A- Be Efficient=============
1) Tabulate your patients and add new events daily.
Develop a good sheet/table to keep track of your patients’ information/daily labs/ ‘to do’ list in a way making it easy for you to answer questions in the morning round and give sign-out notes in the evening to the oncall team.
2) Pre-round: 7:00-8:30AM
Make sure that your previous day progress notes are in the charts before rounds and make a raeview about the night/oncall course of the patient and write an additional note if necessary. Make you new daily patient list so you can work on the new orders/labs/consultations/procedures after the round. Use same notes daily, mention any clinical changes or events and update the labs/procedure results and medication changes. Any new instructions/managements given during the rounds add them.
How to write Progress Note
Date:
Room number:
Pt name:
Code status:
Follow the SOAP Notes Format
Subjective:
Describe your impressions of the patient. For example: Mr. XYZ feels better today, calmer, no CP or SOB, no N/V, NPO for cath. at 11: 30 AM.
This section should be utilized to report subjective information of clinical significance.
Objective:
This section is where you will report the measurable and observable information that you obtain from the patient and the chart.
Vital Signs:
36.2-74-18-129/42
SpO2 95% on 3 L
Overnight events (telemetry,SOB, CP, N/V/D... )
A/P: Assessment of pt and your plan for the day
LABS (Check Maxwell Quick Medical Reference to see how to fill this figure):
HEENT: NC/AT
LUNGS: CTA (B)
HEART: Clear S1S2, RRR
ABDOMEN: Soft, NT, ND, +BS
EXTREMITIES: no edema
ASSESSMENT:
-CAD - stable angina S/P PTCA 10 yrs ago-> positive persantine stress test
3/10/05-> cath. today
Cardiac CRP increased
-HTN
PLAN:
-H/H at 8 PM
-I/O
-CBCD, BMP in AM
-Consults:
-MEDICATIONS:
1) Atenolol 12.5mg po qdaily
2) ASA 162mg po qdaily
3) Lisinopril 10mg po qdaily
4) Lovastatin 40mg po qdaily
5) Lovenox 60mg SC BID
Signature
IMG Survivor
Its better to mix Assessment and Plan together:
1) CAD: Pt presented with CP and non-specific EKG changes. No CP since admission. Treadmil stress + for moderate proximal inferior septal reversible defect and small fixed inferior wall defect with EF 68%. Troponin x 3 negative. Pt was started on Lovenox since admission. After discussion with cardiology pt pending cath/angio tomorrow. Pt was started on ASA, metoprolol, lisinopril and statin.
a) continue ASA, metoprolol, lisinopril, statin
b) pending cath/angio tomorrow at 1:00pm
c) hold AM lovenox
d) NPO after midnight with IV fluid at 100cc D5NS
2) Asthma: Baseline on 10mg prednisone. Was started on 40mg prednisone on presentation 2/2 mild wheezing. Pt was started on12.5mg metoprolol last night. Pt on QVar, combivant and albuterol. No wheezing overnight.
a) taper prednisone slowly
b) continue on QVar, combivant and albuterol
c) continue on metoprolol as pt tolerates.
3-Post-round:
Give Priority to your “to do” list. Call consults, order new studies and replace electrolytes early. Always take care of your sickest patients first.
4-Be nice to nurses, clerks, PT, OT, RT and all other medical staff because they can make your life a lot easier. Interns are sleep-deprived and stressed, but remember to keep your cool. If you run into problems with a staff member call your resident/attending.
B- Learn how to solve the common daily problems (this section is not yet reviewed and may need correction, please follow up soon)
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i. Potassium: Each 10 mEq is equivalent to 0.1 increase on the lab level.
1.Supplement all potassium below 3.8-4.0 unless pt has renal failure (3.0-3.4 may be acceptable, check with resident
2.KCl 10mEq IV (run over one hour)
1.If pt has a central line you can run IV per protocol
2.Can give 1ml of 1% lidocaine with each 10mEq bag if it’s painful: be careful with pts with cardiac conditions
3.K-Dur 10mEq PO (tablet)
4.K-Lyte 25mEq PO (liquid)
a.Has a lot of bicarb so if pt has alkalosis give KCl
5.K-Phos 2 tabs PO
6.K-Phos 10mmol IV (run over one hour)
7.Give 10mEq for every 0.1 below 4.0
8.Watch potassium closely in pts on lasix.
9.You can add 20mEq KCl to each 1L bag of IV fluid
10.Remember K+ will not correct unless you replace Mg
11. Make sure to correct potassium cautiously in patients with renal disease, particularly those with end-stage renal disease.
ii. Magnesium
1.Supplement all Mg below 2.0 unless pt has renal failure (around 1.6 is fine, check with resident)
2.For every 0.5 deficit, you can give 1 g of Mg Sulfate
3.Magnesium Sulfate 1 g IV (run over 1 hour) or 400mEq MgOxide PO BID or TID
iii. Phosphorous
1.Consider supplement if less than 2.0
2.Particularly important for patients in respiratory distress (ATP).
3.K-Phos 2 tabs PO q daily
4.Neutra-Phos 2 packs PO q daily
a.only helps if pt is taking po
b.give it with meals
5.K-phos 10mmol IV
6.Na-phos 10mmol IV
iv. Calcium
1.check albumin to correct level
2.calcium carbonate
a.Tums: 500mg tab = 25 mEq cal
b.Os-Cal: 650mg = 13 mEq cal
v. Bradycardia (New Onset)
1. If the patient is symptomatic or hemodynamically unstable place the patient in Trendelenberg position and follow ACLS protocols (See ACLS: Bradycardia).
2. If ECG show either type II 2nd-degree or 3rd-degree AV block consider trans-cutaneously pacing the patient/consult cardiology fellow ad/or ICU/CCU Team.
3.If the patient is stable look for clues from the patient's Chart/medications list. Take focused history and do physical exam/vital signs.
Causes of bradycardia:
-Medications: Beta blockers (even if eye drops timolol which may interact with calcium channel blockers e.g Verapamil), calcium channel blockers, digoxin, amiodarone, clonidine
-Cardiac: Sick sinus, inferior MI, vasovagal, 2nd or 3rd degree heart block, junctional rhythm
-Instrinsic cardiac causes: Idiopathic degeneration (aging), infiltrative diseases (sarcoid, amyloid), collagen vascular disease, surgical trauma, endocarditis
-Autonomic: Vasovagal syncope, carotid-sinus hypersensitivity, coughing, micturition, defecation, vomiting
-Misc: Hypothyroidism, hypothermia, increased intracranial pressure (Cushing�s reflex), hyperkalemia, hypokalemia, obstructive sleep apnea, normal variant
NB: If the bradycardia is secondary to medications, be careful discontinuing them. Stopping rate control meds could cause a rebound tachycardia and precipitate myocardial ischemia.
vi. Tachycardia (New onsetand/or complicating preexisting cardiac problem?)
1.If the patient symptomatic or unstable follow ACLS protocols (see ACLS: Tachycardia), and get a crash cart into the room ASAP.
2.Obtain an ECG and examine the patient.
3.It is almost always prudent to slow down a stable narrow-complex supraventricular tachycardia (including suspected rapid a-fib or a-flutter) to make a definitive diagnosis of the rhythm.
-Prior to slowing the rhythm down, obtain continuous telemetry or ECG.
-Consider a vagal maneuver such as carotid massage (press for > 15-30 seconds)
-Deliver adenosine 6 mg rapid IV push, repeat with 6 mg, then 12 mg if no response. Be sure to warn the patient of flushing and chest pain associated with adenosine. Theoretic danger of bronchospasm but rarely seen.
Tachycardias are classified according to whether they have a regular rate and whether the QRS on ECG is wide or narrow. They are listed below with diagnostic clues and treatments. When in doubt, call for back up (e.g. cardiology, medicine, or ICU consult).
Narrow QRS, regular rate:
Sinus tachycardia
-Multiple causes (pain, anxiety, hypoxia, hypovolemia, myocardial dysfunction, fever, anemia, meds, pericarditis, hyperthyroidism, PE, alcohol withdrawal).
-Compare ECG with priors, if available. Maximum HR = 220 � age.
-Treat the underlying cause.
AV nodal re'entrant tachycardia (AVNRT) more common than AVRT or AT (see below)
-Caused by existence of dual AV pathways with differing refractory periods, with circuit rhythm set off by a premature atrial contraction (PAC).
-Diagnosis: look for isolated R, pseudo S, or inverted P on ECG. HR typically 180 � 20.
-Treat with AV nodal block (carotid sinus massage, adenosine, B-blockers, calcium channel blockers, or digoxin).
AV re�entrant tachycardia (AVRT)
� Caused by presence of accessory pathway causing large circuit rhythm.
� Diagnosis: short RP interval (i.e. RP <> PR). HR typically <250 .="" map=" CO" svr=" HR"> 80 mmHg and a palpable carotid pulse indicates SBP > 60 mmHg.
� For tamponade, you must call a cardiology consult to perform an echo and pericardiocentesis.
� For pneumothorax, don�t wait for a CXR. Insert 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 minuntes (diluted dose�different from �code blue� dose), Benadryl 50 mg IV, hydrocortisone 100 mg IV. Consider nebulizers for bronchospasm or intubation for respiratory failure.
� For sepsis, rapid administration of antibiotics and pressors will be crucial.
6. If patient has evidence of shock (end-organ damage), 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, creatnine, glucose, LFT's, blood cultures), get ECG, CXR, ABG.
� Consider Foley to measure urine output.
� Consider invasive monitoring (CVP or PA line, arterial line).
Principles of Criticle Care. Hall JB, Schmidt GA, Wood LDH eds. New York 1998: 277-301.
HYPERTENSION
High BP seldom warrants acute intervention. 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 physician(s) during the daytime.
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 (� blockers, ACE inhibitors, central alpha blockers)
� Increased intracranial pressure (Cushing�s reflex)
� ESRD, 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, and kidney) whereas hypertensive urgency implies an elevated BP of > 200/120 but no evidence of end-organ damage. Ask about and examine:
� Brain: headache, confusion, lethargy, stroke
� Eye: blurred vision, papilledema, flame hemorrhages
� Heart: chest pain, SOB, S3, S4, ECG strain or ischemic changes
� Kidney: low urine output, edema, hematuria
5. Hypertensive emergencies require admission to the ICU and reduction of BP by 25% over 6-12 hours with IV medications. Your choices include:
� Nitroprusside 0.3 mcg/kg/min and titrate up (requires arterial line BP monitoring and ICU stay).
� Labetolol 20 mg IV q10 min until BP down; alternatively, infusion dosed at 0.5 � 3.0 mg/min.
� Nitroglycerin 5 mcg/min and titrate up (use when heart disease present; requires ICU stay).
6. For hypertensive urgencies, 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); see Sliding Scales: Nitropaste; captopril 6.25-25 mg po TID (check K, Cr, allergies before); Clonidine 0.1 mg po bid.
� Avoid short-acting nifedipine (increased mortality).
7. 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 <> 38.5� C and in neutropenic, organ transplant, and dialysis patients, T > 38.0� C.
2. Your differential diagnosis is fairly broad.
� Infection (lung, heart, brain, urine, sinuses, prostate, abdomen, skin, lines)
� Inflammation (collagen vascular disease, neoplastic disease, mucositis)
� Drug fever (beta lactam antibiotics, amphotericin, and chemotherapy are frequent offenders)
� Pulmonary embolism or DVT
� Neurologic (spinal cord injury, hypothalamic injury, intracranial hemorrhage, seizures, subdural hematoma)
� Endocrine (adrenal insufficiency, thyrotoxicosis)
� Miscellaneous (aspiration, blood product reaction, atelectasis, hematoma, pancreatitis, MI)
3. After day 3 of hospitalization, the incidence of nosocomial infection and drug-induced fever goes up substantially. Note that nosocomial meningitis is exceedingly rare in the absence of head injury or neurosurgery.
� Common nosocomial infections: UTI (especially in patients with Foley catheters), pneumonia, vascular catheter related infections, wound infections, antibiotic-associated colitis
� Less common: decubitus ulcers, acalculous cholecystitis, nosocomial sinusitis
4. As stated above, drug-induced fevers are quite common in hospitalized patients. Clues are relative bradycardia, presence of a rash, eosinophilia, and the patient being subjectively unaware of fever despite high temperatures. Always look at the medication record!
5. Work-up: first determine whether the patient is stable or unstable
� Look at other vital signs and examine the patient
� Blood pressure is the most important vital sign � monitor frequently for development of hypotension and septic shock. Also worrisome is tachypnea (often an early sign of sepsis).
� If unstable, you may want to call for backup and arrange for an ICU transfer.
� 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 are often indicated).
� Determine whether blood cultures have been drawn within 48 hours. If so, there is generally no need to draw additional cultures.
6. Treatment:
� In most cases, it is prudent to withold empiric antibiotics unless obvious sign of infection (e.g. new infiltrate on CXR). An exception to this rule is patient who is hemodynamically unstable or with other signs of sepsis or septic shock.
� Most bone marrow transplant units have an antibiotic algorithm to follow. Consult your local hospital�s pharmacy for more information.
� Antipyretics:
- Tylenol 650 mg PO or for suspected neoplastic fevers, naproxen 375 mg PO q12h.
- Remember that fever can augment the host defense system and routine antipyretics can mask the disease process and may delay diagnostic evaluation or changes in antibiotics. Therefore, unless there is a good reason for treating with antipyretics such as extreme pt discomfort, AMS due to fever (common in the elderly), or cardiac disease vulnerable to the hypermetabolic state, consider resisting the temptation to lower the temperature.
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 patient appears dead.
2. Risk factors for hypothermia:
� Extremes of age: infants have greater body surface area relative to mass; elderly have lower metabolic rate and poor temperature sensation
� Submersion in cold water: rapid thermal conduction in water
� Alcohol ingestion: vasodilation, impaired shivering and awareness, hypothalamic dysfunction
� Sepsis: 39% of consecutive patients with hypothermia studied at San Francisco General Hospital were bacteremic
� Endocrine disorders: hypothyroidism, hypopituitarism, hypoadrenalism, diabetes, hypoglycemia
� Head injury: central core temperature dysregulation
� Drug ingestions (especially phenothiazines and barbiturates)
3. Classification:
� Mild (T 34�-36�):
- Initial increase in metabolic rate and shivering.
- Increased HR, BP, cardiac output, respiratory rate.
- Impaired judgment, mild lethargy, confusion, loss of fine motor coordination.
� Moderate (T 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 (T <> 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 nebulizers, suction, masks, ABGs, oral/nasal airways.
2. 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).
3. Diuretics:
� Consider furosemide in any patient with history or exam consistent with CHF; other processes associated with increased lung fluid (pneumonia, ARDS) may also improve temporarily with diuresis, and a single dose of furosemide is unlikely to do any irreversible damage.
4. Assess potential need for intubation (see Critical Care: Mechanical Ventilation). BiPAP trial may be helpful method of temporizing while making this decision.
5. 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 to the patient immediately; if stable, you can ask the nurse a little about the pain.
2. Take a look at your signout card. Is this at all worrisome for angina or MI? If so, or if the story sounds good (have a low threshold), ask the nurses to get an ECG or at least bring the ECG machine to the bedside during the time it takes you to arrive to see the patient.
3. Upon arriving in patient�s room, look at ECG first (ask for prior ECG from chart) or start obtaining the ECG 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 shortness of breath, diaphoresis, radiation to left jaw/arm, nausea/vomiting, 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, and hypoxia.
� PE: dyspnea, tachypnea, tachycardia, pleuritic chest pain, hypoxia, A-a O2 gradient, hemoptysis.
5. Other etiologies that are sometimes overlooked include pericarditis, pneumonia/pleurisy, GERD, PUD, esophageal spasm, esophageal rupture or tear (Mallory-Weiss), candidiasis, herpes zoster, costochondritis (Tietze�s syndrome), anxiety (a diagnosis of exclusion).
6. Treatment: If angina suspected, start O2 by NC and use sublingual nitroglycerin (NTG 0.4 mg SL q5 min x 3; hold for SBP <100> 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.).
6. Work-up: Renal failure is caused by prerenal, renal, and postrenal causes. Many laboratory indices exist to differentiate these (see Renal: Acute Reversible Renal Dysfunction), 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 is not quite done yet. Do the workup described under the Renal section.
� Always consider hypovolemia, decreased cardiac output, infection or sepsis, contrast nephropathy, and drug toxicity as potential causes because they are very common
� Beware of associated volume overload, acidosis, and hyperkalemia
� Consider increasing the frequency of labs and adjust drug dosages for renal failure as needed
7. 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 furosemide 20-80 mg IV.
� If in renal failure, may require dialysis. Sometimes patients in renal failure can still respond to high dose furosemide while waiting for the renal consult (160-240 mg IV slowly).
8. Complications: acute oliguria is associated with higher rates of infection, gastritis, GI bleeding, AMS, and arrhythmias. Consider prophylaxis and/or closer monitoring of these possibilities.
Klahr S, Miller SB. Acute oliguria. N Engl J Med 1998; 338:671-5.
COMBATIVE OR CONFUSED PATIENT
1. Does the patient have altered mental status or is he/she upset about 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 (for the most part) 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 Neurology: Altered Mental Status). If you suspect an underlying reason for the agitation (pain, sundowning, hypoxia, medication), then obviously treat the underlying reason.
� Always look at the MAR for medications as a cause.
� Remember that agitation and/or confusion can be the harbinger or a more serious underlying medical condition such as sepsis so always look at vitals and consider basic labs.
4. Chemical restraints that are often useful:
� Haldol 1�10 mg IV/IM/PO (a very versatile drug, with minimal respiratory and CNS depression)
� Droperidol 2.5�10 mg IV/IM (if given IM, wait at least 10�15 minutes for its effects).
� Watch for prolongation of QT interval with either droperidol or haldol.
5. If you feel physical 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 a Posey but may be necessary if patient is pulling out lines, etc.
6. ICU psychosis: poor terminology because altered mental status in the ICU is no different from delirium in any other hospitalized patient. Be sure to fully evaluate any significant change in the mental status of your ICU patients. Lack of sleep and the frequent noises/alarms in the ICU have never been proven to be true causes of delirium in the ICU. Common causes include:
Metabolic disturbances: provide adequate nutrition and treat underlying metabolic derangement.
Electrolyte imbalance: monitor and treat as indicated.
Withdrawal syndromes: often missed; treat as indicated.
Acute infection: search for source and treat.
Head trauma, intracranial lesions: evaluate with head CT.
Medications: common medications given in the ICU setting that can cause delirium: propofol, lidocaine, fentanyl, morphine, atropine, anti-convulsants, H2 blockers, omeparzole, and virtually any antibiotic (including beta-lactams, cephalosporins, macrolides, quinolones, and aminoglycosides). Consider minimizing the number of medications and/or use alternative meds.
McGuire BE, Basten CJ, Ryan CJ, Gallagher J. Intensive care unit syndrome: a dangerous misnomer. Arch Intern Med 2000; 160:906-9.
Practice guideline for the treatment of patients with delirium. American Psychiatric Association. Am J Psychiatry. 1999 May;156(5 Suppl):1-20.
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?).
� Was this a syncopal episode, a mechanical fall, or related to altered mental status?
� 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 PT/PTT 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 disease.
� 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.
4. Helpful hints:
� Although witnesses' (including nurses' and family member) accounts of the fall can be helpful, remember to evaluate the patient as objectively as possible.
� Have a low threshold for head CT if the patient hit their head during the fall. If the patient has a focal neurologic deficit that is new, you must get a head CT. If the patient lost consciousness or doesn�t remember falling, strongly consider a head CT.
� Extrapolating from the ER literature, any patient with loss of consciousness and any one (1) of the following characteristics should get a head CT: headache, vomiting, age > 60, intoxication, short-term memory deficits, physical evidence of trauma above the shoulders, or seizure.
� Serial neuro exams after the fall are a must to rule out progressive neuro deficits from head injury (i.e. subdural hematoma).
� By law, you are required to write a note in the chart and fill out an incident report.
Haydel MJ, Preston CA, Mills TJ, Luber S, Blaudeau E, DeBlieux PM. Indications for computed tomography in patients with minor head injury. N Engl J Med 2000; 343:100-5.
INSOMNIA
1. 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. Obtain a brief history and evaluate the patient to see if there is any underlying problem that is causing the insomnia (e.g. pain).
Differential diagnosis: psychological (anxiety, grief), physical (pain, decreased mobility, dyspnea), delirium, infection, metabolic, polyuria (diuretics given at night), incontinence, underlying medical condition, sleep apnea.
Medications that can cause insomnia (only a partial list): anticholinergics, beta-agonists, clonidine, steroids, caffeine, nicotine, phenylephrine, dilantin, SSRI's, theophylline, synthroid.
3. 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).
4. Low dose trazodone is often effective. Sedative doses usually 25-50 mg po qhs prn although some patients may need up to 100-200 mg. Especially useful in elderly patients.
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. Medication dosing: normal vs. elderly or cirrhotic patients
Trazodone: start at 50 mg, max 300 mg. If age > 65 or (+) cirrhosis, start at 25 mg, max 100 mg.
Ativan: start at 0.5-1.0 mg, max 4 mg. If age > 65 or (+) cirrhosis, start at 0.25 mg, max 1 mg.
Restoril: start at 15 mg, max 30 mg. If age > 65 or (+) cirrhosis, start at 7.5 mg, max 15 mg.
7. If above measures do not work, you may want to evaluate patient first before giving more powerful sedatives. In addition, in any patient in whom you think sedation is potentially dangerous (e.g. end- stage liver disease, severe COPD) evaluate the patient and consider not treating the insomnia.
TO BE CONTINUED VERY SOON
