Night Calls
Deepu Nair, M.D.
Thomas E. Baudendistel, M.D.
1. If possible, in any patient in whom you are worried about symptomatic bradycardia, try to have atropine and Zoll® pads at the bedside before the patient gets unstable. Always ask yourself the following two questions in the bradycardic patient:
· Is the patient symptomatic or hemodynamically unstable? If so, place the patient in Trendelenberg and follow ACLS protocols (See ACLS: Bradycardia).
· Does the ECG show either type II 2nd-degree or 3rd-degree AV block? If so, consider trans-cutaneously pacing the patient and prepare for possible transvenous pacer (consult Cardiology).
2. If the patient is relatively stable hemodynamically and symptomatically and there is no sign of a dangerous form of AV block, you have some time to do a quick chart biopsy and look for clues from the patient’s med list and admitting diagnoses. Causes of bradycardia:
|
Category |
Examples |
|
Meds |
ß blockers, calcium channel blockers, digoxin, amiodarone, clonidine (look at the MAR and remember to consider any eye drops—e.g. timolol) |
|
Cardiac |
Sick sinus, inferior MI, vasovagal, 2nd or 3rd degree heart block, junctional rhythm |
|
Instrinsic causes |
Idiopathic degeneration (aging), infiltrative diseases (sarcoid, amyloid), collagen vascular disease, surgical trauma, endocarditis |
|
Autonomically mediated |
Neurocardiogenic syncope, carotid-sinus hypersensitivity, situational: coughing, micturition, defecation, vomiting |
|
Other |
Hypothyroidism, hypothermia, increased intracranial pressure (Cushing’s reflex), hyperkalemia, hypokalemia, obstructive sleep apnea, normal variant |
3. 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 at night. However, have a low threshold to get an ECG in bradycardic patients and consider ischemia in any patient at risk.
4. 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.).
5. If you believe the bradycardia is secondary to medications, 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).
6. Transcutaneous pacing can be quite uncomfortable. If there's time, short-acting analgesics and/or sedatives may be worthwhile considering.
7. In asymptomatic patients with bradycardia, the class I indications for pacemakers are as follows:
· 3rd-degree AV block with asystole lasting > 3 seconds or with escape rates < 40 while awake.
· 3rd-degree or 2nd-degree type II AV block in patients with chronic bifascicular or trifascicular block
Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000; 342:703-9.
1. Is the patient symptomatic or unstable? If so, follow ACLS protocols (see ACLS: Tachycardia), 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 ECG and go to examine the patient.
4. 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).
· 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.
· 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, ß blockers, calcium channel blockers, or digoxin).
· Caused by presence of accessory pathway causing large circuit rhythm.
· Diagnosis: short RP interval (i.e. RP < PR interval), retrograde P wave.
· Treat with AV nodal blocking (see above).
· Caused by enhanced automaticity of atrial tissue or ectopic atrial pacemaker(s).
· Diagnosis: long RP interval (i.e. RP > PR). HR typically <250.
· Treat with calcium channel blocker.
· Similar to atrial fibrillation. Usually some heart disease present.
· Diagnosis: flutter waves in inferior leads, ventricular rate some multiple of 300 ± 5. When the HR is about 150, always consider atrial flutter.
· Treat with cardioversion, AV nodal blocking.
Narrow QRS, irregular rate
· Causes: see Cardiology: Atrial Fibrillation.
· Diagnosis: relatively straightforward. Look for absence of P waves and flutter waves in all leads. Atrial fibrillation is the most common cause of an irregularly irregular rhythm.
· Treatment: see Cardiology: Atrial Fibrillation.
· Often difficult to distinguish from atrial fibrillation.
· 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.
· Treat with AV nodal blocking, cardioversion.
· Caused by multiple ectopic atrial pacemakers. Usually associated with pulmonary disease. Also seen in hypomagnesemia, hypokalemia.
· Look for three distinct P wave morphologies in the same lead and three separate PR intervals.
· Treat underlying dysfunction—verapamil may be useful.
Wide QRS, regular rate
Wide QRS, irregular rate
Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332:162-73.
1. Start with the ABC's and whether or not the patient is 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.
2. Key questions if the patient is relatively stable:
· Is this BP real? Measure the BP manually yourself with the correct sized cuff. Get all of the vitals and make sure they are current (never presume they were recently done).
· Is it any different from prior values? If the patient usually lives around 80/40, then the acuity may be decreased somewhat.
· Is the mean arterial pressure (MAP) < 60 mmHg? MAP = (SBP + 2(DBP))/3. MAP less than 60 signifies hypoperfusion to vital organs.
· Is there associated hypoxemia?
· Consider early on the need for central venous access or PA line.
3. MAP = CO x SVR = HR x SV x SVR (where SV is a product of preload and contractility). Therefore, hypotension can only be caused by one or more of the following:
· Heart rate: look at ECG for pathologic tachycardia, bradycardia.
· Decreased preload: assess JVP, volume status, and consider hypovolemia, tension pneumothorax, PE, tamponade, RV infarct, pulmonary hypertension.
· Decreased contractility: listen for gallop, murmurs, rales and consider myocardial dysfunction, valvular dysfunction (AS, AI, MR), aortic dissection, drugs.
· Decreased SVR: warm extremities, flushing; consider sepsis, anaphylaxis, spinal shock, adrenal insufficiency, drugs.
4. Start with the hypotension algorithm as your initial approach in order to make a rapid empiric diagnosis of the cause of hypotension. Once this is done, consider the following:
· Overlap syndomes: get more data with a PA line or echocardiogram + CVP.
- Sepsis + cardiogenic, sepsis + hypovolemia, cardiogenic + hypovolemia.
· Consider other causes of hypotension as listed above and as follows:
- Increased cardiac output without sepsis: ESLD or fulminant hepatic failure, severe pancreatitis, trauma with SIRS, thyroid storm, AV fistula.
- Increased CVP without LV failure: pulmonary hypertension, PE, RV infarct, tamponade.
- Nonresponsive hypovolemia: adrenal insufficiency, anaphylaxis, cold sepsis.
5. Helpful hints:
· Above all, stay calm. Crashing patients are scary. Don’t try to manage shock by yourself.
· Remember that the BP cuff can markedly underestimate BP in low flow states; therefore, an arterial line can be invaluable for better BP monitoring.
· If BP is undetectable, palpate for pulses. A palpable femoral pulse indicates systolic blood pressure (SBP) > 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.
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 (ß 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 < 220/110.
Vaughan
CJ, Delanty N. Hypertensive emergencies. Lancet 2000; 356:411-7.
1. Defined as T > 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.
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 < 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.
· Perform secondary survey to check for trauma and to remove wet clothing.
· Patients should be on continuous monitoring and telemetry since hypothermic hearts are irritable. Do not handle roughly as patients can develop VF/VT. In fact, the use of an esophageal temperature probe and/or nasogastric lavage can precipitate VF/VT.
· 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.
· 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 pack, peritoneal lavage, and extracorporeal rewarming (dialysis).
· Patients tend to be dehydrated due to hypothermic diuresis. Therefore, give warmed IV fluids empirically unless contraindicated.
· Severely hypothermic hearts (T <30°) have poor response to cardioactive stimuli, especially those used in ACLS (lidocaine, epinephrine, procainamide, pacer stimulation, defibrillation). Avoid multiple dosing of meds leading to toxic levels. Remember, rewarming is the solution.
Differential diagnosis:
1. Pulmonary:
· Pneumonia – cough, fever, sputum.
· Pneumothorax – acute onset, pleuritic CP. Consider in any intubated patient.
· PE – often difficult to rule in or out by history/exam. Consider this early.
· Aspiration – common problem in patients with decreased consciousness or AMS.
· 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 diagnosis (e.g. sepsis).
2. 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 right heart failure.
3. Metabolic:
· Sepsis – dyspnea can be an early, non–specific sign of systemic infection.
· Acidosis – patients become tachypneic to blow off CO2 in compensation.
4. Hematologic:
· Anemia – easy to miss this by history/general exam.
· Methemoglobinemia – rare; consider in patients taking dapsone or certain other meds with cyanosis/low sat, normal PO2.
5. Psychiatric:
· Anxiety – common, but a diagnosis of exclusion!
Evaluation of the patient:
1. History:
· Acuity of onset of dyspnea.
· Associated symptoms (cough, chest pain, palpitations, fever).
· New events or medications given (including IV fluids!) around the time of onset.
· Relevant PMH and admitting diagnosis.
2. Physical exam:
· Vital signs: You should ask for these (including an O2 sat) as soon as you hear that the patient is complaining of shortness of breath. This will help you decide how quickly you need to respond.
· Lungs: wheezes, rales, stridor, symmetry of breath sounds. Remember that adventitial lung sounds may be absent in someone with severe airflow limitation.
· Cardiac: JVP, carotids, rate/rhythm, and murmurs or rubs.
· Extremities for edema (unilateral vs. bilateral) and perfusion (cool vs. warm, capillary refill, cyanosis).
· Mental status:
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.
3. Labs/studies:
· CXR, ECG, and ABG. CBC if clinically indicated.
· These 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.
Initial management:
1. Oxygen:
· 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 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.
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). 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 or CHF).
· Nitropaste (see Sliding Scales: Nitropaste).
· If patient is not already on aspirin and has no contraindications, have patient chew and swallow ASA 325 mg.
7. 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. ECG may show evidence of ischemia in RCA distribution if dissection is proximal.
8. If pneumothorax suspected, get CXR and call surgery for chest tube placement. If tension pneumothorax, don’t wait for the CXR! Insert a 14 gauge angiocath into the 2nd intercostal space at the midclavicular line on the side of the pneumothorax.
9. If high suspicion for pulmonary embolism, get chest CT with PE protocol or V/Q scan if available. Begin anticoagulation (if there are no contraindications) while you are waiting for the results.
10. Be sure to obtain post-pain ECG and document the event.
Lee TH,
Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med 2000;
342:1187-95.
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. The abrupt absence of urine output altogether (anuria) most often suggests obstructive uropathy. Other causes to consider if obstruction is not the case are:
· Progression of preexisting renal failure
· Renal cortical necrosis
· Necrotizing glomerular disease (RPGN)
5. Rule out obstructive uropathy early by checking 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.).
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.
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:
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.
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.
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. Obtain a brief history by asking the nurse or evaluating the patient yourself to see if there is any underlying, potentially treatable problem that is causing the insomnia (e.g. pain).
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
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.
Lenhart SE, Buysse DJ. Treatment of insomnia in hospitalized patients. Ann Pharmacother 2001; 35:1449-57.