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&sectionRank

=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