheumatic, congenital, CHF
o Order of valves commonly affected: MV, Aortic, MV + Aortic, TV, PV(rare)
Clinical manifestations: Symptoms and signs can be explained by pathophysiology. They
include:
1) Constitutional symptoms (Fever, chills, weight loss…)
2) Valve destruction (regurgitation, murmurs…)
3) Conduction abnormalities
4) Embolization (septic emboli, Janeway lesions)
5) Immunologic phenomena: (Osler nodes, Roth spots, glomerulonephritis…)
Modified DUKE Criteria--NPV >98%, Spec. 99%
o Definite IE: 2 Major Criteria OR 1 Major + 3 Minor Criteria OR 5 Minor Criteria
o Possible IE: 1 Major and 1 Minor, or 3 Minor Criteria
Major Minor
1. Positive Blood Cx with typical
organism (Staph, Strep viridans
and bovis, Enterococcus,
HACEK): 2 separate cultures or
persistently positive blood cx
Single positive blood culture for
Coxiella burnetti or positive
serology, titer >1:800
2. Evidence of endocardial
1. Predisposing heart condition or
IV drug use
2. Fever
3. Vascular phenomena—Janeway
Lesions, septic pulmonary
infarcts, mycotic aneurysm
4. Immunologic phenomena—
Osler’s Nodes (tender), Roth’s
spots, glomerulonephritis, RF
involvement: + Echo with
oscillating mass/abscess or new
regurgitation
5. Microbiologic evidence—Positive
Blood Cx not meeting major
criteria
Choice of Echocardiography (TTE v/s TEE)
o If the clinical suspicion is relatively low, perform a TTE
o TEE recommended for patients with prosthetic valves, rated at least “possible IE” by
clinical criteria, complicated IE, paravalvular abscess, difficult transthoracic
imaging/anatomy as in patients with COPD, obesity, or previous thoracic surgeries.
o TTE at completion of therapy to establish new baseline for valve function and
morphology and ventricular size and function.
THERAPY:
-Cultures are positive in 90% of patients. However, for empiric therapy while awaiting cultures,
use Vancomycin 15-20 mg/kg/dose every 8-12 hours (don’t exceed 2g per dose).
o Native Valve Endocarditis: antibiotics for usually 4-6 weeks +/- surgery
o Virridans group strep or Strep bovis a) PCN susceptible organism: PenG x 4 wks OR Ceftriaxone 2 g/day x 4 wks
Short therapy regimen: {PenG OR Ceftriaxone} + Gent x 2 wks
*If PCN allergy: Vanco x 4 wks
b) PCN resistant organism: Amp + Gent x 4-6 wks,
*If PCN allergy: Vanco+ Gent x 6 wks
o OSSA: Nafcillin/Oxacillin x 6 wks, with optional Gent for 3-5 days for L sided &
complicated R sided, 2 wks for uncomplicated R sided IE
o Enterococcus/Pseudomonas: uncommon in NVE, possible in IVDU, often
require surgery
o MRSA: Vanco x 6 weeks
o HACEK: Ceftriaxone or Amp/Sulbactam or Ciprofloxacin x 4 wks
o Culture negative: Amp/Sulbactam+ Gent x 4-6 wks
o Prosthetic Valve Endocarditis: antibiotics for 6 weeks & more commonly require surgery
1. PCN susceptible strep: PenG or Ceftriaxone x6 wks +/- Gent x 2 wks (Vanco if PCN
allergy)
2. PCN resistant strep: Pen G or Ceftriaxone + Gent x 6 wks (Vanco if PCN allergy)
3. OSSA: Nafcillin + Rifampin x 6 wks or longer + Gent x 2wks
4. MRSA: Vancomycin + Rifampin x 6 wks or longer + Gent x 2 wks
5. Enterococcal: Amp + Gent x 4-6 wks (PCN allergy/resistance: Vanco+ Gent x 6 wks)
6. HACEK: Ceftriaxone or Amp/Sulbactam or Ciprofloxacin x 6 wks
7. Culture negative:(< 1 year)Vanco+Cefepime+Rifampin x6 wks+ Gent x 2 wks
8. Candida/Aspergillus: both surgery and Amphotericin B necessary
Surgical Indications: necessary in 15-25% of IE overall
1. Acute aortic/mitral insufficiency with failure
2. CHF refractory to medical therapy
3. Valvular rupture/perforation
4. Perivalvular abscess, valve dehiscence
5. New heart block
6. Persistent vegetation after systemic embolization--esp anterior mitral valve
leaflet
7. Fungal IE (except histo)
8. Persistent sepsis after 7 or more days of appropriate antibiotics
9. ≥ 1 embolic event during the first 2 wks of appropriate
therapy
10. Early prosthetic valve endocarditis (e.g. within 60 days of valve surgery)
11. Size > 15mm or >10 mm with systemic embolization
Antibiotic Prophylaxis for IE
o Highest risk patients: prosthetic cardiac valve or material, previous IE, unrepaired or
residual defects of repaired cyanotic congenital heart diseases.
o Highest risk procedures: dental procedures that involve manipulation of gingival tissue or
perforation of oral mucosa, respiratory procedures with biopsy, procedures involving
infected skin or musculoskeletal tissue, or surgery to place heart valve/material
o No longer needed for GI/GU procedures
o Regimen: Amoxicillin 2 g or Cefazolin 1g , 30 to 60 min before procedure, Clindamycin
600 mg or Azithromycin 500 mg for PCN allergy
References:
1. "Infective Endocarditis: Diagnosis, Antimicrobial Therapy, and Management of
Complications" Circulation 2005 (AHA guideline Endorsed by IDSA)
2. "Prevention of Infective Endocarditis" Circulation 2007 (AHA guideline endorsed by
IDSA)
Hyponatremia
Objectives
1. Describe the 3 basic types of hyponatremia
2. Therapy for hyponatremia
CC: Seizures
HPI: SZ is a 36 year-old male who resides in a psychiatric group home. He was found on the
floor of his room unresponsive and incontinent. He was breathing spontaneously and his pulses
were full. He had last been seen one hour prior to this with no abnormalities noted. Pt. had
complex seizure in the ED, responsive to diazepam.
PMH: Schizophrenia
Allergies: NKDA
Meds: Chlorpromazine (thorazine)
Social: No tobacco or EtOH. Lives in group home
PE:
Vitals: T: 99.2, BP: 125/76, P: 90, R: 16, Wt: 83kg
HEENT: Atraumatic, EOMI, PERRL
Neck: No bruit, no adenopathy, and no thyromegaly
CV: RRR with murmur
Lungs: CTA bilaterally
Abd: soft, non-tender, non-distended
Ext: No c/c/e
Neuro: GCS 3; not following commands, does not withdrawal to pain, no
spontaneous movement of extremities
Labs
BMP: Na 109, K 3.6, Cl 77, CO2 17, BUN 20, Cr 1.0, Glu 120, Osm 224
CBC: WNL
Urine: Osm 300, Na 75, Cr 25
Reference
Adrogue HJ, Madias NE. Hyponatremia. NEJM 2000;342:1581-1589.
Hyponatremia
Overview:
● Sodium disorders typically due to changes in total body water, not really changes in
total body sodium
● Hyper- or hypo-osmolality causes rapid water shifts resulting in changes in brain cell
volume, ultimately which cause mental status changes or seizures
● Key hormones are ADH and Aldosterone
o ADH: regulates sodium concentration
▪ Stimuli: hyperosmolality, low effective arterial volume, angiotensin II
▪ Action: increases aquaporin-2 channel in collecting ducts = passive
water absorption
❖ Urine osmolality is an indirect functional assay of the ADH-renal axis
o Aldosterone: regulates total body sodium amount, and therefore total body
water amount
▪ Stimuli: hypovolemia via renin and angiotensin II, hyperkalemia
▪ Action: reabsorption of sodium for exchange (excretion) of K+ or H+
Pathophysiology
● Excess of water relative to sodium: 3 scenarios
1. ↑ ADH may be appropriate (hypovolemia or hypervolemia with reduced effective
arterial volume)
2. ↑ ADH may be inappropriate (SIADH)
3. ↓ ADH, appropriately low, but kidneys unable to maintain normal Na
concentration. Occurs when water ingestion exceeds and overwhelms the diluting
ability of the kidney. Kidney’s need solute to excrete water! Minimum
concentration of urine (maximal diluting ability) = UOSM: 60 mOsm/L. If normal
dietary solute = 750 mOsm/d, then can urinate ~12L.
▪ Primary polydipsia (>12L/d H2O intake) = high volume intake
● Ingestion of high volume H2O overwhelms maximal diluting
ability = retain free H2O
▪ Tea & Toast & Beer Potomania = poor solute intake
● Reduced solute intake ± increased free H2O = can’t excrete as
much H2O and thus retain
History
● Acute vs Chronic (< 24 - 48h = acute)
● Symptoms
o Nausea, vomiting, anorexia, malaise (mild: Na 130-135)
o Headache, lethargy, restlessness, weakness, disorientation (Na 125-130)
o Seizures, coma, respiratory arrest (Na < 115-120)
● Risk for neurologic complications
o Alcoholism, malnourished, cirrhosis, age, thiazides, hypoxia, hypokalemia
● Tailored PMHx:
o recent GI illness, diarrhea, vomiting
o recent bowel obstruction, pancreatitis, peritonitis,
o heart failure, cirrhosis, kidney disease
o pulmonary disease
o CNS disease, head trauma, tumor
o hypopituitarism, hypothyroidism, adrenal insufficiency
Physical
● Volume status!
o Orthostatics, skin turgor, mucous membranes, JVP, pitting edema
● Altered mental status, lethargy, depressed reflexes
Etiology Algorithm
Treatment of Hyponatremia
● Depends on:
o Symptomatic
o Volume Status
o Acuity (Acute = < 24-48 hr)
Rate of Correction:
● Asymptomatic or chronic symptomatic
o Slow correction: Na ≤ 0.5 mEq/L/h
● Acute symptomatic
o Initial correction rapidly at 2 mEq/L/h x 2-3h until symptoms resolved
▪ Raising the serum sodium by just 4 to 6 meq/L should alleviate symptoms
and prevent brain herniation.
o Rate of correction should definitely not exceed 12meq/L in 24 hours, and
probably shouldn’t exceed 9meq/L in 24h and 18meq/L in 48h to reduce chances
of CPM.
Methods of Correction:
● Hypertonic Saline (3% HTS)
o “Emergent” treatment
▪ Acute, symptomatic (mild or severe): give 100mL bolus 3% HTS
o “Nonemergent” treatment
▪ Acute, asymptomatic: give 50mL bolus 3% HTS or slow continuous
infusion (see below)
▪ Chronic with moderate, severe symptoms (dizziness, forgetfulness, gait
disturbance, nausea, vomiting, confusion, and lethargy): slow continuous
infusion 3% HTS at 15-30mL/h or 50mL bolus
If Na = 110 mEq/L in a 70 kg Male
IVF type Na content
Increase in Na if
1L IVF given
Rate to increase Na by
0.5 mEq/L/h
3% NaCl 513 mEq/L 9.4 mEq/L ~50 mL/h
0.9% NaCl 154 mEq/L 1 mEq/L ~500 mL/h
● Fluid Restriction
o Chronic with mild/no symptoms
o Underlying disorders: Heart Failure, Cirrhosis, SIADH, primary polydipsia
o Usually < 800mL/day
● Salt Tabs (SIADH)
● Frequent lab draws (initially q1-2 hours, then q3-4h)
Central pontine myelinolysis (CPM):
● shrinkage of neurons away from the myelin sheaths due to the osmotic shift of water out
of the cells; symptoms include flaccid paralysis, paraplegia, dysarthria, dysphagia
Overly Rapid Correction of Hyponatremia
● Treatment: emergently reversed with D5W to prevent CPM! Re-dilute the sodium, then
can correct sodium slowly!
Specific Therapies for the Underlying Disorders
● Hypovolemic Hyponatremia w/ hypotension:
o First correct hemodynamic instability with isotonic saline to restore tissue
perfusion
● Hypervolemic Hyponatremia:
o Restriction of Na & water intake
o Loop diuretics to excrete more water than Na
● SIADH
o Free H2O restriction <800mL/d – first line
o Correct the underlying cause
o Salt Tablets – give if chronic, no CHF, and unresponsive to free H2O restriction
o Hypertonic saline +/- loop diuretic if symptomatic or if Free H2O restriction fails
▪ 1L of 3% HTS will increase Na by ~10mEq
▪ 50 mL/h of 3% HTS will rise Na by ~0.5 mEq/L/h
▪ 100-200 mL/h of 3% HTS will rise Na by ~1-2 mEq/L/h
o Conivaptan, Tolvaptan – not commonly used
o Demeclocycline – causes nephrogenic DI
Practical Approach to Hyponatremia
References:
1. Adrogue HJ, Madias NE. Hyponatremia. NEJM 2000;342:1581-1589.
http://content.nejm.org/cgi/reprint/342/21/1581.pdf
2. Cooper D et al. Disorders of Sodium Concentration. The Washington Manual of Medical
Therapeutics, 32nd Ed, 2007.
3. “Hyponatremia”, Jon Pankow, MD
4. UpToDate
5. Pocket Medicine 5th
edition
Hypernatremia
Objectives:
1. Symptoms of Hypernatremia
2. Causes of Hypernatremia
3. Therapy for hypernatremia
CC: Confusion
HPI:
SS is a 72 yo female nursing home resident. Staff reports the patient has had increased confusion
and agitation over the last day or so. She punched a nurse on one occasion, breaking her jaw.
Patient has needed both chemical and physical restraints to control her behavior. No reports of
vomiting, and vital signs have been stable in the facility per staff.
PMH:
Dementia
Hypertension
COPD
Osteoarthritis of hips – wheelchair bound
Allergies: NKDA
Meds: Haloperidol 1mg IM q8 hours prn, HCTZ, Acetaminophen 1 gm po q6 hours
Social Hx: Retired professional bowler, distant tobacco use, no EtOH. Living in nursing home
for 2 years secondary to dementia and behavior problems.
FMHx: dementia and CAD
ROS: decreased appetite for the last few days. No diarrhea or vomiting. No recent head trauma
or falls
Physical Exam:
Vitals: T 96.8 R20 P110 BP 90/67; orthostatic vitals
Gen: WD, NAD
HEENT: Dry mucous membranes, PERRL, EOMI, bruising to left eyebrow without
deformity
CV: Tachycardic without murmur
Lungs: Decreased breath sounds throughout, no crackles or rhonchi
Abd: soft, non-tender, non-distended
Ext: No c/c/e
Labs:
CBC: WNL
BMP: Na 165, K 4.0, Cl 117, CO2 34, BUN 40 Cr 1.3
UA: negative for infection; specific gravity of 1.030
CXR: negative
Hypernatremia
Pathophysiology of Hypernatremia
● Generally, represents a water deficit in relation to the body’s sodium stores; all
hypernatremic pts are hypertonic (by definition)
o Usually a loss of hypotonic free water (dehydration)
o Rarely, iatrogenic from hypertonic saline
● Usually occurs b/c of impaired access to free water
o Intubation, altered mental status, elderly
Workup
● Volume Status (vital signs, orthostatics, JVP, skin turgor)
● UOSM, UNA, Renal panel
Causes/Etiology
● Extrarenal H2O loss (UOSM > 700-800)
o GI H2O loss: vomiting, osmotic diarrhea, NGT drainage, fistula
o Insensible loss: fever, exercise, ventilation
● Renal H2O loss (UOSM < 700-800)
o Diuresis: loop diuretics, osmotic (glucose, mannitol, urea)
o Diabetes Insipidus
▪ Central DI: ADH deficiency
● Hypothalamic or posterior pituitary disease (tumors, trauma)
● Hypoxic encephalopathy, brain herniation, anorexia, alcohol
▪ Nephrogenic DI: ADH resistance
● Congenital mutation of V2 or aquaporin 2 receptors
● Lithium, amphotericin, demeclocycline, foscarnet, cidofovir
● Hypercalcemia, hypokalemia, protein malnutrition
● Postobstructive AKI, recovering ATN, sickle cell, Sjögrens,
amyloid, pregnancy
● Other (UOSM > 700-800)
o Na overload: hypertonic saline (NaHCO3 rususcitation), mineralocorticoid excess
o Seizures, increasing exercise
Signs and Symptoms of Hypernatremia
● Elderly - intense thirst initially, followed by blunting of the thirst response, muscle
weakness, confusion, coma, and death
● Infants – hyperpnea, muscle weakness, restlessness, high-pitched cry, insomnia, lethargy,
coma, and death
● Both – orthostatic hypotension / hypotension and tachycardia (due to hypovolemia)
● Rapid sodium loading (usually iatrogenic) or rapid correction of hypernatremia can cause
seizures
Patients at Risk for Hypernatremia
● Impaired thirst, limited access to water
● Febrile illnesses, elderly, frail nursing home residents, and hospitalized patients
● Infants – secondary to diarrhea
● Altered mental status
● Intubated
Management of Hypernatremia
● Address the underlying cause
o Replacing/stopping GI losses, controlling fever, correcting hyperglycemia,
correcting the feeding preparation
● Restore access to H2O: daily requirement is >1L H2O/d
Goals for Correction of Serum Sodium
● If hypernatremia develops quickly over hours (<48 hours):
o Rapid correction is desirable (improves outcomes, no increased risk of cerebral
edema)
o Goal correction rate: 1mEq/L/h; target Na 145
o 5 % D5W IV 3-6 mL/kg/h, monitor glycemia and Na every hour until Na = 145
o When Na=145, decrease rate to 1 mL/kg/h until Na = 140
● If hypernatremia develops over longer periods of time or unknown:
o Slow correction indicated due to risk of cerebral edema
o Maximum correction rate <0.5 mEq/L/h; target 10 mEq/L/day reduction
o 5 % D5W IV 1.35 mL/kg/h, recheck Na every 4-6 h then every 12-24 h when
target is attained
o Modify the infusion rate to attain target
● Include in replacement the anticipated volume of ongoing losses
● Follow labs closely: q1-4 hrs initially to monitor effect of therapy
Fluid Choice
● Normal Saline if hemodynamically compromised…
o Only appropriate in the symptomatic hypovolemic patient needing to correct
hemodynamic status.
o After hemodynamics stable, then switch to hypotonic saline
Fluid tonicity Infusate Na+ ECF %
5% Dextrose in water (D5W) 0 40
D5 ¼ NS 34 55
D5 ½ NS 77 73
LR 130 97
NS 154 100
Estimating Change in Serum Sodium
● Use the following equation to estimate the effect of one liter of infusate fluid on the
serum Na+
Calculating the Amount of Fluid Needed
● Free Water deficit
● Goal: 50% correction in first 24 – 36h, and complete correction over 3-7 days
● For Na overloaded pt:
o D5W + Diuretic
References
1. Adrogue HJ, Madias NE. Hypernatremia. NEJM 2000;342:1493-1499.
http://content.nejm.org/cgi/reprint/342/20/1493.pdf
2. Cooper D et al. Disorders of Sodium Concentration. The Washington Manual ofMedical
Therapeutics, 32nd Ed, 2007.
3. Pocket Medicine: 5th
Edition
Meningitis
CC: Headache, fever
HPI: Patient is a 31-year-old Caucasian female who presents to the ED for headache and fever
of 36 hours duration. She describes her headache as dull, occasionally pounding, and primarily
frontal in location. Patient denies relief of symptoms with acetaminophen or ibuprofen. She had a
fever of 102 degrees yesterday. During the past 12 hours she has noticed increased difficulty
flexing her neck and states it is painful to do so. She is experiencing photophobia, increasing
fatigue and nausea with vomiting. She has had three previous similar episodes; these resolved
after 2-3 weeks with narcotics and antibiotics. She denies sick contacts, tick or mosquito bites,
or travel outside the U.S.
PMH: Meningitis on three separate occasions (1985, 1994, 1997)
PSH: Cesarean section x 2
Allergies: NKDA
Meds: 1. Depot progesterone Q 3 months
2. Acetaminophen prn
3. Ibuprofen prn
FH: Father – migraine headaches
SH: Denies tobacco; social alcohol use; no illicit drug use. Married with three children.
Recently moved to Wichita from Ohio. Homemakers.
ROS: Denies change in weight, visual disturbance, sore throat, difficulty swallowing, chest pain,
SOA, change in abdominal symptoms, or rash.
PE: T 100.9 BP 101/55 P 88 RR 20 O2 sat 99% RA
GEN: Lethargic. Appears uncomfortable.
HEENT: NC, atraumatic. PERRLA but obvious sensitivity to light. Anicteric sclera.
Oropharynx: non enlarged tonsils, no oral thrush
NECK: Rigid, no LAD. No JVD.
CV: RRR no m/r/g
LUNGS: CTAB
ABD: soft/NT/ND, + BS in all 4 quadrants. No hepatosplenomegaly.
EXT: no c/c/e. Pedal pulse 2/4 bilaterally.
SKIN: warm, no rash.
NEURO: Lethargic. CN II –XII intact. Motor strength 5/5 in all 4 extremities. Sensation intact
grossly in all 4 extremities. DTR 2/4 in upper and lower extremities.
LAB:
CBC: WBC 6.5 -- Diff 60% seg 30% lymphs
HGB 12.8 HCT 26.4
Platelets 211
CMP: WNL
LFTs WNL
CSF: Color clear/colorless
Cells WBC 78 (1% segs, 99% lymphs)
RBC 0
Glucose 48
Protein 66
Gram stain no organisms
Bacterial culture pending
Viral HSV PCR positive
Meningitis Objectives
1. Overview of pathophysiology
2. Recognize signs and symptoms of meningitis
3. Recognize causes of meningitis
4. Interpret CSF findings
5. Treatment of meningitis
Pathophysiology
● Bacterial meningitis is generally the result of nasopharyngeal colonization with causative
organisms organisms gain access to bloodstream organisms infect choroids plexus
epithelial cells CSF infection. The host immune response causes the classic symptoms
of meningitis.
Signs and Symptoms
● Signs/Symptoms
o Almost all either have fever or hypothermic. Very rarely normal temp
o Severe headache
o Nuchal rigidity (88%)
▪ Assessed with neck flexion, active or passive (not lateral flexion or
rotation)
▪ Brudzinski’s (95% specific)
● Spontaneous flexion of hips with passive flexion of neck
▪ Kernig’s
● Inability to allow full extension of knee when hip is flexed to 90
o AMS (78%)
o Nausea, vomiting, seizures, photophobia, petechiae, arthritis
Viral meningitis
● Rarely presents with mental status change (lethargy may occur) or focal neurologic
deficits. Headache in viral meningitis is often frontal or retroorbital in location; pain with
eye movement is also common. Abdominal pain, diarrhea, myalgia and anorexia are
frequent.
● Signs of viral meningitis include the above with the exception of altered mental status or
focal neurologic deficits. Kernig’s and Brudzinski’s sign are often negative in viral
meningitis. Of note, HSV meningoencephalitis often mimics bacterial meningitis.
Causes of meningitis
● Meningitis is the result of bacterial, viral, or fungal infection. The following is a list of
the most common etiologies and conditions that predispose to each infection.
● Bacterial meningitis
9. S. pneumoniae (70%)
a. pneumococcal pneumonia, chronic sinusitis and otitis media, diabetes
mellitus, alcoholism, splenectomy, hypogammaglobulinemia
10. N. meningitides (12%)
a. C5-9 deficiency, splenectomy
11. Listeria monocytogenes (4%)
a. Age > 50, immunocompromised status
12. Group B streptococcus (7%)
a. Most commonly in neonates
13. Haemophilus influenzae (<6%)
a. splenectomy, hypogammaglobulinemia, sinusitis, pneumonia, otitis media
14. Enteric organisms (Klebsiella, E. coli, Serratia marcescens, Pseudomonas aeruginosa,
Salmonella)
a. diabetes mellitus, chronic UTI, cirrhosis, alcoholism, neurosurgical patients,
neonates and elderly
15. Staphylococcus aureus
a. neurosurgical patients (shunt), diabetes mellitus, alcoholism, head trauma,
ESRD, malignancies, IV drug use
● Viral (aseptic) meningitis
o Enteroviruses (90%) – include echovirus, coxsackievirus
o Herpes virus family – include HSV-1 and 2 (HSV-2 > HSV-1), HHV-6, EBV,
VZV, CMV
o Arboviruses
o Lymphocytic choriomeningitis virus (LCMV)
o HIV
o Other – Mumps, St. Louis Virus, West Nile Virus
● Miscellaneous causes of meningitis
o M. tuberculosis
o Fungal etiologies – include cryptococcus, coccidioidomycosis, histoplasmosis,
aspergillus, blastomycosis
o Spirochete infection – includes T. pallidum and B. burgdorferi
o Parasitic – includes amebic, cysticercosis
o Tick born – includes Rocky Mountain Spotted Fever, erlichiosis
Diagnosis
● *Lumbar puncture & consider CT head
● Blood cultures
o Positive in 50-90%
● Indications for CT head before LP:
* Immunocompromised state (eg, HIV infection, immunosuppressive therapy, solid organ
or hematopoietic stem cell transplantation)
* History of CNS disease (mass lesion, stroke, or focal infection)
* New onset seizure (within one week of presentation)
* Papilledema
* Abnormal level of consciousness
* Focal neurologic deficit
● Initial differentiation among bacterial, viral, and fungal/atypical meningitis is
accomplished via CSF evaluation:
o Cell count available within hours
o Remember to correct WBC for traumatic tap
CSF FINDING BACTERIAL VIRAL FUNGAL/MYCOBACTERIA
L
Opening pressure Elevated (> 180
mmH20)
Normal Normal, slightly ↑ (high with
cryptococcus)
WBC 10- >1000; PMNs 10-1000;
lymphocytes
5-100;
lymphocytes/mononuclear
RBC Absent
(nontraumatic)
Absent except
HSV-1
Absent (nontraumatic)
Glucose Decreased (<40) Normal Decreased (20-40)
Protein Elevated (>45) Normal, slightly ↑ Elevated (10-500)
Gram Stain Positive (>60%) Negative Positive (AFB 10-40%)
Positive (India ink for
cryptococcus)
Treatment/Management
EMPIRIC ANTIBIOTIC THERAPY
● Corticosteroids
o Start on all adult patients
o Proven to decrease mortality & neurologic complications
o Only give if before antibotics, preferably 15-20 minutes prior
▪ Not beneficial if given after abx
o Decadron 0.15mg/kg q 6hrs for 4 days only
o 2013 meta-analysis showed that benefit was only for s. pneumo, so d/c steroid if
another agent is confirmed
Empiric therapy
Predisposing factor Common bacterial pathogens Antimicrobial therapy
Age
2-50 years N. meningitidis, S. pneumoniae Vancomycin plus a third-
generation cephalosporin
>50 years
S. pneumoniae, N. meningitidis, L.
monocytogenes, aerobic gram-negative
bacilli
Vancomycin plus ampicillin
plus a third-generation
cephalosporin
Head trauma
Basilar skull fracture S. pneumoniae, H. influenzae, group A Vancomycin plus a third-
beta-hemolytic streptococci generation cephalosporin
Penetrating trauma
Staphylococcus aureus, coagulase-negative
staphylococci (especially Staphylococcus
epidermidis), aerobic gram-negative bacilli
(including Pseudomonas aeruginosa)
Vancomycin plus cefepime;
OR vancomycin plus
ceftazidime; OR vancomycin
plus meropenem
Postneurosurgery
Aerobic gram-negative bacilli (including
P. aeruginosa), S. aureus, coagulase-
negative staphylococci (especially S.
epidermidis)
Vancomycin plus cefepime;
OR vancomycin plus
ceftazidime; OR vancomycin
plus meropenem
Immunocompromised
state
S. pneumoniae, N. meningitidis, L.
monocytogenes, aerobic gram-negative
bacilli (including P. aeruginosa)
Vancomycin plus ampicillin
plus cefepime; OR
vancomycin plus ampicillin
plus meropenem
● * Dose of rocephin is 2g Q12h
Treatment duration:
1. 7 days: Haemophilus, Neisseria
2. 14 days: Streptococcus Pneumonia
3. 14-21 days: group B strep
4. 21 days: Listeria, gram negatives
Viral meningitis is self-limiting. Supportive therapy is the standard of care.
If HSV suspected, treatment is acyclovir 10mg/kg IV q 8 hours x 10-14 days.
Prognosis • 10-20% mortality
o Higher with strep pneumo, lower with N. menigitides
References: 1. Roos, Karen L. and Kenneth L. Tyler. “Meningitis, Encephalitis, Brain Abscess, and Empyema.” Harrison’s
Principles of Internal Medicine. 18th
ed.
2. De Gans J, Van de Beek D: Dexamethasone in adults with bacterial meningitis. N Eng J Med 347:1549, 2002 IDSA Guidelines: Practice Guidelines for the Management of Bacterial Meningitis. CID 2004: (39), 1267-1284
Hyperkalemia
Objectives:
1. Don’t panic – assess the patient
a. Hemolyzed specimen?
b. Tests to assess patient stability
2. Immediate therapies
3. Acute therapy
4. Etiology and work-up
CC: Hypertension follow-up
HPI: KK is a 55 yo female with hypertension. She has been well controlled on HCTZ for
years but recently had systolic BPs in the 160s despite following diet and exercise
prescriptions. Lisinopril was started one week ago. Today she presents to clinic for
lab and BP checks.
PMH: Hypertension
Arthritis
Chronic kidney disease with baseline creatinine 1.6
All: NKDA
Meds: HCTZ 25 mg po daily
Lisinopril 10 mg po daily
Ibuprofen prn
Soc: No history of smoking or alcohol use, she is a retired bird breeder.
FMH: Hypertension and CAD in her father who died of an acute MI at age 66.
ROS: No chest pain or dyspnea, occasional palpitations for the last 2 days, no nausea or
vomiting. Denies any change in bowel or bladder habits.
PE: Vitals: T 99.1 BP 168/87 P90 R16
HEENT: EOMI, PERRL @ 5 mm
Neck: No carotid bruit, supple, no JVD
CV: RRR, no murmur, no edema, PP 2/4 in all extremities
Lungs: CTAB
Abd: soft, nontender and nondistended with +BS
Ext: No clubbing or cyanosis, no joint erythema or warmth
Labs: CBC: WNL
BMP: Na 140, K 7.5, Cl 104, CO2 18 BUN 38 Cr 4.0
EKG: See Below
Hyperkalemia
Definition: A serum potassium greater than 5 mmol/L
Classification of Hyperkalemia
o Spurious Hyperkalemia
o Artificial elevation of the measured serum potassium due to hemolysis of the
sample or cellular lysis
➢ Excessive time or tightness of the tourniquet during venepuncture
➢ Muscle activity during venepuncture
➢ Aged specimen
➢ Severe thrombocytosis or leukocytosis
o Transcellular Shift of Potassium
o The following can occur alone, but usually are present in combination, causing
an increase in the serum potassium
Acidosis
• Usually metabolic acidosis
Hyperosmolality
• Severe hyperglycemia
Insulin deficiency
• Type I Diabetes Mellitus
o Increased Potassium Intake
o Increased intake, even iatrogenic, rarely causes hyperkalemia unless there is
underlying impairment in the kidney’s ability to excrete potassium
Iatrogenic hyperkalemia
• Infusion of potassium containing solutions
• Oral potassium supplementation
Unrestricted access to food high in potassium in patients with renal failure
• Salt substitutes (Nu-salt)
o Decreased Renal Excretion of Potassium
o Mineralocorticoid deficiency
Addison’s disease
Aldosterone deficiency or resistance
• Aldosterone antagonists (spironolactone, etc.)
Renin deficiency
• Diabetic nephropathy
Drugs
• Aldosterone antagonists – as above
• ACE inhibitors/ARBs – block renin effect, decrease aldosterone
• NSAIDS
• Trimethoprim (bactrim)
o Can cause hyperkalemia in the face of renal insufficiency
o Usually occurs with IV dosing, but can occur with oral dose
o Type 4 renal tubular acidosis (RTA)
Clinical Manifestations
o Often asymptomatic
o Severe hyperkalemia (potassium > 6.5mmol/L)
o Generalized weakness
o Paralysis
o Cardiac arrhythmia, cardiac arrest
o Sudden death
Assessment of the Hyperkalemic Patient
o EKG – changes in the EKG indicate a MEDICAL EMERGENCY
o Peaked T waves (mild to moderate hyperkalemia)
o PR prolongation (severe)
o QRS widening (severe)
o Loss of P wave with widened QRS (severe)
o Sine wave EKG (very severe)
o Ventricular Fibrillation (very severe)
o Confirm the hyperkalemia
o Only performed AFTER the EKG has been reviewed and appropriate actions
taken
o Search for cause of Hyperkalemia
Management of Hyperkalemia
o Immediate Therapies
o IV Calcium – cardiac membrane stabilization (does not actually lower the
potassium)
-Calcium chloride or gluconate can be given as a slow IV bolus (usually 1-
2 grams)
o Insulin and D50 – shifts potassium INTO the cells
-Give 10 units of regular insulin IV, followed by 50mL bolus of D50
-A longer infusion of Dextrose and insulin can also be used
• (250ml of D20 + 25 units of regular insulin IV over 30 min)
o Continuous nebulized albuterol inhalation
-Beta-agonist activity of albuterol causes intracellular shift of potassium
o Acute Therapies
o Correct acidemia
-Bolus or continuous infusion of sodium bicarbonate for metabolic
acidosis
• Bicarbonate administration controversial, but acute correction of
acidosis may be beneficial
-Ensure adequate perfusion
• Re-expansion of the circulating volume is essential
-Treat respiratory acidosis if present (a less common cause)
-Correction of the acidosis causes potassium to shift intracellularly
o Potassium removal
-Sodium polystyrene resin (Kayexalate)
RARELY used. Usually not effective immediately and does not appear to
be more effective in removing potassium from the body than laxative
therapy. Although uncommon, can produce severe side effects,
particularly intestinal necrosis, which may be fatal
Only use kayexalate in patient who meets all of the following criteria:
▪ Potentially life-threatening hyperkalemia
▪ Dialysis is not readily available.
▪ Other therapies to remove potassium (eg, diuretics, rapid restoration of kidney function)
have failed or are not possible.
-Loop diuretics
• Enhance potassium excretion in patients with adequate
circulating volume
-Hemodialysis
• Useful in severe hyperkalemia or if the above therapies are
ineffective
• Renal failure
• Generalized tissue injury/breakdown (rhabdomyolysis)
o Ongoing Treatment and Prevention
o Aimed at treating the underlying cause
-Replace mineralocorticoids
-Discontinue offending agents/drugs
-Dietary potassium restriction References
1. Rastergar A, Soleimani M. Hypokalemia and hyperkalemia. Postgrad Med J 2001;77:759-764. o http://pmj.bmjjournals.com/cgi/reprint/77/914/759.pdf
2. Gennari FJ. Disorders of potassium homeostasis: Hypokalemia and hyperkalemia. Crit Care Clin 2002 Apr;273-288.
Delirium
Objectives
1. Know the most common causes for an acute delirium
2. Identify patients at high risk for developing delirium
3. Know the most common medications associated with delirium
HPI: A 92 year old woman is admitted to the skilled nursing unit after a hospital course for
pneumonia in order to receive physical therapy and reconditioning. The nursing staff has called
to say that the patient is having mental status changes and seems lethargic. The family has
noticed these changes as well. She did not participate in physical therapy today.
Past Medical History:
1. Osteopenia with T-Score of –1.9.
2. Hypertension diagnosed >25 years ago.
3. Osteoarthritis mostly involving the hips and knees.
4. Chronic constipation.
5. Mild renal insufficiency with baseline creatinine of 1.8.
Meds: Calcium/Vitamin D
Alendronate
Atenolol
Chlorthalidone
Ibuprofen PRN
Tramadol PRN
Docusate
Allergies: NKDA
Soc: Widowed, lives alone. She has never smoked and drinks alcohol only on holidays.
FH: Unremarkable
ROS per nursing and family - no falls, no fever/chills, no N/V, no diarrhea, no GI bleed, no
chest pains, no polyuria/polydipsia
Physical Exam
Vitals: Afebrile, Sa02 94% on RA
Gen: Arousable but sleepy. She has normal amount of muscle wasting for her age.
HEENT: NC, AT, PEERLA, oral cavity is pink and wet
Neck: Supple, no lymphadenopathy or JVD, normal carotid upstrokes with no bruit
CV: RRR with SEM at right superior costal margin without radiation, no S3
Lungs: CTA with poor inspiratory effort
Abd: Soft, NT, ND, no mass, BS+
Ext: No C/C/E
Neuro: Oriented x2 to person and place but not time. Strength 5/5 in all
extremities. DTRs 2/4 in biceps, patella, ankles bilaterally. No cerebellar
signs. Babinski is downgoing.
Labs
CBC: WBC 9.5 Hgb: 12.5
BMP: Na 142, K 3.7, Cl 110, CO2 23, BUN 25, Cr 1.6, Glu 79
Delirium
Definition
● Transient, usually reversible, cause of cerebral dysfunction manifesting clinically with a
wide range of neuropsychiatric abnormalities most notably for decreased attention span
and waxing and waning confusion
● Usually occurs in the elderly and have pre-existing compromised mental status.
DSM-V Criteria:
● Disturbance in attention/awareness: can’t focus, direct, nor sustain attention
● Acute (hours to days) change from baseline; fluctuates during day (worse at night, better
in AM)
● Disturbance in cognition: dysfunction in memory, language, visual-spatial abilities,
perception
● Evidence from H&P or labs to suggest cause by a medical condition, substance
intoxication/withdrawal, or med-related effect
● Behavioral disturbances (hypoactivity, hyperactivity, dysfunctional sleep pattern)
● Variable emotional disturbances (fear, depression, euphoria)
Causes
Meds/Toxins Opiates, benzodiazepines, antipsychotics, muscle relaxers,
antihistamines
Drugs of abuse: EtOH, heroin, cocaine
Withdrawal from benzodiazepines or EtOH
Side effects: fluoroquinolones (seizures), serotonin syndrome
Poisons/Toxins (carbon monoxide, cyanide)
Infections Sepsis, UTI, meningitis, encephalitis, abscess
Metabolic Hypoxia, Hypercarbia
Electrolytes (Na, Ca, Mg, Phos), hyper- and hypoglycemia
Thyroid dysfunction
Wernicke's encephalopathy
Brain Seizures, injury, hypertensive encephalopathy
Multi-Organ
Failure
Renal failure (↑BUN), liver failure (↑NH3), respiratory failure (↑CO2,
↓O2)
Other Burns, hyperthermia, hypothermia
Or you can use the acronym: DIE
● Drugs - 40% of all cases (above)
● Infection – any acute infection may cause delirium in the elderly patient
● Electrolyte disturbance / Everything Else
o Metabolic, Endocrine, CNS trauma, Hepatic or Resp failure
Risk Factors
● Change in environment – hospitalization
● Post operative
● Additional physical or mental illness, especially underlying dementia, depression, and
other medical comorbidities
● Age - children and the elderly are most susceptible
● Sensory impairments - visual or hearing deficits
Workup by Etiology
● Important: understand that delirium is a medical diagnosis with medical etiologies that
are presumed to be reversible.
● Conduct a thorough history and detailed medication review, then physical to guide
further workup below.
UDS, EtOH Illicit drugs, toxins, medications
Serum medication levels Digoxin, lithium, quinidine, risperidone OD
CBC, UA w/ Cx, BCx, LA, ESR, CRP Infection, sepsis
ABG, pulse oximetry, CXR Hypoxia, hypercarbia, respiratory failure
Renal panel Electrolyte disturbances
LFTs, Ammonia Hepatic encephalopathy, liver failure
TSH ± free T4; B12 Thyroid storm/dysfunction; B12 deficiency
CT or MRI brain Head trauma, intracranial hemorrhage
LP Meningitis
EEG Seizures
DDX for Delirium
1. “Sundowning”
o Behavioral deterioration at night, typically demented & institutionalized patients
o Suspect delirium if new, but sundowning is impaired circadian rhythm regulation
in environment
2. Focal Syndromes
o Wernicke’s aphasia, frontal brain lesions (mutism, lack of judgment, no or labile
emotions)
3. Nonconvulsive status epilepticus
4. Dementia (Alzheimer's, Lewy body)
o Cognitive changes are insidious, progressive, do not fluctuate much, occurs over
months to years
o Attention is intact, older memories intact (early stages)
o Lewy Body Dementia: may have fluctuations and visual hallucinations
5. Primary psychiatric illnesses
Management
● Identify and treat the underlying cause! (see above for causes)
● 1st line: Environmental/Preventative measures
o Improve familiarity & frequent reorientation (clocks, calendars, adequate lighting,
quiet atmosphere, consistency, familiar objects and photographs)
o Frequent visitation by family and friends – encouraged to help re-orient
o Sleep protocol: consistent sleep-wake cycles w/ reduced interventions
o Optimize comfort, minimize lines and catheters if possible
o Glasses and hearing aids if needed
o Early mobilization
o Minimize physical restraints if possible
● 2nd
line: Medical treatment – for the combative patient failing 1st line measures
o Haloperidol (Haldol): 0.5-10mg IM q3-6h – oldest and best line
o Ziprasidone (Geodon): 10mg IM q2h or 20mg q4h (max: 40mg/d)
o Olanzapine (Zyprexa) 5-10mg IM q2-4h (max: 30mg/d)
o Quetiapine (Seroquel): 50mg PO bid (initial)
o Get an EKG! Check for QTc prolongation!
o Avoid benzodiazepines (Diazepam, Lorazepam) except in EtOH withdrawal and
Seizures
o For severely combative patients with QTc prolongation (esp if >475-500):
▪ Telemetry, optimize Mg2+ to 2.0 and K+ to 4.0 and consider lower doses
of antipsychotics if absolutely needed
▪ May need to resort to soft wrist restraints and trial of benzos
● 3rd
line: soft wrist restraints – may need to have security help
Important notes on Court Holds:
● A common misunderstood process involves Court Holds. You can NOT take out a Court
Hold on a delirious, combative patient without a co-existing psychiatric illness (suicidal
depressive, actively manic or psychotic, schizophrenia, bipolar etc).
o You may be pressured by nurses, police, etc. to take out a Court Hold on a
combative, delirious patient wanting to leave AMA. A Court Hold is designed to
hold psychiatric patients who lack capacity and are likely to cause harm against
their will until they are court committed by a judge. There can be co-existing
delirium too, but there must be an underlying psychiatric problem necessitating
the court hold.
● For severely delirious, combative patients lacking capacity without an underlying
psychiatric illness, you can medically restrain them with antipsychotics or soft restraints
as noted above. You may need security, but you do not need a court hold.
Assessing Capacity
● Cognition is a key component of capacity—any condition or treatment that affects
cognition may impair decision-making capacity
● Is not static—cognition can improve with treatment, especially in hospitalized pts
● MMSE may help, but is not a substitute
● Any physician can determine capacity. The judge determined competence.
Decision-Making
Ability Definition Sample Questions
Understanding Ability to state the meaning of "can you tell me in your own words
relevant information: dx, risks,
benefits, indications, options
what I have told you"
Expressing a
choice
Ability to make a decision "which option do you choose?"
Appreciation Ability to explain how the
information applies to him-/herself
"Tell me what your medical problem
is and do you think your option could
possibly benefit or harm you?"
Reasoning Ability to compare information and
infer consequences
"How could your choice affect your
daily living? How is it better than the
other options?"
References:
1. UpToDate
2. Brown TM, Boyle MF. Delirium. BMJ 2002;325:644-647.
3. DSM-V
4. Algorithm on the Combative Patient, 2016, Jon Pankow, MD
Diabetic Ketoacidosis (DKA) CC: Diffuse abdominal pain, nausea with vomiting
HPI: Patient is a 24-year-old Caucasian male who presents to the ED complaining of abdominal
pain. He began “feeling ill” with diffuse myalgias and nausea 36 hours ago. The patient was
unable to eat because of his nausea and discontinued his insulin; he has not taken his blood
sugar. Approximately 24 hours ago, the patient began vomiting and was able to drink only small
sips of water. He had the acute onset of diffuse abdominal pain 12 hours prior to presentation.
The pain is described as dull with occasional sharp sensations in the epigastric region. The
patient had a single episode of loose stools. The patient denies any fever, chills, hematemesis,
melena, hematochezia, chest pain, or shortness of air.
PMH: 1. Diabetes mellitus type 1 diagnosed at age 12
2. Three previous hospitalizations for DKA
3. Diabetic nephropathy with baseline creatinine ~ 1.1
PSH: 1. Appendectomy at age 9
Allergies: NKDA
Meds: 1. Lantus 20 units qHS
2. Novolog 6 units with breakfast and lunch, 8 units with dinner
3. Acetaminophen prn
FH: Father – diabetes mellitus type 2, non-insulin requiring
Mother – HTN
SH: + 5 pack year history of tobacco; occasional alcohol (social); no illicit drugs. Single
without children. Lives alone. Student at WSU.
ROS: Denies weight change, visual changes, sore throat, difficulty swallowing, or dysuria.
PE: T 100.1 BP 94/58 P 119 RR 23 O2 sat 99% 2L NC
GEN: awake, A & O x 3. Mild respiratory distress.
HEENT: PERRLA, anicteric sclera. Fundi not well visualized. Oropharynx with dry mucous
membranes. Dentition reveals several caries. Fruity smelling breath.
NECK: supple, no LAD, no thyromegaly. No JVD.
CV: tachycardic, regular rhythm. No murmur/rub/gallop.
LUNG: tachypneic, CTAB.
ABD: Thin. soft/TTP diffusely without guarding or rebound/ND. Bowel sounds present in all 4
quadrants. No hepatosplenomegaly.
EXT: no c/e/e. Pedal pulse 2/4 bilaterally.
SKIN: no rash. Dry.
NEURO: CN II – XII intact. Strength 5/5 in upper extremities and lower extremities bilaterally.
Gross sensation intact in upper extremities bilaterally; decreased gross sensation in feet
bilaterally. Reflexes 2/4 in upper and lower extremities bilaterally. Proprioception intact
bilaterally. Babinski negative bilaterally. Mild wide based gait bilaterally.
LAB:
CBC: WBC 12.0 Diff – WNL
HBG 16.2 HCT 40.3
Platelets 386
BMP: Na 128 K 5.3 Cl 94 CO2 11 BUN 25 Cr 1.3 Glucose 567
Magnesium 2.4 Phosphorus 1.8 Calcium 8.2 Albumin 3.4
LFTs WNL
ABG: 7.15/25/98
UA: Glucose 4+, Protein 1+, ketones 2+, 0-1 WBC, 0-2 RBC
EKG: Sinus tachycardia; no ST/T wave abnormalities
CXR: no acute cardiopulmonary process
Objectives: 1. Recognize causes of diabetic ketoacidosis
2. Understand management of DKA
3. Recognize potential complications of DKA therapy
Overview Diabetic ketoacidosis (DKA) is an acute, life threatening complication of diabetes mellitus.
Symptoms include polydipsia, polyuria, fatigue, lightheadedness, shortness of air, nausea,
vomiting, abdominal pain, and neurological symptoms ranging from mild confusion to stupor to
coma.
Signs include tachycardia, tachypnea, hypotension (if severe), evidence of decreased volume
status (sunken eyes, dry mucous membranes, poor skin turgor, absence of jugular distension),
Kussmaul’s respirations, and fruity breath. Altered mental status on the above noted spectrum
may also be observed.
Mortality is ~ 2% per episode.
Pathophysiology
DKA is initiated by a lack of insulin (either production or external supplementation). In the
absence of insulin, counterregulatory hormones (glucagon, growth hormone, ACTH,
catecholamines) enhance triglyceride breakdown into free fatty acids. Beta oxidation of the free
fatty acids results in the formation of ketone bodies (beta-hydroxybutyrate and acetoacetate) and
academia. In addition, these hormones induce gluconeogenesis. The resultant hyperglycemia
causes an osmotic diuresis.
Etiology 1. Inadequate insulin treatment or medication noncompliance (25%)
2. Acute illness
a. Infection – UTI, pneumonia, sepsis…
b. AMI
c. CVA
d. Acute pancreatitis
e. Cocaine use
f. Trauma
g. Surgery
3. Medications
a. Olanzpine/clozapine
b. Lithium
c. Terbutaline
4. Idiopathic
Diagnostic Criteria for DKA
FEATURE Mild Moderate Severe
Plasma glucose >250 >250 >250
Arterial pH 7.25-7.30 7.00-7.24 <7.00
Serum bicarbonate 15-18 10-14 <10
Serum sodiuma 125-135 125-135 125-135
Serum ketones Positive Positive Positive
Urine ketones Positive Positive Positive
Serum Osmolality* Normal Normal/↑ Normal/↑
Anion gap^ >10 >12 >12
Altered mental state Alert Alert/drowsy Stupor/coma a
These represent measured serum sodium levels. Recall that with significant hyperglycemia
(>200), actual serum sodium is calculated by {Na + [(glucose – 100) x 0.016]}
* Serum osmolality = [(2 x Na) + (BUN/2.8) + (glucose/18) + (EtOH/4.6)] ^ Anion gap = Na (measured) – (Cl + CO2)
Management 1. Assess patient stability (ABCs). The patient may require intubation if he/she has altered
mental status.
a. Monitor mental status, vital signs and urine output hourly
2. Fluid resuscitation
a. Patients with DKA have 6-8 L fluid deficit. The initial fluid resuscitation 0.9%
saline. Generally, rate of infusion is 500 mL to 1 L over the first hour then 300-
500 mL/hr for the next 12 hours.
b. If the corrected sodium (1.6 meq reduction in Na for each 100 mg/dL rise in the
serum glucose) is low, continue using 0.9% saline until sodium normalizes (be
cautious regarding the rate of sodium correction given the risk for central pontine
myelinolysis).
c. If the corrected sodium is normal or high, change infusion to 0.45% saline 200-
300 mL/hr. (A normal serum sodium in the setting of DKA indicates a more
profound water deficit).
d. When serum glucose <250-300, change hydrating solution to D5 ½ NS.
3. Insulin replacement
a. Begin insulin drip. Initially, patient should be given a regular insulin bolus of
0.15units/kg then place on constant infusion of 0.1units/kg/hr.
The goal is to decrease glucose by ~80mg/dL/hr.
b. Monitor serum glucose hourly while on insulin drip.
c. When serum glucose approaches 250mg/dL, decrease insulin infusion rate by 1-3
units/hr. Continue this rate until the patient has received adequate fluid hydration,
serum CO2 is >15, and Anion Gap has closed.
d. When above criteria met, start the patient on subcutaneous insulin (either previous
home insulin dosing or 0.5 to 0.8 U/kg/day), give a dose of subcutaneous insulin
prior to discontinuing the insulin drip (~ 2 hour prior).
4. Electrolyte replacement
a. Monitor electrolytes (BMP, magnesium, phosphorus) every 2-4 hours upon
admission. The electrolytes generally drop dramatically with treatment.
b. Potassium replacement: substantial K deficit due to urinary/GI losses, but K may
be high due to shifting of K, insulin deficiency, and hyperosmolality.
i. Start repleting K when levels fall below 5.3
ii. If levels <3.3 give KCl before insulin
iii. Add KCl to IVF (usually 40mEq/L)
c. Magnesium replacement orally as necessary. IV formulations if levels are
extremely low.
d. Phosphorus replacement: insulin therapy often unmasks phosphate deficiency;
phosphate replacement can cause hypocalcemia and hypomag.
i. Routine replacement not recommended unless cardiac dysfunction,
hemolytic anemia, respiratory depression
ii. If serum phosphorus <1.5 mEq/L, give 0.16 mmol/kg of Kphos IV over 6
hours. (Rapid infusion causes hypocalcemia.)
e. Bicarbonate replacement is contraindicated in DKA (worsen hypokalemia and
cerebral edema). Treatment of the underlying condition will resolve the acidosis.
Can give if pH <7.0
i. If pH 6.9-7.0: 1amp HCO3 + 10KCl in 200cc H20
ii. If pH <6.9: 2amps HCO3 + 20KCl in 400cc H20
References:
1. Abbas, E.K., Haleh Haerian, Burton Rose. “Clinical features and diagnosis of diabetic
ketoacidosis and hyperosmolar hyperglycemic state in adults.” www.utdol.com.
2. Powers, Alvin C. “Diabetes Mellitus.” Harrison’s Principles of Internal Medicine. 18th
ed. Ed. Kasper, et.al. New York: McGraw-Hill (2005), 2152 –2180.
Alcohol Withdrawal
Objectives
1. Recognize signs and symptoms of uncomplicated alcohol withdrawal
2. Risk factors for prolonged or complicated withdrawal
3. Drugs of choice for alcohol withdrawal
4. Management of alcohol withdrawal including seizures and delirium tremens.
CC: “I need help to stop drinking”
HPI: 44 year-old African American male presents with shaking and tremors. He denies any
nausea, vomiting, fevers, chills, or GI bleeding. He reports drinking only three beers
yesterday and today. His brother is present and indicates his alcohol intake is well over
that amount, but is unable to quantify exactly. He has been in alcohol abuse treatment
programs in 2000 and 2001, but he continues to drink.
PMH: Alcoholism
Renal Insufficiency
Hepatitis C
Hypertension
Thrombocytopenia
Anemia of chronic disease
All: PCN (Unknown reaction)
Meds: Diltiazem
Soc: Smokes 1-ppd x 20 years. He drinks alcohol daily. Remote history of IVDU.
FH: Father - Diabetes Mellitus, hypertension, stroke; Mother – hypertension
ROS: Denies any chest pain or SOA. Denies any hemoptysis or blood in the stool. Denies any
abdominal or lower extremity swelling.
PE:
Vitals: T 97 P 100 BP 179/117 RR 20 SaO2 98% on RA
Gen: Moderately obese AA male with poor hygiene, tremulous
HEENT: EOMI, PERRL, sclera are moderately icteric
Neck: WNL
Lungs: CTA bilaterally
CV: RRR, no murmur
Abd: Soft, slightly distended, +BS, TTP. No fluid wave. No hepatosplenomegaly.
Neuro: Awake and oriented x 3, moving all four extremities, no focal deficits
Labs:
CBC: WBC 4.4 Hgb 11.2 MCV 102 Plts 34
BMP: Na 135 K 2.9 Cl 95 CO2 22 BUN 8 Cr 1.1 Glu 116
LFT: AST 27 ALT 30 AP 88 BiliT 2.0 Alb 2.6
EtOH: 60
CXR: WNL, no infiltrates or effusions
1. Evaluate if the patient at risk for alcohol withdrawal:
● Recent drinking history including frequency, amount and time of last drink
● Past history of withdrawal or seizures, hallucinosis, or delirium tremens
● Needing medications for detoxification in the past
● Concurrent use of benzodiazepines or barbiturates (may increase tolerance and risk of
serious withdrawal phenomena, requiring higher benzodiazepine doses and a prolonged
detoxification process)
2. Spectrum of Alcohol Withdrawal
● Minor alcohol withdrawal: tremulousness, irritability, anorexia, nausea; sx may appear
within a few hours after reduction/cessation of alcohol and usually resolve within 48hr
● Alcohol withdrawal seizures: typically one or a few brief generalized convulsions
occurring 12-48hr after cessation of alcohol intake. Must exclude other causes for the
seizures, but antiepileptic drugs are generally not indicated
● Severe withdrawal or delirium tremens: tremulousness, hallucinations, agitation,
confusion, disorientation, and autonomic hyperactivity (fever, tachycardia, diaphoresis);
typically occurs 72-96 hrs after cessation of alcohol. Can be associated with up to 5%
mortality. Lasts up to 5 days.
3. General patient management concerns:
● Make sure patient is fully and adequately hydrated (use IV fluids containing glucose)
● Correct magnesium, calcium, and other electrolyte imbalances
● Thiamine 100 mg IM or IV daily for 1-3 days, then PO daily
● Folic acid 1 mg PO daily, multivitamin PO daily
● If history of seizures, institute routine nursing seizure precautions
● If withdrawal is severe or very high doses of benzodiazepines are administered, attend to
pulmonary hygiene and consider constant observation or transfer to ICU.
4. Assessment of Severity of Withdrawal
● A regular systematic assessment should be made of the patient's status using a validated
instrument, such as the Clinical Institute Withdrawal Assessment for Alcohol Scale
(CIWAS-Ar), to measure withdrawal severity
5. Treatment of Alcohol withdrawal:
● Withdrawal prophylaxis- Patients with a history suggestive of alcohol withdrawal who
presents with minimal current withdrawal symptoms are suitable for withdrawal
prophylaxis. The benzodiazepine options include oral chlordiazepoxide (Librium), oral
oxazepam (serax) or oral, sublingual, intramuscular, or intravenous lorazepam (Ativan).
The prophylaxis track has three levels: mild, moderate, and severe, based on assessed
risk, with corresponding benzodiazepine doses.
● Symptom-triggered therapy- involves providing medication only when a patient has
symptoms. Requires close monitor/re-assessment of patient using assessment tool (i.e.
CIWAS-Ar) so that medications can be dosed accordingly. [Studies have shown that
symptom-triggered therapy leads to less overall medication and a shorter treatment
period.]
● Throughout the detoxification process, closely monitor for excessive sedation, and hold
doses until sedation clears.
● Recommended Benzodiazepines:
o Chlordiazepoxide - 50-100 mg PO/IV PRN. One of the preferred agents for
prophylaxis. Avoid in elderly and liver disease (decreased albumin, increased INR).
Usual maximum dose is 300 mg/24 hr.
o Oxazepam –only PO. Another preferred agent for prophylaxis, safer in liver
disease, 10-30 mg po TID to QID, must monitor LFTs if using long term.
o Lorazepam -PO, SL, IV, IM. Preferred for elderly, liver disease, NPO (SL or IV)
and severe or rapidly escalating withdrawal. Do not give bolus lorazepam in doses
greater than 4 mg. Shorter half-life helpful in avoiding oversedation.
● Do not mix benzodiazepines (e.g. Librium scheduled with Ativan prn). Select
a single agent and titrate as needed. May switch over to another
benzodiazepine if indicated, e.g., Librium to Ativan if withdrawal is severe
and escalating, requiring frequent IV dosing.
● For refractory DT: can consider phenobarbital or propofol with benzodiazepines
●
● Once the patient is stabilized for 24 hours:
o Reduce the total 24-hour dose by 25% per day over next 2-3 days.
o If IM or IV lorazepam was used to stabilize the patient, consider change to oral
chlordiazepoxide or oxazepam as soon as possible.
References:
1. Hoffman R, G Weinhouse. Management of moderate and severe alcohol withdrawal
syndromes. Up to Date, 2014.
2. Kosten TR, O’Connor RP. Management of drug and alcohol withdrawal. NEJM
2003;348:1786-95. http://content.nejm.org/cgi/reprint/348/18/1786.pdf (for subscribers)
Leaving AMA
● Approximately 1%-2% of hospital discharges occur AMA. Patients who leave
AMA have significantly higher readmission rates and may be at increased risk of
serious adverse health consequences when compared with normally discharged
patients.
● The use of a standardized protocol to address issues of decision-making
capacity, follow-up arrangements, and communication may help reduce the risk
of errors when patients are discharged AMA.
● Discharge AMA does not absolve the physician of responsibility for poor
outcomes; as always, good clinical care and careful documentation are of
paramount importance.
● Proper AMA Discharge
○ Given the prevalence of AMA discharges and the serious problems that they present, emergency physicians should make every attempt to prevent a patient from leaving AMA.[3] However, if it is unavoidable, three requirements should be met for the AMA process to confer optimal legal protection.
■ First, a patient should be deemed to have the capacity to refuse care.
■ Second, all potential risks should be disclosed. ■ Third, the AMA consent should be properly documented in the
chart.
References:
1.How Signing Out AMA May Create Significant Liability Protection for Providers Frederick Levy, MD, JD; Darren P. Mareiniss, MD, JD; Corianne Iacovelli, JD. J Emerg Med. 2012;43(3):516-520.
2.Discharge Against Medical Advice. Commentary by Stephen W. Hwang, MD, MPH. https://psnet.ahrq.gov/webmm/case/96
Pain Management
Case 1:
Opioid titration
Mr. White is taking 100 mg of sustained release morphine every 12 hours. For the past two days,
he has taken an additional eight, 15 mg doses of immediate release morphine because his pain
was not controlled.
What are his new sustained release morphine and rescue (immediate release) doses?
Case 2:
Changing an oral opioid to the IV/SQ route
Ms. Brown was taking 150 mg oral sustained release morphine every 12 hours. She developed a
pathologic femoral fracture and has required additional 150 mg of oral immediate release
morphine daily for the past two days, achieving good pain control. She will go to the operating
room tomorrow for internal fixation and will require intravenous pain control.
What is the parenteral morphine drip rate that is equivalent to the oral medication she
currently takes? What is her new rescue dose and how often can it be given?
Case 3:
Changing to another oral opioid
Ms. Reed is taking sustained release oxycodone, 100 mg every 12 hours, but has developed
intolerable sedation. She would like to try hydromorphone, an immediate release opioid agent.
What is the equivalent dose of hydromorphone?
Case 4:
Changing from an oral opioid to transdermal fentanyl
Ms. Doe is taking 100 mg sustained release morphine every 12 hours. She is having difficulty
swallowing pills and would like to use transdermal fentanyl.
What is the equivalent dose of transdermal fentanyl?
Case 5:
Change opioid agent and route
Mr. Topper is having nightmares and hallucinations on 150 mg oral sustained release morphine
twice per day. Because he is to be hospitalized for an operation, he will need a parenteral opioid.
A decision is made to switch him to parenteral hydromorphone.
What is the equivalent mg/hour parenteral hydromorphone dose, and what is his rescue
dose?
Pain Management
1. Evaluate/monitor pain in all patients using a 0-10 scale (mild 1-4, moderate 5-7, severe 8-10)
2. Base the initial choice of analgesic on severity and type of pain
Mild non opioid
Moderate non opioid and opioid
Severe opioid and non opioid
If neuropathic component, also start adjunctive therapy with a TCA or anticonvulsant
(amitriptyline 25mg qhs, Neurontin 100mg TID, increase doses as tolerated)
3. Non Opioids
Acetaminophen- often first choice, use full doses (3-4g/day), do not exceed 2g/day in
alcoholics or patients with chronic liver disease
NSAIDs- naproxen 375-500mg BID, ibuprofen 400-800mg TID; can combine with
acetaminophen for better pain control, caution/contraindicated in patients with GERD,
kidney disease
4. Opioids
Parenteral- Morphine drug of first choice, Dilaudid drug of second choice
Oral- use this route whenever possible
short-acting- oxycodone, morphine, hydromorphone
long-acting- OxyContin, MS contin
Transdermal- fentanyl
Notes- add laxative for all patients on opioids
Add prn antiemetics for nausea/vomiting
If pain is uncontrolled: increase opioid dose by 25-50% if pain is of moderate intensity, and
by 50-75% if pain is of severe intensity
5. Specific situations
Musculoskeletal- use acetaminophen and/or NSAID, if severe an opioid may be required
initially
Sickle cell crisis- opioids are the drug of choice, add or continue NSAIDs
6. Adjuvant therapy: should also be used where appropriate (muscle relaxants, tricyclics,
anticonvulsants, steroids, radiotherapy, topical agents)
7. Miscellaneous:
a) Avoid writing only prn orders, write for scheduled pain meds with hold orders if patient is
sedated or respiration depressed, or scheduled med with a prn for breakthrough pain.
b) Always consider using non-drug measures: PT, OT, heat, cold, massage, TENS
c) Look for and treat any comorbid conditions, especially anxiety and depression.
d) Treat the underlying cause, but do not delay pain management while doing the workup.
e) Educate your patient and their family about his/her pain and the management plans.
f) Continuously review and re-adjust your management plans
Key points for administering opioids
● Use opioids in combination with nonopioids for patients who have moderate/severe pain.
● Use orally administered analgesics whenever possible. Intravenous and subcutaneous
administrations are preferred over intramuscular administration.
● For moderate or severe pain, titrate the opioid dose upward by 50% to 100% until the
pain is relieved.
● Consider lowering the rate of opioid escalation in the presence of renal or hepatic
insufficiency.
● Consider lowering the initial dose and rate of opioid escalation for opioid-naive and
elderly patients.
● For pain occurring between opioid doses of sustained release opioids, give 10% of the
total daily opioid dose in an immediate release form (rescue dose).
● Treat episodic pain, pain with movement or activity (with little or no pain at rest) with
short-acting opioids on an as-needed basis.
● For chronic pain, consider a dosing regimen that anticipates the need to treat pain
continuously, rather than treating pain after it becomes problematic.
● Use the "Dosing and conversion chart for opioid analgesics" when introducing a new
opioid, choosing a different administration route or calculating a rescue dose.
● Consider incomplete cross tolerance when switching between different opioids. Decrease
the calculated dose of the new opioid by at least 25%.
● Use immediate release opioids to treat breakthrough pain. Transdermal fentanyl is slow
to achieve therapeutic levels and has a prolonged elimination time after removal.
● Consider adjuvant therapy
Equianalgesic dosing
When switching opioids, you should follow these five steps:
1. Add the total dose of each opioid given during 24 hours. If both parenteral and oral doses
were given, calculate the 24-hour total for each.
2. Determine the conversion ratio for each type of opioid and each route by using the
“Dosing and conversion chart for opioid analgesics”. Calculate the conversion ratio as the
equianalgesic dose of the current opioid (or route) divided by the equianalgesic dose of
the alternative opioid (or route).
3. Divide the 24-hour dose of the current opioid (or route) by the conversion ratio to
estimate the 24-hour dose of the alternative opioid (or route).
4. Modify this estimate based upon the clinical situation.
5. Divide the estimated dose by the appropriate dosing interval for the appropriate opioid
(or route) based upon the “Dosing and conversion chart for opioid analgesics.”
Sources:
Pain Management for the Internist. ACP Internist. 2009.
http://www.acpinternist.org/archives/2004/12/pain/toc.htm
Answer case 1: To determine his new sustained release morphine dose, calculate the total opioid taken by adding
the amount of sustained release morphine and immediate release morphine consumed in 24
hours. Divide this quantity by 2 and administer every 12 hours:
(100 mg x 2)+(15 mg x 8)=320 mg
320 mg/2=160 mg sustained release morphine every 12 hours New rescue dose of morphine is estimated as 10% of the new total daily sustained release dose:
320 mg x 0.10~30 mg of immediate release morphine
Answer case 2: Calculate the total amount of oral opioid taken per 24 hours:
(150 mg x 2)+(150 mg)=450 mg/day
Use the "Dosing and conversion chart for opioid analgesics" to calculate the equivalent total
daily parenteral dose. Divide that amount by 24 to derive the hourly drip rate.
According to the "Dosing and conversion chart for opioid analgesics," the conversion ratio of
oral to parenteral morphine is 3:1.
450 mg/3=150 mg
150 mg/24 hours=6.25 mg/hour To determine the parenteral rescue dose, calculate 10% of the daily parenteral opioid dose:
150 mg x 0.10=15 mg The peak effect of intravenous morphine is reached in approximately 30 minutes. Provided there
are no concerning side effects, the rescue dose can be given every 30 minutes until the pain is
adequately controlled.
Answer case 3:
Patients can develop intolerable side effects to an individual opioid. In most cases, another
opioid will not cause side effects to the same extent. To safely change opioids, you must
prescribe the correct dose of the new agent. The "Dosing and conversion chart for opioid
analgesics" will help you calculate the equivalent dose of the new opioid. However, you must
allow for incomplete cross tolerance to opioid side effects.
After patients take the same opioid dose for a week or two, they become tolerant of the opioids
sedative and respiratory depressive effects. When another opioid is substituted for the original
opioid, however, patients will not be completely tolerant to the new opioids side effects. That can
lead to over-sedation or confusion, although respiratory depression is unusual except with
methadone. You must carefully calculate the equianalgesic dose of the new opioid and then
reduce that dose by 25%-50%.
Fentanyl is the single exception to this rule. The equianalgesic tables for fentanyl have been
adjusted, so you can use the doses given in the "Morphine to fentanyl equivalents" conversion
tables without further adjustment.
Calculate the total daily dose of oxycodone:
100 mg x 2=200 mg Use the "Dosing and conversion chart for opioid analgesics" to calculate the equivalent oral
hydromorphone dose (the conversion ratio of oxycodone to hydromorphone is 20:7.5, or 2.6:1):
200 mg oxyodone/2.6=77 mg oral hydromorphone (round off to 75 mg) Adjust the total 24-hour oral hydromorphone dose downward by 25%-50%:
75 mg x 2/3=50 mg Divide the total daily dose of hydromorphone into appropriate intermittent doses based on the
"Dosing and conversion chart for opioid analgesics":
50 mg/6 doses per day~8 mg every 4 hours
Answer case 4:
Calculate the total dose of oral sustained release morphine:
100 mg x 2=200 mg/day Determine the equianalgesic dose of transdermal fentanyl by using the "Morphine to fentanyl
equivalents" chart.
For a patient taking 100 mg sustained release morphine every 12 h (200 mg daily) the equivalent
fentanyl patch dose is 100 µg/h. Remember that the "Morphine to fentanyl equivalents" chart has
already been adjusted for side-effect tolerance and presents the actual dose to be given to the
patient.
Answer case 5:
Calculate the total sustained release morphine dose:
150 mg x 2=300 mg per day Calculate the conversion from oral morphine to IV/SQ morphine using the "Dosing and
conversion chart for opioid analgesics." The conversion ratio of oral to parenteral morphine is
3:1:
300 mg sustained release morphine per day/3=100 mg/day parenteral morphine Convert morphine to its equivalent hydromorphone dose using the "Dosing and conversion chart
for opioid analgesics" (the conversion ratio of IV morphine to IV hydromorphone is 10:1.5, or
6.6:1):
100 mg IV morphine/6.6=15 mg IV hydromorphone Adjust the dose for incomplete cross tolerance by reducing by 25%-50%:
2/3 of 15 mg=10 mg IV hydromorphone per day Divide dose by 24 to obtain dose per hour:
10 mg/24 hours~0.4 mg/hour hydromorphone Calculate rescue dose by multiplying total daily dose of hydromorphone by 10%:
10 mg x 0.10=1 mg
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