RESIDENT SURVIVAL GUIDE

2004-2005

Introduction

Welcome to residency. You are about to start one of the busiest, most fulfilling times of your life. Your fear is probably appropriate — a lot is going to be expected of you. But, try to keep it in check. You are here for a reason. You have passed all the tests, clerkships, and other hurdles you needed to graduate from medical school. This is another part of your learning experience. Many have gone before you and many will go after you—you can do this! Remember, you are not a superhero. Exercise, eat well, and take time to enjoy the things that help you relax. Residency is a marathon and not a short sprint. We have written this guide because many of our residents thought it would be helpful to have a quick reference for those inevitable questions and pimping sessions. This is based on the Resident Survival Guide produced by EVMS for its residents as well as the University of California at San Francisco’s Housestaff Handbook. This is not meant to be an exhaustive explanation for everything that goes on at each site or how to deal with every nurse’s call at night but it will hopefully help make your transition into residency easier. We have gone to great lengths to ensure the accuracy but it is not guaranteed. If you see something that is incorrect, please make a note of it so when we collect suggestions and changes for next year, we can update it correctly. Have a great year!

General

Team Lists: Each team has a list of its patients. Generally, updating the list is the responsibility of the students but students need clear instructions on what your expectations are for the list. Try to find out what your senior resident’s preferences are for the list and convey that to the students. Ultimately, the list usually needs to be further updated by the intern during the wee hours of the morning on call nights. Students should always have a copy of the list for the attending at the beginning of rounds. Sample Progress Note: This is a pretty thorough format and may not pertain to every patient but if you cover this on most patients, you should satisfy all of the attendings in the department. Time/Date PGY-1 Progress Note S: Events over last 24 hours. Complaints. N/V/CP/SOB/po intake? Address the reason why they were admitted. (For example, no chest pain since admission.) O: Tm Tc RR HR BP O2 sat (on RA, etc.) (Include ranges of any abnormal vital signs but also include the current value for all vitals.) I/O: Time/ Accuchecks listed Gen: CV: Resp: Abd:

List current meds in the margin

Extrem: (Also include any system that is pertinent to the diagnosis.) Labs: Micro: list dates and results--check daily X-ray/PVL/ECHO, etc. results A/P: (or you can separate them into two categories) 1. chest pain - . . . 2. HTN, controlled - . . . 3. hypokalemia - replete 4. DM type II, moderate control - increase AM regular Your signature Pager Number/Stamp ICU Note Format: Please note-some attendings prefer the note be by system. Other attendings prefer this format. Admit Date:_____ ICU Day: _____ ABX and Day #:_______ IV Lines & Day #:____ Meds:_____________ Problem List:___________________________ _____________ ____________________________ _____________ ____________________________ _____________ ____________________________ 24 Hour Events: PE: Vitals: (include current values and ranges) I/O Total:_________ Gen: Lungs: FiO2:_____ CVP:_____ CV: AC/IMV:_____ PA:_____ Abd.: Vt:_____ PAWP:_____ Extrem.: PSV:_____ CO/CI:_____ Neuro: SpVt:_____ SVR:_____ PEEP:_____ SvO2:_____ Labs: CBC/Chem/ABG/etc. Micro: CXR: Assessment & Plan: Pulm.: CV: include volume status Heme: GI: Renal: acid-base status Neuro: ID: F/E/N: (fluids, electrolytes, and nutrition) Misc: stress ulcer & DVT prophylaxis; appearance of lines Sample Admit Orders: Of course, you will develop your own style but this may be helpful in the beginning when things seem overwhelming. (ADC VANDALISM)

Admit to Medicine (stepdown or telemetry, if needed) Attending - name Resident - name Intern - name and pager number Diagnosis: 1. main reason why they are being admitted 2. list all other diagnoses in order of importance Condition: stable/fair/guarded/critical, etc. Vitals: routine with pulse ox q12 hours Allergies: medication-reaction Nursing: Call MD for T >100.5 or <96.0, SBP >180 or <95, DBP >95 or <45, HR >120 or <55, RR >24 or <12, O2 sat <93% Diet: cardiac, ADA, etc. Activity: ad lib Labs: now labs and AM labs IVFs: heplock or fluid and rate Special: x-rays, EKG, PVLs, 2D-ECHO, stress tests, etc. (Don’t write “special”.) Meds: -try to avoid PRN meds unless you know they are needed -list all home meds that they will need as an inpatient -stop meds that are causing problems All old records to floor. Example Format for Discharge Orders: 1. D/C (or transfer) to . . .(home, nursing home) 2. D/C IVs and/or catheters 3. Dx: 1. main reason for admission 2. list all other diagnoses 4. Condition: (good, stable, etc.) 5. D/C Instructions: 1. Diet: 2. Activity: 3. Meds: 4. F/U: (arrange F/U with all services that were following the patient) 5. Call MD or go to ER if SOB/CP, fever, (list symptoms pertaining to his/her admitting diagnosis), or any other concerning symptoms develop. Some other things that may need to be included: -dressing change instructions and or F/U for specific lab draws - Fax copy of D/C note to clinic where patient is following up. Make sure to list the fax number. Example Format for Discharge note: This primarily needs to be done for people who are following up within 2-3 weeks of discharge because the discharge dictation will not make it to the office for F/U by that time. Either fax it yourself or write an order to have the D/C note faxed to the clinic where the patient is following up. Keep it brief (1-2 pages max). This is a great thing to have the student do while you are running around getting other things done. Admitting Date: Discharge Date: D/C Dx: list all in order of importance Attending: Residents: Consults: list name and service

Procedures and Studies: briefly state date and results Reason for Hospitalization: include brief presentation, pertinent labs, and physical findings. Hospital Course: Briefly address what happened during hospitalization D/C Condition: Dispostion: home, name of nursing home, etc. Discharge Instructions: Diet: Activity: D/C Meds: list names and dosage F/U: Pending issues: list any studies that are pending at discharge or specific issues that you want to make sure are not missed at F/U. (Labs/tests that are not back yet.) Example Format for Discharge Dictation: This information can be in any order you prefer. Of note, a good discharge note makes this very easy. Say your patient’s name and SSN, your name, and the attending’s name. Admission and Discharge Date: Admitting diagnoses: Discharge diagnoses: Reason for hospitalization: Procedures and Studies during Hospitalization: Consultants: Hospital Course: It is usually best to address this by listing the systems but you can dictate the overall hospital course when the patient does not have many medical problems or had a very short stay. D/C Condition: Disposition: D/C Instructions: 1. Diet: 2. Activity: 3. Meds: F/U: Deaths: Unless the attending of record is present at the death and completes the paperwork, the medicine intern on call pronounces all deaths. When a nurse calls to let you know of a death, go see the patient in as timely fashion as possible. Check for response to verbal/painful stimuli, fixed/dilated pupils, lack of pulse, and use your stethoscope to check for heart sounds/breath sounds. Note the time you pronounced the person dead. Write a progress note that describes the above findings and documents that you notified the attending and the next of kin (the attending may do this).

COMMON FLOOR CALLS

BRADYCARDIA 1. If possible, have atropine and Zoll pads (Transcutaneous Pacer/Defibrillator 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 1. Do you believe the BP? Ask the nurse 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 cardiologist to arrange for 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 .25 mcg/kg/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 (also check ID section for fever workup)

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, anticipate this problem with your patient – leave explicit instructions in case of fever in your patients.

V. If your suspicion of infection is high, determine if antibiotics should be started. However, it is tricky starting new drugs on patients unless you are specifically told to do so at checkout. Think long and hard; there may be a good reason why the primary team didn’t

use antibiotics 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, especially in geriatric and immune compromised population.

• 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 patient lists. 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.

Most recommend a statin as well, checking the LFT and fasting lipid profile.

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)

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. Zolpidem (Ambien) 5 – 10 mg is another good choice and the nurses’ favorite.

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

TOPICS IN INTERNAL MEDICINE

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 = 1.5 x [HCO3] + 8 ± 2

Metabolic alkalosis: pCO2 = 0.7 x [HCO3] + 20 ± 5

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

chronic: HCO3 increases 4 for every 10mmHg change in pCO2

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

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

In short , the respiratory disorders can be determined using “Dr. McGinley’s box”:

Acidosis AlkalosisAcute 1 1 Chronic 4 5

This box helps help you remember the change in HCO3 for every 10 mmHg change in pCO2. Remember, it is always ±3.

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)

• 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, CPK & CK-MB q6 - 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. This is usually done in the ER. 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. Statin. Check FLP, LFT. 12. 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.

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’):

a. Prolonged anginal pain or repetitive episodes of angina at rest or during minimal exercise in the previous 12 hours.

b. 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.

c. 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: 300 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. In the VA, 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):

a. ST elevation (greater than 0.1 mV, two or more contiguous leads) b. 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.

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 – “IV Drug Abuser 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" even though many doubt such effect exists)

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

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

29% 100%

wave

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

• Arrhythmi

sudden syncope, injury

14 (4–38) Brady=sinus node dz, 2nd/3rd HB,

as 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.

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.

4. MDIs: steroids Fluticasone 2 p BID

Beclmethasone 2–10 p BID-QID

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 or your Palm for predicted peak expiratory flow.

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

CHEST TUBES (Although surgions and ICU attendings usually put them in, you may be able to help if you ask nicely.)

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)

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. In Tidewater area, 15 - 25% of pneumococcus shows intermediate resistance to PCN (which is still covered by ceftriaxone) If patient likely has pneumococcus and is critically ill, consider using vanco.

3. According to data 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 (6ml/kg if ARDS suspected)

Mode: AC or SIMV, rate of 12

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 5 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) < 105

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, ACS (Acute Coronary Syndrome), 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 some 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. There are IV heparin drip order forms that guide you through all of the important decisions in therapeutic anticoagulation.

4. 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. (1.5mg/kg qd can be used for DVT and PE treatment.) 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, CrCl <30)

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- 80 u/kg for PE, and 70 u/kg for ACS.

B. Heparin infusion-13 u/kg/hr for ACS and 18 u/kg/for for DVT/PE.

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.

BLOOD COMPONENT THERAPY (Check the guidelines on SNGH computer system for assistance to avoid the wrath of Dr. Ray Tahhan who is affectionately referred to as the “Blood Nazi”.)

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. 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).

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.

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)

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.

IV DRUG USER 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 IV drug users 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.

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

RA

Gout/pseudogout

SLE

Bacterial

TB

Aseptic necrosis

SLE

Rheumatic fever

Scleroderma

PMR

E nodosum

PAN

Amyloid

Scleroderma

Dermatomyositis & polymyositis

Viral arthritis

TB

Ankylosing spondylitis

Seronegative spondylo-arthropathies

Psoriatic arthritis

Rheumatic fever

Behçet’s syndrome

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, fungal, Cryptococcal antigen (CrAg), India Ink (check with lab or with ID to see if it is available), oligoclonal bands, MBP, Lyme titers, HSV PCR.

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– Clear or cloudy

N slight I <100 Mostly lymph

N

Barré

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.

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.

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.

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. DOT (direct observation therapy) is mandatory for most patients. Consult the Health Department if DOT is needed.

9. Incarcerated patients need to be cleared by the jail medical team 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. Although Demerol it is the 'textbook' favorite, it can cause seizures and is often avoided.

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.

9. Treat specific complications as they arise.

• Dehydration: pour in the fluids.

• Electrolytes: replete as necessary.

• Infection: DDX pancreatic necrosis, abscess, infected pseudocyst, aspiration pneumonia. Culture everything, consider CT abdomen, and cover bowel flora.

• Pseudocyst: suggested by persistent pain and high amylase. May resolve spontaneously after weeks of bowel rest with TPN or may need surgical intervention.

• Pulmonary: atelectasis, effusion, ARDS.

• Renal failure: from severe intravascular volume depletion.

RANSON'S CRITERIA (taken from NEJM 1994, 330: 1198)

Admission 48 hrs

Non–gallstone pancreatitis

Age >55 Decrease in Hct >10

WBC >16K Increase in BUN >5 mg/dl

Glucose >200 mg/dl

Ca <8 mg/dl

LDH >350 U/l pO2 <60

AST >250 u/l Base deficit >4 mM

Fluid deficit >6 l

Gallstone pancreatitis

Age >70 Decrease in Hct >10

WBC >18K Increase in BUN >2 mg/dl

Glucose >220 mg/dl

Ca <8 mg/dl

LDH >400 U/l Base deficit >5 mM

AST >250 u/l Fluid deficit >4 l

Risk factors

Mortality

1–2 < 1%

3–4 15%

6–7 100%

*severe acute pancreatitis if >/= 3 Ranson OR if any of the following:

shock, renal insufficiency, pulmonary distress.

ALCOHOLIC HEPATITIS

1. Presenting symptoms: Anorexia (87%), fever (50-75%), N/V (55%), weight loss (60%)

2. More specific symptoms: tender hepatomegaly, jaundice, ascites, edema, encephalopathy, bilateral parotid enlargement.

3. Labs: Leukocytosis, hypoalbuminemia, elevated alk phos, AST/ALT > 2 with AST <600.

4. Mortality is 20-65% at 6 months.

5. Treat by stopping EtOH (good luck!), supporting nutrition.

6. Role of steroids examined by Maddrey (Gastroenterology 75: 193). Note that this practice remains fairly controversial, as several large studies have produced discordant results--basically, if the alk hep is severe enough that you are considering using steroids, you should probably involve the GI service.

If you decide to use them: calculate the discriminate function (4.6 x PT + TBili). If >32, or patient has encephalopathy, short term improvement in mortality from taking 40 mg/day prednisone or equivalent for 4 weeks.

ASCITES (partially based on Runyon, NEJM 1994, 330: 337-342)

1. Diagnostic workup generally involves paracentesis.

• Two popular approaches for paracentesis are midline and right lower quadrant.

• If doing a midline approach, be sure to have patient empty bladder first.

• Do not tap near sites of previous abdominal surgery or overlying infection.

• Coagulopathy or thrombocytopenia are not contraindications except in presence of DIC or fibrinolysis; however, if pt is coagulopathic, use a 16 gauge or smaller needle.

2. Decide on therapeutic versus diagnostic paracentesis.

• Generally, for new onset ascites, a diagnostic paracentesis is safest.

• Do therapeutic paracentesis if there is compromise in respiratory function or tense/painful ascites.

• One may safely remove up to 5-6 liters of fluid providing it is removed slowly (30-90 min) and you place patients on fluid restriction to prevent hyponatremia. Some people advocate volume expansion with 5% albumin IV to prevent hypotension - dosage is 10g/L of ascites fluid removed - although this is typically done only on the LTU.

3. Send samples routinely for cell count and diff, culture, albumin, protein.

• Sensitivity of cultures is enhanced by inoculating blood culture bottles directly with ascites, although the labs now say this is unnecessary.

• Consider also sending tubes for glucose, LDH, amylase, Gram stain if ascites not thought to be due to cirrhosis. Send a serum LDH and albumin.

• If suspicion of TB or malignancy (bloody ascites?), AFB stain or cytology may be valuable.

4. Differential diagnosis based on serum ascites-albumin gradient (difference between serum and ascites albumin). High gradient implies portal HTN (accuracy 97%).

High gradient (> 1.1 g/dl) Low gradient (< 1.1 g/dl)

Cirrhosis Peritoneal

Alcoholic hepatitis

Cardiac failure

Massive liver metastases

Fulminant hepatic failure

Budd–Chiari syndrome

Portal vein thrombosis

Veno–occlusive disease

Fatty liver of pregnancy

Myxedema

"Mixed" ascites

carcinomatosis

Peritoneal TB

Pancreatic ascites

Biliary ascites

Nephrotic syndrome

Serositis

Bowel obstruction/infarction

5. Total protein concentration of ascites predicts risk of SBP (< 1 g/dl is high risk).

6. Medical treatment generally involves preventing reaccumulation of fluid and prevention of infection.

• sodium restriction. Goal of ~0.5kg decrease in wt/day.

• diuretics (start 40 mg Lasix to maximum of 160 mg/d and 100 mg spironolactone po to maximum of 400mg/d - increase as BP allows; increase dose only after waiting at least 2-3 days). Consider addition of metolazone 5-10 mg/day if unable to achieve desired diuresis.

•consider antibiotics for SBP prophylaxis (see section below)

CHILD-PUGH CLASS FOR CHRONIC LIVER DISEASE

Points scored

1 2 3

Encephalopathy grade

None 1–2 (mild confusion or lethargy)

3–4 (marked confusion or coma)

Bilirubin (mg/dl)* <1.5 1.5–2.3 >2.3

Ascites None Easily controlled Poorly controlled

Albumin (mg/dl) >3.5 2.8–3.5 <2.8

PT (sec >control) <4 4–6 >6

* Does not apply to primary cholestatic liver disease (e.g. primary biliary cirrhosis)

Total points Classification

5–6 Class A

7–9 Class B

10–15 Class C

CONSTIPATION

Some words of advice:

1. Afterload before preload. Avoid anything po if patient is impacted or obstructed.

Afterload = Dulcolax supp., Fleets enema, mineral oil enema, “Hog” enema (250 cc water, 125 cc mineral oil, 125 cc glycerin)

Preload = MOM 30 cc po qid prn

Inotropy = Lactulose 30 cc q2h until stools, Mag citrate 1 bottle.

Stool softeners = Colace 100-250 mg po bid.

2. All patients on chronic narcotics should be on a bowel regimen.

3. Do not give magnesium-containing products to patients with renal dysfunction (e.g. MOM).

GI BLEED

1. Site of bleeding can often be suggested by H&P. Note these are not hard and fast rules (e.g. brisk upper GI bleeding can cause BRBPR). Presumed location of bleed will help guide appropriate studies: EGD, colonoscopy, sigmoidoscopy, angiography, radionuclide scan, etc.

Upper Lower

Hematemesis BRBPR

Melena Hx diverticulosis

Epigastric pain Bowel surgery

NSAID use Colon Ca

Liver disease/EtOH abuse/varices IBD

Peptic ulcer disease Angiodysplasia

Esophagitis

Mallory Weiss

• Other relevant history includes prior bleeds, prior abdominal surgery, prior aortic surgery, PMH, trauma, coagulopathy, anticoagulant meds.

2. Clinical risk stratification guidelines (before endoscopy) - But remember: clinical judgment always comes first. The general goal is to use clinical criteria to determine timing of endoscopy and a combination of clinical criteria plus endoscopic criteria to determine need for admission and floor versus ICU. Moderate risk patients generally are admitted to the floor/tele or stepdown unless there are high risk endoscopic features. High risk patients are always admitted to the ICU.

Low risk

Moderate risk High risk

Age <60 Age >60

Initial SBP >100; vital signs now normal

SBP <100 on admission and/or mild ongoing tachycardia

Current SBP <100 and/or severe ongoing tachycardia

Transfusion req <2 units

Transfusion req >2 units

Transfusion req >5 units

No active major co–morbid disease*

Stable major co–morbid disease*

Unstable major co–morbid disease*

No liver disease Liver disease without coagulopathy or encephalopathy

Decompensated liver disease

No moderate or high–risk clinical features

No high–risk clinical features

* Major co–morbid disease defined as CAD, CHF, ARF, sepsis, disseminated malignancy, AMS, pneumonia, COPD, asthma

3. Evaluation and stabilization in the ER

Low risk Moderate risk High risk

• Vital signs q30 min

• Single IV OK

• Continuous ECG

• Vital signs q15 min with BP and O2 sat

• Two IVs with isotonic fluid

• T&C 2–4 PRBC

• Continuous ECG

• Vital signs q15 min with BP and O2 sat

• Two IVs with isotonic fluid

• T&C 2–4 PRBC

• Foley catheter

• Transfuse if no response to crystalloid

• Consider airway protection if massive hematemesis or AMS

• Surgical consult

For all patients, remember the following:

• Orthostatics are unreliable.

• Get CBC (can be misleading initially with "falsely high" HCT), coags, lytes, renal panel, LFTs, ECG if CAD or >45 years

• NG aspirate with 50-100 cc NS or tap water; don't lavage! Leave NGT in. OK to place NGT if patient is coagulopathic or has suspected varices. Remember that it is often helpful to use Hurricane spray or Lidocaine jelly before inserting NG's. If the ER has not already placed an NGT, you may want to check with the GI attending on call before placing an NGT. Many of them prefer that you not place an NGT if the patient is going to get an EGD on the same day because it can cause irritation that makes the EGD hard to interpret.

• Abdominal series only if abdominal distention , pain, or peritoneal signs

4. Treatment

• Volume resuscitate with IV NS to correct vital signs; transfuse HCT to >24 (>30 if CAD), platelets to >50. Consider FFP if PT >1.5x control, DDAVP (0.3 mcg/kg IV q12h x 2) if

uremic bleeding.

• Octreotide for patients with acute bleeding & evidence of advanced liver disease or portal HTN. Dosing: 100 mcg bolus then 50 mcg/hr.

• NPO until after endoscopy

• Avoid H2 blockers before endoscopy. Consider proton pump inhibitor (omeprazole at UCSF and SFGH; lansoprazole at VA). Avoid NSAIDs, ASA, anticoagulants.

5. Post-endoscopy treatment - just some reminders

• Ask GI when OK for patient to eat

• Don't forget Helicobacter pylori!

• Generally if patients are admitted they are observed for re-bleeding after endoscopy. Length of time depends on endoscopic and clinical risk criteria but usually =72 hrs

INTRACTABLE HICCUPS

Differential diagnosis

Esophagitis (chemical, infectious)

Drugs

Metoclopramide

Sulfa

Alcohol

Steroids

Barbiturates

CNS disorder (metastases, encephalitis)

Uremia

Pleural or subdiaphragmatic disease

Phrenic or vagal nerve irritation

Psychogenic

Idiopathic

Treatment - largely empiric and paradoxical

Chlorpromazine (Thorazine) or Haldol

Valsalva maneuvers

Lorazepam (Ativan)

Metoclopramide (Reglan)

NAUSEA

First Line: Promethazine (Phenergan) 12.5 to 25 po/pr/im/iv q4-6h prn

Prochlorperazine (Compazine) 10 mg po/im/iv q6h or 25 mg q12h prn

Lorazepam (Ativan) 0.5-2.0 mg po/iv q4-6h prn

Metoclopramide (Reglan) 10 mg po/iv q4-6h prn

Dexamethasone (Decadron) 10 mg po/iv q6h prn

Second Line: Dronabinol (Marinol) 2.5-10 mg po q6h

Ondansetron (Zofran) and granisetron (Kytril) are heavy duty antiemetics typically only for chemotherapy-induced nausea.

General tips:

• Beware neuroleptic malignant syndrome or dystonic reaction with excessive use of Compazine or droperidol (treat with Benadryl 50 mg IV/IM or Cogentin 10 mg IV)

• Compazine, droperidol, marinol are all relatively contraindicated in patients with known seizure disorder.

• A common side-effect of many anti-emetics is drowsiness.

• CRI patients usually have anti-emetics written by the fellows.

• As with other drug therapy, combinations of anti-emetics can sometimes succeed when single agents fail.

SPONTANEOUS BACTERIAL PERITONITIS (SBP)

1. Presents as patient with pre-existing ascites with abdominal pain, fever, decreased bowel sounds, or any deterioration of clinical condition (e.g. worsened hepatic encephalopathy, hypotension).

2. Diagnostic test is based on paracentesis and culture

• ascites WBC > 500/mm3 with PMN > 250/mm3 highly suggestive ->start antibiotics!

• A positive Gram stain is rare but diagnostic

• A positive culture is diagnostic

3. Most common organisms are E. coli, Strep species, and pneumococci.

4. Treat with third generation cephalosporin (e.g. cefotaxime, ceftriaxone). No role for aminoglycoside.

5. The risk of recurrent peritonitis may be decreased by long-term norfloxacin 400 mg qd or ciprofloxacin 400 mg qd. In high-risk cirrhotics (with ascitic protein <1g/dL) SBP prophylaxis should be initiated: norfloxacin, septra (1 DS tab 5x/week, or ciprofloxacin 750 mg/week.

TOXICOLOGY

**Remember with all poisonings, you can always call Poison Control at (or 1-800-222-1222) for assistance, especially helpful with Tylenol overdoses.**

ACETAMINOPHEN OVERDOSE

Check acetaminophen levels and check tox screen for co–ingestions.

Signs/Sx: 2-4 hrs: nausea, vomiting, diaphoresis, pallor.

24-48: RUQ pain, jaundice, clotting abnormalities.

1. Call poison control

2. NGT, lavage with 2 liters NS (useful only within first 2-4 hours).

3. Activated charcoal, if indicated, 1 g/kg po/per NGT typically x1 dose

4. Toxic dose is 140 mg/kg; blood level > 140 mcg/cc after 4 hrs is toxic (consult nomogram or poison control).

5. Give acetylcysteine (Mucomyst) if toxic levels possible

• Dose is 140 mg/kg po x 1, then 70 mg/kg po q4h x 17 doses; can also give IV (consult poison control for recommended duration and IV use)

• Best if within 12 h of ingestion, but start treatment for any toxic level.

6. Vigorous antiemesis if taking acetylcysteine po (treat patient as if receiving chemotherapy).

7. Follow acetaminophen levels q12h, LFT, PT/PTT.

8. Evaluate potential need for liver transplant: pH<7.3, Cr >3.4, INR >6.5, or rapidly rising AST.

9. Plasma half life is 2-4 hrs, but may be prolonged following OD, need to follow levels until no longer toxic.

BETA BLOCKER OVERDOSE

1. Signs/Sx- hypotension, nausea, vomiting, diarrhea, bradycardia, CNS depression, bronchospasm. Hyperkalemia, hypoglycemia, metabolic acidosis.

2. Obtain blood levels 3. EKG- AV block, prolonged QRS, asystole. Sotalol- torsades, VF, VT 4. Treatment

-Gastric lavage (NGT can further increase vagal tone--monitor closely)

-Calcium gluconate or carbonate 10% at 0.2 ml/kg over 10 minutes (watch for hypotension)

-Glucagon 5-10 mg initial dose, then drip of 1-5 mg/hr

-Atropine for bradycaria and hypotension. May need pressors.

-Pacing, IABP for severe poisoning

-Lidocaine, Mg, overdrive pacing for sotalol poisoning

CARBON MONOXIDE INHALATION

1. Symptoms generally depend on CO level (i.e. carboxyhemoglobin)

• 20–40%: Dizziness, headache, weakness, disturbed judgment, decreased visual acuity

• 40–60%: Tachycardia, tachypnea, ataxia, syncope, seizures

• >60%: Coma, death

2. To get CO level, get ABG with carboxyhemoglobin level (this needs to be specifically requested); routine pulse oximetry will be normal

3. Treat with 100% oxygen by tight–fitting mask or endotracheal tube. Hyperbaric rx for pts with coma, seizures, sx not resolving with 100% O2

4. Measure CO level q2–4 hours until <10%.

5. Half life 4-6 hrs when breathing RA, decreased to 40-80 minutes on 100% O2

COCAINE OVERDOSE

Effects

1. Local anesthesia and CNS stimulation via inhibition of catecholamine reuptake, giving generalized sympathetic stimulation.

2. CNS–rigidity, agitation, delirium, psychosis and short–lived seizures, intracranial bleed

3. Cardiac–VT/VF, coronary vasospasm/thrombosis, MI

4. Pulmonary–pneumothorax in ‘crack’ smoker, pulmonary edema

5. Gastrointestinal–mesenteric ischemia/infarction

6. Renal–failure secondary to renovascular spasm/shock/rhabdomyolysis

7. Systemic-hyperthermia common and may be very impressive

8. Effects may be exacerbated by co-ingestion of alcohol

9. Short half life- approx 1 hour

Diagnosis

1. H&P

2. Labs: urine tox screen, CBC, lytes, glucose, CPK, UA for myoglobin

3. ECG, CXR, head CT if suspect cerebral hemorrhage.

Treatment

1. ABCs, vital signs (including rectal T) and ECG monitor.

2. For tachyarrhythmias, try labetalol (alpha plus beta blockade) or calcium channel blocker, as the conventional wisdom is that pure beta-blockers in cocaine-induced syndromes can cause unopposed alpha-stimulation, thereby worsening the underlying problem.

3. For HTN, give ß–blocker plus phentolamine (to prevent paradoxic HTN via ß2 blockade) 1–5 mg iv bolus, may repeat in 5–10 min or as drip at 0.1–2 mg/min; aim for DBP<100–110.

4. For agitation and psychosis, use droperidol and/or lorazepam prn

5. For seizures, give lorazepam (0.1–0.2 mg/kg iv q10–15 min for a total of 30 mg), but if status epilepticus, consider other causes such as continued drug absorption from broken bag of cocaine in GI tract

6. Decontamination via gastric lavage, charcoal and cathartic, or whole bowel irrigation if indicated (consult poison control).

ETOH INTOXICATION/WITHDRAWAL

1. Tremulousness (6–12 hrs. after last drink)

• Irritablity, hypervigilance, tachycardia, HTN, coarse tremor of hands and tongue-"tongue wag"

• Thiamine 100 mg IV, MVI, folate 1 mg IV/PO. Give thiamine before glucose.

• Mg replacement, watch for drop in phosphate

• Ativan 1-2 mg IV q 4-6h, Librium 25–100 mg IV/po, or Valium 5–20 mg IV q4-6h until it stops. Monitor closely for oversedation.

2. Seizures (12–48 hours after last drink)

• If no past h/o seizure, or if seizure is focal in onset, evaluate for other causes of sz.

• If past h/o EtOH seizure, treat as other seizures but loading with anticonvulsants not indicated. May use 1-4 mg Ativan at presentation for prophylaxis.

3. Delirium Tremens–autonomic instability with fluctuating mental status. 2–7 days after last drink, usually with visual hallucinations, perspiration, fever, tachycardia, hypertension. This is a medical emergency. Mortality is approximately 5%.

• Ativan 1-2 mg IV, Librium 25–100 mg IV/po, or Valium 5–20 mg IV at presentation, repeat as needed in 1 hr, then Ativan 1-2 mg q 4-6hr or Librium 25–100 mg q 4–6hr. x 24 hrs. Reduce the initial 24 hr dose by 25% over next 2–3 days in divided doses. Monitor respirations.

• thiamine, folate, MVI iv/po

• replete Mg, K, Ca, PO4

• rule out infection, pneumonia.

• admit to monitored setting.

G-HYDROXYBUTYRATE (GHB) OVERDOSE

1. History of ingestion from friends or witnesses (group parties); check coingestions

2. Symptoms: unconsciousness (GCS typically below 8), vomiting and myoclonic movements with emergence and recovery

3. Signs: bradycardia, hypotension, coingestion of ETOH (30%) or other substances (25%), mild hypothermia, respiratory acidosis

4. Treatment: TIME. Recovery is typically within 2 to 4 hours, occurs spontaneously and correlates with the presenting GCS (lower = longer), usually does not require intubation unless there is a significant coingestion

OPIATE OVERDOSE

Effects

1. CNS–sedation and respiratory depression, seizures with meperidine, propoxyphene and codeine (esp. in renal insuff.)

2. Pulmonary–acute noncardiogenic pulmonary edema.

3. Half life varies: 2-3 hrs for morphine, 22 hrs for methadone

4. Beware co-contaminants used to cut heroin--caffeine, strychnine, phenacetin, quinine.

Diagnosis

1. H&P (pinpoint pupils, hypothermia, CNS and resp. depression)

2. Response to naloxone (be aware of risk for seizure, withdrawl and noncardiac pulmonary edema)

3. Labs: urine tox screen (however, certain synthetic opioids such as fentanyl are not detected by routine tox screen), CBC, lytes, glucose, ABG, CXR, consider acetaminophen/ASA levels if combination drugs ingested, CK if considering rhabdomyolysis.

Treatment

1. ABCs, oxygen.

2. Naloxone (to reverse respiratory depression): 0.1–1 mg iv, may repeat dose q2–3 min up to a total of 10–20 mg. Necessary to monitor at least 3–4 hrs after last naloxone dose which has t1⁄2 of 1 hr vs. most opioids which have longer t1⁄2; recommend 6–12 hr observation after opioid–induced coma and monitor for acute withdrawal syndrome in opiate–dependent pts. Longer monitoring needed if OD on methadone

3. Decontamination via gastric lavage, charcoal and cathartic; consider whole bowel irrigation if drug packets ingested.

SALICYLATE OVERDOSE

Check salicylate level and check tox screen for co–ingestions. Try to determine whether salicylate was regular or enteric–coated (affects pharmacokinetics).

Signs/Sx: hyperventilation->resp alkalosis, metabolic acidosis, tinnitus, vomiting, tachycardia, fever, lethargy, confusion, cerebral and pulmonary edema, seizures.

Rx: 1. Call poison control

2. NGT, lavage with 2 liters NS.

3. Intubate for respiratory depression if indicated

4. Activated charcoal, if indicated, 1 g/kg po/per NGT (consult poison control regarding the use of multiple doses of activated charcoal).

5. Give fluids if hypotensive. Make urine alkaline with IVF: 1⁄2NS & 2 amp NaHCO3/l

at 10–15 cc/kg/hr until urine output good, then D5W + (1–4 amps) NaHCO3/l & 20–40 mEq KCl/l at 1–3 x maintenance requirement.

6. External cooling if febrile (no acetaminophen!)

7. Hemodialysis indicated if level >130 six hrs after ingestion, refractory acidosis, persistent CNS symptoms, and/or if renal failure.

8. Follow salicylate level every 4-8 hrs until falling

9. Correct clotting abnormalities if present- FFP or Vit K

10. Plasma half life 2-3 hrs, 20-36 hrs following OD.

TRICYCLIC ANTIDEPRESSANT OVERDOSE

->remember, Doxepin is a tricyclic.

Signs/Sx: may take up to 6 hrs, anticholinergic (agitation, big pupils, fever, HTN, tachycardia), CNS depression, seizures, arrhythmia including VT, AV block, IVCD, bradycardia.

Rx: 1. Call poison control. Check tox screen for co–ingestions. Measure metabolite levels as well - these are also toxic.

2. NGT, lavage with 2 liters NS. Ipecac contraindicated.

3. Thiamine, Naloxone, D50, intubate, monitor, generous IV access, volume expansion

4. Beware QRS on EKG >0.10 sec; VT, VF, myocardial depression can ensue (Q on T phenomenon).

5. Activated charcoal 50 to 75 g x 1.

6. Bolus with 1 or more amps of NaHCO3 IV push for widening QRS or arrhythmias.

7. Do not use any class IA ( quinidine, procainamide) if VT occurs. No Beta blockade for arrhythmias. Physostygmine only if mild poisoning, NEVER if arrythmia present.

8. Half life 25-30h, but can be longer in OD

ENDOCRINE

MISCELLANEOUS THYROID TIPS

1. TSH alone is usually an adequate screening test (unless you suspect pituitary disease).

2. If TSH is abnormal, get FT4 and T3.

3. When interpreting TFT's,

a. TSH assay precision is higher than precision for FT4 and T3.

b. In a hospitalized patient, remember to think about sick euthyroid syndrome (SES). The TFT's can be varied but the most common variant is low TSH, low or normal FT4. Sick euthyroid usually causes only mild perturbations in thyroid function tests: markedly abnormal values are usually NOT due to SES.

4. IV Synthroid dosing is HALF the po dose.

5. When treating newly dx'ed hypothyroidism, start LOW (unless the patient is in myxedema coma) and go SLOW (don't precipitate AFib, MI). It takes months for TSH levels to reflect effects of therapy.

6. Thyroid storm is a life-threatening emergency (get endocrine consult). This condition occurs in Graves' disease, and can be precipitated by stress, infections, and iodine loads (e.g. CT contrast). Mainstays of treatment are propranolol (beta-blocking effect plus decreased peripheral conversion of T4 to T3), PTU or methimazole, potassium iodide (after the propranolol and PTU is on board, since neg feedback on T4/T3 release by thyroid), steroids (increases conversion of T4 to T3), and treating the underlying cause. These patients have a high mortality and should be in the ICU.

CORTROSYN STIMULATION TEST

1. Screens for primary and secondary adrenal insufficiency. Patient cannot be taking glucocorticoids at the time of the test. If given steroids, must be off cortisol more than 24 hrs. If you suspect adrenal insufficiency in an unstable patient, give steroids and test later. Decadron is the one option for "stress-dose steroids" that will not interfere with the serum cortisol test later.

2. Start IV and ensure some way to rapidly draw blood (either a central line, expendable peripheral IV, or confidence in your phlebotomy skills).

3. Order 0.25 mg cortrosyn from pharmacy and reconstitute. Low dose tests are also available.

4. Draw baseline cortisol level. Inject cortrosyn and flush IV.

5. Wait 45 minutes, and draw a second cortisol level, send to lab.

6. Normal response is cortisol level >20 mcg/dl. However, the specific value that establishes the dx of adrenal insufficiency is controversial.

INSULIN SLIDING SCALE

*Although in wide-spread use, insulin sliding scales are an inefficient and non-physiologic method of managing diabetes.

Fingerstick qid with Insulin Lispro SQ coverage (Use regular insulin if no other insulin or oral hypoglycemic medication is given in addition to the sliding scale.):

Fingerstick Blood Sugar Action <40 1 amp D50 iv and call HO <60 Give 4oz of juice and repeat in 15 min 61 – 150 No Coverage 151 – 200 2U Lispro insulin SQ 201 – 250 4U Lispro insulin SQ 251 - 300 6U Lispro insulin SQ 301 – 350 8U Lispro insulin SQ 351 – 400 10U Lispro insulin SQ >400 12U Lispro insulin SQ and call HO

Sliding scale advice:

•May need to decrease doses in renal failure (insulin is not as rapidly cleared)

•May need to increase doses for patients who are septic or treated with steroids (insulin resistance)

•Patients on TPN/PPN may need an insulin drip (insulin can be added to TPN)

•Mild hyperglycemia is better than hypoglycemia.

•Patients/nurses appreciate changing to FS qd once their insulin requirements are established

•Do not discharge patients on insulin sliding scales; instead, find an appropriate outpatient regimen before discharge.

Oral hypoglycemics in the hospital:

•It's often easiest to just take patients off of these when they are admitted and put them on a insulin regimen, since patients' po intake in the hospital is unpredictable and rarely the same as their usual diet. Once patients are stabilized/awaiting placement, it may make sense to put them back on their oral agents.

•Hold Metformin when patients are admitted, since it's hard to predict who may be getting a large IV contrast load at some point (and Metformin plus IV contrast may equal renal failure & lactic acidosis--these are bad)

•Hold sulfonylureas when patients will be NPO for any reason

DIABETIC KETOACIDOSIS

*Of note, DKA can occur with glucoses as low as 250-300. The key to the diagnosis is, as the name suggests, the presence of ketones and acidosis.

1. Volume replacement: More important than insulin, allowing pt to pee out glucose/ketones! NS to treat hypovolemia (fluid deficits may be on the order of >5 liters), then follow with NS or 1/2NS at 150-400 cc/hr to keep urine output >30 cc/hr. Watch for pulmonary edema and volume overload, esp for pts w/CAD or renal insufficiency.

2. Insulin: loading dose of 0.2 u/kg IV (usually 10 units IV is the amount needed to saturate all receptors) followed by maintenance drip of 0.1 u/kg/hr. Try to decrease glucose by 75-100 mg/dl/hr. You can change to sq insulin using a modified sliding scale once the anion gap closes. Some points to remember about this are:

•Divide the amount of insulin the patient would be getting on the insulin drip into NPH and regular, using the following formula:

2/3 as NPH, 1/3 as regular

2/3 in the morning, 1/3 in the evening

This is also a good way to determine a home regimen for a newly diagnosed diabetic who has been on a sliding scale in the hospital.

• Only d/c the insulin drip 1-2 hrs AFTER starting the sliding scale to prevent rebound hyperglycemia and DKA. For instance, once the anion gap is closed and the patient is eating, give the first dose of NPH about an hour before their meal, then let them eat, then d/c the insulin/D5 drips about an hour later.

3. The goal is to close the anion gap, not to reduce hyperglycemia. Usually, the serum glucose will normalize before the gap is closed. At this point, you still need the insulin drip to promote metabolism of ketones. When serum glucose decreases to 250-300 mg/dl, remember to change fluids to include D5 or even D10; continue insulin drip at slightly lower rate (e.g. 2-4 u/hr). Note that the anion gap is a better indicator of patient's status than ketones, as the lab test for ketones at most of the hospitals misses betahydroxybutyrate (the primary ketone in DKA).

4. Patient may still be in DKA when anion gap closes if bicarb still low.

5. Potassium replacement: potassium will initially be falsely elevated due to acidosis, but can drop quickly. Wait until potassium is 4.0-4.5, then begin replacement aggressively e.g. add 20 mEq KCl to each liter of fluid (you may also need to give K orally or through a different line).

6. Patient should usually be in the unit/stepdown unit for close observation and frequent labs. Make sure that you have good IV access; it is often convenient to establish an arterial or central line for frequent blood draws.

7. Do a work-up for a precipitating cause: Infection, infarction, no insulin, incision (surgery), and/or intoxication.

8. If a patient is admitted with DKA as their first presentation with diabetes, make sure they get adequate diabetic teaching before discharge (nursing staff can help with this).

HHS (HYPERGLYCEMIC-HYPEROSMOLAR STATE)

This is treated much the same way as DKA (mainstays of treatment are fluids, insulin drip, and careful monitoring and repletion of electrolytes such as potassium). Some additional things to remember are:

1. The glucoses are usually much higher than in DKA; as a result, these patients' fluid deficits can be up to 10 liters.

2. Calculating the free water deficit is the best way of gauging the type of fluid you are giving and also how fast you should give it. Use the corrected sodium (corrected for hyperglycemia) as a way of measuring this.

3. It may be useful to place an NG tube to give free water boluses. This way, you can avoid repleting free water solely IV (you won't have to use as much NS, or worse, wage the war between D5W and the insulin drip), and can theoretically lessen the risk of pulmonary edema and volume overload.

4. Note that severe AMS and coma really only occur once serum osm >340--if the patient is altered with a serum osm less than 340, you should investigate other causes of AMS.

RENAL

ACUTE RENAL FAILURE

I. What is acute renal failure? There are multiple definitions, including:

• an increase in serum creatinine of 0.5 or more above baseline

• a 50% or greater increase in the serum creatinine

• a reduction in the creatinine clearance by 50% or more

II. Etiology:

A. Prerenal causes – 70% of all ARF, can progress to ATN (a continuum)

1. Hypovolemia – vomiting, diarrhea, diuretics, hemorrhage, osmotic diuresis (DKA, hypercalcemia), burns, Addisonian crisis

2. Decreased effective intravascular volume – CHF, cirrhosis, nephrosis, shock, pancreatitis

3. Commonly precipitated by renal vascular changes: ACEI, cyclosporine, NSAIDs

B. Postrenal causes

1. Urethral obstruction - BPH, prostate CA

2. Neurogenic bladder, spinal cord injury

3. Ureteral obstruction – retroperitoneal fibrosis, bilateral calculi, colorectal CA, cervical CA

4. Intratubular obstruction – various crystals (uric acid, calcium oxalate, acyclovir, crixivan)

C. Intrinsic renal causes – classified according to site of injury

1. Acute tubular necrosis (ATN):

• ischemic (50%):

• any prolonged prerenal or hypotensive state

• vascular obstruction: renal artery stenosis, TTP–HUS, large-vessel vasculitis, atheroembolism, renal vein thrombosis

• toxic (35%): radiocontrast dye, aminoglycosides, cyclosporine, ampho, rhabdo, hemoglobin, acyclovir, chemotherapeurics (cisplatinum, MTX, mitomycin C),…

2. Acute interstitial nephritis (AIN):

• allergic (most common): PCNs, cephalosporins, sulfas, NSAIDs, rifampin, diuretics, many other rare causes

• infections: pyelonephritis, HIV, leptospirosis, Legionnaire's, hantavirus, …

• autoimmune disorders: some SLE, Sjogren’s, cryoglobulinemia

• infiltrative diseases, including sarcoid

• amyloid, myeloma

3. Glomerulonephritis (GN): sub-classified by serologies:

• Anti-neutrophil cytoplasmic autoantibody (ANCA) positive: Wegener’s, Churg-Strauss, microscopic polyarteritis, ANCA-associated crescentic GN

• Anti-GBM Ab positive: Goodpasture’s (with lung involvement), anti-GBM GN (renal involvement alone)

• Immune complex GN (low C3, C4): SLE (ANA+), post-strep/peri-infectious GN (ASO+), cryoglobulinemic GN (HCV+/cryo+), IgA GN, MPGN

III. Diagnostic evaluation:

1. Place Foley to relieve obstruction – especially if anuric

2. Examine the urine!!!:

• prerenal: bland, hyaline casts (nonspecific)

• ATN: pigmented granular casts and renal tubular cells (nonspecific)

• AIN: WBC, WBC casts, eos (all specific but insensitive) – WBCs with (-) LE is classic for eos

• GN: dysmorphic RBCs, RBC casts (also specific but insensitive)

• proteinuria: raises suspicion for GN (especially if nephrotic-range (>3gm/24h) or in combination with hematuria). <1-2gm/24hr often seen in AIN.

3. Check BUN/Cr ratio: >20 implies prerenal (beware other causes of increased BUN, e.g. GIB), <15 implies intrinsic renal disease

4. Calculate FENa (developed for oliguric (<400mL/24h) renal failure, but often applied with less validity to nonoliguric renal failure): <1% favors prerenal, >1% favors intrarenal/ATN (decreased concentrating capacity).

5. for acute on chronic renal failure, plot 1/Cr vs time

6. obtain renal ultrasound to look for:

• hydronephrosis (obstruction)

• asymmetric kidney size (renal artery stenosis)

• bilateral small kidneys (chronic medical renal disease) – Bx of little yield in these patients

• large kidneys (DM, amyloid including myeloma, lymphoma, PCKD, HIV)

7. serologies (especially complement) if GN is high in DDx

8. 24hr urine for Cr and protein to quantify creatinine clearance and proteinuria

9. Bx may guide management in AIN and GN

10. Observe UOP: oliguric (<400mL/24h) renal failure is a/w worse prognosis, except with contrast nephropathy (typically oliguric with good recovery)

IV. Principles of Treatment: Specific treatments depend on etiology. Some possibilities (consult nephrology!):

• fluid challenge: prerenal

• bicarbonated IVF (1/2 NS + 2amps NaHCO3/L or D5W + 3amps NaHCO3/L at 100-150mL/hr, titrate to high volume UOP with urine pH>6): rhabdo and acute uric acid nephropathy

• steroids: some AIN, SLE, some GN

• cytotoxic agents (cyclophosphamide, chlorambucil): some GN

• plasmapharesis/plasma exchange: anti-GBM, TTP

• renal dopamine (1.5-3 mcg/kg/min): very controversial

•.manage fluids carefully, especially if oliguric (give IVF for prerenal states, but beware volume overload and pulmonary edema)

• watch electrolytes, especially K, Mg, HCO3, Phos, and Ca (be careful with IV Ca in hyperphosphatemia – CaPhos products >70 can cause metastatic calcification)

• D/C contributing drugs (ACEI, NSAIDs, nephrotoxins)

• Renal dose all meds (see below for reminders)

• Treat bleeding with PRBC (Hct>30 has better outcome in uremic bleeding), dDAVP (0.3mcg/kg, round up to nearest 4mcg – note rapid tachyphalaxis), estrogens (+/-), platelets, and hemodialysis (best therapy)

• Aggressively treat infections, a major cause of mortality – patients may not mount fever

INDICATIONS FOR DIALYSIS

The mnemonic AEIOU is often used for indications for emergent dialysis:

A cidosis, especially if severe (pH < 7.2 and refractory to HCO3 or unable to give HCO3 due to volume overload) or symptomatic (arrhythmias).

E lectrolytes, especially potassium with EKG changes. Temporize with Ca, D50, insulin, bicarb, kayexalate.

I ngestions, especially those that cause renal failure such as salicylates or ethylene glycol

O verload, i.e. volume overload causing pulmonary edema. Temporize with nitrates and mega doses of Lasix (160–200 mg IV) – push slowly to avoid ototoxicity.

U remia, i.e. confusion, pericarditis, seizures, platelet dysfunction with severe bleeding, intractable N/V

CHRONIC RENAL FAILURE

Keep the following considerations in mind when writing orders on renal patients:

• Renal diet (low Na, low K, low PO4) – low protein is controversial

• Nephrocaps 1 po qd to replace water-soluble vitamins lost in HD

• Calcium binders (see hyperphosphatemia section)

• Renally adjust all medications (your friendly pharmacist can help)

• Avoid magnesium containing compounds such as MOM, Mylanta, Fleets enema.

• Be careful with maintenance IVF – ESRD pts may not need any

• On exam, check access sites: catheters without infection, thrill over shunt?

• Do not use current or potential UE shunt sites for blood draws and IVs

• Do not take BP in extremity with a shunt

PERITONEAL DIALYSIS (PD)

I. Uses peritoneum as the dialysis membrane

A. Continuous ambulatory PD (CAPD): 2-3L abdominal dialysate changes 4-5x/day

B. Continuous cycling PD (CCPD): automated exchanges during sleep, may use CAPD in addition

II. Fluid removal is controlled by concentration of dialysate (1.5%, 2.5%, 4.25% glucose) and frequency of exchanges (max fluid removal with 4.25% q2h)

III. Complications:

A. Peritonitis: usually managed as outpatient with intraperitoneal abx. Send fluid for cell count, diff, Gm stain, Cx. Admit for recurrent infection, failure to respond to appropriate abx, abscess, organ perf, sepsis (could these be any more obvious?)

B. Catheter and exit site infections: may need to remove peritoneal dialysis catheter

C. Hyperglycemia: use escalating doses of SQ NPH or intraperitoneal insulin at 1.5 to 4 times SQ doses

CONTINUOUS VENOVENOUS HEMOFILTRATION (CVVH) AND HEMODIALYSIS (CVVHD)

• Used primarily in patients who cannot tolerate conventional HD due to hypotension (fluid shifts are minimized in CVVHD)

• Good for removing large volumes of fluid

• Fluid removal is on a mL/hr basis (typical starting point is 100mL/hr). May run "net even" for hemodialysis without ultrafiltration.

• CVVHD is slower than conventional HD for acute solute removal (overdose, severe hyperkalemia)

• Requires ICU care

• May have higher drug clearances than conventional HD – dose most drugs for GFR=20mL/mi

DRUGS REQUIRING ADJUSTMENT IN RENAL FAILURE

(Disclaimer: this list is not complete!!!)

•Antibacterials, antifungals, antituberculars, antivirals: always check Sanford’s

•ACEI’s: most except fosinopril

•Atenolol needs renal dosing, but not metoprolol

•Acetaminophen: q6h if GFR<50, q8h if GFR<10

•Use glipizide instead of glyburide

Acetazolimide Ethosuximide Phenobarbitol

Alendronate Famotidine Primidone

Allopurinol Flecainide Procainamide

Bretylium Gemfibrozil Pravastatin

Buspirone Glyburide Ranitidine

Carbamazepime Hydralazine Simvastatin

Chlordiazepoxide Lithium Sotalol

Codeine Meperidine Spironolactone

Cimetidine Metformin Terbutaline

Clofibrate Methyldopa Theophylline

Digoxin Metoclopramide Valproic acid

Disopyramide Morphine Venlafaxine

Verapamil

NEUROLOGY/PSYCHIATRY

SEIZURES

1. If patient is still seizing--remember your ABC's:

• Give O2, position patient on side to prevent aspiration. Suction airway as needed. Do not try insert airway.

• Prevent patient from injuring himself/herself.

• If seizures continue after 2-3 minutes, try to start an IV and abort the seizure with Ativan 2 mg. Alternatively, Ativan IM q5 minutes to maximum of 8 mg or Valium PR 20mg.

• Give thiamine 100 mg IV first, then 1 amp D50.

• If seizure does not stop in 30 minutes, patient is in status and will need ICU management.

2. Once seizure stopped,

• Place oral airway. Get ABG if patient appears cyanotic.

• Establish IV access and send basic labs (CBC with diff, lytes, BUN, creatinine, glucose, Ca, Mg, albumin, antiepileptic levels).

• Evaluate if this is status: continuing seizing for >30min, no consciousness after 30 minutes, if pt seizes again without achieving normal consciousness. If status, pt to ICU, Neuro consult.

3. Load with phenytoin 15-20 mg/kg in 3 divided doses at 50 mg/min (usually 1 g total).

• Remember, phenytoin is not compatible with glucose-containing solutions or with Valium. If you have given these meds earlier, you need a second IV.

4. Consider common causes of seizures (work-up generally involves basic labs and a head CT for new onset seizures).

• Alcohol withdrawal

• CNS lesion (tumor, CVA, head injury, meningitis/encephalitis, etc.)

• Meds (Demerol, benzo withdrawal, penicillin, lidocaine toxicity, INH, ASA, TCA, cocaine, Benadryl, amphotericin, theophylline, etc.)

• Metabolic (low glucose, Na, Ca, or Mg)

• Other (HIV, malignant hypertension, hypoxia, uremia)

5. If an inpatient, write for seizure precautions. Watch for metabolic acidosis and rhabdomyolysis.

6. Remember that all patients with medical conditions which could potentially affect their ability to safely operate a motor vehicle (i.e. seizures, syncope) has to be informed by their physician that the seizure must be reported to the DMV.

ALTERED MENTAL STATUS (AMS) (if patient has AIDS, see "AIDS and AMS")

The mnemonic "MOVE STUPID" can jog your memory of the various causes of AMS:

Metabolic – B12 or thiamine deficiency (more rarely, Wilson’s dz or niacin deficiency)

Oxygen – hypoxemia is a common cause of confusion. Also, anemia and decreased cerebral blood flow (e.g., from low cardiac output), CO poisoning

Vascular – CVA, intracerebral hemorrhage, vasculitis, TTP, DIC, hyperviscosity, hypertensive encephalopathy

Endocrine – hyper– or hypoglycemia, hyper– or hypothyroidism, high or low cortisol states and Electrolytes, particularly sodium or calcium

Seizures – pts are often confused when post–ictal, and can be unresponsive in status epilepticus. Also think of Structural problems such as lesions with mass effect, hydrocephalus

Tumor, Trauma, or Temperature (either fever or hypothermia)

Uremia – A related disorder is hepatic encephalopathy.

Psychiatric – this is a diagnosis of exclusion. ICU psychosis and "sundowning" are commonly seen in the hospital. Rarely, Porphyria can cause confusion.

Infection – any sort, including CNS, systemic, or a simple UTI in an elderly patient

Drugs – including intoxication or withdrawal from alcohol, illicit or prescribed drugs. This is common in hospitalized pts, particularly elderly. Degenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s cause a slower decline in cognitive function.

Initial Evaluation of AMS:

-Some standard therapies include:

• thiamine, 100 mg IV

• glucose, 1 amp of D50, after thiamine (to prevent precipitation of Wernicke's) if you can't get a rapid finger stick (i.e. at SFGH)

• naloxone (Narcan), usually 0.4-1.2 mg IV if there is any possibility of opiate OD

• oxygen by nasal cannula or mask, with oropharyngeal airway if necessary

-Neuro exam: pupils, doll's, gag (if neg, intub?), moves away from midline w/painful stim = purposeful movement

-Have a low threshold for getting a head CT in any patient that has focal neurologic signs or is at risk for CVA. If you think pt is herniating (blown pupil), call neurosurgery and consider dexamethasone, hyperventilation and mannitol.

-The old truism about LP's applies here: If you think about it, you should probably do it--particularly in any patient with fever or meningeal signs, or any patient who is immunosuppressed. (see ID section for more details)

GLASGOW COMA SCALE

Total score is the sum of eye + verbal + motor. The range of scores is from 3 (totally unresponsive) to 15 (normal). Intubated patients cannot have verbal responses, so they are scored as the sum of eye + motor, followed by a T and the maximum score is thus 10T.

Eye opening Verbal response Motor response

Spontaneous 4 oriented 5 follows commands 6

to voice 3 confused 4 localizes pain 5

to painful stimuli 2 inappropriate words 3 withdraws from pain 4

Never 1 unintelligible sounds 2 flexor response 3

none 1 extensor response 2

none 1

MINI MENTAL STATUS EXAM (MMSE)

Orientation Language

Name: season/date/day/month/year (5) Repeat "No ifs, ands or buts." (1)

Name: hosp/flr/town/state/country (5) Follow three step command (e.g. take this

Registration paper, fold it in half and hand it to me) (3)

Name two objects (2) Write "close your eyes" & ask pt to obey

Recall written command (1)

Three words immediately (3) Ask pt to write a sentence (1)

and then in 3min (3)

Attention Ask pt to copy a design (intersecting

Serial 7s or "world" backwards pentagons) (1)

or days of week backwards (5)

Total=30

CORD COMPRESSION

Suspect this diagnosis in patients with new weakness or change in sensation (especially if they have a demonstrable level), new bowel/bladder retention or incontinence. Prognosis is dismal for pts w/no function for >24h. Prognosis is best for pt new, incomplete loss (i.e. weakness). This is a surgical disease--call Neurosurg early. That having been said,

- Stabilize the spine: i.e. collars for C-spine, Turtle shells (TLSO) for T/L-spine.

- Dexamethasone (40mg qD, then 20mg qD)--not always indicated (in case of traumatic fracture, for instance)

- If tumor, radiotherapy.

FORMULAS

Electrolytes/acid–base

Na correction: for every 100 mg/dl increase in glucose > 150, sodium decreases 1.6 mEq/l

Ca correction: for every 1 g/dl decrease in albumin below 4.0, Ca decreases 0.8 mg/dl

Plasma osmolality = 2 [Na] + [Glu]/18 + [BUN]/2.8; normal 270–90.

Osmolal gap = measured osm – calculated osm

>10 abnormal, <0 is usually calculation or lab error. Increased osmolal gap caused by alcohol, renal failure, methanol, ethylene glycol (check urine under woods lamp), mannitol, hyperlipidemia, hyperproteinemia

Anion gap = [Na] – [Cl] – [HC03] Normal 12 ± 2

Delta AG/Delta HCO3: value > 1 suggests coexistent metabolic alkalosis or compensation for respiratory acidosis; value < 1 suggests a coexistant hyperchloremic metabolic acidosis or compensation for respiratory alkalosis

Urine Anion Gap = [Na] + [K] – [Cl]

NH4 is the major unmeasured cation, so a strongly negative UAG suggests high urine NH4 and therefore GI source for acidosis; Positive # suggests RTA

Winter’s formula: predicted pC02 = 1.5 [HC03] + 8 ± 2

Water deficit = 0.6 [body weight in kg] [(Na/140)–1]

Cardiology

Cardiac output = HR x stroke volume

Fick equation: (75 cc O2/min/m2)(BSA in m2)

CO = –––––––––––––––––––––––––––––––––

8.5 x (1.36[Hb][SaO2]–1.36[Hb][Sv02])

SVR = [(MAP – CVP)/CO] x 80; normal = 700–1600 dynes/s/cm2

PVR = (Ppamean – PCWP)/CO; normal = 45–120 dynes/s/cm2

Other normal values for hemodynamic monitoring:

CVP, RAP: 0–8 cm

PASP: 15–30 cm

Ppa mean: 9–16 cm

PCWP: 3–12 cm

Pulmonary

A–a O2 gradient = FiO2 x (pATM - pH20) - (pCO2/R) - pO2

= FiO2 x (760 - 47) - (pCO2/0.8) - pO2

= [150–1.25 x pC02]–pO2 (sea level on RA) (normal 10 - 20)

increases with age; approximate adjustment = (age/4) + 4

Hematology

Reticulocyte index = (% retic/2)([Hct]/[Normal Hct])

Normal = 1; adequate reticulocyte response = 2–6.

Mentzer index = MCV ÷ RBC count.

If >13, favor iron deficiency over thalassemia.

Renal

Estimated cretanine clearance = (140)-age) (weight in kg) (0.85 if female) serum Cr x 72 Creatinine clearance = [Urine Cr] x Urine volume

(from 24hr urine collection) [Serum Cr] x 1440 Fraction Na excretion (FENa) = Urine Na x Serum Cr x 100% Serum Na x Urine Cr Transtubular K gradient = Urine K / Plasma K = Urine K x Plasma osm

Urine osm / Plasma osm = Plasma K x Urine osm

Normal value 7-12; if <7 suggests renal inability to secrete K (type IV RTA, adrenal insuff)

Endocrine

Average serum glucose = Hemoglobin A1C x 20

ACLS PROTOCOLS

VF (OR PULSELESS VT)

Check carotid or femoral pulse. If no pulse initiate CPR (± precordial thump for witnessed arrest).

1. Defibrillate

• Check rhythm. If still VF or VT,

• Defibrillate 200 J. Check pulse

• Defibrillate 300 J and recheck pulse

• Defibrillate 360 J and recheck pulse and rhythm

• CPR if still no pulse, IV access, intubate.

2. Epinephrine (1:10,000)

• 1 mg IV/ET and repeat q3–5 min or escalate dose 1-> 3-> 5 mg

• After each drug dose, defibrillate again with 360 J and recheck

or

Vasopressin

• 40 U IV, one time dose. (wait 10-20 minutes before starting epi)

3. Amiodarone

• 300mg IV push.

• May repeat once at 150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs.)

• After each drug dose defibrillate with 360 J and recheck

4. Lidocaine

• 1–1.5 mg/kg IV push.

• Can then give 0.5 mg/kg boluses q3–5 min up to 3 mg/kg total

• After each drug dose defibrillate with 360 J and recheck

5. Consider

• Magnesium 1–2 gm iv (refractory VF, Tosades, hypo Mg)

• Procainamide 30 mg/min, NTE 17 mg/kg

• Sodium bicarbonate 1 meq/kg iv (each amp has 44 or 50 meq of bicarb.)

ASYSTOLE

1. CPR until asystole confirmed in 2 or more leads.

2. IV, intubate

3. Consider causes: hypoxia, hyper/hypokalemia, acidosis, drug OD, hypothermia

4. Consider pacing

5. Epinephrine 1 mg IV/ET q3–5 min

6. Atropine 1 mg IV/ET, repeat in 3–5 min

7. Consider sodium bicarbonate 1 meq/kg iv

PEA/EMD

1. CPR, IV, intubate

2. Consider causes: hypovolemia, hypoxia, cardiac tamponade, tension pneumothorax, hypothermia, PE, drug OD, hyperkalemia, acidosis, MI

3. Epinephrine 1 mg IV/ET q3–5 min

4. Atropine 1 mg IV/ET if HR <60 bpm

BRADYCARDIA

1. Vitals, IV access, O2, monitor, pulse oximeter

2. Serious signs or symptoms (chest pain, SOB, AMS, hypotension, shock, CHF, AMI)

• Atropine 0.5–1 mg IVP

• Transcutaneous pacing (Zoll pads)

• Dopamine 5–20 mcg/kg/min IV

• Epinephrine 2–10 mcg/min IV

• Isoproterenol 2–10 mcg/min

3. Type II or complete heart block, no symptoms

• Transcutaneous pacing (Zoll pads)

• Transvenous pacer

4. Sinus, junctional, or Type I, no symptoms

• Observe

TACHYCARDIA

A. Unstable (i.e. symptoms of CP, SOB, AMS, SBP <90, CHF, ischemia/infarction)

1. If HR >150, prepare for immediate cardioversion

2. O2 by face mask; ensure airway, IV access

3. Consider trial of meds based on specific arrhythmia

4. Consider sedation unless patient hemodynamically unstable (hypotensive, pulmonary edema, unconscious)

5. Synchronized cardioversion

Atrial flutter/PSVT

Atrial fibrillation

VT

50 J 100 J 100 J

100 J 200 J 200 J

200 J 300 J 300 J

300 J 360 J 360 J

360 J

B. VTach, stable

1. O2 by face mask; ensure airway, IV access

2. Lidocaine 1–1.5 mg/kg IVP

3. Lidocaine 0.5–0.75 mg/kg IVP q5–10 min to total dose 3 mg/kg

4. Procainamide 20–30 mg/min IV up to 17 mg/kg total dose

5. Bretylium 5–10 mg/kg IV over 8–10 min, up to 30 mg/kg total dose

6. Synchronized cardioversion as though unstable

C. Wide–complex tachycardia, stable

1. O2 by face mask; ensure airway, IV access

2. Lidocaine 1–1.5 mg/kg IVP

3. Lidocaine 0.5–0.75 mg/kg IVP q5–10 min to total dose 3 mg/kg

4. Adenosine 6 mg rapid IVP

5. Adenosine 12 mg rapid IVP

6. Adenosine 12 mg rapid IVP

7. Procainamide 20–30 mg/min IV up to 17 mg/kg total dose

8. Bretylium 5–10 mg/kg IV over 8–10 min, up to 30 mg/kg total dose

9. Synchronized cardioversion as though unstable

D. PSVT, stable

1. O2 by face mask; ensure airway, IV access

2. Vagal maneuvers

3. Adenosine 6 mg rapid IVP

4. Adenosine 12 mg rapid IVP

5. Adenosine 12 mg rapid IVP

6. If narrow complex and stable, consider:

• Verapamil 2.5–5 mg IV, then 5–10 mg IV in 15–20 min

• Digoxin, diltiazem, ß blocker

• Synchronized cardioversion

7. If wide complex and stable, presume VT

• Lidocaine 1–1.5 mg/kg IVP

• Procainamide 20–30 mg/min IV up to 17 mg/kg total dose

• Synchronized cardioversion