INTRODUCTION

Okay, you’re starting your internship. Many things are going through your head. You are one of TWO TYPES: Either,

You are so afraid of the lack of sleep that you’ve been unable to sleep; you are about to take ACLS and this makes you even more afraid; you haven’t found an apartment yet; you have already noticed that your memory is failing; you have just taken ACLS and are even more afraid than you were before; you are thinking of buying a palm–size computer to make up for your memory loss.

or

You have bought notecards and a box of binder rings.

No, both types are NOT wrong; both are RIGHT! This IS terrifying. You WON’T sleep. Your memory IS failing. You DO need binder rings.

All we can do is give you some advice:

1) Remember that you are a young person in the prime of your life.

2) Most of your patients will get better no matter what you do.

3) Wear your pager on buzz.

4) The longer you stay, the longer you stay.

5) Know the contraindications to a rectal exam.

6) Be humble before what you see.

7) Exercise.

8) Try not to dwell on the fact that you are a young person in the prime of your life.

But seriously…This year is a big change for everybody, and change can be difficult. It’s important to know that your residents WANT you to ask questions (it makes them feel they’ve learned something). ANYTIME you don't know something, ASK! There are lots of other people around the hospital who are experts in lots of things, from nurses to lab techs to ward secretaries, and they can save you a lot of time and trouble as well.

Remember, all the housestaff are pulling for you. We know what it’s like; we’ll help you whenever we can.

Survival hints:

· Go see direct floor admits first, as nothing will happen for these patients until you do. Order a STAT chest X-ray and send admit labs STAT.

· Coumadin orders must be rewritten daily, even if the patient is on a stable dose.

· Plan discharges early with the social workers. This will expedite matters greatly.

Organization: Pre-round on your patients before 8 AM. Your resident will round separately with each intern and the NP on the team. Check labs early (back around 9:30-10:00) and write orders and replete blood products as needed. When rounding with your R2, try to only see the sicker patients and round individually or your scut time will be eroded. Try to write notes before attending rounds. Rounds with the attendings begin at 10:30, with sporadic teaching rounds as time permits. All interns should attend 12 noon Medicine conference! Afternoons are for unfinished notes and scut. There is supposed to be a CRI conference three afternoons per week, but this can be attending-dependent.

Survival Hints:

· Chemo usually goes for 4 days. The patients start getting sick on days 4–14.

· Bone Marrow Transplants: Autologous transplants will get their own stem cells. They generally do well, and are in house for 2–3 weeks. Allogeneic transplants get someone else’s stem cells, and will get very sick due to immunosuppression and GvHD (skin, gut, liver). They are in house for >1 month.

· Protocols for dealing with prophylactic antibiotics, transfusions, treating GvHD, or chemotherapy side–effects are posted in the workroom on 11L and are explained in the CRI handbook. Ask your fellow for a copy if you’re interested. Some common orders you may need to know about:

• Routine mouth care

1. Amphotericin mouthwash 10–15 cc swish and swallow TID

2. Salt and Soda rinses TID

3. Chlorhexidine (0.12%) 30 ml swish and spit out TID

• Fever and neutropenia – see section under Infectious Disease

• Common antiemetics– see section under Gastroenterology

· On this service more than others, you are cheap labor for the attendings. You have very little autonomy, and the sooner you get used to it the easier it will be. To break the tedium, insist on teaching from the attendings or the fellow.

· To deal with the many sick patients, get efficient and organized.

• Since the plan for most patients rarely changes from day to day, write notes before attending rounds and fill in the data later.

• Look up labs early (usually they will be back by 10 AM or so) so you can replete blood products early. You can also add on labs that have not been ordered.

• Round with your resident individually so the other intern can be doing work while you round.

• If you’re in a rush, the most important vital signs are Tmax and weight.

· The nurses on this floor are superb and will save your butt.

THE LIVER TRANSPLANT UNIT (LTU)

Survival Hints:

· The LTU Housestaff Orientation Manual is the guide for most questions. Always keep it handy. The LTU Syllabus is also very helpful, if you get the time to read it.

· Efficiency and organization are the keys! Write notes before rounds if possible, and then fill in the data and plan during the day. Schedule tests early in the morning, fill out TPN orders in the AM, and anticipate transfers to and from the unit early.

· You are never required to go to the OR.

· Being alone in-house with SICK patients on call can be scary. Never be shy about calling the fellows or curbsiding the senior medicine housestaff (e.g. CCU or ICU resident) with any questions.

· Pediatric patients can be very difficult to manage. They should be shared between all interns. Consult the peds transplant fellow with questions, and use the peds residents for help. Peds bloods should be drawn by the pediatricians and standard orders (e.g. feeding, electrolyte repletion) should be written by the peds service.

CCU–CARDIOLOGY

Survival Hints:

· Rounds consume a large part of the morning, so use the free time (i.e. time that you are not presenting) to schedule tests, write important orders, and consult other services.

· If you are post call, bring the patients’ EKGs to rounds (other days as well if there are changes).

· The CCU has special order sheets for CCU patients that must be filled out for each admission. 10 South (stepdown unit) has special order sheets for 10S patients that must be filled out when transferring patients to 10S. 10 Long (regular floor with telemetry) has a special telemetry sheet that must be filled out for all patients on telemetry. Get used to being a glorified secretary.

· The nurses will greatly appreciate you letting them know early in the day about patients leaving the unit.

· Take advantage of the month to improve your bedside diagnostic skills. Dr. Chatterjee (the God of UC cardiology) is especially good at demonstrating / teaching physical findings.

ADMISSION ORDERS

Always notify the primary MD of admission (courtesy, plus it helps with dispo)!

1. ADMIT to floor, service, intern name and beeper

2. DIAGNOSIS

3. CONDITION (good, fair, stable, guarded, critical, etc.)

4. VITALS (q shift, with pulse ox, per routine etc.)

5. ACTIVITY (bedrest, bed to chair, bathroom privileges, as tolerated, etc.)

6. NURSING (oxygen, strict I&Os, daily weights, telemetry, foley to gravity, etc.)

7. DIET (low sodium, low cholesterol, 1800 cal ADA, renal, etc.)

8. IV (heplock, TKO, or fluid e.g. D51/2NS at 75 cc/hr)

9. ALLERGIES

10. MEDS (therapeutic and prn meds): It is a HUGE help to your fellow interns if you write prn orders for most of these things so that your cross-coverage will not be bothered by the nurses asking for Tylenol...

Pain: Tylenol 650 mg po q4h prn fever, pain, headache (not to exceed 2 gm/d for liver patients)

GI: See section in GI on nausea orders.

Maalox 30 cc po qid prn indigestion (do not use in renal failure). Alternatively, use Maalox ES 20 cc po qid prn

Consider pepcid or famotidine 20 mg po/iv bid or sucralfate 1 gm po qid for ulcer prophylaxis.

Sleep: See section in Night Float on insomnia

Stool: See section in GI on stool orders.

DVT: prophylax with SCD/TED hose or heparin 5000 units SQ bid or enoxaparin 30 mg sq bid if patient bedbound

11. LABS (including admit and qAM labs, but don’t go crazy with qAM labs that don’t need to be followed forever)

12. CALL HO for T<35.5 or >38.5, BP<90/50 >180/100, HR<55 >100, RR>30 <10, O2 sat < 92%, and adjust as necessary.

DEATHS AND DOCUMENTATION

1. When called for a patient’s death, ascertain that the patient is unresponsive to verbal and tactile stimuli, without spontaneous respirations (visually and by auscultation), is pulseless and without heart sounds, and that pupillary reactivity is absent. Furthermore, ensure that you have the correct name by ID bracelet.

2. Notify the primary resident and/or attending MD, unless the death was expected and you were specifically informed that this wasn’t necessary.

3. Request the "death packet" or paperwork from the nursing station/ward clerk; this usually has a set of instructions for physicians, and all you have to do is follow these.

4. Notify the next of kin and determine whether an autopsy is desired. Some people feel that unless the death was expected (i.e. DNR/DNI or comfort care), this should not be done over the phone--some people call the family and inform them that the patient is not doing well and suggest that they come into the hospital, then inform them when they arrive. You will develop your own style. Also determine whether the family would like to view the body prior to transport to the morgue. It may help the family member to inform them that the patient died peacefully, etc., if this was the case. Have the family sign the release of body (even if they have not yet made funeral arrangements; they can call the hospital the following day for the funeral arrangements, but they must sign the form in person), autopsy request/refusal, etc. Additionally, check your packet carefully for the organ donation form; you are required to call the hotline, within one hour in some cases, for all deaths. They will let you know if the patient is suitable for organ donation; you can then discuss the issue with the patient’s family. Do this ASAP so the family can grieve in peace.

5. Call the coroner if the cause of death is unknown, or due to an accident, homicide, suicide, injury, criminal act, hospital procedure, poisoning, inpatient < 24 hours or occupationally related. Furthermore, call the coroner if the person is unidentified, a prisoner, or never regains consciousness in the hospital. There are some other criteria for notifying the coroner (see the death packet); but when in doubt, call them and run the case by the deputy medical examiner and document that this was done in your note (i.e. take down the coroner’s name and badge number).

6. Fill out the PDP and other paperwork. If death is imminent for one of your patients, please leave a completed PDP upon signout as a courtesy to your colleagues--but do NOT leave this at the bedside or nursing station where it could potentially be seen by the pt's family or visitors. The death packet varies by hospital. Ask the nurses for help.

7. All deaths require a "death note" documenting the events immediately leading to the patient’s death (if appropriate), your exam, the conversation with the coroner, and the conversation with the patient’s family (i.e. "Patient’s daughter, xxxx xxxxx was notified and declined autopsy.").

8. All deaths must be dictated regardless of length of stay.

9. The attending must fill out the death certificate (leave this in the packet for them to fill out the next day).

DISCHARGING—PLAN AHEAD!

The four hospitals have slightly different discharge paperwork.

1. Fill out the PDP or patient discharge planning form. This requires a diagnosis (you CANNOT abbreviate – i.e. AIDS is not acceptable), short hospital course summary, tests performed, and discharge medications to be dispensed. Frequently, nurses (and your resident) appreciate you doing this the day before anticipated discharge.

2. At Moffitt and SFGH, medicines written on the PDP are not dispensed. Discharge medicines require a separate form. At Moffitt, your friendly team pharmacist will call the patient’s pharmacy and speed up the discharge meds.

3. Fill out prescriptions (On weekdays, the pharmacist does this at Moffit). Unless filled at the hospital pharmacy, this requires a license except at the VA. Narcotics require triplicates (only attendings and R3’s have these) except at the VA. Do this a day in advance!

4. Ensure follow–up appointments. Usually the ward clerk will help you. At both SFGH and Moffitt, this can be done by writing a specific order (e.g. "Schedule Chest clinic appt. for next available date). This is very useful for routine appointments, but remember that you can usually get earlier appointments if you call yourself.

5. Ensure that the patient has transportation. You may need to enlist the social worker’s help (Moffitt, SFGH). At the VA, this usually means filling out the blue "Report of Contact" form (don’t ask why). Again, at the VA, things can be expedited (would you believe it?) by contacting the Travel Office directly.

6. Write the "Discharge to (home, Laguna Honda, hospice)" order in chart, and D/C IV, telemetry if appropriate--otherwise they will never actually leave!

7. At SFGH and Moffitt you must write a brief discharge note (yes, it counts as your progress note for that day).

PRE–ROUNDING AND NOTES IN THE ICU

Presenting can be attending specific – check with the ICU residents - but is usually done in this UCSF system-based format. You'll get used to it. Usually, the data is first presented (example below); after you present the data, you then run a problem list and plan. Here’s a sample format:

Events:	talk with pt's nurse and the cross-coverage	MEDS
Neuro:	subj and exam=pain, mental status, neuro, tremor	opiates, benzos,
	intubation	other sedatives, anti-
		seizure meds, psych
Resp:	vent settings, resp rate	bronchodilators,
	ABG,CXR	steriods
	exam=rales/rhonchi, symmetry, sputum
CV:	BP, MAP, HR, rhythm, ectopy/activity on	cardiac meds,
	telemetry	pressors
	hemodynamics, EKG, cardiac enzymes
		IV fluids (type/rate)
Renal:	I&Os, CVP	diuretics, dopa
	lytes/BUN/Cr, acid-base status, urine lytes
	exam: edema, anasarca
		TPN or TF
GI:	NGT, stool output,	H2 blocker or PPI
	abd films, LFT's, pancreatic, PT
	abdominal exam
		Vitamin K, heparin,
Heme:	CBC, smear, coags, transfusions, blood in bank	coumadin, DDAVP,
		chemo/immunosupp.
ID:	Tcurrent, Tmax, skin, decubitus ulcers	Abx day #
	WBC, diff, cultures, sensitivities, CXR,UA, lines
	abx levels
		Insulin, thyroid
Endo:	glucose, TFT, adrenal function, osmalarity,	steroids
	ketones, gap
ICU:	DVT and GI prophylaxis
	Lines (condition & day #)

PROCEDURES AND DOCUMENTATION

Procedure notes should be written for any invasive procedure.

1. Consent the patient. Explain the procedure, indications, risks, and benefits, to the patient or surrogate. One may obtain consent from the DPOA/family member via telephone if the patient is not competent to do so, but be sure that the conversation is witnessed. Place the signed consent form on the chart.

2. After the procedure, write a concise procedure note documenting the date, time, indication, consent, prep, type and amount of anesthesia or sedation, details of the procedure, yield, studies sent, and complications or lack thereof.

Example: Diagnostic thoracentesis performed for new pleural effusion. Patient consented, right rear lower thorax prepared with betadine, anesthetized with lidocaine 1% 5 cc. 20 cc straw colored fluid drained. CBC and diff, LDH, albumin sent. Chest x–ray revealed no pneumothorax and patient tolerated procedure well.

3. Remember to fill out an entry in your procedure book or on the web-based E-Value system--you will thank yourself later.

SIGN–OUT CARDS

Writing sign–out cards is more an art than a science. Cross–cover may be called for problems unrelated to your patient’s illness. However, do not weigh your card down in details. This becomes easier with experience. Try not to reuse the same card eternally if everything has been crossed out and scratched through, though it may be tempting. Also, don't forget to pick up your sign-out cards from the night float when you come in each morning--he or she may have important overnight information to share with you.

1. On a 3 x 5 index card, write your name and pager number and your resident’s name and pager number, along with your patient’s name, medical record number, and location. At UC, these cards are pre-printed with spaces for you to fill out.

2. Include a bullet on your patient and other anticipated problems for which cross–cover may be called, so that he or she doesn't have to reinvent the wheel.

3. Include pertinent medications and/or allergies, and current illness status.

4. If there are things to do, write in a box so that cross–cover can check it off when done. Note that it is poor form to sign out tasks that require a major management decision (i.e. don’t say "Check the results of the LP and start appropriate antibiotics"). It is also a burden to your friendly cross-coverage to sign out things that are irrelevant to overnight management (i.e. "check abdominal CT results" if nothing will be done with them overnight).

5. Include: CODE STATUS!, need for culture, and need for I.V. It is often helpful to specify what kind of cultures you would want (i.e. does the patient have known dx of pneumonia and unknown organism and so just needs blood cultures OR is it a patient with a totally unrelated problem like angina who should get pan-cx'd, CXR, UA etc if febrile)

6. It is often helpful to leave some space for cross–cover to write notes in case he/she is called.

7. If you are on the CRI, write the antibiotic(s) to be given if the patient spikes or looks septic (follow CRI protocol).

8. If your patient will likely die overnight, please fill out at least the PDP (see above section "Deaths and Documentation") and leave family contact numbers prominently displayed on the card.

9. If your patient may be transferred out of the ICU/stepdown or has a high likelihood of being "bumped" overnight, write transfer orders and leave them upside down in the chart.

Example:

R1 Ilovemyjob (650)997-help

R2 beenthere 719-yeah

Jones, J #111222333 Rm11L–22

95 y.o. male admitted with COPD exacerbation. Sundowns. On prednisone taper, nebulizers, and written for Haldol qhs. Day 3 ceftizox/erythro. Stable.

If spikes, penicillin allergic.

[ ] Check K+ level on 8 PM labs and replete if necessary

+ Cx DNR, + intubation + IV

GENERAL TIPS--BALANCING EFFICIENCY AND COMPULSIVENESS

--If you have a question about how to do something, if you're worried about a patient, if you start feeling overwhelmed by a situation--don't hesitate to call your resident or backup. He or she is there to help, and it's always better to call early in a deteriorating situation rather than late.

--Order important and lengthy tests (CT scans, ultrasounds, etc) and perform procedures early in the day. This will insure that you will not be waiting around at 6 pm post-call for the results of that head CT or signing it out to your unfortunate cross-cover intern; your resident will also appreciate this. The same goes for important consults.

--Don't forget to check each patient's cultures each day. They will usually call you or the unit clerk with the first positive culture, but it's best to avoid the embarassment of finding out two days later that Pseudomonas also grew out of that blood culture in addition to the Staph epi.

HOW TO BE THE WORLD’S BEST NIGHT FLOAT

GENERAL COMMENTS AND HINTS

1. When you arrive, page the on call interns and get the sign out cards. They will appreciate your help immensely.

2. Nip bad signout in the bud. "If .., then consider" statements can be particularly helpful in focusing your thoughts when called for an acute problem. If something has been unclear to you overnight or you feel some important information was left off the card, it won't get better unless you talk respectfully with your fellow intern the next morning.

3. Make a "scut" list. Refer to this occasionally during your plentiful free time to ensure you have done everything that needs to be done.

4. You may wish to verify that all labs or studies that are signed out to you have been ordered. If not, then you have some time to re–order them.

5. Identify your backup resident before an emergency arises. He or she will be instrumental if things get out of hand.

6. Identify worrisome patients who are unstable or sick. You may wish to round with your backup resident on these patients as well as all unit patients.

7. Try to make yourself available to the regular ward interns from 7 AM to 8 AM for signout.

8. When going to evaluate patients, always double check that you are seeing the right person. It is potentially embarrassing to evaluate Mr. J for abdominal pain when he called you for insomnia and his neighbor perforates his stress ulcer.

9. Remember, you are the night float. You may encounter many fascinating clinical scenarios; however, your main job is to keep everyone alive and stable until the primary team comes in the next morning. Although it may sound crass, don’t get too bogged down with a huge diagnostic workup. Just the basics will do for the most part.

10. Never ask yourself if it can get any worse... it can. But remember, no matter how bad it gets, you're done at 8 am. Night float is a somewhat thankless job--but we all thank you.

COMMON NIGHT FLOAT CALLS

BRADYCARDIA

1. If possible, have atropine and Zoll pads at the bedside before the patient gets bradycardic.

2. Is the patient symptomatic? If so, get patient in Trendelenberg and follow ACLS protocols. Now is a good time to call the resident.

3. Do a quick chart biopsy and look for clues from the patient’s med list and admitting diagnoses. Some common causes of bradycardia appear below:

Meds	ß blockers, Ca blockers, digoxin, amiodarone
Cardiac	Sick sinus, inferior MI, vasovagal, 2nd or 3rd degree heart block, junctional rhythm
Other	Hypothyroidism, increased intracranial pressure (Cushing’s reflex), normal variant

4. In general if the patient is not symptomatic and this is not a significant change from prior days/nights, then an exhaustive workup is unnecessary. However, if your suspicion of cardiac disease is high and this is a change from prior vitals, then an EKG at the minimum may not be a bad idea.

5. Take a focused H&P. Focus on signs and symptoms to distinguish the above (chest pain, prior MI, straining or other maneuvers prior to bradycardia, altered mental status, hypothermia, BP, etc.)

6. If you believe the bradycardia is secondary to meds, be careful discontinuing them. Remember, treat the patient, not the numbers. Stopping rate control meds could cause a rebound tachycardia and precipitate myocardial ischemia (a bad thing).

7. Transcutaneous pacing can be quite uncomfortable. If there's time, short-acting analgesics and/or sedatives may be worthwhile considering.

TACHYCARDIA

1. Is the patient symptomatic or unstable? If so, follow ACLS protocols, call a resident and get a crash cart into the room ASAP.

2. Does this merit investigation, i.e. has the patient been tachycardic all week and has this been noted in the regular team’s progress notes?

3. Obtain an EKG and go to examine the patient.

Tachycardias are classified according to whether they have a regular rate and whether the QRS on EKG is wide or narrow. They are listed below with diagnostic clues and treatments. Generally, you will want to call a resident if you want to treat, since this may involve calling a code.

Narrow QRS, regular rate

1. Sinus tachycardia

A. Multiple causes (pain, anxiety, hypoxia, hypovolemia, myocardial dysfunction, fever, anemia, meds, pericarditis, hyperthyroidism, PE, alcohol withdrawal).

B. Compare EKG with priors, if available. Maximum HR = 220–age.

C. Treat the underlying cause.

2. AV nodal re–entrant tachycardia (AVNRT): more common than AVRT or AT (see below)

A. Caused by existence of dual AV pathways with differing refractory periods, with circuit rhythm set off by PAC.

B. Diagnosis: look for isolated R, pseudo S, or inverted P on EKG. HR typically 180 ± 20.

C. Treat with AV nodal block (carotid sinus massage, adenosine, ß blockers, Ca blockers, digoxin).

3. AV re–entrant tachycardia (AVRT)

A. Caused by presence of accessory pathway causing large circuit rhythm.

B. Diagnosis: short RP interval (i.e. RP < PR interval), retrograde P wave.

C. Treat with AV nodal blocking (see above).

4. Atrial tachycardia (AT)

A. Caused by enhanced automaticity of atrial tissue or ectopic atrial pacemaker(s).

B. Diagnosis: long RP interval (i.e. RP > PR). HR typically <250.

C. Treat with Ca blocker.

5. Atrial flutter with regular block

A. Similar to atrial fibrillation. Usually some heart disease present.

B. Diagnosis: flutter waves in inferior leads, ventricular rate some multiple of 300 ± 5. When the HR is about 150, always consider atrial flutter.

C. Treat with cardioversion, AV nodal blocking.

Narrow QRS, irregular rate

1. Atrial fibrillation. See also expanded section in Cardiology.

A. Causes: see expanded section in Cardiology.

B. Diagnosis: relatively straightforward. Look for absence of P waves and flutter waves in all leads.

C. Treatment: see expanded section in Cardiology.

2. Atrial flutter with variable block

A. Often difficult to distinguish from atrial fibrillation.

B. Look in inferior leads for flutter waves at approximately 300 per minute. May increase AV block transiently with adenosine or carotid sinus massage to reveal flutter waves.

C. Treat with AV nodal blocking, cardioversion.

3. Multifocal atrial tachycardia (MAT)

A. Caused by multiple ectopic atrial pacemakers. Usually associated with pulmonary disease. Also seen in hypomagnesemia, hypokalemia.

B. Look for three distinct P wave morphologies in the same lead and three separate PR intervals.

C. Treat underlying dysfunction--verapamil may be useful.

4. Frequent PACs

Wide QRS, regular rate

1. Ventricular tachycardia (VT) versus supraventricular tachycardia (SVT) with aberrancy. Aberrancy refers to either dysfunction of the His–Purkinje system or presence of an accessory pathway.

2. Given the seriousness of VT, in any patient with heart disease with a wide QRS tachycardia you must assume VT until proven otherwise. See ACLS section for treatment.

3. The Brugada criteria (see Cardiology section) is a useful tool to distinguish VT from SVT with aberrancy.

Wide QRS, irregular rate

1. VT versus atrial fibrillation with aberrancy. Actually, any condition causing an irregular rate in the presence of aberrancy will cause this.

2. Generally treated with cardioversion, either electrical or with procainamide.

HYPOTENSION (concept shamelessly stolen from Dan Lerner)

1. Do you believe the BP? Ask the nurse/PCA to repeat the measurement (or repeat it yourself). In fact, get all of the vitals and make sure they're current (never presume they were done just before you were called). Also, make sure the correct sized cuff was used.

2. Is it any different from prior values? If the patient usually lives around 80/40, then the acuity is decreased somewhat.

3. Is the patient symptomatic? You determine this by looking for evidence of shock (i.e. inadequate tissue perfusion), tachycardia, tachypnea, pre-renal oliguria, altered mental status, etc. If shock is present, then evaluation should proceed sooner rather than later. You should strongly consider calling a resident and preparing for ACLS.

4. Hypotension can only result from low cardiac output or low systemic vascular resistance. Your differential diagnosis is extensive but can be generally thought of in the following categories:

A. Low cardiac output

• Cardiac (MI, valvular disease, cardiomyopathy, arrhythmia)

• Obstruction (tamponade, tension pneumothorax, massive PE)

• Hypovolemia (e.g. bleeding, diuresis, burns, GI losses, third spacing, pancreatitis)

B. Low vascular resistance

• Meds, e.g. vasodilators, morphine, demerol

• Infection, i.e. sepsis

• Anaphylaxis, Neurogenic shock

• Autonomic dysfunction, e.g. in diabetics, spinal cord injury

• Endocrine (thyroid or adrenal insufficiency)

5. Take a focused H&P and a chart biopsy to rule out the above diagnoses. In particular, don’t forget:

MI	prior heart disease, chest pain, ischemia on EKG
Tamponade	pulsus paradoxus, distant heart sounds, JVD, electrical alternans on EKG
Pneumothorax	unequal breath sounds, tracheal deviation away from side of pneumo, JVD
PE	dyspnea, JVD, hypoxia, RV heave, loud P2
Anaphylaxis	flushed skin, urticaria, stridor, wheezing
Bleeding	think of bleeding into retroperitoneum, abdomen, pancreas, thigh, GI tract

6. If patient has shock, act quickly. Some basic steps:

• Treatment is aimed at the underlying cause, but almost all cases call for fluid resuscitation. If suspicion of CHF is low, then pour in the fluids.

• Start O2, put patient in Trendelenberg, draw basic labs (CBC, lytes, BUN, creat, glu, LFT, blood cultures), get EKG, CXR, ABG.

• Consider Foley to measure urine output.

• Consider invasive monitoring (CVP or PA line, arterial line).

7. Other specific notes:

• For tamponade, you must call the CCU fellow to perform an echo and pericardiocentesis.

• For pneumothorax, don’t wait for a CXR. Shove a 14 or 16 gauge needle into the second intercostal space at the midclavicular line ASAP.

• For anaphylaxis, give epinephrine 0.2-0.5 ml (0.2-0.5 mg) of 1:1000 SC/IM q20 min, Benadryl 50 mg IV, hydrocortisone 250 mg IV. Consider albuterol nebulizers for bronchospasm or intubation for respiratory failure.

• For sepsis, rapid administration of antibiotics and pressors will be crucial.

8. Above all, stay calm. Crashing patients are scary. Don’t try to manage patients in shock by yourself.

HYPERTENSION

High BP seldom warrants acute intervention, especially from a night float. Your only concern should be whether this represents a hypertensive emergency or whether the hypertension reflects a more serious underlying process. Anything else should be managed by the primary team.

1. Do you believe the reading? Take BP yourself if in doubt; use the right size cuff.

2. Do a chart biopsy and note the time course of hypertension. Has it been constant since admission, or has it developed suddenly?

3. Rule out underlying conditions causing hypertension based on a chart biopsy and focused H&P. Treat the underlying condition rather than the BP.

• Alcohol withdrawal (tachycardia, tremor, confusion)

• Drug overdose (cocaine, amphetamine)

• Drug interactions (MAO inhibitors, tricyclics)

• Drug withdrawals (ß blockers, ACE inhibitors, central alpha blockers)

• Increased intracranial pressure (Cushing’s reflex)

• Renal failure, renal artery stenosis

• Eclampsia, pre–eclampsia (is the patient pregnant?)

• Coarctation of the aorta, aortic dissection (unequal BP in arms?)

• Pheochromocytoma (episodic nature; associated with flushing, diaphoresis, tachycardia)

• Endocrine (Cushing’s syndrome, thyrotoxicosis)

4. Hypertensive emergency exists when elevated BP is associated with end–organ damage (brain, eye, heart, kidney). Ask about and examine:

• Brain: headache, confusion, lethargy

• Eye: blurred vision, papilledema, flame hemorrhages

• Heart: chest pain, SOB, S3, S4, EKG strain or ischemic changes

• Kidney: low urine output, edema, hematuria

Hypertensive emergencies require admission to the ICU and reduction of BP over 6-12 hours with IV medications--although you may use nifedipine 10 mg po q30 min as needed to acutely bring down the BP while waiting for the paperwork to go through. Your choices include:

• labetolol 20 mg IV q10 min until BP down

• nitroglycerin 5 mcg/min and titrate up (use when heart disease present; causes headache and ICU stay)

• nitroprusside 0.3 mcg/kg/min and titrate up (requires arterial line BP monitoring and ICU stay)

5. If no underlying condition, is there a hypertensive urgency (BP > 220/120, no end–organ damage)? Remember that in a patient who has "lived at this level" of hypertension for a while, a large acute reduction in BP may change an asymptomatic patient into a symptomatic one (precipitate cerebral/myocardial ischemia). If you decide to intervene, suggestions include:

• nitropaste is easy and can be easily removed (but can cause HA)

• captopril 6.25-25 mg po tid (check K, Cr, allergies before)

• nifedipine 10 mg po tid

• clonidine 0.1 mg po bid

6. Special situation: In patients with an acute CNS process (i.e. during/post-CVA), HTN is usually compensatory and should be permitted as long as the BP is < 220/110.

FEVER

I. Your differential diagnosis is fairly broad.

• Infection (lung, heart, brain, urine, sinuses, prostate, abdomen, skin, lines)

• Inflammation (collagen vascular disease, neoplastic disease)

• Mucositis

• Atelectasis

• Blood product reaction

• Drug fever (beta lactam antibiotics and amphotericin are frequent offenders)

• PE or DVT

II. Determine whether the patient is stable or unstable (i.e. look at other vital signs and examine the patient). If unstable, you may want to call the resident and/or the ICU resident to arrange an ICU transfer.

III. Take a focused H&P. Remember drug allergies! Determine whether additional studies to rule out the above diagnoses are indicated (e.g. CXR, U/A).

IV. Determine whether blood cultures have been drawn within 48 hours. If so, there is generally no need to draw additional cultures. Also, look on your signout card. If they were made correctly, they will indicate whether cultures are needed.

V. If your suspicion of infection is high, determine if antibiotics should be started. On the CRI, there is an antibiotic algorithm to follow and is posted in the charting room across from the nursing station on 11Long. However, it is tricky starting new drugs on patients unless your signout card specifically gives you some choices. Think long and hard; there may be a good reason why the primary team didn’t use cefawonderful on this patient.

HYPOTHERMIA

1. "They’re not dead until they’re warm and dead." Significant depression of vital signs and mental status occur, so do not delay resuscitation if pt appears dead.

2. Risk factors for hypothermia:

• Extremes of age: infants have greater body surface area relative to mass; elderly have lower metabolic rate and poor temperature sensation

• Submersion in cold water: rapid thermal conduction in water

• Alcohol ingestion: vasodilation, impaired shivering and awareness, hypothalamic dysfunction

• Sepsis: 39% of consecutive patients with hypothermia at SFGH were bacteremic

• Endocrine disorders: hypothyroidism, hypopituitarism, hypoadrenalism, diabetes, hypoglycemia

• Head injury: central core temperature dysregulation

• Drug ingestions (especially phenothiazines and barbiturates)

3. Classification:

• Mild (temp 34°–36°)

Initial increase in metabolic rate and shivering

Increased HR, BP, CO, RR

Impaired judgment, mild lethargy, confusion, loss of fine motor coordination

• Moderate (temp 30°–33.9°)

Pupillary dilation, severe lethargy and confusion

Decrease in BP and HR, cessation of cardiovascular activity

Atrial fibrillation and other arrhythmias common

• Severe (temp <30°)

Progressive bradycardia and hypotension, decreased respirations

Muscle rigidity, loss of consciousness, absent DTRs or brainstem reflexes

Cardiac irritability with high risk of VF or asystole.

4. General principles:

• Obtain accurate core temperature. Gold standard is esophageal probe but rectal probe is acceptable. Tympanic temperatures should be noted with suspicion.

• Patients should be on continuous monitoring and telemetry since hypothermic hearts are irritable. Do not handle roughly as patients can develop VF/VT.

• Rapid core rewarming is key. Do not warm the extremities because this will cause peripheral vasodilation and return of cold blood to core. Use warmed IV fluid, warm humidified O2, heat lamps, hot water bottles or packs. Consider peritoneal lavage with warmed fluid.

• Perform secondary survey to check for trauma and to remove wet clothing.

• Patients tend to be dehydrated due to hypothermic diuresis.

• Look for the J wave (Osborne wave) on ECG–second upward wave immediately following the S wave. Seen best in V3 or V4 but classically in II, present in 80% of hypothermic patients, increases in size with more severe hypothermia.

• Severely hypothermic hearts (T <30°) have poor response to cardioactive stimuli, especially those used in ACLS (lidocaine, epi, procainamide, pacer stimulation, defibrillation). Avoid multiple dosing of meds leading to toxic levels. Remember, rewarming is the solution.

LOW URINE OUTPUT

1. Normal urine output is typically at least 0.5 cc/kg/hr. Oliguria is defined as urine output <400 cc/day, and anuria is <100 cc/day.

2. First, do you believe the numbers?

• if patient has a Foley, flush tubing to make sure it is not clogged.

• if patient does not have Foley, ask about urine output. Look for daily weights.

3. Examine the patient and assess volume status. Some places to look especially:

• mucous membranes, skin pallor/dryness, edema, complaints of thirst

• neck veins (to assess CVP), crackles in lungs (pulmonary edema)

• bladder palpable on abdominal exam

• prostate exam

4. Check a post–void residual by inserting Foley after patient voids. If volume >200 cc then leave the Foley in; this indicates significant residual bladder volume indicating urinary retention. Some reasons for urinary retention include prostatic hypertrophy, anticholinergic side–effects of medications (narcotics, Benadryl, anesthetics, etc.).

5. Renal failure is caused by prerenal, renal, and postrenal causes. Many laboratory indices exist to differentiate these (see section under Renal), but if patient is not volume overloaded or obstructed and has no history of CHF, then a fluid challenge is usually appropriate (250–500 cc NS IV bolus). If they respond, however, your job isn’t quite done yet. Do the workup described under the renal section.

6. If patient is in CHF or is volume overloaded, initiate diuresis. Remember, though, that unless the patient is truly volume overloaded, diuresis just for the sake of increasing urine output is pointless--treat the patient, not the numbers.

• patients with working kidneys and overaggressive hydration usually will diurese themselves just by lowering the IV fluid rate.

• if in CHF or with symptoms, use Lasix 20–80 mg IV.

• if in renal failure, may require dialysis. Sometimes people in renal failure can still respond to high dose Lasix while waiting for the renal fellow (160–240 mg IV).

DYSPNEA

I. Differential Dx (5 major categories of disease to consider)

A. Pulmonary

pneumonia – cough, fever

pneumothorax – acute onset, pleuritic CP. Consider in any intubated pt.

PE – often difficult to rule in or out by hx/exam. Consider this early.

aspiration – common problem in patients with decreased LOC.

bronchospasm – can occur in CHF, pneumonia as well as asthma/COPD

upper airway obstruction – often acute onset, stridor/focal wheezing

ARDS – usually in pts hospitalized with another dx (e.g. sepsis)

B. Cardiac

MI/ischemia – dyspnea can be an anginal equivalent

CHF – common in elderly pts on IVF, or due to ischemia

arrhythmia – can cause SOB even without CHF/ischemia

tamponade – consider when pt has signs of isolated R heart failure

C. Metabolic

acidosis – pts become tachypneic to blow off CO2 in compensation

sepsis – dyspnea can be an early, non–specific sign of systemic infection

D. Hematologic

anemia – easy to miss this by history/general exam

methemoglobinemia – rare; consider in pts taking dapsone or certain other meds with cyanosis/low sat, nl PO2

E. Psychiatric

anxiety – common, but a diagnosis of exclusion!

II. Evaluation of the Patient

A. History: you need to know about the acuity of onset of dyspnea, any associated symptoms (cough, chest pain, palpitations, fever), any new events or medications given (including IV fluids!) around the time of onset, as well as the relevant PMH and admitting diagnosis.

B. Physical exam: start with the vital signs. You should ask for these (including a sat) as soon as you hear that the patient is complaining of SOB; this will help you decide how quickly you need to respond (and/or call your resident for help!). A good lung exam for wheezes, rales, stridor, symmetry of breath sounds, as well as a full cardiac exam with attention to JVP, carotids, rate/rhythm, and murmurs or rubs are crucial. Remember that adventitial lung sounds may be absent in someone with severe airflow limitation. Also look at the extremities for edema (unilateral vs. bilateral) and perfusion (cool vs. warm, cap refill, cyanosis). The mental status is important because it gives you an idea of cerebral oxygen delivery; also, if the patient is mentating poorly, intubation for airway protection should be considered.

C. Labs/studies: CXR, ECG, ABG, +/- a CBC. These 4 basic studies will give you a great deal of information, and help you sort out what might be going on with your patient if it’s not clear from the above. Certainly, in any patient you don’t know well, you should almost always get all of these.

III. Initial Management

A. Oxygen: this should be your initial intervention for any patient who is dyspneic. Even CO2 retainers need oxygen, and it takes longer than the few minutes you need to evaluate them for significant respiratory depression to develop. Your goal is a PO2 > 60, or O2 sat > 92%. If nasal cannula isn't doing the trick (max FIO2 is ~40%), try a simple mask (up to 50%), non–rebreather (70%), or high–humidity mask (90%). Remember that the RT is your friend; call early if you’re having any trouble, and they will help with nebs, suction, masks, ABGs, oral/nasal airways.

B. Diuretics: certainly consider Lasix in any patient with history or exam consistent with CHF; other processes associated with increased lung water (pneumonia, ARDS) any also improve temporarily with diuresis, and a single dose of Lasix is unlikely to do any irreversible damage.

C. Beta agonists: patients with wheezing from any etiology can benefit from bronchodilators. Remember that wheezing can occur in many conditions other than asthma (e.g., CHF, pneumonia).

D. Assess potential need for intubation (see Pulmonary section).

E. Once you have the patient stabilized and the results of your initial studies, you can initiate therapy directed at the specific etiology of the patient’s dyspnea.

CHEST PAIN

1. Ask for vital signs on the phone immediately, including O2 sat. If the patient is unstable, go right away to the patient (think about calling your resident); if stable, you can ask the nurse a little about the pain.

2. Take a look at your signout card. Is this worrisome for angina or MI (have low suspicion)? If so, or if the story sounds good (again, have a low threshold), ask the nurses to get an EKG during the time it takes you to arrive or at least bring the EKG machine to the bedside.

3. Upon arriving in patient’s room, look at EKG first (ask for prior EKG from chart) or start obtaining the EKG as you’re asking history.

4. Directed history and physical. This will comprise the bulk of your diagnostic workup. You will need to rule out bad stuff rather than diagnose definitively. The major killers are:

•MI typically "pressure" pain associated with SOB, diaphoresis, radiation to L jaw/arm, N/V, cardiac risk factors present; remember, MI can present atypically, and not only in women and diabetics

•Aortic dissection "tearing" pain, associated with HTN, smoking, radiation to back, unequal pulses

•Pneumothorax COPD, trauma, decreased breath sounds, hyperresonance, deviation of trachea away from side with pneumothorax, hypoxia

•PE dyspnea, hypoxia, A–aO2 gradient, hemoptysis, pleuritic chest pain

Other etiologies that are sometimes overlooked include pericarditis, pneumonia/pleurisy, GERD, PUD, esophageal spasm, candidiasis, herpes zoster, costochondritis (Tietze’s syndrome), anxiety (a diagnosis of exclusion).

5. If angina suspected, start O2 by NC and use sublingual nitroglycerin (NTG 0.4 mg SL q5 min x 3; hold for SBP <100). Remember, just because the chest pain responds to NTG does not automatically rule in angina. If ineffective, try other antianginals including:

• morphine 2-4 mg iv (watch bp and for oversedation)

• metoprolol 5 mg IV q5 min x 3 (avoid in COPD/asthma)

• nitropaste (see sliding scale in Cardiology section)

If patient is not already on aspirin and has no contraindications, have patient chew and swallow ASA 325 mg.

6. If suspecting dissection, transfer to ICU to reduce BP and inotropy with ß–blocker. Arrange for emergent CT scan or echo and call vascular surgery. EKG may show evidence of ischemia in RCA distribution if dissection is proximal.

7. If pneumothorax suspected, get CXR and call surgery for chest tube placement. If tension pneumothorax, don’t wait for the CXR! Shove a big angiocath into the 2nd intercostal space at the midclavicular line (on the side with the pneumo, dummy!).

8. If PE suspected, get ABG to confirm hypoxia. Consider V/Q and anticoagulation.

9. Be sure to obtain post–pain EKG and document event.

COMBATIVE OR CONFUSED PATIENT

1. Does the patient have altered mental status or is he/she upset over something?

2. If there is any question of physical injury, call security. No matter how many years of commando training you have, it is not your responsibility to restrain patients in a safe manner. Also, patients generally tend to calm down when they are confronted by overwhelming numbers of people who are responsive to their needs or anxieties.

3. Try to do as much of an altered mental status workup as you can (see section under Neurology). If you suspect an underlying reason for the agitation (pain, sundowning, hypoxia, medication), then obviously treat the underlying reason.

4. Chemical restraints that are often useful:

• Haldol 1–10 mg IV/IM/PO (a very versatile drug, with minimal respiratory and CNS depression)

• Droperidol 2.5–10 mg IV/IM (if given IM, wait at least 10–15 minutes for its effects. Very effective for the agitated patient and is a housestaff favorite at the Mish)

5. If you feel restraints are needed, there are always forms that need to be completed specifying the type of restraint and the reasons for initiating. They must be renewed every 24 hours. Generally, try to initiate the least restrictive type of restraint; after all, would you want to be tied down? Further, restraints have actually been shown to increase the rate of falls and injuries in delirious patients.

• Posey vests prevent patients from leaving the bed but leave the arms and legs free.

• Four point cloth restraints limit the movement of arms and legs. They are more restrictive than Poseys but may be necessary if patient is pulling out lines, etc.

FALLS

1. Assess patient for any injury. Any focality on exam must be worked up in the appropriate manner (e.g. head CT, plain films, immobilization, etc.). In particular, look for:

• ecchymoses, abrasions, fractures, pain, asymmetry, deformity, decreased range of motion.

• look at head, hands, shoulders, hips, knees, feet.

• do a complete neuro exam including gait, strength, and cerebellar tests.

• mental status testing may be necessary if patient is confused or altered.

2. Try to find out the circumstances of the fall.

• witnessed? By whom?

• loss of consciousness (does patient remember hitting the ground?)

• mechanism (getting out of bed, going to bathroom, standing up, turning around, etc.)

• associated symptoms (premontory aura, incontinence, dizziness, headache, visual symptoms, palpitations, chest pain, dyspnea)

• preceding actions (coughing, urinating, straining, standing suddenly)

• past medical history (diabetes, heart disease, CVA, sensory deficits, Parkinsonism, arthritis, depression, new medications, prior falls)

• check chart for recent platelets and coags to try to determine risk for bleed

3. Broad differential diagnosis, with appropriate workup. Don’t forget the following:

• Neuro: seizures, CVA/TIA (bleed, embolus, ischemia), gait disorder, Parkinson’s, vertigo, dementia, normal pressure hydrocephalus, poor proprioception

• Cardiac: arrhythmia, MI, vasovagal, hypovolemia, orthostasis, valvular dz

• Meds: sedative/hypnotics, antidepressants, vasodilators, alcohol, diuretics (requiring frequent trips to bathroom)

• Musculoskeletal: arthritis, pain, deconditioning, weakness

• Other: anemia, poor eyesight, dim lighting, room change, bed rails left down, wet floor

INSOMNIA ("Doctor, your patient needs a sleeper!")

1. Ask nurse to check patient’s allergies and/or other meds (for potential interactions). Think also about the patient’s underlying medical conditions (i.e. does the patient have renal or hepatic dysfunction that is going to affect the clearance of what’s being given?).

2. Generally start with antihistamine, e.g. diphenhydramine (Benadryl) 25–50 mg or hydroxyzine (Atarax or Vistaril) 50–100 mg po qhs prn insomnia. Watch out for anticholinergic side–effects, especially in older patients (e.g. dry mouth, blurry vision, urinary retention, wackiness).

3. If patient is elderly or tentative mental status, may want to try chloral hydrate 500–1000 mg po qhs prn insomnia. Generally not good for alcoholics or patients with liver disease.

4. Low dose trazodone (Desyrel) is often effective. Sedative doses usually 25–50 mg po qhs prn although some patients may need up to 100–200 mg.

5. If above ineffective, benzodiazepines are often used next. Most commonly, medium half–life benzos are used such as temazepam (Restoril) 15–30 mg or lorazepam (Ativan) 0.5–1 mg po qhs prn insomnia.

6. If above measures do not work, may want to evaluate patient first before giving more powerful sedatives.

ACID/BASE AND ELECTROLYTES

ALGORITHM FOR ACID BASE DISORDERS

1. Establish data base: ABG, chem7, anion gap.

2. Identify the main disorder.

Disorder	pH	pCO2	HCO3
respiratory alkalosis	>7.40	<40
respiratory acidosis	<7.40	>40
metabolic alkalosis	>7.40		>24
metabolic acidosis	<7.40		<24

3. Evaluate compensation using nomogram or formulas (see below). For respiratory disorders, this will determine chronicity. If compensation does not match expected values, there is a mixed acid-base disorder.

4. Determine the anion gap (AG, NL=12). If the AG is 20 or greater, then a metabolic acidosis exists regardless of pH or HCO3.

5. If there is an AG, determine whether this alone accounts for the change in HCO3. Calculate the gap-gap (delta-gap) = patient’s anion gap – 12 (normal anion gap). Add this to the measured HCO3. If the result is >30, then an additional metabolic alkalosis exists. If the result is <23, then an additional non-gap metabolic acidosis exists.

Table from Goldberg M et al, JAMA 223: 269-275, 1973; via The Primer on Kidney Diseases, 2nd ed.

COMPENSATION FORMULAS

Metabolic acidosis: pCO2 decreases 1.0-1.3 for each mmol/L change in HCO3, or

pCO2 = last two digits of pH

Metabolic alkalosis: pCO2 increases 0.6-0.7 for each mmol/L change in HCO3

Respiratory acidosis: acute: HCO3 increases 1.0 for every 10mmHg change in pCO2

chronic: HCO3 increases 3-3.5 for every 10mmHg change in pCO2

Respiratory alkalosis: acute: HCO3 decreases 2.0 for every 10mmHg change in pCO2

chronic: HCO3 decreases 4-5 for every 10mmHg change in pCO2

Differential diagnosis for each disorder:

I. Respiratory alkalosis: CNS disorders, hypoxia, pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), anxiety, drugs (ASA, theo), liver failure, sepsis, recovery phase of met acidosis

II. Respiratory acidosis: respiratory center inhibition (opiates, myxedema, O2 in CO2 retainer), neuromuscular disorder (Guillain–Barré, myasthenia gravis, botulism, hypokalemia), chest wall disorder, airway obstruction, acute and chronic lung disease

III. Metabolic alkalosis

A. Chloride–responsive (urine Cl– <10): vomiting, NG drainage, diuretics, post–hypercapneic, cystic fibrosis, villous adenoma, congenital chloride diarrhea

B. Chloride–resistant (urine Cl– >20): primary aldosteronism, secondary aldosteronism (CHF, cirrhosis & ascites, Cushing’s, Bartter’s), congenital adrenal hyperplasia, Liddle’s, licorice

C. Miscellaneous: poorly resorbed anion (PCN, carbenicillin), refeeding alkalosis, administration of alkali (e.g. antacids, overshoot from Rx of acidosis, massive transfusions with citrate anticoagulant, milk alkali)

IV. Metabolic acidosis (gap) - there is an unmeasured anion:

M ethanol

U remia

D iabetic ketoacidosis/starvation or EtOH ketoacidosis

P araldehyde

I NH, iron toxicity

L actic acidosis

E thylene glycol

Rhabdomyolysis

S alicylates

Anion Gap notes:

• Adjust for hypoalbuminemia: the AG NL range (12 +/- 2) decreases (see "Formulas")

• A modest increase in AG is often seen with volume contraction metabolic alkalosis.

• If an AG is present, calculate the osmolar gap to narrow the DDx to methanol, ethylene glycol, isopropyl alcohol, and ethanol.

• DDx of low AG: hypoalbuminemia, halide (Br-, I-) intoxication, severe hyperlipidemia, multiple myeloma (via hyperparaproteinemia).

V. Metabolic acidosis (nongap)

Clinically, the major distinction is between renal and extrarenal (usually GI) causes. To differentiate, calculate the urine anion gap (UAG) = UNa + UK – UCl. A negative UAG (more Cl than Na + K) implies the kidney is appropriately compensating for acidosis by secreting NH4+ (the unmeasured cation), further implying a nonrenal cause. A high UAG implies urinary loss of unmeasured anion (a primary renal acidosis, or RTA).

A. Nonrenal causes of nongap metabolic acidosis:

• Bicarb wasting:

--GI: diarrhea, ileus, fistula, villous adenoma

--urinary tract diversions: ureterosigmoidostomy, ileal conduit

• Administration of chloride-containing acid: NH4Cl, HCl, TPN, cholestyramine

• posthypercapnia (transient)

B. Renal causes…

RENAL TUBULAR ACIDOSIS

	Type I	Type II	Type IV
Location	Distal	Proximal	Distal
Defect	H+ secretion	HCO3 resorption	Inadequate aldo
Urine pH	>6.0	Variable	<5.5
Urine K+	Very low	Low	High
HCO3	Very low	Moderately low	Usually >17

Type I RTA: drugs (ampho, Li), chronic pyelonephritis, obstructive uropathy, nephrocalcinosis, autoimmune (SLE, Sjogren’s, thyroiditis, cryoglobulinemia, chronic active hepatitis, PBC), amyloidosis, myeloma

Type II RTA: primary (hereditary), myeloma, amyloidosis, Sjogren’s, PNH, acetazolamide, hyperglobulinemia, heavy metals (Pb, Cd, Hg, Cu, others)

Type IV RTA: inadequate aldo activity

• Low aldo levels with normal/increased renin levels: Addison’s dz, isolated decreased aldo synthesis a/w heparin or LMWH, ACEI, ARB, CSA, critically ill patients

• Low aldo levels with low renin levels: DM (most common), NSAIDs, HIV

• Aldo antagonists: aldactone, TMP, pentamidine, amiloride

• Miscellaneous: obstructive uropathy, sickle cell disease, amyloidosis, AIN

ELECTROLYTES

Except for hypo/hypernatremia (which are usually water problems), electrolyte abnormalities can be thought of as too much/too little in, too much/too little out, or intra-corporeal shifts.

HYPONATREMIA

Definition: A water disorder due to excess water retention in relation to solute. Start by verifying serum osmolality, then address volume status:

I. Iso-osmotic hyponatremia (pseudohyponatremia, Sosm 280-295): lab artifact due to hyperproteinemia or hyperlipidemia - rare to nonexistent with modern assays.

II. Hyperosmotic hyponatremia (Sosm >295): due to hyperglycemia (no osmolar gap) or IV infusions (mannitol, glycine - a/w osmolar gap)

III. Hypo-osmotic hyponatremia ("true" hyponatremia, Sosm < 280): except for polydipsia, these disorders are characterized by high ADH levels and high urine osms (verify urine osm > serum osm). First assess volume status:

A. Hypovolemic: "appropriate" ADH secretion in an effort to maintain intravascular volume.

1. Renal sodium/volume losses (UrNa>20): diuretics, salt-wasting nephropathy, hypoaldosteronism

2. Extrarenal sodium/volume losses (UrNa<10): GI (emesis, diarrhea), skin (burns), hemorrhage, surgical drains. Also remote diuretic use.

B. Hypervolemic: third-spacing with functional intraarterial volume depletion. DDx: cirrhosis, CHF, low-albumin states (nephrotic syndrome)

C. Euvolemic: preserved sodium/volume regulation.

1. Rule out hypothyroidism with TSH

2. Rule out adrenal insufficiency with cortisol or cortrosyn stim test

3. Rule out psychogenic polydipsia and beer potomania with simultaneous urine and serum osms. (These are low ADH states with low urine osms.)

4. SIADH is a Dx of exclusion, usually with UrNa > 20 and low serum uric acid. DDx:

- pulmonary: PNA, abscess, TB, aspergillosis, asthma, CF, CA

- CNS: post-op pain, infxn, abscess, tumor, CVA, DT’s, trauma, Guillain-Barre, subdural

- neoplastic: bronchogenic, mesothelioma, pancreatic, sarcoma, bladder, prostate, GI, lymphoma

- drugs: chlorpropamide, dDAVP, oxytocin, psychotropics, carbamazepime, TCA’s, opiates, vincristine, cytoxan, colchicine, NSAIDs

5. Reset osmostat (rare)

Treatment:

• Hypovolemic: replete volume with NS until hemodynamically stable. Then calculate sodium deficit and replace half of that deficit with NS (154 mEq Na/L) over the first 12-24 hours (max 1-2 mEq/hr, if asymptomatic 0.5 mEq/hr).

Na deficit (mEq) = pt mass (kg) * (0.6 L/kg for men, 0.5 L/kg for women) * (140-Na)

140

• Hypervolemic/euvolemic: fluid restrict to 1.0-1.5L/24hr.

• If symptomatic (Sz, AMS), replace with 3% NaCl (513mEq/L) at 1-2 mEq/L/hr until Na=120 or Sx resolve:

3% NaCl gtt rate (mL/hr) = pt mass (kg) * (0.6 or 0.5 L/kg) * (1 to 2 mEq/L/hr)

0.513mEq/mL

• Correction too fast may result in central pontine myelinolysis (flaccid paralysis, dysarthria, and dysphagia)

• Demeclocycline is rarely indicated

HYPERNATREMIA

May result from excess water loss (common) or Na gain (rare). Requires insufficient water intake (e.g. altered mental status or sedation) to be sustained.

I. Diagnosis: assess volume status, urine volume, urine osm, and urine Na.

A. Excess Na gain (hypervolemic, high UOP, Uosm>500, UNa>100): usually occurs in pts with osmotic water diuresis (e.g. DKA) replaced with NS. May also occur with hypertonic NaCl or NaHCO3 infusions, dialysis with hypertonic dialysate, or (rarely) NaCl tabs.

B. Extrarenal water losses (hypovolemic, UOP<500mL/24h, Uosm>500, UNa<10): GI (emesis, diarrhea) or insensible losses (skin, exercise, heat exposure, burns, mechanical ventilation).

C. Renal water losses (hypovolemic, UOP>1L/24h, Uosm>500): diuretics or osmotic diuresis. Osmotic diuresis defined by urine solute excretion rate (urine volume * urine osms) > 900 mosm/24h.

D. Diabetes insipidus (euvolemic, UOP>>>1L/24h, Uosm<300): verify Uosm<300 during water restriction, then differentiate causes of DI with dDAVP trial (10mcg intranasally):

1. Central DI (Uosm increase with dDAVP): CNS trauma, tumors (primary hypothalamic, metastatic, leukemia, lymphoma), aneurysms, CVA, Sheehan’s, infections (basilar or other meningitis, encephalitis, TB, syphilis), granulomatous dz (sarcoid, histiocytosis), autoimmune

2. Nephrogenic DI (no change in Uosm): drugs (lithium, demeclocycline, propoxyphene, methoxyflurane, ampho), hypercalcemia, hypokalemia, obstructive uropathy, chronic tubulointerstitial renal dz (not technically DI)

II. Treatment:

• reduce water losses and (if due to Na gain) excess IVF

• correct volume depletion with NS until hemodynamically stable

• calculate free water deficit:

FW deficit (L) = pt mass (kg) * (0.6 L/kg for men or 0.5 for women) * (Na-140)

140

• replace half of deficit over 24 hours with either H2O po/pNGT or 1/2NS IV. (Note that only 1/2 of 1/2NS volume contributes to "free water.") Replace remainder of deficit over 48-72 hours. (Too fast may cause cerebral edema.)

• CDI: intranasal dDAVP

• NDI: eliminate drug causes, low Na diet, thiazide diuretics

HYPOKALEMIA

I. Causes:

A. Inadequate intake

B. Excessive loss

1. GI losses: vomiting, diarrhea, laxative abuse, fistula

2. Renal losses: drugs (diuretics, gentamicin, amphotericin, carbenicillin), excess mineralocorticoids (Cushing’s, hyperaldosteronism, hyperreninemia), congenital (Bartter, Liddle), RTA types I and II, hyperglycemia (excessive diuresis)

C. Cellular shifts: metabolic alkalosis, acute hyperventilation, drugs (insulin)

II. Diagnosis: There are several ways to approach diagnosing the specific cause of hypokalemia, if you care. All methods are best before supplementation, are poor in chronic renal failure, and are fraught with technicalities. Normal values vary with dietary intake.

	Urine K	FEK (like FENa)	TTKG
Renal	>20	>10%	>8
Extrarenal	<20	<10%	<6

III. EKG: T wave flattening ± inversion, U waves, arrhythmias (e.g. PSVT, Afib), and ST changes, pseudo–prolonged QT.

IV. Treatment:

Check creatinine first - supplement patients with renal insufficiency cautiously.

Replete Magnesium

Supplement to keep near 4.0 following the scale below

Serum potassium rises roughly 0.1 for every 10 meq of supplementation.

po K causes GI upset - give max 40 mEq at a time

IV K should be given no faster than 10mEq/hr through a peripheral IV or 20mEq/hr through a central line.

In the ICUs, you will save sleep by writing a sliding scale (only when renal function is normal):

Serum K mEq KCl to give PO/IV

3.7-3.8 20

3.5-3.6 40

3.3-3.4 60

3.1-3.2 80

<=3.0 100

HYPERKALEMIA

I. Causes:

A. Spurious: hemolysis during phlebotomy, greatly increased platelets or WBC

B. Excessive intake: ingestion, iatrogenic

C. Insufficient loss: renal failure, type IV RTA, adrenal insufficiency or other hypomineralocorticoid state, drugs (spironolactone, ACE inhibitor, digitalis overdose)

D. Cellular shifts - acidosis, cell death (rhabdomyolysis, burns, tumor lysis), retroperitoneal hemorrhage

II. EKG: tall peaked T waves, PR prolongation followed by loss of P waves, QRS widening

III. Treatment:

A. STAT EKG

B. Verify with a repeat lab draw

C. Immediate Rx (works in minutes): for EKG changes, stabilize myocardium with 1-2 amps Ca gluconate (lasts 30-60 minutes)

D. Temporary Rx (shift K into cells):

1. 2 amps D50 plus 10u regular insulin IV: decreases K by 0.5-1.5 mEq/L and lasts several hours

2. 2 amps NaHCO3: best reserved for non-ESRD patients with severe hyperkalemia and acidosis

3. B2-agonists: effects similar to insulin/D50

E. Long-lasting elimination:

1. Kayexalate 30g po (repeat if no BM) or retention enema

2. NS and lasix

3. Dialysis - note that CVVHD corrects K more slowly than conventional HD

HYPOMAGNESEMIA

I. Causes:

A. Decreased intake or absorption: malnutrition, malabsorption, diarrhea, NG aspiration

B. Increased excretion: hypercalcemia, osmotic diuresis, hyperparathyroidism, drugs (loop diuretics, aminoglycosides, amphotericin, cisplatin, cyclosporine, alcohol, pentamidine)

II. Signs:

• lethargy, confusion, tremor, fasciculations, ataxia, nystagmus, tetany, seizures

• hypokalemia, hypocalcemia

• PR and QT prolongation

III. Treatment: supplement to keep 2.0 or greater except in renal failure patients. Oral preparations differ from one hospital to another. Note that oral preparations cause diarrhea in larger doses.

Hospital	Tablets available	Dose per tablet	Typical dose
Moffitt	Mag complex	300 mg elemental Mg	1–2 tab qd
VA	Mag oxide	420 mg (240 mg elemental Mg)	1–2 tab qd
SFGH	Mag gluconate	500 mg (27 mg elemental Mg)	1–2 tab qd

For parenteral therapy, MgSO4 IV comes in amps, 1 amp = 1 gram (8 mEq). Give each gram over one hour. You may write a sliding scale in the ICUs:

Serum Mg	gm of MgSO4 to give IV
1.8–1.9	1
1.6–1.7	2
1.4–1.5	3
1.2–1.3	4
<1.2	5

HYPERMAGNESEMIA

I. Causes:

A. Insufficient excretion: Renal failure

B. Excess intake: Overaggressive replacement.

II. Signs (rarely present until Mg >4 mEq/l): areflexia, lethargy, weakness, paralysis, respiratory failure, hypotension, bradycardia, heart block, asystole

III. Treatment:

A. Asymptomatic: hold magnesium supplementation

B. Symptomatic: 1 amp Ca gluconate IV over 10 minutes to antagonize Mg. Support ventilation and heart rate if necessary. Definitive therapy requires dialysis if no renal function, or Ca gluconate infusion to promote Mg excretion.

HYPOCALCEMIA

Correct for low albumin (see formula section). Especially if albumin is <2, measure ionized Ca. Note that alkalosis augments Ca binding to albumin, thus decreasimg the amount of ionized (effective) Ca and increasing severity of symptoms at a given level.

I. Causes:

A. Insufficient intake: hypoparathyroidism or pseudohypoparathyroidism (PTH resistance), vitamin D deficiency, renal failure (vit. D deficiency)

B. Excessive secretion: critically ill patients, severe hypomagnesemia hypermagnesemia

C. Intra-corporeal shifts: acute pancreatitis, rhabdomyolysis, tumor lysis syndrome

D. Meds: For instance, foscarnet (and others)

II. Signs: paresthesias, tetany (especially carpopedal spasm), lethargy, confusion, seizures, Trousseau’s sign, Chvostek’s sign, QT prolongation

III. Treatment:

• po: CaCO3 500-1000mg tid between meals (to maximize absorption) - also consider vitamin D

• IV: max 10mEq/hr. CaCl2 has 14mEq/amp, Ca gluconate only 4.5mEq/amp (one amp = one gram). Give 5-15mEq at a time, more if necessary.

• Correct hypomagnesemia

HYPERCALCEMIA

I. Causes: 90% due to hyperparathyroidism or malignancy. Initial w/u may include Ca, Phos, albumin, ionized Ca, alkaline phosphatase, and PTH. Also consider vit D levels, PTHrP, SPEP, TSH, and imaging (CXR, bone scan, bone survey, CT scans, ...). All etiologies are due to a combination of increased bone resorption, increased GI absorption, and decreased renal excretion:

1. Primary hyperparathyroidism: 85% adenoma, 15% hyperplasia, 1% carcinoma

2. Malignancy:

• PTHrP-mediated (humoral): especially with renal tumors and squamous cell carcinomas: lung, head/neck, esophageal, bladder, ovarian

• local osteolytic destruction (mediated by local cytokines): multiple myeloma, lymphoma, leukemia, some solid solid tumor mets (e.g. breast cancer)

3. Granulomatous disease: sarcoidosis, fungal, TB

4. Vitamin D toxicity

5. Milk-alkali syndrome

6. Thiazide diuretics

7. Renal failure: note that ARF usually causes hypocalcemia - beware ARF as a result of hypercalcemia

8. Other endocrine: hyperthyroidism, adrenal insufficiency, VIP-producing tumor

9. Immobilization

10. Familial hypocalciuric hypercalcemia

11. Lithium

12. Estrogens and anti-estrogens

13. Aluminum intoxication

II. Signs: "Stones, moans, groans, with psychic overtones"

•Renal: polyuria, nephrolithiasis, renal failure, ectopic calcification

•GI: anorexia, nausea, vomiting, constipation

•Neuro: weakness, fatigue, confusion, stupor, coma

•EKG: shortened QT

III. Treatment:

A. IVF volume resuscitation and saline diuresis: at least 3-4L in first 24 hours

B. IV lasix after volume repleted (urine Na and Cl > 90). Keep I =O.

C. Calcitonin salmon: 4-8u SQ/IM q6-12hr. Works within hours, but weak effect (1-3 mg/dL) that wanes after 2-3 days.

D. Pamidronate: 90mg IV over 24hr (for Ca>13.5). Treatment of choice in hypercalcemia of malignancy. Side effects include decreased Mg and phos and low-grade temperature

E. Glucocorticoids: hydrocortisone 200-300mg IV qd for 3-5 days, or prednisone 20-50mg po bid with taper. Most effective for myeloma, hematologic malignancies, sarcoid, and vitamin D intoxication

F. Experimental: plicamycin (mithramycin), gallium nitrate.

HYPOPHOSPHATEMIA

I. Causes:

A. Decreased intake: vitamin D deficiency, malabsorption, vomiting, steatorrhea, phosphate binders, alcohol abuse/withdrawal

B. Shifts from serum into cells: respiratory alkalosis, sepsis, hepatic coma, salicylate poisoning, gout, severe burns, recovery from hypothermia, refeeding, hyperalimentation, recovery of DKA, effects of insulin/glucagon/androgens

C. Increased urinary secretion: hyperparathyroidism, renal tubular defect, (aldosteronism, SIADH, steroids, diuretics), hypomagnesemia

II. Signs (generally seen only with total body depletion and serum PO4 <1 mg/dl): weakness, rhabdomyolysis, respiratory compromise/failure, CHF, paresthesias, dysarthria, confusion, stupor, seizures, coma, hemolysis, platelet dysfunction, metabolic acidosis

III. Therapy:

• po: 1-2 tabs tid-qid:

--Neutraphos (250mg tab = 75mL solution) contains 8mmol phos + 7mEq Na + 7mEq K

--K-Phos (250mg tab = 75mL solution) contains 8mmol phos + 14mEq K

• IV: 15mmol Kphos (contains 22mEq K) or NaPhos (22mEq Na) over 2-6 hours

• Follow Ca, K, and Mg levels

HYPERPHOSPHATEMIA

I. Causes:

A. Increased intake: overzealous PO4 replacement

B. Decreased excretion: renal failure

C. Cellular shifts: tumor lysis, hypoparathyroidism/pseudohypoparathyroidism, acidosis

II. Signs: hypocalcemia, ectopic calcifications if Ca x PO4 product >70

III. Treatment: bind Phos in the gut (give meds with meals to maximize binding). Avoid Ca-containing compounds if serum Ca is also high.

• CaCO3 (OsCal, tums): 500-1000mg (or more) po tid with meals

• Ca acetate (PhosLo): one-two tabs (667mg each) po tid with meals

• Aluminum hydroxide (Amphogel): 600mg po tid with meals. Most effective, but expensive, and can cause bone and CNS toxicity with long-term use (>1-3 weeks)

`100

Phosphorous is poorly dialyzed.

CARDIOLOGY

RULE OUT MYOCARDIAL INFARCTION (without EKG changes)

1. Admit to telemetry (call HO for >6 PVC/min, Afib, Vfib, >3 beat run of VT, R on T).

2. Bed rest until ruled out (yes, this means bedpan, although bedside commode OK for soft rule out).
3. NPO except meds if possible cath or functional study in am (most patients).
4. Oxygen via NC at 2 L/min.
5. EKG on admission and qAM; CXR on admission (portable OK).
6. Labs: troponin I q12h x 2 or alternatively CK&MB q8 x 3, basic labs including coags, cholesterol panel if no previous workup, and HgA1C if DM.
7. Enteric coated ASA 325 mg po qd. Have patient chew and swallow first dose for rapid absorption.
8. NTP q6h to chest wall according to sliding scale, after 24 hrs wipe off q night 12am-6am.

SBP	Action
< 100	wipe off
100–120	1"
121–140	2"
>140	3"

9. Beta–blocker if no contraindications as these have been shown in many randomized trials to reduce mortality. (Typically, metoprolol which can be given as a starting dose of 25mg po bid. Alternatively, a trial of 5mg IV q5min x3 can be given initially. If this IV dose is tolerated you can usually start 25mg po bid, but be sure to write hold parameters.)
10. Colace 250 mg po bid – hold for loose stools
11. Chest Pain Protocol: VS, EKG, NTG 0.4 mg SL q5 minutes x 3, call HO. When seeing patient for persistent chest pain, can give morphine in 1–2 mg boluses. It’s always a good idea to call a resident.

ACUTE CORONARY SYNDROMES – This term encompasses the clinical entities of unstable angina (negative enzymes), non-Q-wave MI (non-ST-elevation, positive enzymes), and acute MI (ST elevation, positive enzymes). The following guidelines reflect the necessary considerations for antiplatelet, antithrombotic, and reperfusion therapies in these patients. Of course, these are only guidelines. Because the exact pathophysiologic process is often unclear, especially at presentation, each patient must be evaluated individually to determine the most appropriate management and the need for CCU level care. Remember, the cards fellow will know the patients and will be around most of the time to help with any difficult decisions regarding thrombolysis, risk stratification, etc. (See Theroux et al., NEJM 1998, 28: 1488-1497 and Yeghiazarians et al., NEJM 2000, 342:2, p101).

UNSTABLE ANGINA/ NQWMI

(Most patients with non-ST-elevation EKG changes)

1. Rule out MI as above, including aspirin, beta-blockers, and nitrates (if need for nitro gtt for persistent chest pain, see below under Acute MI).
2. Antithrombotic therapy with Enoxaparin (Lovenox) 1mg/kg SQ BID vs. unfractionated heparin drip (see anticoagulation section). Remember to ask pt about bleeding risks. Note: Enoxaparin cannot be used in renal failure (Cr clearance <30) or in pts weighing >100 kg.
3. Glycoprotein IIb/IIIa inhibitor- Tirofiban (must be given with either Heparin or Enoxaparin) start 0.4 mcg/kg/min x 30 min, then decrease to 0.1 mcg/kg/min.

• PRISM-PLUS indications for using Tirofiban and Heparin are as follows (must have ‘a’ plus‘b’ and/or ‘c’):

1. Prolonged anginal pain or repetitive episodes of angina at rest or during minimal exercise in the previous 12 hours.
2. ST-T changes including ST elevation or depression of 0.1mV or more in any lead, T-wave inversion of 0.3mV or more in 3 or more limb leads or 4 or more precordial leads excluding V1, or psuedonormalization of 0.1mV or more.
3. An elevation of CK-MB (we use troponin-I).

• PRISM-PLUS exclusion criteria were the following:

ST-segment elevation lasting more than 20 minutes, thrombolysis in the previous 48 hours, PTCA within the previous 6 months, CABG within the previous month, angina caused by identifiable factors, a h/o platelet disorder or thrombocytopenia, active bleeding or a high risk of bleeding, stroke within the previous year, platelet count below 150,000 and serum creatinine >2.5.

1. Clopidogrel (Plavix) if planned stent: 150 mg PO x 1, then 75 mg qd.
2. Consider ACE-I if blood pressure still elevated.
3. Risk stratification ASAP: functional study vs. cath.

ACUTE MYOCARDIAL INFARCTION

1. Admit to CCU, rule out MI as above (make sure aspirin has already been given).
2. PTCA preferable to thrombolysis when available (GUSTO trial).
3. Consider Thrombolytics- Inclusion Criteria (according to AHA Executive Summary on MI, 1996). Indications include ‘a’ or ‘b’ w/ time to therapy 12 hours or less (ideally < 6hours):

1. ST elevation (greater than 0.1 mV, two or more contiguous leads)
2. Bundle branch block (obscuring ST-segment analysis) and history suggesting acute MI.

4. If considering thrombolytic therapy, ask about contraindications:

Relative Uncontrolled hypertension (BP >180/110)

Prolonged CPR

Remote history of CVA or GI bleed

Pregnancy

Hemorrhagic retinopathy

Cardiogenic shock (consider PTCA instead)

Absolute Suspected dissecting aortic aneurysm

Active bleeding

Known intracranial tumor, CVA within 6 months, or head trauma within 1 month

Major surgery/GI bleed/trauma within 6 weeks

Bleeding diathesis or liver disease with portal HTN

5. Heparin gtt (see anticoagulation section).

6. Nitroglycerin gtt for persistent chest pain: start at 5 mcg/kg/min IV and titrate to pain, not to exceed 200 mcg/kg/min. After 24 hrs, give 6h holiday qd to prevent tolerance. Hold for SBP<90-100.

7. Beta-blocker as above (if no contraindications); titrate dose to goal HR 55-70 if BP allows, with hold parameters.

8. ACE-I: usually start with Captopril 6.25 mg PO tid and increase dose as BP allows; should be initiated within 24 hrs of MI. Don't forget those hold parameters.

9. Consider morphine for pain (1-2 mg IV boluses PRN).

COCAINE CHEST PAIN

(If you have never seen this before, you will likely encounter it here during your residency. Cocaine can and does (not infrequently) cause real myocardial ischemia and infarction in young healthy people. Always remember to take a detailed cocaine/crack history in patients with chest pain, especially at SFGH.)

1. Pathophysiology: prevention of NE and DA reuptake leading to alpha-1 activation; increased myocardial demand (increased HR and afterload); coronary and peripheral vasoconstriction; promotes in situ thrombus formation; can lead to premature atherosclerosis and LVH.
2. History: chest pain usually 30m to 4hrs after use, but can occur up to 24hrs after use or even longer with withdrawal.
3. ECG: criteria for lysis often present; abnormal in >50% of patients; many with J point elevation or LVH with repolarization abnormality; may be normal in many patients with MI.
4. Most patients should be admitted; 6% of pts. with cocaine-associated chest pain have MI.
5. Management: (NO randomized controlled trials) benzodiazepines, aspirin, oxygen, NTG for persistent pain, calcium channel blocker vs B-blocker plus phentolamine, thrombolysis vs angioplasty. The conventional wisdom is that beta-blockers should be avoided in cocaine chest pain, since they can lead to unopposed alpha-stimulation and thus, theoretically, worsening of the underlying pathophysiology.

CONGESTIVE HEART FAILURE

1. Admit to floor if pressor support not needed (i.e. patient not in shock).

2. Determine whether patient is in left–sided or right–sided failure or both.

Left–sided CHF	Right–sided CHF
Rales	Elevated JVP
Tachypnea	Hepatojugular reflux
Left–sided S3	Ascites
	Peripheral edema
	Congestive hepatopathy

3. Look in the old records for a prior echo or cath describing prior ejection fraction and presence of systolic versus diastolic dysfunction.

4. If CHF exacerbation, determine possible reason(s) based on H&P.

• Medical noncompliance

• Dietary indiscretion

• Ischemia

• Arrhythmia

• Cardiovascular stress (infection, anemia, pregnancy, hyperthyroidism)

• PE

• Worsening valvular disease (e.g. aortic stenosis)

5. For systolic dysfunction, treatment may include:

A. ACE inhibitor–the mainstay of CHF treatment.

• Start with captopril 6.25 mg po tid and increase dose as BP allows. If one dose is well-tolerated, you can go ahead and increase the next dose; it's not necessary to wait 24h.

• Once stable, switch to equivalent dose of once–daily ACE inhibitor. Consult your local friendly pharmacist for hints, or use a rough conversion based on the following table:

Captopril	Benazepril/ Enalapril Fosinopril/ Lisinopril
6.25 mg po tid	5 mg po qd
12.5 mg po tid	10 mg po qd
25 mg po tid	20 mg po qd
50 mg po tid	40 mg po qd

• Hydralazine plus nitrates can be used in pts that cannot tolerate ACE-I’s.

B. Diuretic–used to reduce symptoms of pulmonary edema.

• The workhorse is furosemide; doses can vary from 20–400 mg IV q6hr.

• When giving furosemide, watch BP carefully.

• To convert IV to po, double the dose (i.e. 20 IV is equivalent to 40 po).

• If furosemide is ineffective, try adding metolazone 5–20 mg po qd (must give 30 min before Lasix dose).

• Watch serum electrolytes (especially K) and replace as necessary.

C. Other important considerations:

• All patients should be on a low salt diet.

• Oxygen by NC or face mask to relieve dyspnea (see Pulmonary section).

• Nitrates as BP tolerates to reduce preload and as antianginal (e.g. start with Isordil 10 mg po tid).

• Morphine 0.5–2 mg IV q4hr to relieve dyspnea.

• Consider digoxin loading if patient not responding well to initial therapy. (see "Atrial Fibrillation" section for instructions on dig loading)

• May wish to rule out MI for CHF exacerbation in which ischemic heart disease is a possibility (almost always the case).

• Chronic therapy also includes both beta-blockers and spironolactone (see below), but these are not usually started in the setting of an acute exacerbation. Poorly compensated heart failure is a contraindication to initiation of beta-blockers.

D. If poorly compensated, may need to be in CCU with dopamine and dobutamine drips.

E. Aldactone: Dose of 25 mg qd now demonstrated by the RALES trial to provide significant improvements in morbidity and mortality in Class III-IV CHF (NEJM 341, 10: 709-17). Note that all patients were on an ACEI and a loop diuretic, and that exclusion criteria included Cr > 2.5 and K > 5.0. Generally not started in the acute setting.

6. For diastolic dysfunction, diuresis and low–salt diet are still applicable. However, drug therapy is aimed at improving ventricular relaxation and decreasing heart rate.

• Beta blocker, e.g. metoprolol 25 mg po bid or atenolol 25 mg po qd; titrate up as BP tolerates.

• Ca blocker, e.g. diltiazem 30 mg po qid or verapamil 40 mg po tid; titrate up as BP tolerates and change to once daily formulation once steady dose achieved.

HEART MURMURS

1. Aortic stenosis: Systolic murmur heard best in the aortic area; rarely at apex. Crescendo–decrescendo, transmitted to carotids. A2 decreased. Paradoxical splitting of S2; narrow pulse pressure. Pulsus parvus et tardus.

2. Aortic insufficiency: Diastolic blowing murmur heard at left sternal border in 3rd and 4th interspace. Wide pulse pressure. Quincke’s sign (capillary pulsations at fingertips), DeMusset’s sign (bobbing head), Muller’s sign (pulsing uvula), Corrigan’s pulse (water hammer). Pistol shot sounds.

3. Pulmonic stenosis: systolic murmur heard in pulmonic area, transmitted to back and neck. A2 is decreased, P2 is delayed, RVH with parasternal lift.

4. Pulmonic insufficiency: High pitched diastolic murmur; heard in pulmonic area; decrescendo; RVH

5. Mitral stenosis: low rumbling diastolic murmur heard best at apex. Opening snap sometimes present.

6. Mitral insufficiency: loud, holosystolic, high–pitched, heard best at apex and transmitted to axilla. Soft S1.

ATRIAL FIBRILLATION

If symptomatic or unstable, cardiovert (see ACLS).

If relatively stable, control rate, anticoagulate and cardiovert (electrically or w/ ibutilide).

Etiologies: PIRATES (pulmonary disease, ischemia, rheumatic heart disease, atrial myxoma, thyrotoxicosis, ethanol, sepsis)

Agents for rate control (caution if giving ß–blocker and Ca–blocker together; may result in excessive AV nodal blockade)

1. Calcium Channel Blockers:

• contraindications: VT, 2d or 3d degree AV block without pacemaker, severe hypotension, cardiogenic shock, bypass tracts, close administration with IV ß blockers

• Diltiazem: 0.25 mg/kg or 20 mg IV over 2 min. Watch for hypotension!

Rebolus in 15 min prn with 0.35 mg/kg or 25 mg.

Drip 5–15 mg/hr if unable to control rate.

• Verapamil (much cheaper): 0.1 to 0.3 mg/kg (up to 5–10 mg) IV over 2 minutes.

Repeat 5–10 mg IV in 15–30 min if needed

Drip 5 mg/hr; may titrate up to 20 mg/hr

2. ß–blocker: Metoprolol 5 mg IV q5 min x3 (contraindicated in COPD, low EF)

3. Digoxin: load 0.5 mg IV x one, then in 6 hours 0.25 mg IV q6h x 2. Starting standing dose usually 0.125–0.25 mg po or iv qday.

• tends to have slower onset of action than Ca– or ß–blockers

• adjust daily dose in presence of renal failure, amiodarone, etc.

LOADING ANTIARRHYTHMICS / CARDIAC MEDS

Procainamide–usually load 1 g IV over 1 hour (750 mg if elderly, etc.) then start (usually) Procan SR 750 mg qid again checking for (1) QTc prolongation as for quinidine, (2) prolongation of QRS > 50%, or (3) hypotension. Follow levels of procainamide + NAPA (a total level of 10–20 is therapeutic).

Amiodarone–amount varies depending on indication. For VT, po load with 400 mg po tid until total of 12 gm, then 400 mg po bid–qd. For IV load, use 1 gm every 24 hrs. Watch for long QTc, bradycardia, hypotension, and torsades. For SVT, generally start 200–400 mg po qd. If patient on digoxin, halve dig dose. IV loading is usually done on telemetry; PO loading is usually done (if tid/qid) on tele for the first 24-72 hours.

Adenosine-for use in assessing the underlying rhythm and/or breaking an SVT. Typical dose is 6-12mg IV push, but if through a central line use 3-6mg IV push.

Lidocaine- load 1 mg/kg IV, then maintain gtt at 1-4 mg/min

ENDOCARDITIS

(See section under Infectious Diseases– "Shooter with a Fever.")

COMMONLY USED PRESSORS

Name	Receptors affected	Dose	Action(s)
Phenylephrine (Neosynephrine)	Alpha1	10–200 mcg/min	Pure vasoconstrictor; causes ischemia in extremities
Norepinephrine (Levophed)	A1, B1	2–64 mcg/min	Vasoconstriction, positive inotropy; causes arrhythmias
Dopamine	Dopa	1–2 mcg/kg/min	Splanchnic vasodilation ("renal dose dopamine")
	B1	2–10 mcg/kg/min	Positive inotropy; causes arrhythmias
	A1	10–20 mcg/kg/min	Vasoconstriction; causes arrhythmias
Dobutamine	B1, B2	1–20 mcg/kg/min	Positive inotropy and chronotropy; causes hypotension

EKG READING MADE EASY

(This is the thumbnail outline of selected criteria for certain ECG abnormalities.)

Note: height: 0.1 mV = 1 mm

duration: 0.04 s = 1 mm

Rate 60–100 bpm normal

<60 bpm bradycardia

>100 bpm tachycardia

QRS Axis: normal axis is –30° to +90°. <–30° is left axis, >90° is right axis

Differential diagnosis of axis deviations (in order of likelihood)

Right Axis	Left Axis
1. RVH	1. LAFB
2. Lateral or anterolateral MI	2. Inferior MI
3. WPW with left freewall pathway	3. WPW with posteroseptal pathway
4. LPFB	4. COPD or PE

Intervals PR normal .12–.20 seconds

QRS normal <.09 seconds, abnormal >.12 seconds

QTc normal <0.45 (measured QT/square root of R–R interval)

Right atrial abnormality

lead II P>.25 mV

lead V1 P is biphasic and the initial phase is >.15 mV

Left atrial abnormality

lead II P >.12 s with notches separated by at least .04 s

lead V1 P is biphasic and the terminal phase is >.04 ms and >.1 mV

Left ventricular hypertrophy (There are numerous criteria; three useful ones are below. All are sensitive, so fulfillment of one set is sufficient for LVH)

RaVL >11 mm (men), >9 mm (women)

RaVL + SV3 >20 mm (women) and >25 mm (men)

SV1 + (RV5 or RV6) >35 mm

Right ventricular hypertrophy (The following findings suggest RVH; there are several others)

Right axis deviation

R:S ratio > 1 in V1 (in absence of RBBB or posterior MI)

RBBB (Right Bundle Branch Block)

QRS >.12 seconds

Wide S wave in I, V5, V6

Secondary R wave (R’) in right precordial leads with R’ greater than initial R (rsR’ or rSR’).

LBBB (Left Bundle Branch Block)

QRS >.12 s, broad R in I and V6, broad S in V1 and normal axis or

QRS>.12 s, broad R wave in I, broad S in V1, RS in V6, and left axis deviation.

LAFB (Left Anterior Fascicular Block): There are several sets of criteria for LAFB; one useful one is below)

Axis is more negative than –45 degrees

Q in aVL, and time from onset of QRS to peak of R wave is >.05 s.

Also helpful is QI, SIII pattern

LPFB (Left Posterior Fascicular Block)

Axis >100 and QIII, SI pattern

Q Waves

Pathologic Q’s are at least 40 ms and 0.1 mV deep; more specific amplitude criteria are available (See T. Evans’ Cribsheets p21 for screening mantra- ANY,ANY,ANY / 20,30,30 / 30,30 / 30,30 / R40, R50).

BRUGADA CRITERIA TO DISTINGUISH SVT FROM VT

(taken from Brugada et al., Circulation 1991, 83:1649–59)

Reqs: Wide complex tachycardia with regular rhythm, 12–lead EKG.

Algorithm: • Proceed along each step in the stated order.

• If the answer is ‘yes’ to any question, then the diagnosis of VT is made with the sensitivity and specificity given at each step.

• If all four criteria below are absent, then the diagnosis of SVT with aberrancy is made.

• Overall sensitivity is 97% and specificity is 99% for diagnosis of SVT; overall sensitivity is 99% and specificity is 97% for diagnosis of VT.

Criteria	Sensitivity for VT	Specificity for VT
1. Absence of an RS complex in ALL precordial leads?	21%	100%
2. R to S interval >100 ms in one precordial lead?	66%	98%
3. A–V dissociation?	82%	98%
4. Morphological criteria for VT present in V1–2 and V6?*	99%	97%

Morphological criteria favoring diagnosis of VT are listed below.

Note that one criteria from V1–2 and one criteria from V6 must be met to diagnose VT.

	Sensitivity for VT	Specificity for VT
Tachycardia with a RBBB–like QRS (i.e. primarily positive in V1)
Lead V1
Monophasic R wave	60%	84%
QR or RS wave	30%	98%
Lead V6
R to S ratio <1	41%	94%
QS or QR wave	29%	100%
Monophasic R wave	1%	100%
Tachycardia with a LBBB–like QRS (i.e. primarily negative in V1)
Lead V1 or V2
Any of the following:	100%	89%
R >30 msec
>60 msec to nadir of S wave
Notched S wave
Lead V6
QR or QS	17%	100%

SYNCOPE

Defined as transient loss of consciousness and postural tone w/o residual neuro deficits.

Causes	Characteristics	Prevalence (range) in %	Examples
Cardiac
• Organic Heart Disease	chest pain, dyspnea, exertional, postop	4 (1–8)	AS, HCM, PE, Pulm HTN, myxoma, MI, coronary spasm, tamponade, aortic dissection
• Arrhythmias	sudden syncope, injury	14 (4–38)	Brady=sinus node dz, 2nd/3rd HB, Pacemaker malfunc, drug–induced Tachy=VT, torsades, SVT (palpitations characteristic)
Reflex–mediated
• Vasovagal	warmth, nausea	18 (8–37)
• Situational	occurs after daily activity	5 (1–8)	cough, micturation, defecation, swallow
• Other	after neck pressure or head turning	1 (0–4)	carotid sinus, neuralgia
Orthostatic hypotension	sxs with standing	8 (4–10)
Medications	sxs with drug use	3 (1–7)
Psychiatric	frequent sxs, lack of injury	2 (1–7)
Neurologic	HA, diplopia, hemiparesis	10 (3–32)	migraines, TIA, subclavian steal (32 is from one study including seizures)
Unknown	negative workup	34 (13–41)

• From 5 pop–based studies ‘84–’90 Ann Intern Med 1997;126:989
• Evaluation: history, PE (including orthostatics), and EKG for all patients; CXR for most patients. Many patients should be admitted to telemetry for 24-48 hrs (first-time syncope with any suspicion of cardiac etiology); if suspicion of cardiac etiology consider echocardiogram, exercise treadmill test, Holter monitoring, electrophysiology study. May consider tilt-table testing, loop monitoring, psychiatric evaluation, EEG, brain imaging (MRI or CT), and/or carotid/transcranial Doppler studies depending on the level of suspicion for specific etiologies.

CLINICAL PEARLS – "Presenting to Nora"

Physical Exam Essentials:

Neck: JVP, A wave and V wave characteristics (remember no A wave in Atrial Fibrillation),

Carotids – intensity and upstroke characteristics

CV: PMI characteristics and location, lifts or heaves, palpable murmurs, gallops or thrills,

rhythm, S1 and S2 characteristics, murmurs including characteristics, location and

radiation, rubs, gallops (remember no S4 if in Atrial Fibrillation)

Abd: Liver – is it palpable, and if so, is it pulsatile (signifying probable high RA pressures w/ TR)

PULMONARY

ASTHMA / COPD EXACERBATIONS

1. Nebs: Albuterol 0.5cc/3cc NS via neb up to q2h prn; Atrovent 0.5 cc/3cc NS via neb up to q6h. If particularly bad, can consider continuous Albuterol nebs. Note that there is no evidence for using Atrovent in acute asthma exacerbations.

2. Steroids: Solumedrol 60–120 mg IV q6–8h. Usually changed after the first day to a rapid prednisone taper if the patient is not chronically on steroids. A reasonable taper is to start with prednisone 60 mg po QD and taper by 10 mg QOD.

3. MDIs: steroids Beclmethasone 2–10 p BID-QID

Fluticasone 2 p BID

ß2 agonists Albuterol 2–4 p QID and PRN

anticholinergic Ipratropium 2–4 p QID (COPD)

--The utility of inhaled steroids in COPD is controversial. Most people feel that they should not be given unless the patient has been proven to have "steroid-responsive COPD" (i.e. PFT's pre and post-weeks to months of inhaled steroids show improvement). Their efficacy in asthma, however, is more well-accepted, when given in addition to systemic steroids.

4. Antibiotics: COPD patients often have chronic bronchitis, and many feel that any exacerbation should be treated (in addition to above) with an antibiotic like doxy or amoxicillin. Consider IV antibiotics with flare that is so severe that pt. cannot take pos.

5. Order bedside peak flow meter to check daily or q shift peak flows. See Pocket Pharmacopeia for predicted peak expiratory flow.

6. Use supplemental O2 VERY cautiously in COPD, as these patients may retain CO2.

CHEST TUBES

1. Indications: pneumothorax, hemothorax, chylothorax, empyema, recurrent pleural effusion. For medical patients the last two predominate.

2. Placement: 5th or 6th intercostal space at mid–axillary line; tube should enter just above the rib. For PTX, tube heads anteriorly toward apex; for fluid removal, tube heads toward posterior costophrenic sulcus.

3. Pleurevac chambers – three sections of note:

A. Collection chamber: collects fluid

B. Water seal chamber: prevents air from being sucked back and bubbles when there is an air leak. Frequently water in this chamber is colored blue.

C. Suction chamber: regulates suction applied to system.

4. Daily management (usually done by surgery service but good to know)

A. Is there bubbling in the water seal chamber? If so, air is coming in from somewhere between the Pleurevac and the pleural space. Clues to location of air leak: if suction is off and bubbles appear when patient coughs, leak is probably from lung into pleural space; otherwise, suspect air leak in the system which can be localized by clamping the tube at exit site from the chest wall, then moving the clamp along the system to more distal locations. Of note, do not allow water to exceed 2 cm line because the higher the water level, the more resistance for air to exit.

B. Is the tube functioning? If on water seal without suction, water level in water seal chamber should fluctuate with patient’s respirations. Suction should be set to give a steady stream of bubbles in the suction chamber (usually 20 cm H2O is sufficient).

C. Quantitate and qualitate drainage daily. Mark reading time and level on Pleurevac. For effusions, when drainage is <50 cc/day, tube may be removed. For empyema, leave tube on suction until drainage <20 cc/day.

D. For PTX, leave on suction until no more air leak, then put to water seal by turning off suction. Check CXR in several hours to determine if PTX has recurred. If not, then clamp tube. Check CXR in several hrs. If still no ptx, pull tube. After pulling tube, again check CXR to ensure PTX has not recurred.

E. Removal of chest tube (generally done by surgery)

a. Have patient take deep breath and hum or Valsalva

b. Pull out tube quickly while preparing to close existing suture holding tube into chest

c. Cover wound with Xeroform dressing

COMMUNITY–ACQUIRED PNEUNOMIA (CAP)

Note: Moffitt has a clinical pathway with suggested treatment regimens--laminated cards on this subject are available in the doctors' room on 12 Long.

Diagnosis: Fever, cough, often with rigors, sputum production, SOB, pleuritic CP. If constitutional and pulmonary symptoms with a normal CXR, pt. has bronchitis but not pneumonia (except in PCP where CXR is normal 10% of the time).

Microbiology of CAP in specific patient populations

Healthy young adult	pneumococcus, Mycoplasma, Chlamydia
HIV positive	pneumococcus, H. influenzae, PCP, TB, aerobic gram–negative rods (E. coli, Klebsiella), MAI, fungi (Cryptococcus, Histo), CMV, Toxo
Smoker (chronic bronchitis)	pneumococcus, H. flu, Moraxella catarrhalis
Alcoholic or nursing home resident	pneumococcus, H. flu, Klebsiella, aspiration, Staph aureus, TB
Neutropenic	pneumococcus, gram–negatives (E. coli, K. pneumonia, Pseudomonas, H. flu, Enterobacter species), S. aureus, fungi (Candida, Aspergillus)

Further Evaluation:

1. Sputum Gram stain is controversial. Pre-antibiotic sputum w/ >25 PMNs and <10 epithelial cells is a good sample. This can be valuable in immunocompromised patients.

2. CBC with diff, CXR. ABG if indicated.

3. Get blood cultures before antibiotics initiated. Good positive predictive value, but positive in only 10% of CAP.

4. Consider testing for Legionella (culture and urinary assay), Mycoplasma (titers limited utility), Chlamydia (acute and convalescent serology), or influenza if clinical course atypical or enigmatic.

5. Poor prognostic factors appear below and influence decision to hospitalize or treat as outpatient.

6. Consider underlying HIV in patients 15 to 54 with CAP (especially if BCX positive).

7. TB: see section under "ID"

Treatment

1. Cover likely organisms based on demographics above. For hospitalized patients, empiric therapy includes a 3rd generation cephalosporin or B-lactam-B-lactamase inhibitor with or without macrolide or a fluoroquinolone (alone). ICU patients double up cephalosporin with macrolide or fluoroquinolone. Initiate treatment in ED as delays greater than 8 hours have an associated increase in mortality.

2. At UCSF, 25% of pneumococcus shows intermediate resistance to PCN (which is still covered by ceftriaxone) and 8% high level resistance. If patient likely has pneumococcus and is critically ill, consider using vanco. Of note, these numbers are much lower at SFGH, where only 2% of pneumococcus shows high-level resistance.

3. At UCSF, 30% of H. influenzae and 94% of Moraxella catarrhalis produce beta–lactamase. Thus, in smokers or patients with bronchitis you should cover with lactamase–resistant antibiotics, or use macrolides, doxy, or Septra.

4. Switch to po antibiotics early (macrolide, fluoroquinolone, or doxycycline) and consider finishing treatment as outpatient if good prognosis based on grading system below.

5. If treatment with initial 3rd generation ceph + doxy seems to be failing, consider the following organisms this combination misses: MRSA, pseudomonas double coverage, enterococcus, fungi; coverage is fair but not ideal for anaerobes.

Special note for HIV positive pts:

• PCP: >95% of pts. w/ PCP have CD4 <200 but PCP can occur in CD4 >200 if splenectomized, pregnant or postpartum. Many are hypoxic, many have high LDH. Classically bilateral interstitial infiltrates, but can really look like anything (although the teaching is that PCP never presents with a pleural effusion).

--Dx: induced sputum; if negative and highly suspicious, BAL.

--Rx: TMP/SMX IV, dosed at 15 mg TMP/kg qd, in 3-4 divided doses (i.e. for a 70 kg person, total of 1050 mg/day, dosed as 265 mg IV q6h). For sulfa-allergic, use dapsone + TMP (see Sanford for dosing). If pO2 < 70, add steroids, first dose 15-30 minutes before antibiotics: Prednisone at 40 mg po bid x 5 days, then 40 mg qd x 5 d, then 20 mg qd x 11d. Many times you will treat empirically when clinical suspicion is high. See ID section for further details.

• TB: Although pts. w/ high CD4 counts have typical TB sx, pts. with severe immunosuppression can have atypical presentations, so r/o TB in any HIV pt. with apparent pna, constitutional sx, and TB risk factors. See section in ID under TB for more details.

Risk factors for mortality

Demographic factor	Points
Nursing home resident	10
Coexisting illnesses
Neoplastic disease	30
Liver disease	20
Congestive heart failure	10
Cerebrovascular disease	10
Renal disease	10
Physical exam findings
Altered mental status	20
Respiratory rate > 30/min	20
Systolic BP < 90 mm Hg	20
Temp < 35° or > 40°	15
Pulse > 125/min	10
Laboratory and radiographic findings
Arterial pH < 7.35	30
BUN > 30 mg/dl	20
Na < 130 mmol/l	20
Glucose > 250 mg/dl	10
Hct < 30%	10
pO2 < 60 mm Hg	10
Pleural effusion	10

(from Fine, MJ et al, NEJM 1997; 336:243)

Total score = age (or age – 10 for women) + points above

--Score < 70 has low mortality (0–0.9%) and can consider outpatient therapy assuming patient can take oral antibiotics and can be compliant with regimen.

--Score 71–90 consider brief hospitalization (mortality 0–2.8%).

OXYGEN THERAPY

Modes of O2 delivery (remember room air is FiO2 21%):

• Nasal cannula – up to 6 liters, with each liter getting roughly +3% FiO2. Actual FiO2 depends on minute ventilation.

• Simple mask – maximum FiO2 is approximately 50%. Again, actual FiO2 depends on minute ventilation.

• Venturi mask – FiO2 preset at 24, 28, 31, 35, 40, and 50%

• Non–rebreather – max FiO2 up to 90%

• High humidity – max FiO2 almost 100%

• Face tent – similar FiO2 to high humidity but more variable; tends to be less claustrophobic

PLEURAL EFFUSIONS

Check B/L decubitus films prior to thoracentesis; if effusion is small enough that you don't feel comfortable tapping it blindly, get ultrasound guidance.

Light's criteria: to be an exudate, an effusion must meet only one of the following criteria, although specificity goes up with the number of criteria met.

1. Pleural fluid LDH > 2/3 the upper limit of normal at your hospital lab

2. Pleural fluid/serum LDH ratio > 0.6

3. Pleural fluid/serum total protein ratio > 0.5

Transudative: CHF (90%), cirrhosis, nephrotic syndrome, peritoneal dialysis, myxedema, acute atelectasis, constrictive pericarditis, SVC syndrome, PE

Exudative: PNA (parapneumonic), CA, PE, empyema, TB, CTD, chronic atelectasis, pancreatic disease, uremia, chylothorax, sarcoidosis, drug reaction, post MI syndrome, Meigs, viral/fungal/rickettsial/parasitic

Differential diagnosis of exudative effusions:

Glucose <60	Complicated parapneumonic effusion/empyema, rheumatoid (<10), malignancy, TB, parasitic
pH <7.2	Empyema or complicated parapneumonic, rheumatoid, esophageal rupture (<6), TB, malignancy, hemothorax, systemic acidosis, parasitic
Amylase >normal serum amylase	Esophageal rupture, pancreatitis, malignancy
Bloody (RBC >100K)	Trauma, malignancy, pulmonary embolism or infarction, TB
Lymphocytes >50%	Lymphoma or other malignancy, TB or fungi, sarcoidosis, postpericardiotomy

Consider pleural biopsy if CA or TB suspected

PULMONARY EMBOLISM

S/sx: dyspnea (73%), pleuritic pain (66%), cough (37%), leg pain or swelling (27%), hemoptysis (13%); tachypnea >20 (70%), rales (51%), tachycardia (30%), loud P2

Studies: Think of this dx in patients with dyspnea and/or hypoxia with no good explanation on CXR, EKG, CBC.

--ABG: mean paO2 70mmHg, <60 (25%), <80 (74%)

--CXR: abnormal 84%: atelectasis, effusion, basilar opacity, elevated diaphragm, oligemia, Westermark’s sign.

--ECG: SI, QIII, TIII plus RAD, RBBB insensitive (sensitivity increases with PAP>20). More common is sinus tach.

--LE U/S if positive can be useful in a patient with an intermediate V/Q by avoiding PA gram

--Spiral CT: sensitivity 91%, specificity 97% for LARGE PE's (may not detect subsegmental, after 3rd division of pulm arteries). Requires relatively large bore (20 gauge or larger) peripheral IV; central lines, PICCs, and external jugulars are not acceptable. These are more available at night at most hospitals than V/Q's.

--V/Q Scan: a normal/low probability V/Q excludes clinically significant PE while a high probability virtually rules in PE. See stats from the PIOPED study below.

	Sensitivity	Specificity	PPV	NPV	(+) LR
High Intermediate Low Normal	41% 42 16 2	97% 55 59 90	87% 32 16 10	12% 66 80 88	14 1 0.4 0.2

RESPIRATORY FAILURE / MECHANICAL VENTILATION

Indications for intubation

Uncorrectable hypoxemia (pO2 < 70 on 100% O2 NRB)

Hypercapnia (pCO2 > 55) with acidosis (people with COPD often live with pCO2 50–70 +)

Ineffective respiration (max insp force < 25 cm H2O)

Fatigue (RR>35 with increasing pCO2)

Airway protection

Upper airway obstruction

Modes of ventilation:

--AC: assist control. At AC 12 with TV 700, patient will get at least 12 breaths/minute, each of which will have a volume of 700. If the pt initiates a breath on his/her own, that breath will still have a volume of 700.

--SIMV: synchronized intermittent mandatory ventilation. On SIMV of 12 with TV 700, the pt will get at least 12 breaths, each with TV 700. If pt initiates a breath over and above the rate of 12, the volume delivered will be as much as the patient can pull. This setting prevents over-ventilation in pts with rapid respiratory rates, who may develop respiratory alkalosis if on AC; however, it also requires more respiratory muscle work than AC.

--CPAP/PS: Continuous positive airway pressure, also known as pressure support. (This is a weaning setting, not appropriate for initial setting post-intubation). This just means that there is a certain level of pressure delivered during inspiration (whenever pt initiates a breath) to overcome the resistance of the endotracheal tube and/or to allow pts to begin to wean despite being somewhat weak. For example, on PS 10/PEEP 5, during inspiration, pt has 10 cm of pressure blown in, and during expiration, only 5 cm pressure (to stent open collapsing airways, theoretically).

--BiPAP: NON-invasive mechanical ventilation--like a gas mask that straps onto the patient's face but otherwise functions much like a regular vent on PS setting. Often used in CF patients or other pts with chronic lung disease (who are often DNR/DNI) for brief periods to relieve hypercarbia or improve oxygenation. Most people find it quite uncomfortable and therefore not suited for longterm ventilation. RT will help you with the settings, since they are quite different from invasive vent settings.

Initial ventilator settings–be careful in COPD and asthma because of auto–PEEP

VT = 10 ml/kg (less if on ARDS protocol of low TV, high RR)

Mode: AC or SIMV, rate of 12

I:E ratio: no less than 1:2, up to 1:4

FiO2 = 1.0 (wean down as rapidly as possible to avoid oxygen toxicity)

PS (pressure support) = 0–10 (often 5 to overcome resistance of ET tube )

PEEP (positive end-expiratory pressure) = 0–15 (usually 0 initially)

Adjusting ventilator settings: a simplistic approach. Note that this is NOT the intern's job in 9ICU.

--Oxygenation can be thought of as determined by the amount of alveolar membrane exposed to oxygen and the amount of oxygen available. Therefore, if the pO2 is too low: increase the FiO2 or the PEEP (recruits more alveoli to improve oxygenation, but be careful as too much PEEP can decrease cardiac output). Your goal is to oxygenate the patient with an FiO2 of ≤ 0.6; if necessary, add PEEP in order to wean the O2 down to that level.

--Ventilation can be thought of as determined by the amount of ventilated/perfused lung (i.e. non-dead space) available to get rid of CO2 and the frequency by which that gas exchange occurs. Therefore, if the pCO2 is too high: increase the rate or increase the tidal volume, as these are the determinants of ventilation

Weaning parameters

•medically stable, alert; sedation weaned to minimal level

•original condition requiring intubation reversed

•adequate pO2 on < 40% FiO2

•minute ventilation < 10 l/min

•dead space < 50%

•adequate ABG after 30 min CPAP or T–piece trial

•MIF (maximal inspiratory force) < –20

•RR <20

•Tobin index: Resp rate (spontaneous) < 100

Tidal volume

HEMATOLOGY / ONCOLOGY

ANEMIA

In order to determine the etiology, know the reticulocyte count, MCV, and morphology on peripheral smear. If you suspect iron deficiency (the most common form of anemia), order a ferritin. If necessary, you can then add additional lab tests to further the workup (don't forget that many of these studies must be drawn before the patient is transfused). If you're worried that the patient is losing blood or may need blood, send a type and screen or type and cross, and check the hematocrit more frequently. Consider guaiac of all stools and possibly a second IV.

Causes:

I. Decreased reticulocyte count, i.e. decreased production

A. Low MCV (microcytic, hypochromic) - Mentzer index may be helpful (see formulas).

1. iron deficiency (send serum Ferritin, if <15 virtually diagnostic).

Rx:325mg FeSo4 qd-tid; also requires workup if not in menstruating woman.

2. sideroblastic anemia (hereditary and acquired causes)

3. thalassemia

4. anemia of chronic disease

B. Normal MCV (normocytic, normochromic)

1. Primary bone marrow failure

a. aplastic anemia

b. red cell aplasia (hereditary, e.g. Blackfan-Diamond or acquired)

c. myelophthisis

2. Secondary bone marrow failure

a. uremia

b. endocrinopathy

c. anemia of chronic disease

d. anemia of liver disease

C. Increased MCV (macrocytic)

1. Megaloblastic

a. B12 deficiency (send serum B12)

b. folate deficiency (send Folic Acid)

c. myelodysplasia: refractory anemia/erythroleukemia

d. drug-induced (chemo, Dilantin, phenobarb, alcohol, AZT and other HIV drugs)

2. Non-megaloblastic

a. liver disease

b. hypothyroidism

c. reticulocytosis

II. Increased reticulocyte count, i.e. increased destruction, hyperproliferative

A. Acute blood loss

B. Hemolysis (send LDH, bili, and possibly haptoglobin and coombs tests)

1. Extrinsic cause

a. antibody-mediated

b. trauma (valve, microangiopathic)

c. cellular toxins (malaria, Clostridium)

d. hypersplenism

2. Membrane defect

a. spur-cell anemia

b. PNH

c. hereditary spherocytosis, elliptocytosis

3. Intrinsic defect

a. enzyme defect (G6PD deficiency, etc.)

b. hemoglobinopathy

c. sickle cell disease

d. thalassemia

e. HbC disease

ANTICOAGULATION - DVT, PE, AFIB, UNSTABLE ANGINA, MI

1. DVT prophylaxis should be addressed in all inpatients; early ambulation encouraged and PT when indicated. Options for prophylaxis include intermittent pneumatic compression devices, elastic stockings, low dose Heparin, LMW Heparin.

2. The work-up of DVT/PE includes lower extremity Doppler ultrasound of the affected limb(s). If initial clinical suspicion is high for PE or remains high despite a negative u/s, should proceed directly to V/Q scan or spiral CT, with pulmonary angiogram as the gold standard. In choosing test, take into consideration the pt's baseline CXR and the hospital site specific radiologic expertise. D-dimers do not have a high negative predictive value at our hospitals, since the labs use the latex agglutination test, not the ELISA. Draw an extra blue top tube prior to starting heparin if concerned about a hypercoaguable state since heparin will interfere with assays for antithrombin III and the lupus anticoagulant. Protein C, S, anticardiolipin antibodies, homocysteine, prothrombin and Factor V Leiden mutations can be sent on pts on heparin. Note that Proteins C + S are vitamin K dependent factors and will thus be lowered by warfarin therapy. In addition, antithrombin III, Protein C + Protein S may be transiently depressed during the acute event, and only persistent lupus anticoagulants are associated with hypercoagulability. Therefore, any abnormal test should be repeated in the future to document an accurate diagnosis.

3. At UCSF Moffitt-Long Hospital there is a IV heparin order form that guides you through all of the important decisions in therapeutic anticoagulation. This form must be used for all IV heparin used on the Medicine and Cardiology services.

4. There has recently been a treatment guideline published at UCSF for venous thromboembolism, including outpatient management of DVT and PE. This is reprinted in the next section.

5. Risk factors for bleeding on heparin:

1) Surgery, trauma, or stroke within the previous 14 days.

2) History of peptic ulcer disease, GI bleeding or GU bleeding.

3) Platelet count less than 150K

4) Age > 70 yrs.

5) Hepatic failure, uremia, bleeding diathesis, brain metastases.

6. In many patients, instead of regular heparin you may consider low molecular weight heparin (enoxaparin) instead of unfractionated heparin. This eliminates the need to monitor PTT and adjust dosages. LMWH is also associated with a lower incidence of thrombocytopenia. The typical dose is 1 mg/kg sq bid. Unfractionated (regular) heparin may be preferable if:

• Patients require prolonged hospitalization (cost savings over enoxaparin)

• Rapid neutralization with protamine may be necessary (e.g. possible surgery)

• Patient has renal insufficiency (creatinine > 2)

Per hematology, LMWHs are relatively safe in obese patients; the 1 mg/kg q12h dosing with enoxaparin has been shown to be safe in patients weighing up to 150 kgs. In cases of pregnancy with changing weight and plasma volume, renal insufficiency, or advanced age wiht a resultant calculated CrCl < 30 ml/min, you can monitor therapy with anti-Xa levels (a send out test with a turnaround time of approximately 24 hours).

7. Patients should be therapeutically anticoagulated as soon as possible (within 24 hours). Thus, it is better to overshoot and risk bleeding than to undershoot and risk further embolic/thrombotic events.

A. Heparin bolus-150 u/kg for PE, and 80-100 u/kg for most other conditions.

B. Heparin infusion-15-25 u/kg/hr depending on bleeding risks. Patients at high risk should receive 15-18 u/kg/hr and patients at low risk should receive 22-25 u/kg/hr.

C. Sliding scale-adjust heparin to keep PTT in therapeutic range (60-80).

PTT Bolus Hold Adjust Heparin Rate

<50 70 u/kg 0 Increase 200 u/hr

50-59 0 0 Increase 100 u/hr

60-80 0 0 No change

81-99 0 0 Decrease 100 u/hr

>100 0 60 min Decrease 200 u/hr

Note: If the 1st PTT after loading dose is > 100 sec do not change the infusion rate unless evidence of bleeding. Recheck the PTT in 4-6 hrs.

D. The PTT should be checked 4-6 hrs after a new bolus or any change in the infusion dose. The UCSF Moffitt-Long heparin protocol calls for a PTT check q4 hrs until 2 consecutive PTTs are therapeutic, then qAM.

E. Other labs to check include stool guaiac qd and CBC qd

8. Duration of heparin: Pts with DVT or PE should receive 5 days of heparin (even if the INR is therapeutic earlier in hospital course). The anticipated length of stay for pts with DVT/PE is 5 days.

9. Warfarin dosing: The first dose of warfarin should be given on Day 1 (if long term anticoagulation desired). Usually 5-7.5 mg po at night (to ensure absorption on an empty stomach) on Day 1, then 2.5-7.5 mg po qhs (most often 5 mg). Increase in the INR of >0.3-0.4 units per day should result in a dose reduction (otherwise an INR overshoot is likely). Information about the pt's past warfarin dosing history will help you titrate the current dose. Conditions such as CHF, liver disease, vitamin K deficiency and a variety of drugs may influence warfarin response. Duration of coumadin must be tailored to each individual case, with range of Rx from 3 months to life-long anti-coagulation.

10. Therapeutic range of warfarin: INR of 2.5-3.5 for mechanical prosthetic valves or recurrent systemic thromboembolism; INR of 2.0-3.0 for most other indications.

OUTPATIENT THERAPY FOR VENOUS THROMBOEMBOLISM

(After Moffitt-Long treatment guidelines)

1. Inclusion criteria:

• Clinically stable patients with DVT or PE documented with imaging study

• Patients must be motivated and interested in home self-injection and frequent follow-up

2. Exclusion criteria:

• Comorbid conditions: Active peptic ulcer disease, bleeding in last 14 days, brain metastases, CVA in last 10 days, blindness, CNR or cord injury/surgery in last 10 days, family bleeding diathesis, patient weight

<35 kg, platelets <80K or fall of >40%

• Anesthesia: Spinal or epidural anesthesia in past 3 days

• Medication conflicts: prior sensitivity to heparin, concomitant thrombolytic therapy, need for high-dose NSAIDs other than ibuprofen, naproxen, or Celebrex. Vioxx may result in warfarin sensitivity.

• Cognition problems: inability to maintain diary, inject medications, reliably follow medication schedules, recognize change in health status, or understand directions from home health team

3. Initial therapy with enoxaparin (1 mg/kg sq q12h) plus coumadin (5 mg po qhs; 7.5 mg po qhs if >85 kg). May have acetaminophen, codeine, ibuprofen, naproxen, or Celebrex for pain.

4. Patient education materials available from 10L and 12L nursing stations

5. Maintenance algorithm

• Continue enoxaparin until patient has received 5 days of enoxaparin and two consecutive INR > 2.0

• Coumadin to keep INR from 2-3 (or 3-3.5 when anticardiolipin and recurrent thrombosis present)

• PT/INR check daily after day 2 until patient is on stable dose of coumadin

6. Followup should be with the following:

• Home health nurse if home-bound

• Anticoagulation clinic (353-2143 at Moffitt, 206-8492 at SFGH)

• Hematology clinic (353-2421)

• Primary care provider

• Consider Follow-up Service appointment

BLOOD COMPONENT THERAPY

Premedications usually include Benadryl 25 mg po/iv & Tylenol 650 mg po/pr prior to each unit.

1. Packed red blood cells (PRBC): most plasma removed. One unit should raise Hct 3 points or Hgb 1 g/dl.

• leukopoor red blood cells have most WBC removed to make it less antigenic. Use in patients prone to transfusion reactions and in patients requiring multiple transfusions (bone marrow transplant, leukemia, chemotherapy).

• washed red blood cells have WBC virtually completely removed. Use as for leukopoor RBC; note that they are more expensive.

• irradiated blood cells have stem cells killed, decreasing likelihood of GvHD.

• CMV negative blood used for patients who should not be exposed to CMV (CMV negative pre-transplant or post-transplant patients).

2. Platelets: One unit should ideally raise platelet count by 10K; there are usually 6 units per bag ("six-pack"). For dysfunctional platelets (e.g. in uremia), ddAVP is usually given at 0.3 mcg/kg iv q12-24 hrs x 2.

• use when platelets <10-20K in nonbleeding patient.

• use when platelets <50K in bleeding pt, pre-op pt, or before a procedure.

• cross-matched platelets may be used when patient has been sensitized to random-donor platelets and no longer increases platelet counts after transfusion; cross-matching typically takes 1-2 days and requires Lab Medicine approval.

3. Fresh frozen plasma (FFP)

• contains all factors.

• use when patient in DIC or liver failure with elevated coags and concomitant bleeding. Correction of the prothrombin time is transient due to the short half-life of factor VII.

4. Cryoprecipitate

• contains factor VIII, von Willebrand factor, and fibrinogen

• Use is generally reserved for patients with quantitative fibrinogen deficiency (e.g. DIC) and qualitative fibrinogen deficits (e.g. acquired dysfibrinogenemia associated with liver disease). Its use in patients with hemophilia A (factor VIII deficiency) and von Willebrand disease has been supplanted by the use of specific factor products that are safer and more efficacious.

• you can replete with less volume than FFP

NEUTROPENIC FEVER (ANC<500).

(If patient has AIDS, see 'AIDS and Fever')

1. Panculture: Blood x 2, urine, sputum (also for Gram stain), stool for C.difficile if pt. has been on antibiotics. On the CRI, if the patient has a central line send one set of blood cultures from central line and one peripherally. Get a CXR.

2. Patients on the CRI have an antibiotic algorithm which is is posted in the charting room on 11 Long. If you are called for cross-cover, appropriate antibiotics should have been included on the sign out card.

3. On the CRI, you typically draw a set of central line blood cultures every 24 hours. You only need to draw peripheral cultures if this is the first spike or patient is very sick.

4. If not on the CRI, consider monotherapy with broad-spectrum antibiotics such as ceftazidime, cefipime or anti-pseudomonal B-lactam (most common pathogens to cover: GNB including Pseudomonas, Staph aureus, Strep viridans *also consider fungal, MRSA).

•Alternative Rx is duotherapy to double cover Pseudomonas either with addition of an aminoglycoside or if concern re: renal toxicity, a FQ such as ciprofloxacin

•Duotherapy with vancomycin if: suspected IV catheter infection, known colonization with MRSA/PRSP, +blood culture for GPC, hypotensive patient.

•If suspicious of fungal infection, consider amphotericin B (typically 1 mg/kg iv qd).

5. If not on the CRI, order for neutropenic precautions, neutropenic diet, mouth care with Peridex 10 cc sw/sp bid, Nystatin 10 cc sw/sw qid or Mycelex troche 1 qid, and Tylenol 650 mg q4-6h prn

SICKLE CELL PAIN CRISIS

These patients are typically well-known to the hospital staff for their frequent admissions for pain crises. You should not be surprised by a massive opiate tolerance and the need to escalate rapidly in the amount of analgesia required to bring relief. Often these patients have a specific pain protocol worked out; page the Heme fellow or the Pain consult (usually a pharmacist) to get the exact details. Remember that physicians typically undertreat pain.

Typical orders:

1. Aggressive hydration: D51/2 NS at 150-250 cc/hr

2. NPO; advance diet as tolerated

3. O2 0-4 L/min by NC. If respiratory status is compromised, remember to think of acute chest syndrome.

4. CBC, retic count, cultures, lytes, BUN, creatinine, bilirubin, UA, CXR. Draw tube for type and hold.

5. Folic acid 1 mg po qd

6. Analgesic du jour.

• Try to avoid Demerol (these patients will inevitably require huge doses, thus greatly increasing the risk of seizures).

• At Moffitt, frequent flyers have explicit pain protocols written down on 12 Long. Look there for the appropriate dose of opiates. When in doubt, page the Heme fellow or Pain consult. At SFGH, protocols are available in the ED, or call the heme fellow.

7. Try to determine precipitating factor(s): stress, dehydration, drug use, infection, hypoxia, MI, etc. Remember that although many of these patients come in and out of the hospital for "routine" pain crises without specific precipitants, there always is the potential for something bad to be going on. Of note, pain crisis often presents with elevated WBC and low-grade fever; therefore complete w/up of concomitant infection important.

8. If pain crisis (ie acute vaso-occlusive crisis) leading to stroke, priapism or intractable pain - consider exchange transfusion.

9. If patient with frequent episodes of pain crisis, consider hydroxyurea as prophylaxis.

THROMBOCYTOPENIA

Defined as platelet count <150K. Generally, platelets >50K are not associated with significant bleeding, and spontaneous bleeding rarely happens with platelets >10-20K in the absence of coagulopathy or qualitative platelet defect.

• avoid IM injections, rectal exams, suppositories, and enemas

• avoid drugs that interfere with platelet function (e.g. NSAIDs/ASA, certain beta-lactam antibiotics)

• presence of petechiae indicate a significant risk for intracerebral hemorrhage

• check for signs/sx: ecchymoses, petechiae, purpura, GI bleed, epistaxis, etc.

Causes of thrombocytopenia

I. Decreased production

--Aplastic anemia

--Megaloblastic anemia, i.e. B12 or folate deficiency

--Hematologic malignancies (e.g. myelodysplasia, leukemia, myeloma)

--Marrow infiltration (lymphoma, myelofibrosis, metastatic tumor, TB, Gaucher's disease)

--Alcoholism

--Drug-induced (e.g. thiazides, estrogens, Septra, chemo, cimetidine, famotidine)

--Paroxysmal nocturnal hemoglobinuria (PNH)

--Infections (mono, influenza, rubella, hemorrhagic fever, etc.)

II. Increased destruction

A. Immune mediated:

--Idiopathic thrombocytopenic purpura (ITP)

--Neoplasia-associated (e.g. CLL)

--Drug-induced (e.g. quinidine, heparin, rifampin, sulfa, indomethacin, gold)

--SLE, RA

--HIV-associated thrombocytopenia

--Post-transfusion purpura

B. Non-immune mediated:

--Disseminated intravascular coagulation (DIC): increased PT/PTT and D-dimers, decreased PLT/fibrinogen.

--Hemolytic uremic syndrome (HUS)

--Thrombotic thrombocytopenic purpura (TTP): increased LDH, decreased PLT, normal coags.

--Pre-ecclampsia/ecclampsia

--Toxic shock syndrome

--Vasculitis

--Infections (rickettsial, CMV, EBV, malaria, sepsis, etc.)

--Sequestration (hypersplenism)

TRANSFUSION REACTIONS

Signs: sudden fever, diaphoresis, hypotension, urticaria, wheezing, chills, tachycardia.

Treatment:

1. Stop blood product immediately.

2. Consider workup for severe transfusion reactions: blood cultures, hemolysis labs including purple top for Coombs and red top for repeat T&C. If you call the Blood Bank, they will help out with this; besides, they are required to get involved.

3. Benadryl 25-50 mg and Tylenol 650 mg for mild transfusion reactions.

4. Hydrocortisone 50-100 mg IV for severe reactions.

5. If hemolysis occurs, maintain diuresis with IVF and furosemide; consider alkalinization of urine with bicarb to prevent renal failure. Watch K, CK.

6. Many hospitals will have a protocol to follow and tons of paperwork to fill out.

BONE MARROW TRANSPLANT--POTENTIAL COMPLICATIONS

Days post-BMT Complication

-7 to 21 Toxicity of preparative regimens (nausea, vomiting,

diarrhea, alopecia, mucositis, renal failure, skin

breakdown, ARDS, cardiomyopathy)

0 to 21 HSV reactivation

Hepatic veno-occlusive disease

0 to 28 Diffuse alveolar hemorrhage

0 to 49 Bacterial and fungal infections

28-70 CMV infection

14 to 100 Acute GvHD

49 to 100 Interstitial pneumonitis

100 to 180 Chronic GvHD

VZV

Pneumocystis carinii pneumonia

BMT--ACUTE GRAFT VS HOST DISEASE STAGING AND GRADING

(Adapted from Armitage, NEJM 1994, 330:827-838)

Stage Skin Liver GI

1+ Maculopapular rash on <25% BSA Tbili 2-3 mg/dl 500-1000 cc diarrhea/day

2+ Maculopapular rash on 25-50% BSA Tbili 3-6 mg/dl 1000-1500 cc diarrhea/day

3+ Generalized erythroderma Tbili 6-15 mg/d >1500 cc diarrhea/day

4+ Generalized erythroderma Tbili >15 mg/dl Severe abd pain ± ileus

and desquamation

Use staging information above to determine clinical grade on chart below.

Clinical grade Skin Liver GI Decrease in clinical performance

I 1+ to 2+ 0 0 None

II 1+ to 3+ 1+ 1+ Mild

III 1+ to 3+ 2+ to 3+ 2+ to 3+ Marked

IV 2+ to 4+ 2+ to 4+ 2+ to 4+ Extreme

INFECTIOUS DISEASE / AIDS

ANTIBIOTICS

1. For complete antibiotics recommendations, refer to Sanford or the UCSF handbook. The following are some general thoughts and practical tips.
2. Get the cultures you need before first antibiotics dose. It’s OK to start broad (e.g. Zosyn) while waiting for culture results, but start to think about what pathogens you are suspecting given the clinical scenario and try to tailor your regimen in an appropriate fashion.
3. If your patient continues to spike through antibiotics, review your regimen and look for gaps in coverage. These may include (but are not limited to) fungi, atypical bacteria, resistant organisms (e.g. MRSA), organisms that sometimes require double coverage (e.g. Pseudomonas). Also consider hidden abscesses, drug fever and other non-infectious causes of fever. (See "Fever of Unknown Origin" section)
4. Each of our three hospitals has different antibiotics on formulary, including some that require approval from ID before any doses will be dispensed. To save yourself (and the ID fellow) some potentially painful 3 a.m. calls, here is a list of anibiotics that currently require approval at our hospitals:

a. Moffitt: Linezolid, Synercid, liposomal Amphotericin

b. VAMC: Ciprofloxacin, Levofloxacin, Ceftazadime, Cefotetan, Ceftriaxone, Fluconazole, Gancyclovir, anti-retrovirals for HIV. (ID approval also required for more than 3 days of Vancomycin or Tobramycin)

c. SFGH: Imipenem, iv Ciprofloxacin, iv Fluconazole, Zosyn, iv Rifampin, iv Levofloxacin, iv Capreomycin, iv Chloramphenicol, Itraconazole.

OSTEOMYELITIS

1. Infections of bone can be caused by hematogenous spread of bacteria (think IVDU or elderly patient), spread of adjacent infection (think prosthetic joints or decubitus ulcers) or skin breakdown secondary to vascular insufficiency (think diabetics).
2. When the osteo has been caused by hematogenous spread of bacteria, a patient may present acutely with fever, bony pain and tenderness but other mechanisms may result in a more indolent clinical course.
3. If you can probe down to bone on physical exam, the patient has osteomyelitis.
4. Plain films may be normal early in the course of osteo, and an MRI or nuclear bone scan may be necessary to make the diagnosis. MRI (if readily available) is the preferred modality as soft tissue involvement can also be observed.
5. A positive blood culture or bone aspiration/biopsy is necessary to identify the causative organism and select antibiotics. Some common pathogens include Staph. aureus (IVDU, spread from adjacent infection) and Staph. epi (adjacent infections). In IVDU, gram-negative organisms (Pseudomonas, Serratia) are also common. Don’t forget to consider fungi and AFB, especially with insidious onset of symptoms.
6. Treatment consists of debridement of bone and prolonged antibiotics, typically starting with 4-6 weeks of iv antibiotics.

SHOOTER WITH A FEVER

1. Standard Fever workup–Blood culture x3 –separate 1 set of cultures by at least 1 hour (95–99 % sensitive for endocarditis, 2 cultures is only 85–90% sensitive for endocarditis), UA and culture, CXR.

2. Careful skin exam for abscess, cellulitis and peripheral stigmata of endocarditis (indicating left sided disease).

• petechiae – on conjunctiva, palate, buccal mucosa

• splinter hemorrhage – subungual linear streaks

• Roth spots – oval retinal hemorrhages

• Osler nodes – small tender nodules on fingers or toes

• Janeway lesions – small, nodular. painless hemorrhages on palms or soles

3. Palpate bones, especially spine for osteomyelitis and epidural abscess

4. Pelvic exam in women to r/o PID as source of fever

5. EKG on arrival and qd; PR interval prolongation may indicate ring abscess

6. Treatment: nafcillin 2 gms IV q 4 hr plus gentamicin 1 mg/kg IV q 8 hrs. If concerned about MRSA, consider Vancomycin. The treatment of endocarditis is extremely complicated and depends on the organism, the sensitivities, the site infected, and the response to therapy. If you diagnose endocarditis, ID wants to be consulted.

7. Almost all shooters with fever should be admitted to the hospital. However, if you find no source of infection and your clinical suspicion is low, it is acceptable to observe without antibiotics. If the patient defervesces quickly off antibiotics, it may not be necessary to wait 48 hrs for culture results prior to discharge (SFGH protocol is 24 hours without fever if no antibiotics started and cultures are negative).

8. Get echo if new murmur, hemodynamically unstable, PR prolongation, or not responding to therapy.

MORE ON ENDOCARDITIS

1. Other than IVDU, risk factors for endocarditis include recent iv catheter, recent dental procedures or GI/GU instrumentation, abnormal valves (e.g. sequelae of rheumatic heart disease, calcified or sclerotic valves).
2. Common pathogens in non-IVDU patient with native valve: Strep. viridans (60%), Staph. aureus (20%), Enterococci (5-10%).
3. Common pathogens in IVDU patient with native valve: Staph. aureus (60% of all cases and 80-90% of cases involving tricuspid valve) and unusual gram-negative bacilli and fungi are more common.
4. Common pathogens in patients with prosthetic valve: Coagulase positive and negative Staph., gram-negative organisms and fungi if valve is NEW (<2 months). After 2 months, pathogens similar to native valve except more coagulase negative Staph.
5. When blood cultures are negative, consider fungi, slow-growing organisms (HACEK) and organisms requiring special growth media (e.g. Legionella, Bartonella)
6. Treatment includes 4-6 weeks of antibiotics for L-sided endocarditis, 2 weeks for purely R-sided staph aureus endocarditis, and may also include valvular surgery if patient develops valvular regurgitation/acute heart failure refractory to medical treatment or has an abscess.
7. Don’t forget prophylactic antibiotics for patient with valvular abnormalities or prosthetic valves before dental, GI or GU procedures.

8. Diagnosis rests on Duke Criteria (Durack et al., Am J Med 1994; 96: 200). Need 2 major, 1 major + 3 minor, or 5 minor to diagnose infectious endocarditis (IE).

Major Criteria:

1 Positive blood culture (BCX):

A. Two positive BCX for organisms typically causing IE (S. viridans, S. bovis, HACEK organisms, S. aureus, or Enterococcus) in the absence of other sources for infection.

B. Microorganisms consistent with IE from persistently positive BCX. At least two positive BCX >12 hrs apart, or at least 3 of 4 positive BCX.

2. Evidence of endocardial involvement:

A. Positive echocardiogram

• Oscillating intracardiac mass on valve or foreign body, or in path of regurgitant jets

• Abscess

• Partial dehiscence of prosthetic valve

B. New valvular regurgitation (worsening or changing of previously existing murmur not adequate)

Minor Criteria:

1. IVDU or pre–existing heart condition.

2. Fever > 38°

3. Vascular phenomena (septic pulmonary emboli, major arterial emboli, intracranial hemorrhage, Janeway lesions, mycotic aneurysms, conjunctival hemorrhages)

4. Immune phenomena (Roth spots, glomerulonephritis, Osler’s nodes, rheumatoid factor)

5. Microbiology evidence (positive BCX or other serologic tests consistent with infection but not meeting major criteria)

6. Echocardiography consistent with IE but not meeting major criteria.

SEPTIC ARTHRITIS

1. Suspect septic arthritis with acute onset of joint pain in a patient with bacteremia, history of IVDU, damaged or prosthetic joints.
2. Staph. aureus is the most common non-gonococcal pathogen. Group A & B Strep are also common. In IVDU, also suspect gram-negative organisms.
3. For diagnosis, get blood cultures and synovial fluid. Blood cultures are positive in about 50% of patients with septic arthritis. See following table for assistance in interpreting synovial fuid and differentiating from inflammatory joint disease:

	Normal	Noninflammatory	Inflammatory	Septic
Color	Colorless	Xanthochromic	Yellow	Variable
Clarity	Transparent	Transparent	Translucent	Opaque
Viscosity	High	High	Low	Low
WBC/mm3	<200	200–3000	3000–50,000	>50,000
PMN	<25%	<25%	>50%	>75%
Culture				May be +
Crystals			May be +
Examples		Osteoarthritis Trauma Charcot joint Aseptic necrosis SLE Rheumatic fever Scleroderma PMR E nodosum PAN Amyloid	RA Gout/pseudogout SLE Scleroderma Dermatomyositis & polymyositis Viral arthritis TB Ankylosing spondylitis Seronegative spondylo-arthropathies Psoriatic arthritis Rheumatic fever Behçet’s syndrome	Bacterial TB

4. Treatment consists of appropriate antibiotics and repeat aspiration of affected joint if fluid re-accumulates rapidly. For joints that are difficult to access/aspirate (e.g. hip), surgery may be necessary.

MENINGITIS

1. Indications for Lumbar Puncture:

A. When infection (meningitis, encephalitis) suspected. Exception is if brain abscess or space–occupying lesion suspected

B. To determine if bleeding has occurred (e.g. subarachnoid hemorrhage)

C. When CSF chemistries have diagnostic value (e.g. MS)

D. Cytology in malignancies

E. Therapeutics (e.g. intrathecal chemotherapy, Cryptococcal meningitis)

2. Contraindications: (Remember, DON’T DELAY ANTIBIOTICS even if you must delay tap!)

A. Infection at LP site

B. Severe thrombocytopenia (platelets <30–50) or bleeding diathesis

C. Mass lesion suspected (e.g. brain abscess, tumor, subdural hematoma, intracranial hemorrhage). In this case, do CT or MRI first.

D. In the presence of papilledema, consult Neurology first.

3. Tests to order:

Tube 1: Cell count and differential

Tube 2: Total protein and glucose

Tube 3: Culture and Gram stain

Tube 4: Cell count and differential

Depending on the clinical situation, may also order: cytology, VDRL, AFB stain/culture (often requires lab medicine approval), fungal stain (fungal cultures often require lab medicine approval), Cryptococcal antigen (CrAg), India Ink (no longer done at SFGH), oligoclonal bands, MBP, Lyme titers, HSV PCR. FYI: at SFGH, lab medicine approval is required for HSV and TB.

4. Interpretation of results (general guideline – use your common and clinical sense)

Condition	Appearance	Glucose (mg/dl)	Protein (mg/dl)	Cell Count	Differential	Pressure (cm H2O)
Normal	Clear	50–75% serum	<50	<5	100% lymph	5–20
Hemorrhage	Bloody or xantho	N or D	I but <1000	RBC and WBC	Same as blood	Usually I
Bacterial meningitis	Cloudy or purulent	< 40% serum	45–500	100–100K	>80% PMN	Usually I
Fungal meningitis	Clear or cloudy	20–40	25–500	25–1000	Inc mono and lymph	N or I
Aseptic/viral meningitis	Clear or cloudy	N or D	50–200	10–500	Inc mono and PMN early, then lymph	N or I
TB meningitis	Cloudy	<40	100–2000	50–500	Mostly lymph, some PMN	Usually I
Herpes encephalitis	Bloody or xantho	N or D	50–100	20–500	Mostly lymph	N or I
Neoplasm	Clear or xantho	40–80	50–1000	<100	Mostly lymph	Usually I
Guillain– Barré	Clear or cloudy	N	slight I	<100	Mostly lymph	N
Neurosyphilis	Clear or cloudy	N	40–200	200–500	Mostly lymph & mono	N or I

Abbreviations: N – normal; D – decreased; I – increased

•Note: > 99% certainty of bacterial meningitis if any of the following:

-- CSF glucose < 34 mg/dl,

-- CSF/blood glucose ratio < 0.22,

-- CSF protein > 220 mg/dl

-- >2000 CSF wbc

-- >1180 CSF neutrophills

•Common pathogens:

-- 15-50 y.o: Strep. pneumoniae, N. meningitis, Listeria

-- >50 y.o. or debilitated: Above, plus H. flu and Pseudomonas

-- AIDS: Cryptococcus, bacterial meningitis, Herpes, Coccidiodes (For info, see "AIDS and Altered Mental Status)

--Post-surgical or post-traumatic: Staph. aureus, pneumococcus, and gram negatives

•Empiric bacterial meningitis treatment – (doses for adults with normal renal function)

-- Ceftriaxone 2gm IV q12h + Vancomycin 1g (15 mg/kg) IV Q12h (+/- Ampicillin 2gm IV q4h if Listeria is considered). Remember, do not use vanco and steroids together.

•Remember: NOSOCOMIAL MENINGITIS EXTREMELY RARE IN NON-SURGICAL PATIENTS

AIDS AND ALTERED MENTAL STATUS

The differential includes the following:

Parenchymal	Meningeal	Other
Toxoplasma	Cryptococcus		Metabolic
CNS lymphoma	Bacterial		CVA
PML	Syphilis		Drugs
HSV encephalitis	TB meningitis		Systemic infection
AIDS dementia	Lymphoma		Psychiatric

Less common: Bacterial abscess, tuberculoma, fungus (histo, cocci), CMV. Ideally, save an extra tube of CSF whenever possible in case extra PCR studies are desired for CMV, HSV, or TB.

Standard procedure includes the following:

1. CT or MRI: MRI more sensitive for Toxo, lymphoma, ADC (AIDS dementia complex), PML, HSV, and meningeal enhancement, but get CT if you can’t get MRI in 12–24 hrs or you need pre–LP screen.

2. LP: opening pressure, glu, prot, cell count, CSF CrAg, VDRL. Also send serum CrAg and VDRL as well. Even if no cells are present, send cultures: bacterial, fungal, and cytology; in the worst cases of crypto, there are often <5 WBCs because of poor inflammatory response. If high clinical suspicion, send AFB and viral cultures.

a. lymphocytosis: Crypto, TB, syphilis, fungal, viral, lymphoma

b. neutrophils: bacterial, CMV polyradiculopathy

c. low glucose: bacterial, TB, fungal, syphilis, lymphoma meningitis

d. high protein: any of above

e. RBCs: subarachnoid bleed, HSV or traumatic tap.

3. If fever present, do routine fever workup.

4. Treatment

a. Ring–enhancing lesions: toxo versus lymphoma.

• if serum toxo IgG+ and no Septra prophylaxis, treat empirically for toxo. This consists of Pyrimethamine 200 mg on day 1, then 100 mg po qd plus sulfadiazine (1.5 gms q6 hrs) or Clinda (600 mg po or IV q 8 hrs). Rescan within 7-9 days. If no improvement clinically and radiologically, patient may need biopsy.

• if serum toxo IgG negative, or patient taking Septra, single lesion on MRI, or lesion crossing midline, consider early stereotactic biopsy.

• if lymphoma, use XRT (need tissue diagnosis first).

b. Cryptococcus:

• low risk pt. (normal MS, no HA, no N/V, nl opening pressure): Fluconazole 400 mg po qd. That being said, 99% of inpatients with crypto meningitis require 14 days of IV Amphotericin.

• high risk (includes those with any of the following: AMS, N/V, HA, elevated OP, CSF WBCs < 20, or CSF CrAg > 1:1024): Ampho 0.75 mg/kg IV qd x 14 days. When using amphotericin, give pre and post-hydration with 500 cc NS. If creatinine is rising increase to 1L pre and post. Avoid other nephrotoxic agents, and watch for significant K+ and Mg++ wasting. In pateints with normal renal function, begin Amphotericin with 20 meq PO bid of KCL and Mg 500 mg PO q day. An RTA will inevitably develop with Amphotericin. Hydrocortisone is only needed (as 25 mg in the bag of ampho) if patients continue to have rigors after day 3 or 4 that don't respond well to morphine. Morphine is just as effective as demerol for rigors and is the first line for rigors at SFGH.

c. Neurosyphilis (CSF VDRL positive or serum VDRL positive with CSF lymphocytosis and high protein): PCN G 2–4 million units q 4 hrs. x 10 days.

d. Cerebral edema or mass effect: Decadron 4 mg IV q 6 hrs. If herniation, use mannitol 1.5 – 2 gms/kg IV

e. TB (lymphocytosis, low glu, high prot, or AFB): INH, Rifampin, Ethambutol, PZA, and Decadron.

f. PML, ADC: HAART is the treatment of choice. Contact the AIDS consult service for advice on initial or salvage regimens. Experimental protocols are available for PML via the AIDS consult service.

AIDS AND SHORTNESS OF BREATH

Initial work–up would include the following:

1. Chest x–ray (rule out infiltrates, pneumothorax), ABG, EKG, supplemental oxygen

2. Initial labs should include lytes, BUN, creatinine, Ca, Mg, Phos, CBC, diff, plts, LDH

3. Blood cultures x 2, sputum for gram stain and C & S

4. Induced sputum for PCP, if c/w clinical presentation (CD4 usually less than 200 but certainly not always). Remember to make patient NPO after midnight and submit forms to RT.

5. Strongly consider placing patient on respiratory precautions and obtaining sputum x3 for AFB to rule out TB.

6. Consider empiric anti–PCP Rx. Septra is always the treatment of choice. Pentamidine is another option for severe disease. Other agents: Clindamycin / Primaquine, Trimethoprim / Dapsone, Atovaquone (for mild disease only).

7. Corticosteroids in addition to anti–PCP antibiotics if the PaO2< 70 (dose: 40 mg po bid x5d, 40 mg po qd x5d, then 20 mg po qd for 11d. Give first dose 15-30 minutes before 1st dose of TMP/SMX).

8. Start antibiotics for bacterial or fungal pneumonia if clinically indicated.

9. Consider obtaining a pulmonary consult to expedite bronchoscopy if needed. This is often required anyway if getting sputum induction as need BAL to definitively r/o PCP.

10. As with all acutely ill pts with poor prognosis you should establish code status.

MORE ON TUBERCULOSIS

1. Volumes have been written on this disease, which should be strongly considered in patients presenting with cough, fatigue, fever, weight loss and night sweats. The following points are intended to help manage cases of suspected or documented TB in the hospital.
2. Chest X-ray findings in primary TB include small homogenous infiltrates, hilar and paratracheal lymphadenopathy and segmental atelectasis. Reactivation TB can manifest in many ways, but typical findings include apical cavitary disease and pneumonic infiltrates in the apical or posterior segments of the upper lobes. Remember that with HIV, the radiographic presentations can vary greatly from the "classical" findings, especially when CD4 < 100, when lower lobe disease and mediastinal/hilar LAN are more common.
3. ANY patient with a good story for TB and/or suggestive chest X-ray should be placed in respiratory isolation. As a general rule, it’s always easier to take patients out of isolation after discussion with the attending than to (sheepishly) put them in after they have spent the night coughing AFB onto other patients and the staff.
4. To rule out contagious TB, obtain three morning sputum samples (keep patients NPO after midnight while collecting). If patient does not have a productive cough, sputum must be induced by RT. Intubated patients can have three sputums collected 8 hours apart through the ET tube. SFGH has a protocol hanging in the residents' room.
5. After three NEGATIVE sputums have been collected, you may take patients out of respiratory isolation. If suspicion for TB is still high, consider bronchoscopy for diagnostic washings +/- transbronchial biopsies. Standard cultures take 6-8 weeks to grow TB.
6. For HIGH-RISK patients (prisoners, HIV patients with moderate to high clinical and radiographic evidence, immunocompetent patients with high clinical and radiographic evidence, particularly if they share close living quarters with others), anti-TB treatment should be started on the first day of hospitalization and, depending on the clinical scenario, continued until cultures (not smears) return negative.
7. Treatment for TB typically involves 4-drug therapy with INH, Rifampin, Pyrazinamide and Ethambutol. Doses and length of treatment varies given local drug-resistance patterns and immune status of patient.
8. Consider DOT (direct observation therapy) for patients who may have difficulty completing treatment as outside the hospital.
9. Incarcerated patients need to be cleared by TB clinic and the jail medical team (Dr. Goldensen) prior to going back to jail if they were admitted for r/o TB.

AIDS AND NEW FEVER

Initial work–up would include the following:

1. If patient has concomitant SOB or pulmonary Sx’s, then work–up as for "AIDS–shortness of breath."

2. CXR

3. Consider head CT (if clinically indicated, then chest or abdominal CT)

4. Blood cultures x2, blood culture for AFB including MAC (this requires green top tubes at SFGH but can be part of a regular blood draw, as it is not a sterile culture). Stool for C. difficile (if h/o antibiotics), fecal WBC, stool culture, and O&P x3 if patient has diarrhea.

5. Consider LP; send CSF for cell count, protein, glucose, and CrAg (all STAT). Also send CSF for C&S, VDRL, and viral culture (if high clinical suspicion).

6. Labs should include lytes, BUN, creatinine, CBC, diff, plts, LDH, LFTs, hepatitis serologies (if suspected or unknown), serum CrAg.

7. Consider empiric antibiotic therapy.

8. Examine the skin carefully. If lesions are present, they can facilatate a prompt diagnosis e.g. cryptococcus, histoplasmosis, mycobacterial disease, and bacilliary angiomatosis

8. Consider consults (AIDS, pulmonary, infectious disease, heme/onc).

9. As with all acutely ill pts with poor prognosis you should establish code status.

FEVER OF UNKNOWN ORIGIN (FUO)

Classicially defined as three weeks of illness with T>38.3 on several occasions and failure to reach diagnosis after one week of inpatient evaluation.

1. In adults, infections count for 25-40% of classic FUO, with TB and endocarditis (see previous sections) being the most common systemic infectious diagnoses. Primary HIV or OI associated with AIDS can also present as FUO. Occult abscesses are localized infections that commonly cause FUO. Sneaky places that abscesses hide include bone, spleen, kidney, brain, liver.
2. Cancer accounts for another 25-40% of FUO, especially lymphoma and leukemia.
3. Autoimmune disorders causing FUO (10-20%) include Still’s disease, lupus, cryoglobulinemia and polyarteritis nodosa.
4. For patients who develop FUO in the hospital (i.e. nosocomial FUO), also consider line infection, recurrent pulmonary embolus, transfusion-related viral infection, Clostridium difficile and drug fever.
5. In neutropenic or HIV FUO, consider atypical/opportunistic infections and the more mundane catheter infections, sinusitis, groin and perianal abscesses. Some HIV drugs can also cause fever: Septra, abacavir, dapsone are common offenders.
6. FUO work-up includes repeat blood cultures (preferably including some when the patient has been off antibiotics for a few days), chest X-rays, CT of abdomen and pelvis and chasing ANY abnormal clinical findings (e.g. LP and head CT for headache, echo for murmur). Bone marrow biopsy tends to be low-yield in FUO EXCEPT in HIV patients, in whom mycobacterial infiltration of marrow is a more common cause of FUO. Radionuclide studies (e.g. tagged wbc scan) can be frustrating in a patient without localizing syptoms given high rate of false-positive and negative results.
7. Empiric treatment with antibiotics is indicated if infectious disease is strongly suspected but "shotgun," broad-spectrum approach should be avoided unless patient is rapidly deteriorating.
8. In patients with CD4 < 50 and FUO with or without pancytopenia and/or abdominal pain, empiric treatment (not prophylaxis) for MAC is appropriate. Obtain at least 1 culture first (90%) sensitivity and then start 2 drugs- Clarithromycin 500 mg bid and ethambutol at 15 mg/kg/day. Even appropriately treated MAC can cause fevers for 5 days to 8 weeks.

GASTROENTEROLOGY

ACUTE PANCREATITIS

1. Your main goals are to rest the pancreas and to provide supportive care.

2. DDx: Alcohol and gallstones. Rare causes: hypertriglyceridemia, hypercalcemia, various meds, and the dreaded scorpion sting.

3. Use Ranson's criteria (see below) to assess prognosis (i.e. whether pt. needs ICU bed).

4. Get an IV in and start IV rehydration. Be aware that fluid shifts and sequestration are common.

5. Keep patient NPO until pain-free and off narcotics.

6. NG tube suction is needed only for nausea/vomiting.

7. Morphine is commonly used for analgesia, although in theory it can cause spasm of the sphincter of Oddi. Try to avoid meperidine as it is not available at SFGH and can cause seizures in large amounts, although it is the 'textbook' favorite.

8. Labs to send off include CBC, lytes, BUN, creatinine, glucose, Ca, LDH, amylase, LFT. Consider a lipase level if the diagnosis is uncertain. Get ABG and CXR if any evidence of respiratory compromise.