HouseStaff Handbook

This highlights key topics that all SAMC Family Medicine residents are recommended to acquire during their residency training. The topics included are routinely updated to reflect guideline changes and best practice recommendations. Other nuance topics that pertains to inpatient and outpatient rotations are included for guidance and expectations. Please utilize this handbook during your rotations.

General Information

General Information

Food

Free lunch at physician lounge West wing first floor (Code 135). Need to show ID Badge.

Lunch hours: 
Monday - Thursday 11.30am to 2pm
Fridays - 11.30am to 1:30pm

One Main cafetaria and grill (first floor)

You can pay with your badge money
Hours: Monday to Sunday
Breakfast 6am - 11am
Lunch 11am - 1.30pm for chef table ; Grill 11am - 4pm
Dinner 5pm - 7.30pm for chef table and grill
Grill will reopen again from 8.30pm to 11.30pm
Cyber cafe Starbucks (2nd floor)
Hours : Monday to Friday from 6am to 2pm
You can pay using your badge money 

General Information

Parking

Hospital Parking
Park in the parking garage. Usually the gate open before 7AM but when it's closed, you will need your badge to open the gate. DO NOT park in the physician parking area or you will get ticket. 

MAP (see Legend 6)

Northwest Clinic Parking

4770 W Herndon Ave, Suite 110
Fresno, CA 93722
(559) 450-0463
(559) 450-0464 (fax)

Use badge to access front side entry on clinic facility.  Parking is available for physicians and staff on the east facing lot as marked.  

parking_nw.jpg
General Information

Library

It is located on the 2nd floor near the Starbucks cafe, North Wing.  Badge access is necessary.  Assistance to literature resources and references for research is provided.  

Online assistance to OPEN-Athens, Pubmed, and UptoDate setup

Monday-Friday
Librarian: Judith J. Kammerer
judith.kammerer@samc.com

8:30 a.m.-4 p.m
(559) 450-3322
(559) 450-3315 (fax)


General Information

Important Door Codes

Our Rounding room : 085#

Sleeping Quarter: 4th floor 611#

6th floor doctors’ lounge 33115

From elevator on 6th floor 425#

From COVID area to 6th floor 425 

ED lounge and bathroom code 5051#

General Information

Sick, PTO, and Emergencies

If you need to take a sick day, PTO, and other emergencies, please contact our program coordinator via doc halo/email (doc halo faster), and please inform your attending that you are sick or have other emergencies. If it happens during our clinic days, then you need to also inform Eileen Robles (office coordinator), Dr. Kim and Dr. Ruelan so that they are aware and can reschedule your patients. 

How To

How To

Call Schedule AMION

  1. go to Amion.
  2. Click secure login
  3. Type password: saintagnes 
  4. When you need to make a consult and wants to know the attending on call, click on the pink arrow on the top left of screen
  5. To consult nephrology on call during inpatient, dial 559-960-0010
  6. To see the schedule for the residents and attending on call for our program, click on the "call". The jeopardy residents, PCC resident and PCC attending also can be found here
  7. To see the residents in the clinic and preceptors, click "clinic" tab 

Login for all departments
saintagnes

Login for FM department
samcgme! 

How To

Didactics

Didactics is scheduled every Wednesday starting at 1PM

Location is Nursing conference in 1st floor West Wing near the endoscopy.  Virtual MS Teams link will be streamed and recorded at:

Virtual Didactics TEAMS Link
Lecture Slides, Materials Access Link

Grand rounds are held either on MS Teams or Nickerson.  Please check email notifications. 

View GOOGLE Didactics Calendar 
Download the iCal format to native mobile App

You are required to Sign-In for attendance

Inpatient Service

Inpatient Service

Signouts

Inpatient Service

Call Days

Inpatient Service

Admission Orders

  1.  Place admit order within 1 hour
  2.  Go see the patient
  3.  Do Medical reconciliation
  4.  Place appropriate general orders
  5.  Present and see the patient with your attending
  6.  Modify orders as appropriate
  7.  Repeat for next admit and curse the heavens that it arrived so soon
Inpatient Service

Procedure Notes

  1.  Perform the procedure
  2.  Find the appropriate procedure note in the EMR
  3.  Complete the procedure note
  4.  Sign and send the note to the attending you did the procedure with
Inpatient Service

Death and Documentation

  1. When called for a patient’s death, ascertain that the patient is unresponsive to verbal and tactile stimuli without spontaneous respirations (visually and by auscultation), is pulseless and without heart sounds, and that pupillary reactivity is absent. Furthermore, ensure that you have the correct name by ID bracelet.
  2. Notify the attending MD, unless the death was expected and you were specifically informed that this wasn’t necessary.
  3. Notify the next of kin and determine whether an autopsy is desired, also determine whether the family would like to view the body prior to transport to the morgue. It may help the family member to inform them that the patient died peacefully, etc., if this was the case. Have the family sign the release of body (even if they have not yet made funeral arrangements), autopsy request/refusal, valuables forms. Do this ASAP so the family can grieve in peace.
  4. Call the coroner according to the reasons below. If in doubt, call the coroner. If a case is felt to be a coroner case, neither you nor the family may touch anything immediately surrounding the patient. It is considered tampering. 
  5. Fill out the discharge summary, discharge orders, death note in the chart, death certificate which must be done by a licensed physician (if death is imminent for one of your patients, please leave a completed discharge paperwork upon signout as a courtesy to your colleagues). Ask the nurses for help.

 

Deaths reportable to Coroner (California Government Code section 27491)

  1. If patient has not been seen by a physician (or palliative care RN) in the past 20 days
  2. If death <24hr in hospital
  3. Suspected criminal act
  4. Accidental poisoning
  5. Controlled substance
  6. Occupational disease
  7. Contagious disease as the cause of death
  8. Death in OR or not fully recovered from anesthesia
  9. Prisoners (in custody)
  10.  Unidentified people
  11.  Cases where physician is unable to state the cause of death.

Common Calls From The Floor

Common Calls From The Floor

Bradycardia

Evaluation

Management

Common Calls From The Floor

Tachycardia

Narrow complex tachycardia

Evaluation

Management

Wide Complex Tachycardia

Evaluation

Management

 

Common Calls From The Floor

Hypotension

Evaluation

Decreased SVR: Exam = warm extremities, sometimes flushing

Decreased preload: Exam= cold extremities

Decreased contractility

Management

  1. Is the patient stable?
  2. Have low threshold to transfer a hypotensive patient to the ICU for better nursing support, pressors and/or intubation
  3. Treatment is aimed at the underlying cause but almost all cases call for fluid resuscitation. If suspicion of CHF is low then give rapid isotonic fluid resuscitation
  4. If there is concern for mixed cardiogenic and septic shock, let your volume exam guide treatment. Keep fluid boluses small (i.e 200ml and reassess). Trend lactate.
  5. In general, start O2, additional large bore peripheral IVs, put patient in trendelenburg, draw basic STAT labs (CBC, lytes, BUN, creatinine, glucose, LFTs blood/urine culture), STAT EKG, CXR, ABG/lactate

If the patient stable then ask this question

  1. Is this BP real?
  2. Is the BP different from prior values? if the patient usually has a BP 80/40 then the acuity may be decreased somewhat
  3. Is there associated hypoxemia, AMS, or increased RR (reasons for intubation)?
  4. Is the MAP <60? MAP less than 60 results in significant risk of hypoperfusion to vital organs
Common Calls From The Floor

Hypertension

Evaluation

Physical examination

Lab: not always required. Use selectively to determine cause and whether patient meets criteria for hypertensive emergency.

Management

For hypertensive urgencies: Majority of patient with HTN have no acute end organ damage and their BP can be lowered over days with oral medications. Consider rechecking BP after 30 minutes of quiet rest. Restarting a patient's home med is a good first step. Alternatively, consider starting one or more long acting oral med that can be continued on discharged.

In cases where more rapid lowering and closer tritration of BP is desired, consider shorter acting med

For Hypertensive emergencies

Common Calls From The Floor

Fever

Differential

- Infection (lung, heart, brain, urine, sinuses, prostate, abdomen, skin, joints, lines, etc) 
- Infammation (Collagen vascular disorder, neoplastic disorder) 
- Mucositis
- Atelectasis
- Blood product reaction
- Drug fever (beta lactam antibiotics and amphotericin common causes)
- PE vs DVT 

Is it a true temperature?

-  Is it greater than >100.4 F?
- Quickly chart check and determine if patient is stable vs unstable (look at vitals, etc).  If unstable go to bedside immediately! 

 If unstable:

First:  Brief yet thorough chart check

 Go assess bedside.

Get as much hx as you can - drug allergies, recent infections, blood transfusions, etc. Targeted exam (skin, lungs, extremities, etc). If patient is not responsive or sudden change in mentation, address those first.  
- If you have an idea where the infection is coming from, start targeted antibiotics.   
- If no idea where infection is coming from,  repeat blood culture if > 48 hours since last blood culture. If blood culture performed less than 48 hours ago, usually no need to repeat blood culture.
-Consider pan culture - UA, Urine Clx, line clx, CXR, and EKG on top of repeat blood cultures. 
- Labs to order (based on presentation/suspicion): CBC, CMP, Lactate, Trop, BNP, D-dimer, PT/PTT, etc.
- Also start broad-spectrum antibiotics (Vancomycin/Zosyn) (unless antibiotic allergies)
- ICU consult, Stat. 

If stable:

- Assess where the nurse took temperature, is it in the correct location?
- Have RN recheck temperature in 30 mins and dochalo/ call you. You do not have to act on one temperature, first confirm it. (Exceptions might be if the patient is neutropenic, then consider neutropenic fever). 
- Do a thorough chart check while you wait for a call back:
         - Why was the patient admitted?
         - What was the WBC?
         - What was the urine output?
         - Any recent meds/blood transfusions/surguries?
- If after 30 minutes temperature is confirmed, go assess patient bedside. 
- Get a detailed history from patient. 
- Do a thorough PE, looking for skin infections (including decubitus ulcers), and looking at all lines. 
- If worried about an infectious cause, start appropriate antibiotics. 



Common Calls From The Floor

Low urine output

Normal urine output

- typically at least 0.5 cc/kg/hr. 
- Oliguria: urine output < 400cc/day
- Anuria : urine output < 100cc/day 

Do you believe the numbers? 

- If patient has foley, flush tubing to make sure it is not clogged. 
- If no foley, ask about urine output, look at daily weights, etc. 

 Examine patient bedside.

- Assess volume status: mucous membranes, skin pallor/dryness, edema, complaints of thirst, neck veins (assess CVP), crackles in lungs (pulmonary edema), bladder palpable on exam, prostate exam, etc. 

Check a post-void residual by bladder scan. 

- If volume > 300cc, then insert foley (In and out). If consistent > 300cc, keep foley in. 

 Causes of urinary retention: 

- BPH, anticholiergic medication, side effect of medication:narcotics/benadryl/anestetics

Assess for renal failure (AKI) 

- Prerenal, renal, postrenal causes. 
- Look for fluid overload (CHF), and obstruction (renal US). 
- If both negative, then fluid challenge is acceptable: 500cc L bolus. (Go to AKI for further management). 

CHF/Volume overloaded? Initiate diuresis:

- Working kidneys: lower IVF rate and self-diuresis
- CHF/symptomatic: use lasix 20mg - 80mg IV 
- Renal failure: Dialysis? If kidneys still working, can try high dose lasix - 160mg- 240mg IV Lasix. 

Common Calls From The Floor

Dyspnea

DDx (5 major categories of disease to consider)

Pulmonary

Cardiac

Metabolic

Hematologic

Psychiatric

Evaluation of Patient

History

Physical exam

Labs/Studies

Initial Management

A. Oxygen

B. Diuretics

C. β-Agonists

D. Intubation

E. Other

Common Calls From The Floor

Chest pain


I. DDx (Biggest killers)

Evaluation of Patient

History:

- Learn about acuity of onset of chest pain
- Associated symptoms? (cough, dyspnea, palpitations, fever)
- Review recent events or meds given at time of symptoms onset
- Review relevant PMHx and admitting diagnosis
- Look at initial EKG (from chart if available)
- Focus on ruling out the major killers rather than definite diagnosis

Physical exam:

- Start by asking nurse for vital signs (HR, RR, BP, O2 sat). Ask for second set 15-30 minutes later.
- Ask nurses to get immediate EKG as you walk to patient’s room.
- Lung/cardiac exam 

Initial Labs/Studies to Order

- Ask nurses to get immediate EKG as you walk to patient’s room.
- Crisis panel
- CBC, CMP, troponin x3 q6h, CXR, ABG
- CHF = echo

Management


Suspected Angina/MI 

- Start O2 by NC and give sublingual NTG 0.4mg q5 min x3; hold for SBP < 100
- Remember, if chest pain responds to NTG it does not automatically rule in angina.
- If ineffective, try other antianginals
- Metoprolol 5mg IV q5 min x 3 (avoid in COPD/asthma)
- Nitropaste
- If not already on aspirin/Plavix and has no contraindications, order ASA 325mg and Plavix 300mg x 1
- Further meds = high-dose statin, consider ACE inhibitors

Suspected Dissection

- Call and transfer to ICU to reduce BP and inotropy with beta-blocker
- Order CT scan or echo and call surgery
- EKG may show evidence of ischemia in RCA distribution if dissection is proximal 

Suspected Pneumothorax

- Call surgery for chest tube placement
- If tension pneumothorax, immediate needle decompression at 2nd intercostal space at midclavicular line. Don’t wait for CXR. 

Suspected PE

- ABG confirms hypoxia
- Consider CTPA or V/Q scan and start anticoagulation

Suspected Pericarditis

- NSAIDS and colchicine

Wrap up: 

- Obtain post-pain EKG and document event 

 

Common Calls From The Floor

Combative or Confused patients

  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 (0). 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. If you suspect an underlying reason for the agitation (pain, sundowning, hypoxia, medication), then obviously treat the underlying reason. 

Management

Non-pharmacologic

Pharmacologic

Common Calls From The Floor

Falls

Evaluation/Management

Differential diagnosis. 

Common Calls From The Floor

Insomnia

  1. Trial non pharmacological measures first: sleep hygiene, noise reduction (ear plugs/muffs), reduce lighting, avoid night time interruptions if able, turn off TV/radio/etc. In room
  2. Before using pharmacotherapy, check patient allergies
  3. Melatonin is generally a safe starting point for medications, with 1-3mg PO scheduled at 9 to 10pm
  4. If not effective, can consider trazodone 50mg PO at bedtime (caution with orthostatic hypotension, atrial/ventricular arrhythmias) 
  5. Can also consider benadryl 25-50mg or hydroxyzine 50-100mg PO nightly PRN (safer for elderly) insomnia. Watch for anticholinergic side effects (dry mouth, blurry vision, urinary retention) and use with caution if impaired cognition.
  6. If still ineffective can consider ambien 5-10mg PO nightly
  7. If above measures not effective, evaluate the patient before considering any strong sedatives.

Acid/Base And Electrolytes

Acid/Base And Electrolytes

Hyponatremia

Definition

Evaluation: Order serum osmolality, urine sodium, urine osmolality, TSH, Lipid panel. 

Tips: Free water balance (Urine osmolality) is regulated by ADH. Sodium excretion (urine sodium) is regulated by aldosterone. If a patient has ESRD, the cause of hyponatremia is excess free water intake in the setting of impaired Kidney water excretion, and is not mediated by ADH. 

Step 1: Differentiate from true hyponatremia from pseudohyponatremia. 

Step 2: is ADH high or low? Compare serum osmolality to urine osmolality.

Step 3: If ADH is high, what is the volume status?

If ADH is activated, urine osmolality is usually >100. Urine Na can help to determine RAAS activation, which can narrow the differential in casese where volume status is not clear. A low urine Na (<20) suggests RAAS activation, as seen in hyper or hypovolemia; a high urine sodium may suggest SIADH. 

Hypervolemic: DDx: CHF, nephrotic syndrome, liver failure. 

Hypovolemic: 

Euvolemic:

Management: Repeat BMP q4hr. Goal to increase Na no more than 4 to 6 mEq/L in 24hrs to prevent osmotic demylination syndrome. Start treatment based on volume status

Evaluate and treat severe symptoms emergently in all patients

Select treatment approach based on volume status, severity, and etiology. 

Hypovolemia: 

SIADH: 

Hypervolemia:

If the serum sodium has been overcorrected:

Diagnosis and Management of disorders of body tonicity-Hyponatermia and Hypernatremia

Clinical practice guideline on diagnosis and treatment of hyponatremia

Acid/Base And Electrolytes

Hypernatremia

Definition:

Etiology: 

Renal water loss (U osm <700-800)

Extra-renal water loss (U osm >700-800)

Evaluation: U osm, U Na, volume status

Management

Step 1: calculate free water deficit. Can also use MD Calc

Step 2: Rate of correction

Diagnosis and Management of Disorders of Body Tonicity-Hyponatremia and Hypernatremia

Rate of correcting of hypernatremia

 

 

Acid/Base And Electrolytes

Hypokalemia

Definition:

Etiology: 

Evaluation: 

Review medication list

Order basic labs: Serum BMP, Mg, Serum osmolality, urine electrolytes (Na, K, Cl), Urine osmolality

Distinguish renal from GI losses with urine potassium. 

Severe hypokalemia, get an EKG. Changes include U wave, inverted T wave, ST depression, PR and QRS prolongation and can lead to Vfib.

Management: There is a replacement protocol that can be ordered. So the RN can replaced it based on the hospital protocol. 

Caution in renal failure or ESRD. Always check the creatinine prior to replacing potassium. Give about half the suggested dose of potassium in patient with decreased GFR

Disorders of potassium homeostasis. Hypokalemia and hyperkalemia

Acid/Base And Electrolytes

Hyperkalemia

Definition

Etiology:

Clinical manifestations:

Evaluation:

Management: PowerChart “Hyperkalemia (TH) Protocol”

Approach to Rx:

Treatment aims:

  1. Stabilize the myocardial membrane
  2. Temporarily shift K into cells
  3. Eliminate K from body

Cardiac membrane stabilization:

Temporarily shift K into cells:

Eliminate K from body:

Key Points:

 

 

Acid/Base And Electrolytes

Hypomagnesemia

Definition

Etiology:

Clinical manifestations:

Evaluation:

Management: PowerChart “Electrolyte Replacement Protocol”

Approach to Rx:

Route and dose based on severity of clinical manifestations and degree of hypomagnesemia

Patients with no or minimal symptoms:

 Patients with severe symptoms: tetany, arrhythmias, seizure

For routine IV or maintenance repletion, use the following estimated repletion doses:

(Conversion relationships: 1 mmol = 2 mEq = 24 mg of elemental magnesium = 240 mg magnesium sulfate.)

Key Points:

 

 

Acid/Base And Electrolytes

Hypermagnesemia

Definition

Etiology:

Clinical manifestations:

Symptoms are either cardiovascular vs neuromuscular manifestations or hypocalcemia

Evaluation:

Management: 

Treatment is tailored based on severity and clinical manifestations and renal function

Key Points:


Acid/Base And Electrolytes

Hypocalcemia

Evaluation: 

Causes:

Signs:

Trousseau's sign, Chvostek's sign, decreased cardiac function, QT prolongation

Treatment:

For those with milder symptoms of neuromuscular irritability (paresthesias) and corrected serum calcium concentrations greater than 7.5 mg/dL (1.9 mmol/L) or a serum ionized calcium concentration greater than 3.0 mg/dL (0.8 mmol/L), initial treatment with oral calcium supplementation is sufficient. If symptoms do not improve with oral supplementation, IV calcium infusion is required.

 

https://www.uptodate.com/contents/etiology-of-hypocalcemia-in-adults?search=hypocalcemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

https://www.uptodate.com/contents/treatment-of-hypocalcemia?search=hypocalcemia&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2


Acid/Base And Electrolytes

Hypercalcemia

Evaluation: 

Causes:

Signs:

Treatment:

  1. IV hydration, initial rate is 200 to 300 mL/hour that is then adjusted to maintain the urine output at 100 to 150 mL/hour
  2. In individuals with renal insufficiency or heart failure, careful monitoring and judicious use of loop diuretics (after intravascular volume has been repleted) may be required to prevent fluid overload. IV furosemide
  3. Specific treatment in approximate desirability of use:

 

https://www.uptodate.com/contents/diagnostic-approach-to-hypercalcemia?search=hypercalcemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

https://www.uptodate.com/contents/treatment-of-hypercalcemia?search=hypercalcemia&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2

Acid/Base And Electrolytes

Hypophosphatemia

Evaluation: 

Causes:

Signs: Generally seen with serum phosphate levels below 1 mg/dl 

Therapy:

- Serum level of 1.5 mg/dl (0.48 mmol/L) → give 1 mmol/kg elemental phosphorus (minimum of 40 and maximum of 80 mmol can be given in 4 doses over 24h) 

- Serum level less than 1.5 mg/dl → give 1.3 to 1.4 mmol/kg of elemental phosphorus (up to a maximum of 100 mmol given in 4 doses over 24h) 

  - Serum level of 1.0 to 1.9 mg/dl (0.32 to 0.63 mmol/L) → treat with oral phosphate 

- Serum level less than 1.0 mg/dl → treat with IV phosphate and switch to oral 

- Stop replacement when serum levels is equal to or greater than 2.0 mg/dl

- If the serum phosphate concentration is greater than or equal to 1.25 (0.40 mmol/L), → give 0.08 to 0.24 mmol/kg over six hours (up to a maximum total dose of 30 mmol).

- If the serum phosphate concentration is less than 1.25 mg/dL (0.40 mmol/L) → give 0.25 to 0.50 mmol/kg over 8 to 12 hours (up to a maximum total dose of 80 mmol).

→ measure serum phosphate levels Q6H and switch the oral replacement once serum levels have reached 1.5 mg/dl (0.48 mmol/L)

 

https://www.uptodate.com/contents/hypophosphatemia-evaluation-and-treatment?search=hypophosphatemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H727383

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324571/#:~:text=When%20evaluating%20a%20patient%20with,not%20reliable%20indicators%20of%20total

Acid/Base And Electrolytes

Hyperphosphatemia

Definition

  • Serum Phosphate >4.5mg/dL.

Etiology/Risk Factors

Evaluation

Laboratory tests to order:

Management

Determine urgency of intervention.

Key Points

Acid/Base And Electrolytes

Algorithm For Acid Base Disorders

Before You Begin: Gather Data

What lab tests do you need?

Step 1: Determine Primary Acid-Base Disturbance. 

Step 2a: Calculate and Interpret the Anion Gap

Step 2b: Calculate and Interpret the Excess Anion Gap

Step 3: Evaluate for Compensation

Evaluate for physiologic compensation for the acid-base disorder.

Any values above or below expected suggest an additional acid-base disturbance; a compensation should not normalize or overcorrect the pH.

The following table gives a quick rule-of-thumb for evaluating compensation. More detailed formulas are listed below.

image-1647883802322.png

Common Questions in Metabolic Acidosis

Key Points

 

Acid/Base And Electrolytes

Assessment Of RTAs

Definition

Categories 

Evaluation

Treatment

Key Points

image-1647884743295.png

 

Cardiology

Cardiology

Rule out MI

Admit to Telemetry

Activity

Diet

Nursing

Labs

Medications

If in doubt, discuss with seniors!

Consult with cardiologist (i.e. catheterization, GP IIb/IIIa gtt, CCU care), especially for persistent chest pain in the concerning patient.

References

Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017.

Ibanez B et al. Effect of early metoprolol on infarct size in ST-segment-elevation myocardial infarcation patients undergoing primary percutaneous coronary intervention: the Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) trial. Circulation. 2013;128(14):1495-503.

Meine TJ, Roe, MT, Chen AY, et al. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J 2005;149:1043-1049.

Chen ZM, Pan HC, Chen YP, et al, COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet 2005;366:1622-1632.

Cardiology

CHF

Definition

Classification

Overview of Heart Failure with Reduced Systolic Function

Evaluation of Acute Heart Failure

  1. BNP is released from the heart (mainly the LV) in response to increased wall tension.
  2. BNP measurement has limited utility after a good clinical assessment. If the diagnosis of HF is clinically apparent, a BNP test is not indicated. Measurement of BNP levels should not be used as a screening test. If the clinical picture is consistent with HF, do not let a low or normal BNP level necessarily deter appropriate diagnosis and therapy. 
  3. In one study, BNP < 100 pg/mL was helpful in ruling out cardiac causes of dyspnea (<50 pg/mL had 96% negative predictive value for CHF) while BNP > 400 pg/mL is helpful for ruling in cardiac causes of dyspnea. For values <100 pg/mL and >400 pg/mL, consider other causes of dyspnea as well as CHF.
  4. The level of BNP correlates with the severity of HF.  However, patients who are stable and well-compensated may run high BNP levels chronically. 
  5. Obese patients have decreased BNP levels due to adipose clearance.
  6. Higher baseline levels of BNP are seen in older patients and women. BNP is falsely low in obesity, diuretics, ACEi, beta-blockers, and aldosterone antagonist use. BNP is low in constrictive pericarditis

Acute Management of Heart Failure Exacerbation. 

Therapy should be tailored to the hemodynamic profile (Volume status vs Perfusion) as described below:

  1. Volume Overload (Wet) with Good Perfusion (Warm) -> Most common hospital presentation of CHF. IV diuretics ± nitrates, afterload reduction (ACEI/ARB, hydralazine, nitrates), ± aldosterone antagonists and beta-blockers when optimized. 
  2. Volume Overload (Wet) with Poor Perfusion (Cold) -> Likely requires ICU care. IV diuretics, ± afterload reduction, ± inotropes/inodilators. In severe or refractory cases, sometimes PA catheter-guided therapy* is needed, PUF/CVVH, consideration of advanced therapies (LVAD, transplant evaluation).
  3. Non-volume Overload (Dry) with Poor Perfusion (Cold) -> Represents 10% of cases, challenging to treat. Often associated with cardio-renal syndrome. Inotropes/inodilators, afterload reduction, and advanced therapies can be considered.
  4. Non-volume Overload (Dry) with Good Perfusion (Warm) -> Compensated HF. Usually can be treated as an outpatient. Maintain volume status and prevent disease progression with rx. Chronic management with beta-blockers, ACEI/ARB, aldosterone antagonists, loop diuretics.                                   

In general patients should be closely monitored:

Overview and Specifics of Treatment

  1. Immediate Considerations: Diuresis, Inotropes, Afterload reduction
  2. Guideline Directed Therapy: ACE-i, Beta blockers, Aldosterone antagonists, Hydralazine/Nitrates
  3. Devices: ICD, CRT, CRT-D
  4. Advanced Therapies: Mechanical circulatory support, Transplant

Diuresis:

Loop diuretics:

Ultrafiltration:

Fluid removal with no effect on serum electrolytes, consideration reserved for in cases of acute decompensated heart failure inadequately responsive to aggressive diuretic regimen. Increased risk of serious adverse advents and no difference in weight loss at 96 hours when compared to pharmacologic therapy (CARRESS-HF). 

Optimizing Hemodynamics/Inotropes:

Dobutamine:

Dopamine:

Milrinone:

Digoxin:

Nitrates:

Guideline-Directed Therapy

ACE inhibitors:

Beta-blockers:

Aldosterone Antagonists:

Hydralazine + Nitrates:

ICD and CRT 

Indicated only after medical optimization and removal of applicable vices (no active drug use) – please see applicable section.

Implantable cardiac defibrillator (ICD): Primary prevention of sudden cardiac death in populations at increased risk for life-threatening ventricular arrhythmias. Mortality benefit for NYHA class II-III HF + LVEF ≤ 35% despite optimal medical management for at least 3 months (SCD-HeFT trial).

Cardiac resynchronization therapy (CRT): HF frequently leads to intraventricular conduction delay and ventricular dyssynchrony. Resynchronization (biventricular pacing) improves pump function with mortality benefit, symptom improvement, and decreased hospitalizations for NYHA class II-III HF + LVEF ≤ 35% + LBBB + QRS ≥ 150 ms despite optimal medical management (MIRACLE, CARE-HF, COMPANION, MADIT-CRT trials).

Most patients who meet criteria for ICD also meet criteria for CRT and vice versa. Combination devices (CRT-D) confer superior mortality benefit when compared to ICD or CRT alone (REVERSE, MADIT-CRT, COMPANION trials).

Advanced Therapies

Mechanical circulatory support

  1. Intra-aortic balloon pump (IABP): Temporary treatment for HF refractory to medical management, systolic unloading and improved coronary perfusion, particularly useful in patients with ischemia or mitral regurgitation, placed in cath lab (see corresponding section). 
  2. Left ventricular assist device (LVAD): Can be used as a bridge to recovery, a bridge to transplant, or “destination” therapy for outpatient use. Placed in OR.    

Cardiac transplantation: Consider early involvement of transplant/advanced HF team in patients with new, rapidly progressive, severe HF, or advanced HF refractory to treatment.

Overview and Management of Heart Failure with Preserved Systolic Function

Etiologies

Evaluations

Treatment

Discharge Planning

References

Felker GM et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364(9):797-805.

Jessup M, Brozena S. Heart failure. N Engl J Med 2003 348:2007-2018.

Kadish A, Mehra M. Heart Failure Devices: Implantable Cardioverter-Defribillators and Biventricular Pacing Therapy. Circulation 2005;111:3327-3335.

McMurray JJ, Pfeffer MA. Heart failure. Lancet 2005;365:1877-1889.

Najjar S. Heart Failure with Preserved Ejection Fraction. J Am Coll Cardiol 2009;54: 419-421.

Owan TE et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 2006 Jul 20; 355:251-9.

Rathore SS, Curtis JP, Wang Y, et al. Association of serum digoxin concentration and outcomes in patients with heart failure. JAMA 2003;289:871-878.

 

Cardiology

Endocarditis

 

Overview

Diagnosis requires 2 major, 1 major with 3 minor, or 5 minor criteria from the modified Duke Criteria listed below:

MAJOR CLINICAL CRITERIA:

  1. Persistently positive blood cultures with typical IE organisms. Bacteremia is continuous and high grade. Two blood cultures are positive > 90% of the time. Repeat the blood cultures every 48 hours until sterile. Prevalence of endocarditis among patients with S. aureus bacteremia is approximately (13-25%); TTE is now recommended in all patients with S. aureus bacteremia.
  2. Evidence of valvular vegetation, or abscess, or dehiscence on TEE/TTE.
  3. New regurgitant murmur.
  4. Serologic dx (Coxiella IgG titer >1:800 or positive Bartonella or C.psittaci titers) or single positive culture of Coxiella burnetii (Q fever).

MINOR CLINICAL CRITERIA:

  1. Predisposing condition (see below).
  2. Fever (temperature >38.0 C).
  3. Vascular events (septic emboli, pulmonary emboli, mycotic aneurysm, CNS or conjunctival, and Janeway lesions).
  4. Immunologic events (Osler’s nodes, glomerulonephritis, Roth spots, + Rheum Factor).
  5. Microbiologic data not meeting major criteria.

Etiology / Risk Factors

Predisposing conditions include prosthetic valves, previous IE, IDU, structural heart disease (e.g., valvular abnormalities including MV prolapse), hemodialysis and indwelling catheters.

Evaluation

Management

Key Points

References

Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications: a scientific statement for healthcare professionals from the American Heart Association. Circulation 2015 Oct 13;132(15):1435-86.

Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service.  Am J Med 1994;96:200-209.

Fowler VG Jr, Miro JM, Hoen B, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA 2005;293:3012-3021.

Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocartiditis. Clin Infect Dis 2000;30:633-638.

Murdoch DR et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009;169:463-73.

Hoen B, Duval X. Clinical practice. Infective endocarditis. N Engl J Med 2013; 368:1425–33.

Wang A et al. Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA. 2007;297:1354-61.

Kang et al, Early Surgery versus Conventional Treatment for Infective Endocarditis, N Engl J Med 2012; 366;26: 2466-73.

Iversen K, Ihlemann N, Gill SU, et al. Partial Oral versus Intravenous Antibiotic Treatment of Endocarditis. N Engl J Med. 2019 Jan 31;380(5):415-424.

Cardiology

EKG reading made easy


Rates

Readings

OR

Note:

The cardiac axis 

The cardiac axis describes the overall direction of electrical spread within the heart.

In a healthy individual, the axis should spread from 11 o’clock to 5 o’clock.

To determine the cardiac axis you need to look at leads I, II, and III.

Right Axis deviation

Left Axis deviation

P Wave

The next step is to look at the P waves

Note: A prolonged PR interval suggests the presence of atrioventricular delay (AV block).

If the PR interval is shortened, this can mean one of two things:

QRS Complex

When assessing a QRS complex, you need to pay attention to the following characteristics:

Width can be described as NARROW (< 0.12 seconds) or BROAD (> 0.12 seconds)

Height can be described as either SMALL or TALL:

To assess morphology, you need to assess the individual waves of the QRS complex.

Note – the presence of a delta wave does NOT diagnose Wolff-Parkinson-White syndrome. This requires evidence of tachyarrhythmias AND a delta wave.

Q Wave

Isolated Q waves can be normal.

A pathological Q wave is > 25% the size of the R wave that follows it or > 2mm in height and > 40ms in width.

R Wave

Assess the R wave progression across the chest leads (from small in V1 to large in V6).

The transition from the S > R wave to the R > S wave should occur in V3 or V4.

Poor progression (i.e. S > R through to leads V5 and V6) can be a sign of previous MI but can also occur in very large people due to poor lead position.

ST-Segment

The ST segment is the part of the ECG between the end of the S wave and the start of the T wave.

In a healthy individual, it should be an isoelectric line (neither elevated nor depressed).

ST-elevation is significant when it is greater than 1 mm (1 small square) in 2 or more contiguous limb leads or >2mm in 2 or more chest leads. It is most commonly caused by acute full-thickness myocardial infarction.

ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischemia.

T Waves

T waves are considered tall if they are:

Tall T waves can be associated with:

Inverted T waves in other leads are a nonspecific sign of a wide variety of conditions:

Flattened T waves are a non-specific sign, that may represent ischemia or electrolyte imbalance.

Biphasic T waves have two peaks and can be indicative of ischemia and hypokalaemia.

U Waves

U waves are not a common finding.

The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.

These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide, or amiodarone).

References

  1. James Heilman, MD. Fast atrial fibrillation. Licence:CC BY-SA 3.0.
  2. Michael Rosengarten BEng, MD.McGill. Right axis deviation. Licence:CC BY-SA 3.0.
  3. James Heilman, MD. Mobitz type 2 AV block. Licence:CC BY-SA 3.0.
  4. James Heilman, MD. Complete heart block. Licence:CC BY-SA 3.0.
  5. James Heilman, MD. Delta wave. Licence:CC BY-SA 3.0.
  6. Michael Rosengarten BEng, MD.McGill. Q-waves. Licence: CC BY-SA 3.0.
  7. Michael Rosengarten BEng, MD.McGill. Poor R-wave progression. Licence:CC BY-SA 3.0.
  8. Michael Rosengarten BEng, MD.McGill. Tall tented T-waves. Licence: CC BY-SA 3.0.
  9. T-wave morphology. Licence:CC BY-SA 3.0.
  10. James Heilman, MD. U-wave. Licence:CC BY-SA 3.0.
  11. Michael Rosengarten BEng, MD.McGill. Left axis deviation. Licence:CC BY-SA 3.0.
Cardiology

Syncope

Syncope

  1. Rapid onset of transient loss of consciousness
  2. Inability to maintain postural tone
  3. It may be associated with a fall
  4. Resolves spontaneously and quickly without intervention

Presyncope (Near-Syncope)

  1. Weakness, Dizziness, lightheadedness, or "graying out" of consciousness without loss of postural tone
  2. Evaluate Presyncope with the same vigor as Syncope
    1. Presyncope has the same risks of adverse events as Syncope

Causes: Neural or Reflex Mediated Syncope (no cardiovascular risk, most common, 45% of cases)

  1. Vasovagal Syncope (Vasodepressor Syncope)
  2. Situational Syncope
  3. Carotid Sinus Syncope
  4. Glossopharyngeal neuralgia (uncommon)
  5. Trigeminal Neuralgia
  6. Hypovolemia
  7. Medication-related Syncope (Drug-Induced Syncope, responsible for 5-15% of Syncope causes)
  8. Recreational drug use
  9. Postural Tachycardia Syndrome (POTS)

10. Autonomic failure

Cardiac syncope

Vascular disorders

Myocardial disorders

Examination

Labs

Diagnostics

Imaging

Indications for head imaging include:

Note: The San Francisco Syncope Rule (CHESS Score) or Canadian syncope risk score are used to evaluate the short-term risk of severe outcomes and may reduce the syncope hospitalization rate.

Management depends on the cause

References

  1. Joshi and Dermark (2016) Crit Dec Emerg Med 30(8):3-12
  2. Orman and Mattu in Herbert (2016) EM:Rap 16(3): 9-11
  3. Orman and Mattu in Herbert (2018) EM:Rap 18(6): 10-11
  4. Schauer et al. (2016) Crit Dec Emerg Med 30(9):13-9
  5. Kapoor (2000) N Engl J Med 343:1856-62 [PubMed]
  6. Brignole (2001) Eur Heart J 22:1256-306 [PubMed]
  7. Miller (2005) Am Fam Physician 72:1492-500 [PubMed]
  8. Runser (2017) Am Fam Physician 95(3): 303-12 [PubMed]
  9. Vermeulen (2007) Stroke 38(4): 1216-21 +PMID: 17322078 [PubMed]

Endocrinology

Endocrinology

DKA

 

Diagnosis

DKA vs HHS: 

There may be focal neurological deficits and/or seizures in HHS.

In DKA, there may be nausea, vomiting, and abdominal pain. The delayed gastric emptying and/or ileus caused by acidosis and electrolyte derangement may be a cause for such symptoms.

Kussmaul respirations are indicative of acidosis since this is a compensatory mechanism. A fruity breath may be from acetone, which is one of the three ketone bodies produced.

Infection or inadequate control of DM are the main causes. Sometimes DKA is the first presentation for DM.

 

Laboratory and Ancillary Testing

First assess clinical stability of the patient. Ability to protect airway and mental status assessment are important assessments.

A part of the quick assessment is the following STAT orders… (these should already be ordered by ED, but always make sure these are ordered when you accept an admission)

* remember that in DKA the total water deficits are 6L and for HHS 9L.

 

Common Laboratory Derrangements 

Hyponatremia is often present due to fluid shifting from ICF to ECF. Basically the hyperglycemia causes fluid shifts from ICF to ECF. Be cautious of patients with impaired thirst mechanisms and the summer months where hot weather can cause dehydration.

For every 100 mg/dL increase in serum glucose, expect a 2mEq/L fall in serum sodium.

Hypokalemia or hyperkalemia can be present. Increased osmotic diuresis due to hyperglycemia can cause losses of potassium. Conversely, elevated potassium can be cause by ICF to ECF shifts of potassium due to lack of insulin or significant insulin resistance.

Hypophosphatemia or hyperphosphatemia is present. Dietary causes such as low phosphate intake can be present in uncontrolled DM. Conversely, hyperphosphatemia can be present in metabolic acidosis and hyperglycemia due to ICF to ECF shifts of phosphate.

Lipase and amylase are often elevated and DKA can masquerade as pancreatitis. Clinical judgement is necessary to distinguish the two.

Leukocytosis is present in many DKA or HHS patients. Hypercortisolemia and metabolic potentiators such as excess catecholamines can cause this. Think stress response. Do not forget to think about infectious etiology, WBC > 25K or bandemia with > 10%.

Acute Kidney Injury in the form of increased creatinine or reduced GFR can be present. In this case think dehydration or hypovolemia.

Hyperlipidemia can be present and increased lipolysis can serve as substrates for ketone body generation.

 

DKA and HHS are treated the same for the most part. It is important to think of the four hallmarks of DKA and HHS treatment which are correction of …

 

Use the order set in the hospital

  1. Fluid Replacement

a. In the first 2 hours, isotonic (Normal Saline) fluid boluses (1L/hr in average sized person). Be cautious and individualize care on CHF or fluid intolerant patients.

b. In the 3rd hour, continue fluids using either normal saline or half normal saline. If sodium is below reference range, use NS at 250 to 500 mL/hr. If sodium is normal or above reference range, then half normal.

    2. Insulin gtt (regular insulin)

a. 0.1 units/kg bolus followed by 0.1 units/kg/hr.

b. If no bolus is used, then 0.14 units/kg/hr.

c. Nursing will adjust rate based on serial glucose measurements.

Caution – if potassium is < 3.3, correct the hypokalemia first otherwise you will tank the patient’s potassium which is dangerous.

 

Management and Monitoring

3. Electrolytes – there is a protocol for electrolyte correction on the hospital order set. Be sure to use this.

a. Potassium – again replete potassium first if value is < 3.3. May need to add KCl to replacement fluids above (20 to 40 mEq/hr) if potassium is between 3.3 and 5.5 mEq/L.

b. Sodium – this will correct with correction of hyperglycemia.

c. Phosphorus – Correct when <1. If there is a cardiac history or potential for arrhythmia, correct if < 3. Sodium phosphate can be used.

4. Acidosis – No indication for bicarb unless the pH is ≤ 6.9 or if potassium > 6.4 mEq/L.

a. 100 mEq sodium bicarbonate in 400 mL of water.

b. Keep in mind that bicarb administration can cause hypokalemia or worsen it.

Monitoring includes….

 

Resolution of DKA and HHS

What we look for…

 

CONVERSION TO SUBCUTANEOUS INSULIN

Only initiate subcutaneous insulin if the patient is able to eat and the above criteria regarding resolution of ketoacidosis is met.

HHS

1. Overlap 2 hours of insulin gtt when serum glucose reaches 250 to 300 mg/dL

 

DKA

1. Overlap 2 hours of insulin gtt when serum glucose reaches 200 mg/dL

2. In addition two of the following must be met

a. Anion gap < 12

b. Bicarb ≥ 15

c. Venous pH > 7.30

 

References:

1. Up to Date has the latest and best information

2. SAMC order set for DKA

3. Dr. Michael Moya's DKA Handout 

Endocrinology

Inpatient Diabetes Guidelines

Definitions
  1. Type 1 DM: autoimmune. Patients require exogenous insulin to prevent DKA.
  2. Type 2 DM: insulin resistance and a relative insulin deficiency. Treatment may be with diet, exercise, oral meds, injectable meds, and/or insulin. With severe insulin deficiency, patients also develop DKA.
Physiologic Insulin Regimen
All patients have basal, nutritional, and correctional requirements that must be met with endogenous insulin or with insulin provided to them.

Basal: insulin needed even when the patient is not eating (to control gluconeogenesis).

  • Use glargine (q24, typically at bedtime, preferred for type 1), NPH (qHS or qAM+HS), detemir (BID or q24 for larger doses), or a continuous insulin infusion.

Nutritional: insulin to cover carbohydrate intake from food, dextrose in IVF, tube feeds, TPN.

  • Use rapid-acting insulin (aspart, lispro, or glulisine) or short-acting insulin (regular).

Correctional: insulin given to bring a high blood glucose level down to target range (130-150 pre-meal and 180-200 before bedtime).

  • Use rapid-acting insulin (aspart, lispro, or glulisine) or short-acting insulin (regular).
General Rules
  • Remember that a patient with type 1 DM will always need exogenous basal insulin, even if NPO. Failure to do so will lead to DKA.
  • Using correctional (“sliding scale”) insulin alone is acceptable for initial titration but should be reevaluated daily.
  • Order a carbohydrate controlled meal plan. Each meal contains 60 to 75 grams of carbohydrates.
  • Check blood glucose (BG) before meals and at bedtime, +/- at 2am (if suspect hypoglycemia) in a patient who is eating; check BG q 4 or q 6 hours in a patient who is NPO or is receiving continuous tube feeds or TPN.
  • Involve the diabetes educator, nurse specialist and dietician.
  • Supply glucose meter, lancets, test strips, syringes/pen needles, insulin, glucose tablets, and glucagon kit as discharge prescriptions, if needed. Health insurance dictates which types of supplies will be covered.
  • Oral medications: often, oral diabetes medications are held upon admission to the hospital. Hospitalized patients have the potential for renal impairment and tissue hypoxia or need IV contrast, and these are all contraindications to metformin use. Sulfonylureas should generally be held upon admission if you anticipate NPO status due to high risk of hypoglycemia. If patient’s status improves and is reliably stable, consider restarting non-insulin medications.
  • Nutritional insulin: regular is given within 30 min before meal, rapid-acting within 15 minutes before meal.
  • Infection and glucocorticoids increase insulin needs; renal insufficiency decreases insulin needs.
  • Total daily dose of insulin needed: type 1 patients require approximately 0.5 units/kg/day; type 2 patients vary in their insulin resistance and may require from 0.5 to 2 units/kg/day.
Hypoglycemia Protocol
  • BG <70 mg/dL: if patient is alert and taking PO, give 20 grams of oral fast-acting carbohydrate either as glucose tablets or 6 oz. fruit juice. If the patient cannot take PO, give 25 mL D50 IV push.
  • Check BG every 15 minutes and repeat above treatment until BG is ≥100 mg/dL.
Insulin Regimens
  • The guidelines below may assist with initial determination and subsequent adjustment of insulin doses.
  • Reevaluate insulin doses on a daily basis.

Correctional insulin (rapid or short acting): select between sensitive, average, or resistant based on BMI.

  • Sensitive: BMI <20, or <50 units/day.
  • Average: BMI 25-30, or 50-90 units/day.
  • Resistant: BMI >30, or >90 units/day.

Nutritional insulin (rapid or short acting): continue with home nutritional doses, or can start based on meal consumption and titrate up as necessary. Remember to adjust and increase nutritional dosing as you observe daily insulin requirements. Example:

  • Not eating: 0 units pre-meal dose.
  • Eating <50% of meals: 1 unit pre-meal dose.
  • Eating 50-75% of meals: 2 units pre-meal dose.
  • Eating >75% of meals: 3 units pre-meal dose.

Insulin regimen for a patient controlled only with diet at home, but needing insulin in hospital:

  • Day 1: order correctional insulin based on BMI  (sensitive = BMI<25, average = BMI 25-30, resistant = BMI>30)
  • Day 2: if BG pre-meals are >150 mg/dL, add nutritional insulin based on meal consumption (see above). Also, if AM fasting BG is >150 mg/dL, add bedtime basal insulin dosed 0.1 unit/kg.
  • Day 3: adjust insulin doses based on BG pattern. Increase or decrease basal insulin based on AM fasting BG, and adjust nutritional insulin based on pre-meal BG levels. Approximately half the daily dose should be given as basal insulin, and the other half as divided doses with meals.

Insulin regimen for a patient on oral agent(s) at home:

  • Day 1: start nutritional insulin based on meal consumption (see “Nutritional insulin” above). Also, order correctional insulin based on BMI  (see “Correctional insulin” above).
  • Day 2: if AM fasting BG is >150 mg/dL, add bedtime basal insulin dosed 0.1 unit/kg.
  • Day 3: adjust insulin doses based on BG pattern. Increase or decrease basal insulin based on AM fasting BG, and adjust nutritional insulin based on pre-meal + bedtime BGs.

Insulin regimen for a patient on insulin at home:

  • Assess home BG control, appetite, renal function, and risk for hypoglycemia.
  • Basal insulin: continue home regimen if patient has been well-controlled at home, but consider giving only 80% of home dose to reduce the risk of in-hospital hypoglycemia. Or, start bedtime glargine or NPH dosed 0.2 units/kg.
  • Nutritional insulin: order based on appetite, or consider pre-meal dosing of 0.2 units/kg divided by 3 for the dose at each meal.
  • Correctional insulin: order based on total insulin dose or BMI.

Insulin regimen when a patient is made NPO for a procedure: a patient will always require his or her basal insulin, even while NPO, and should not become hypoglycemic if that basal is dosed appropriately. For safety purposes, however:

  • The night before, give the usual dose of bedtime NPH, or decrease the usual dose of bedtime glargine by 25%.
  • The morning of the procedure decrease the usual dose of morning NPH by 50%, or decrease the usual dose of morning glargine by 25%.
  • Stop nutritional insulin (while patient is not eating), but continue the usual correctional insulin.

Insulin regimen for an ICU or surgical patient who is NPO: consider insulin infusion therapy. See your hospital-specific standardized protocol.

Insulin regimen for a patient starting continuous tube feeds:

  • Consider insulin infusion therapy. See your hospital-specific standardized protocol.
  • Estimate the tube feed formula’s 24-hour carbohydrate load (discuss with nutritionist).
  • Estimate the total daily dose (TDD) of insulin, starting with 1 unit insulin for every 10 grams of carb.
  • Basal need: divide the estimated TDD by 2 for the nightly glargine or total bid NPH dose.
  • Nutritional insulin: divide the estimated TDD by 10 for the total nutritional dose, to be given q 4 hours (rapid acting insulin) or q 6 (regular insulin) hours.
  • Correctional insulin: order based on total insulin dose or BMI.

Insulin regimen for a patient receiving TPN:

  • Standard TPN often contains 25% glucose, which, if 100 ml/hour, yields 25 g glucose/hour; discuss with nutritionist to determine exact glucose load.
  • Basal and nutritional insulin: adding insulin to the TPN can be a safe strategy, as the unexpected discontinuation of TPN will also mean the discontinuation of the insulin. Start with 0.1 unit per gram glucose.
  • If the patient has previously required basal insulin, convert this dose to regular insulin and add to TPN (dose reduce to 80% for safety purposes).
  • Correctional insulin: order based on BMI.

Insulin regimen to transition from an insulin infusion to subcutaneous insulin:

  • Calculate the patient’s TDD of insulin, based on the most recent insulin infusion rate. For safety purposes, take 80% of that dose.
  • Basal need: divide 80% of the TDD by half for basal insulin dose.
  • Nutritional insulin: if the patient is eating, divide 80% of the TDD by half, and then split over three meals. If the patient is receiving tube feeds, divide 80% of the TDD by 10 for the nutritional dose, to be given q 4 hours (rapid acting) or 6 hours (regular).
  • If the patient is not receiving nutrition, do not order nutritional insulin.
  • Correctional insulin: order based on total insulin dose or BMI.
  • Give the first basal insulin SQ injection 1-2 hours before the infusion is discontinued. If the transition is being made in the morning, consider using a one-time AM NPH injection or ½ of daily glargine dose to bridge until bedtime glargine or NPH begins.

Insulin regimen for a patient receiving steroids:

Insulin Adjustments
Reference: Hospitalist Handbook
Endocrinology

Hypothyroidism

Definition

Primary Hypothyroidism: High TSH and Low T4

Secondary (central) Hypothyroidism: Low T4 and TSH that is low

Subclinical Hypothyroidism: High TSG with normal T4

Myxedema coma: severe hypothyroidism causing multi-organ dysfunction. A medical emergency with a high mortality rate

Presentation

Early: Usually asymptomatic,  but may have fatigue, weight gain, cold intolerance, menorrhagia or amenorrhea, constipation, dry skin, thin hair, delayed DTR, diastolic HTN and hyperlipidemia

Late: Slow speech, brawny edema, hoarseness, loss of outer third of eyebrows, puffy face/eyelids, thickened tongue, myxedema, bradycardia, hypotension, and hypothermia

Myxedema coma: Endocrine emergency. Can present with AMS, hypothermia, hypoventilation, hyponatremia, hypoxia, hypercapnia, hypotension, convulsion, confusion, lethargy and coma.

Management

Levothyroxine: Full replacement is approx 1.6mcg/kg/day. Patient not requiring full replacement can be started on lower dose

Monitoring and dose adjustment based on TSH every 4-8 weeks until stable dose achieved

Pregnancy: Goal TSH varies by trimester, consultation with endocrinology is indicated

Elderly with CAD or high risk CAD, long standing untreated hypothyroidism: Start levothyroxine 25mcg/day

Subclinical hypothyroidism: Treatment generally not necessary unless TSH is >10, anti TPO positive, presence of a goiter, pregnancy or other compelling complication. Typically lower doses of levothyroxine are needed. Start with 15-50mcg. Follow up in 4-8 weeks of treatment initiation.

Thyroid Cancer: Patient who had total thyroidectomy for thyroid cancer need higher doses of thyroid hormone to suppress TSH

Myexedema coma:

https://pubmed.ncbi.nlm.nih.gov/23246686/

Hospitalist handbook

Endocrinology

Hyperthyroidism

Symptoms and signs

Work up

Management

Medical Therapy

Symptom Management: Propanolol to control symptoms and tachycardia (blocks adrenergic effects and peripheral conversion of T4 to T3). Beta blockade can be stopped once anti-thyroid treatment takes effect.

Inhibition of hormone synthesis: Methimazole or PTU. Methimazole is generally preferred due to better side effect profile (PTU preferred in pregnancy). Obtain baseline CBC and LFT's

Definitive therapy: Radioactive iodine ablation

Thyroid storm

Hospitalist Handbook


Gastroenterology

Gastroenterology

GI bleed

Etiology

Pre-endoscopic clinical risk stratification

Clinical judgment always comes first.

Picture1.png

  *Major co-morbidity defined as CAD, CHF, renal failure, liver disease, sepsis, disseminated malignancy, altered  

       mental status, pneumonia, COPD, asthma.

Evaluation


Management

Evaluation and Stabilization:

IMG_4956.jpg

Common Management of Upper and Lower GI bleed

  1. metabolic alkalosis (2/2 citrate metabolism) in setting of renal impairment
  2. hypokalemia (precipitated by alkalosis)
  3. hypocalcemia (due to citrate binding)
  4. hypothermia
  5. hyperkalemia (particularly with older blood products)
  6. Avoid NSAIDs, ASA, anticoagulants
  7. Surgery consult if recent surgical procedure or rebleeding (>6u pRBC)
  8. Re-bleeding:
  9. Preferred treatment is repeat endoscopic therapy
  10. If patient has persistent bleeding after endoscopy, consider CT angiogram or IR embolization. For uncontrolled bleeding requiring >6u pRBC there is no significant difference (rates of re-bleeding, subsequent therapy, or mortality) for IR embolization vs. surgical intervention.
  11. Other diagnostic modalities (discuss with GI first)
  12. Tagged RBC scan (can detect bleed rate >0.1cc/min,  localizes bleeding to area of abdomen but variable localization to portion of intestinal tract, can re-scan several times over 24-48h after tagged RBC administration for intermittent bleeding). If positive, consider IR embolization.
  13. CT (mesenteric) angiography (requires >1 cc/min.)


Specific management for suspected variceal bleed

Endoscopy

The following are endoscopic findings that a GI consultant uses to further risk stratify patients:

IMG_4957.jpg

* Risk of (rebleeding, mortality rate)

Key points


Reference: Hospitalist Handook

Gastroenterology

Ascites

Definition

Symptoms

Signs

Most common etiologies

 Labs

Ascites fluid assorted labs

Serum

Imaging

Medication Management

    1. Spironolactone and
    2. Thiazide or Loop Diuretic (diuretic dosage should be adjusted to a daily weight loss of no more than 500 g/day in patients without peripheral edema and 1 kg/day in patients with peripheral edema)
    3. Electrolyte correction
    4. Consider Hepatic encephalopathy management
    5. Paracentesis (consider Albumin)
    6. Antibiotic (therapeutic/prophylaxis for SBP)
    7. Electrolyte replacement, restriction of daily sodium intake to 80–120 mmol 

Executive summary of recommendations

  1. Diagnostic paracentesis in new- onset ascites

    • 1.1. A diagnostic paracentesis is recommended in all patients with new-onset ascites. (Quality of evidence: moderate; Recommendation: strong)

    • 1.2. The initial ascitic fluid analysis should include total protein concentration and calculation of the serum ascites albumin gradient (SAAG). (Quality of evidence: moderate; Recommendation: strong)

    • 1.3. Ascites fluid analysis for cytology, amylase, brain natriuretic peptide (BNP), and adenosine deaminase should be considered based on the pretest probability of specific diagnosis (Quality of evidence: moderate; Recommendation: weak)

  2. Spontaneous bacterial peritonitis

    • 2.1. Diagnostic paracentesis should be carried out without delay to rule out spontaneous bacterial peritonitis SBP) in all cirrhotic patients with ascites on hospital admission. (Quality of evidence: moderate; Recommendation: strong)

    • 2.2. A diagnostic paracentesis should be performed in patients with GI bleeding, shock, fever or other signs of systemic inflammation, gastrointestinal symptoms, hepatic encephalopathy, and in patients with worsening liver or renal function. (Quality of evidence: moderate; Recommendation: strong)

    • 2.3. Ascitic neutrophil >250/mm3 count remains the gold standard for the diagnosis of SBP and this can be performed either by manual microscopy or using automated counts, based on flow cytometry for counting and differentiating cells. (Quality of evidence: moderate; Recommendation: strong)

    • 2.4. Ascitic fluid culture with bedside inoculation of blood culture bottles should be performed to guide the choice of antibiotic treatment when SBP is suspected. (Quality of evidence: moderate; Recommendation: strong)

    • 2.5. Immediate empirical antibiotic therapy should be determined with due consideration of the context of SBP (community-acquired or healthcare-associated), the severity of the infection, and the local bacterial resistance profile. Cefotaxime has been widely studied, but the choice of antibiotic should be guided by local resistance patterns and protocol. (Quality of evidence: moderate; Recommendation: strong)

    • 2.6. A second diagnostic paracentesis at 48 hours from the start of treatment to check the efficacy of antibiotic therapy should be considered in those who have an apparently inadequate response or where secondary bacterial peritonitis is suspected. (Quality of evidence: low; Recommendation: weak)

    • 2.7. Patients presenting with gastrointestinal bleeding and underlying ascites due to cirrhosis should receive prophylactic antibiotic treatment (cefotaxime has been widely studied but the antibiotic should be chosen based on local data) to prevent the development of SBP. (Quality of evidence: strong; Recommendation: strong)

    • 2.8. Patients who have recovered from an episode of SBP should be considered for treatment with norfloxacin (400 mg once daily), ciprofloxacin (500 mg once daily, orally), or co-trimoxazole (800 mg sulfamethoxazole and 160 mg trimethoprim daily, orally) to prevent a further episode of SBP. (Quality of evidence: low; Recommendation: weak)

    • 2.9. Primary prophylaxis should be offered to patients considered at high risk, as defined by an ascitic protein count <1.5 g/dL. However, it is important that the potential risks and benefits and existing uncertainties are communicated to patients. (Quality of evidence: low; Recommendation: weak)

  3. Dietary salt restriction

    • 3.1. Patients with cirrhosis and ascites should have a moderately salt-restricted diet with a daily salt intake of no more than 5–6.5 g (87–113 mmol sodium). This translates to a no added salt diet with avoidance of precooked meals. (Quality of evidence: moderate; Recommendation: strong)

    • 3.2. Patients with cirrhosis and ascites should receive nutritional counseling on the sodium content in the diet. (Quality of evidence: weak; Recommendation: strong)

  4. Diuretics

    • 4.1. In patients with the first presentation of moderate ascites, spironolactone monotherapy (starting dose 100 mg, increased to 400 mg) is reasonable. In those with recurrent severe ascites, and if faster diuresis is needed (for example, if the patient is hospitalized), combination therapy with spironolactone (starting dose 100 mg, increased to 400 mg) and furosemide (starting dose 40 mg, increased to 160 mg) is recommended. (Quality of evidence: moderate; Recommendation: strong)

    • 4.2. All patients initiating diuretics should be monitored for adverse events. Almost half of those with adverse events require diuretic discontinuation or dose reduction. (Quality of evidence: low; Recommendation: weak)

    • 4.3. Hypovolaemic hyponatremia during diuretic therapy should be managed by discontinuation of diuretics and expansion of plasma volume with normal saline. (Quality of evidence: low; Recommendation: weak)

    • 4.4. Fluid restriction to 1–1.5 L/day should be reserved for those who are clinically hypervolaemic with severe hyponatremia (serum sodium <125 mmol/L). (Quality of evidence: low; Recommendation: weak)

    • 4.5. Hypertonic sodium chloride (3%) administration should be reserved for those who are severely symptomatic with acute hyponatremia. Serum sodium should be slowly corrected. (Quality of evidence: low; Recommendation: weak)

    • 4.6. It may be appropriate to consider the use of midodrine in refractory ascites on a case-by-case basis. (Quality of evidence: low; Recommendation: weak)

  5. Large volume paracentesis (LVP)

    • 5.1. Patients should give informed consent for a therapeutic or diagnostic paracentesis. (Quality of evidence: low; Recommendation: strong)

    • 5.2. Ultrasound guidance should be considered when available during LVP to reduce the risk of adverse events (Quality of evidence: low; Recommendation: weak)

    • 5.3. Routine measurement of the prothrombin time and platelet count before therapeutic or diagnostic paracentesis and infusion of blood products are not recommended. (Quality of evidence: moderate; Recommendation: strong)

  6. Use of human albumin solution (HAS)

    • 6.1. Albumin (as 20% or 25% solution) should be infused after paracentesis of >5 L is completed at a dose of 8 g albumin/L of ascites removed. (Quality of evidence: high; Recommendation: strong)

    • 6.2. Albumin (as 20% or 25% solution) can be considered after paracentesis of <5 L at a dose of 8 g albumin/L of ascites removed in patients with ACLF or high risk of post-paracentesis acute kidney injury. (Quality of evidence: low; Recommendation: weak)

    • 6.3. In patients with SBP and increased serum creatinine or rising serum creatinine, infusion of 1.5 g albumin/kg within 6 hours of diagnosis, followed by 1 g/kg on day 3, is recommended. (Quality of evidence: low; Recommendation: weak)

  7. Transjugular intrahepatic portosystemic shunt (TIPSS)

    • 7.1. TIPSS should be considered in patients with refractory ascites. (Quality of evidence: high; Recommendation: strong)

    • 7.2. Caution is required if considering TIPSS in patients with age >70 years, serum bilirubin >50 µmol/L, platelet count <75×109/L, a model for end-stage liver disease (MELD) score ≥18, current hepatic encephalopathy, active infection or hepatorenal syndrome. (Quality of evidence: moderate; Recommendation: strong)

  8. Umbilical hernia

    • 8.1. Suitability and timing of surgical repair of umbilical hernia should be considered in discussion with the patient and multidisciplinary team involving physicians, surgeons, and anesthetists. (Quality of evidence: low; Recommendation: strong)

  9. Hepatic hydrothorax (HH)

    • 9.1. TIPSS should be considered in patients with HH after discussion with the multidisciplinary team. (Quality of evidence: low; Recommendation: strong)

    • 9.2. In patients with HH who are not undergoing a TIPSS and/or a liver transplant evaluation, alternative palliative interventions should be considered. (Quality of evidence: low; Recommendation: strong)

  10. Non-selective beta-blockers (NSBB) and ascites

    • 10.1. Refractory ascites should not be viewed as a contraindication to NSBB. (Quality of evidence: moderate; Recommendation: strong)

    • 10.2. Patients with refractory ascites who are taking NSBB should be monitored closely, and dose reduction or discontinuation may be appropriate in those who develop hypotension or acute/progressive renal dysfunction. (Quality of evidence: moderate; Recommendation: strong)

Reference

  1. Pedersen JS, Bendtsen F, Møller S. Management of cirrhotic ascites. Ther Adv Chronic Dis. 2015;6(3):124-137. doi:10.1177/2040622315580069
  2. Aithal GP, Palaniyappan N, China L, et al Guidelines on the management of ascites in cirrhosis Gut 2021;70:9-29.
Gastroenterology

SBP

Definition

SBP is a bacterial infection of the ascitic fluid.

Diagnosis:

PMN count >= 250 cells/mm3 OR ascitic fluid WBC >= 500 cells/mm3 with a positive fluid culture.

Diagnostic clinical signs: New onset fever, confusion or abdominal pain, hepatic encephalopathy, vomiting, diarrhea.

Diagnosis of Culture-negative neutrocytic ascites: PMN count >= 250 cells/mm3 with a negative fluid culture (subtract 1 PMH for every 250 RBCs).

Pathogens causing SBP: Common organisms are E. coli, Klebsiella pneumoniae, Enterobacteriaceae, Streptococcus pneumoniae, and Enterococcus.

Patients with Cirrhosis: Cirrhotic patients can also get secondary bacterial peritonitis, which usually requires surgical intervention. One should suspect secondary peritonitis with perforation if the ascitic fluid meets 2 or more of the following: Total WBC >10,000, Total protein > 1 g/dl, Glucose < 50 mg/dl OR LDH > 225 milliunits/ml (or higher than upper normal for serum). One should also be suspicious if multiple organisms are cultured or if there is a failure to improve after 48 hours of standard therapy.

Risk Factors for SPB: Severe liver disease, GI hemorrhage, Prior SBP, Ascitic fluid protein <= 1 g/dl.

Diagnosis of SBP: Abdominal paracentesis, send fluid for cell count and differential and send fluid directly in the culture bottles.

Treatment for SBP:

Start antibiotic therapy as soon as the diagnosis of SBP is made based on fluid PMN count OR earlier if clinically indicated.

Use a third-generation cephalosporin (cefotaxime or a similar third generation cephalosporin) HIGH dose 2gm every 8 hours for 5 days.

Any person with cirrhosis and ascites who has signs or symptoms concerning for SBP should be treated with antibiotic therapy regardless of ascites fluid PMN count.

Antibiotic Prophylaxis for SBP: Prophylaxis should be given to persons with cirrhosis with a prior history of SBP or acute GI bleeding and should be considered in those who have renal or hepatic dysfunction if total ascitic fluid protein is less than 1.5g/dL.

Primary and Secondary SBP Prophylaxis: Ciprofloxacin 500 mg daily or trimethoprim-sulfamethoxazole one double strength tablet daily.  If patient has cirrhosis and acute GI hemorrhage, IV ceftriaxone 1 gram daily is recommended for a total duration of 7 days. 

Gastroenterology

Acute Pancreatitis

Definition

indicates inflammation of the pancreas.

Acute pancreatitis: results from the leakage of pancreatic enzymes into pancreatic tissue, leading to autodigestion.

Chronic pancreatitis: causes are varied and lead to destruction of the pancreatic tissue.  Patients may present with pain and/or weight loss due to fat and protein malabsorption.

Clinical Symptoms of Acute Pancreatitis:

sudden onset of epigastric pain that lasts for hours to days and radiates to the back, nausea and vomiting, sweating, weakness, and anxiety. The patient often feels better when sitting up and leaning forward.

Physical examination findings of Acute Pancreatitis:

The patient may be febrile, tachycardic, tachypneic, and hypotensive. The skin of the periumbilical area may be discolored (Cullen’s sign). Flank ecchymoses (Grey Turner’s sign) may be present. The abdomen may have mild distention (because of ileus). Upper abdominal and epigastric tenderness (usually without rebound or rigidity) is often present.

Laboratory findings of Acute Pancreatitis:

Elevated serum amylase and lipase. Blood amylase or lipase levels are typically elevated three times the normal level during acute pancreatitis.

Other findings may include leukocytosis (12,000–15,000/μ‎L), hypoalbuminemia, hyperglycemia, and elevated aspartate aminotransferase (AST, SGOT), alkaline phosphatase, and bilirubin.

 Imaging for Suspected Acute Pancreatitis [but not necessary]:

CT ABDOMEN- PELVIS.

Causes of Acute Pancreatitis:

Biliary stones, Alcohol abuse, Drugs, Hyperlipidemia or Hypercalcemia, Idiopathic or Infectious, Trauma, Surgery (after endoscopic retrograde cholangiopancreatography [ERCP], intra-abdominal surgery) or Scorpion sting.

Ranson’s criteria are used to assess severity and prognosis.

Ranson’s criteria are assessed at admission and during the initial 48 hours.

Ranson’s Criteria During the Initial 48 Hours.  Ranson’s greater than 3 is SEVERE.

Base deficit >4 mEq/L

Calcium <8 mg/dL

Hematocrit decrease >10%

Sequestration of fluid >6 L

Oxygen <60 mm Hg

Blood urea nitrogen (BUN) increase of >5 mg/dL 

As the number of criteria met increases, so does the mortality rate.

 Treatment of Acute Pancreatitis:

Complications of Acute Pancreatitis: 

Gastroenterology

Alcoholic Hepatitis

 3 Histological Stages

MELD SCORE [calculate with mdcalc]

Model for End-Stage Liver Disease (MELD) score is a prognostic scoring system used to predict 3-month mortality due to liver disease

MELD scores range from 6 to 40; the higher the score, the higher the 3-month mortality related to liver disease

MDF SCORE  [calculate with mdcalc]

Maddrey Discriminant Function (MDF) score is a measure of disease prognosis in alcoholic hepatitis (AH) used to identify patients at highest risk of mortality and determine the need for initiation of pharmacologic treatment.

An acute inflammatory syndrome that develops in the setting of chronic liver inflammation w/ alcohol use.

Risk Factors

Amount of alcohol, duration of alcohol use (>5-10 yrs for cirrhosis), gender (F>M), ethnicity (↑risk in AA & Hispanics), HCV (>30x ↑risk for cirrhosis), genetic mutations (PNLPA3) and obesity

Clinical Presentation

Hepatomegaly, jaundice, ascites, encephalopathy and fever. 

Of note: alcohol related hepatitis can lead to portal HTN and varices and ascites in the absence of cirrhosis due to hepatic swelling and portal venous obstruction.

Diagnosis

Treatment for Alcohol Related Hepatitis

Gastroenterology

Nausea

Nausea

Nausea is the unpleasant sensation of about to vomit.  This can occur alone or with vomiting.  Many differentials are associated with nausea depending on patient's symptoms.  

Always check patients electrolytes if they have been having severe vomiting and replete electrolytes if required. Suggestive labs could include BMP (checking electrolytes), UA (checking for ketones and specific gravity).  

Treatment of nausea includes:

Things to prevent nausea include:

Neuroleptic Malignant Syndrome can be caused by excessive use of Compazine or Droperidol (stop antiemetic and start Lorazepam 1-2mg IV 4-6hrs or Dantrolene 1-2.5 mg/kg IV with max dose of 10mg/kg/day).  

Advise all patients that Antiemetics can cause drowsiness

Combination of anti-emetics will resolve patient's nausea if patient is unresponsive to a single medication. 

Gastroenterology

Constipation

Check if patient has Bowel Obstruction before giving anything PO

Stool Softeners - Colace 100-250mg po qd or bid 

Osmotic Laxatives  

Suppository - Dulcolax 10mg qd, mineral oil enema, fleet enema

Patients started on narcotics should be advised about constipation.  Also patient's on chronic narcotics should be on bowel regimen to prevent constipation.

Hematology

Hematology

Anemia

Anemia can be caused by many things but first we should get some basic labs such as CBC that will show MCV, and Reticulocyte count. 

Anemia Workup.pngimage-1649027658986.png

This table from UTD summarizes on the different causes of anemia depending on the MCV.

Increased reticulocyte count (increased red cell breakdown) will also require peripheral smear to narrow differential. 

  1. Acute blood loss 
  2. Hemolysis - including antibody mediated, cellular toxins (malaria, clostridium), trauma (valve), or hypersplenism. 
  3. Intrinsic Defect- including enzyme deficiency such as G6PHD, SCD, or thalassemia 
  4. Membrane Defect- including spur cell, hereditary spherocytosis or PNH

Anemia with decreased reticulocyte count 

  1. Deficiency of Iron, Vit B12, Folate, or copper
  2. Medication that can suppress the bone marrow (such as quinidine, TMP SMX, albendazole)
  3. Primary bone marrow disorders (MDS, Myelofibrosis, or leukemia)
  4. Very recent bleeding (within 5-7 days, before bone marrow compensation has occurred)

If patient has Hgb of <7 in Non cardiac patient or <8 in cardiac patient we should consider blood transfusion (pRBC).  (Let the patient know of the risk's and benefits and also inquire that patient is not a Jehovah's Witness before proceeding with blood transfusion).  

 

Hematology

Sickle Cell Pain Crisis

Treatment:

  1. Oral hydration with 3-4 liters of fluid per day. We sugest to start 0.5 to 1 L NS bolus, then maintainance D51/2NS at 150-250 cc/hr. 
  2. Pain management: These patients are usually on chronic opioids. Start dose of IV morphine based on patient's prior dose requirements, or start with 2-5 mg morphine every 3-4 hours. Convert to PO once IV dose approaches equal analgesic home regimen. Perform assessments every 20 min and escalate as needed. 
  3. Supplemental O2 if hypoxia is present. Provide incentive spirometry. 
  4. Provide stimulant (not osmotic) laxatives. 
  5. Avoidance meperidine (can precipitate seizures), and ketorolac (associated with AKI). 
  6. Evaluate for SCD complications associated with pain (eg, avascular necrosis of the hip, acute chest pain syndrome, splenic sequestration). CBC, retic count, cultures, lytes, BUN, vreatinine, bilirubin, UA, CXR,blood type and screen. 
Hematology

Blood Component Therapy

Packed red blood cells (PRBC):

- Consent: Always consent the patient or family member for transfusion of blood products on admission, unless emergent.
- Dose effect: 1 unit PRBC (volume = 350 cc) should raise Hgb by about 1 g/dl
- Leukocyte filtered/reduced:
WBCs are the chief cause of alloimmunization to HLA antigens, which leads to future febrile transfusion reactions and platelet refractoriness. Indicated for patients who require long term transfusion support (Bone marrow transplant, leukemia, chemotherapy), and are at risk of becoming refractory to platelets, or with recurrent febrile reactions.
- Irradiated blood products:
Products are irradiated to kill donor stem cells which (rarely) cause transfusion-associated GVHD.
Indicated for BMT recipients, immunosuppressed patients, when donor and recipient are blood relatives, and patients receiving HLA matched platelets.
- Saline washed RBC:
RBC washed to remove plasma proteins, electrolytes, and antibodies. Indicated only in patients with history of severe transfusion reactions, hyperkalemia, paroxysmal nocturnal hemoglobinuria. Very expensive!
- Indications:
Active bleeding and one of the following:
1 - Blood loss > 500cc or 15% of blood volume (70 cc/kg body weight)
2- SBP < 100 mmHg or 20% fall in SBP
3- Pulse > 100 bpm
4- General anesthesia and Hgb < 9 g/dl
5- Chronic, symptomatic anemia (generally Hgb < 9g/dl)
6- Chronic transfusions to suppress endogenous Hgb in selected patients with sickle cell disease
7- Hgb < 10 g/dl in patients with known coronary artery disease, unstable angina, or acute MI. No RTC trial data to support this practice. One RCT (n=428) in patients undergoing CABG randomized patients to transfusion only if Hgb < 8 g/dL or standard practice (generally Hgb > 9.0) and found no mortality differences.
9- ICU mortality data with clear evidence for more restrictive transfusion (Hgb<7.0) practices
- Other considerations:
Patients with chronic anemia increase plasma volume in order to maintain an adequate cardiac output.
The volume associated with transfusion will cause overload and must be done slowly to avoid precipitating CHF (4 hours per unit vs. 5-10 min/unit in a hypotensive patient with acute blood loss).
Consider transfusing in splits of ½ volume over same time (4 hours per split is the slowest rate at which blood may be transfused).
Consider Lasix 20-40 mg IV to avoid fluid overload during transfusion of multiple units.

Platelets:

- General:
1- 1 unit single donor platelets (SDP) = 7 units of random donor platelets (a hemostatic dose for bleeding in an adult patient)
2- General dose is 1 unit random donor platelets per 10 kg body weight ≈ 1 unit single donor platelets for a 70 kg person.
3- For every 1 unit of SDP, the patient receives hemostatic levels of coagulation factors equivalent to 1 unit of fresh frozen plasma.
- Indications:
1- Platelet count < 5-10K in ITP or significant purpura
2- Platelet count < 10K in J patients, or patients not predisposed to spontaneous bleeding. No change in bleeding events in RCT when compared to < 20K as transfusion threshold
4- Platelet count < 20K and a clinical factor that would be associated with risk of spontaneous bleeding (Temperature > 38.5°C/Infection, concurrent coagulopathy, DIC, hepatic or renal failure, marked splenomegaly)
5- Platelet count < 50K and surgery or post-op bleeding
6- Platelet count < 50K and invasive procedure (LP, indwelling lines, liver or transbronchial biopsy, epidural puncture)
7- Platelet count < 100K with active bleeding
- Dose effect: 1 unit/kg body weight of platelets (1 unit SDP) should increase platelet count by 50K by 10-60 minutes, and by 40K at 18-24 hours post-transfusion.
- Premedication: Tylenol 650 mg p.o. x 1, Benadryl 25-50 mg p.o. OR IV x 1
- Refractoriness to platelet transfusions: A patient is considered refractory to platelets if 3 transfusions within 2 weeks fail to yield an adequate post-transfusion response. There are specific formulas for calculating an expected response, but in general, each unit should inc platelets by 35-40K.
1- Causes: fever, sepsis, splenomegaly, DIC, drugs, platelet consumption, s/p BMT (likely multifactorial etiology, in one series < 40% post-BMT transfusions resulted in appropriate rise in platelet count), alloimmunization with antibody mediated destruction of circulating platelets (towards HLA class I antigen)
2- Diagnosis: check rise 60 minutes after transfusion.
3- Appropriate rise with decrease over next 24 hours®sepsis, DIC, post BMT, etc. No rise at 60 minutes indicates alloimmunization. Order platelet antibody screening test (results in 2-3 days).
4- Treatment: if test positive, or while results pending, order "HLA matched" platelets and check platelet count 10 minutes to 1 hour following transfusion to document appropriate rise. Minimal options in acute bleed situation.
Effort should be made to avoid alloimmunization in at risk patients through irradiation, leukocyte reduction (comparable in RCT) or both.

Fresh frozen plasma (FFP):

- Description:
FFP is made by separating plasma from a unit of whole blood. Contains all clotting factors. One unit of FFP contains: 200-250 cc volume, 400 mg fibrinogen, 200 units of other factors (factors V, VII, XI, ATIII, Protein C, Protein S)
- Indications:
1- Active bleeding or risk of bleeding if PT and/or PTT> 1.5-1.8x normal.
2- Patient with massive bleeding at high risk for clotting factor deficiency while coags pending. Common causes of factor deficiency: liver disease, vitamin K deficiency, DIC, hemorrhage, TTP (treatment with plasma exchange)
3- Reversal of warfarin therapy. Minimal evidence that FFP can correct mildly elevated INR (< 1.8).
- Guidelines for use:
1- Starting dose 15 cc/kg = 4-6 units (dose needed to replace 25% clotting factors, minimum amount necessary to obtain hemostasis)
2- Maximum effect declines after 2-4 hours, so infuse rapidly at time of bleeding or no more than 1 hour prior to anticipated bleeding.
3- Administer fewer units of FFP when transfusing platelets since 1 unit SDP contains equivalent clotting factors to 1 unit FFP.
4- Consider Lasix IV when multiple units FFP given rapidly to avoid fluid overload.

Cryoprecipitate: (Contains fibrinogen, factor VIII, and von Willebrand factor)

- Indications:
1- Fibrinogen < 100 mg/dl (as in DIC)
2- Preparation of topical fibrin glue for surgical hemostasis
Concentrated factor VIII and von Willebrand factor are preferred treatments of Hemophilia A and von Willebrand's disease since cryoprecipitate not virus inactivated, thus carrying a higher risk for virus transmission.
- Dose effect:
1- Usual starting dose is 10 units. Each unit raises fibrinogen by about 8 mg/dl. Follow fibrinogen levels every 6-8 hours to guide frequency and quantity of administration.

Hematology

Transfusion Reactions

For all reactions (except mild allergic/uricaria): STOP transfusion, send remaining blood product and fresh blood sample to blood bank)

Acute Hemolysis (caused by ABO incompatibility)

- Signs: fever/chills, hypotension, flushing, dyspnea, flank pain. Fever often initial sign (rational for attempting to prevent non-hemolytic transfusion reaction)
- Complications: acute renal failure, shock, DIC, death
- Diagnosis: RUA (hemoglobinuria), Positive direct Coombs' test, Agglutination of RBCs on smear
- Workup: type and cross of donor and recipient blood (post-transfusion blood sample) with order for post-transfusion workup (sample is visually inspected for hemolysis)
- Treatment:
1- Stop transfusion immediately if reaction suspected!
2- Maintain blood pressure and urine output with vigorous NS hydration via new infusion set.
3- Lasix 80-100 mg, or mannitol IV to maintain urine output with goal >100 cc urine/hr.
4- Follow strict I/Os.
5- Close monitoring for any electrolyte abnormalities (hyperkalemia)

Anaphylaxis

- Cause: recipient antibodies react with donor plasma forming immune complexes which activate complement. Reported in patients with congenital IgA deficiency and high titers of anti-IgA IgG.
- Signs: sudden onset flushing and hypertension followed by hypotension, edema, respiratory distress, shock.
- Workup: none (no evidence of RBC incompatibility)
- Treatment: 0.2-0.5 cc of epinephrine 1:1000 SQ/IM. Repeat every 3-5 minutes as necessary. NS infusion to maintain urine output and BP. Treat hypoxia with supplemental O2.
- Prevention: patients with history of anaphylaxis to blood should receive components depleted of plasma (saline washed RBCs).

Acute Lung Injury

- Cause: not completely clear. Likely mediated by leukocyte agglutinating antibodies in donor plasma reacting with recipient leukocytes in pulmonary vasculature
- Signs: acute respiratory distress, cyanosis, fever, bilateral pulmonary infiltrates without other signs of heart failure.
- Onset: within 6 hours of transfusion
- Treatment: ventilatory assistance (i.e. ARDSNET protocol), diuretics, steroids (no data for use of steroids)
- Prevention: assay donor's blood, generally bar donor from future donation.

Delayed Hemolysis

- Cause: patients with undetectable antibodies when typed and crossed develop antibodies to minor antigens, leading to extravascular hemolysis. Sometimes these antibodies persist indefinitely after transfusion or following exposure to fetal antigens during pregnancy.
- Onset of symptoms: 4-14 days post-transfusion
- Signs: fever, jaundice, anemia, hemoglobinuria
- Workup: identify responsible antibody to avoid acute hemolysis in future! Patient should carry a transfusion alert card. Send H/H, total and direct bilirubin, direct Coombs', type and screen of donor and recipient blood.

Bacterial Contamination

- Signs: fever, hypotension
- Onset: within 4 hours of transfusion
- Workup: culture of remaining product and immediate antibiotics for the patient.

Febrile, Non-Hemolytic Transfusion Reaction

- Cause: recipient antibodies to passenger donor leukocytes or donor cytokines produced by stored leukocytes.
- Signs: fever, rigors, nausea, vomiting, back/chest pain, HTN
- Onset: within 2 hours of transfusion
- Workup: similar to hemolytic reaction (difficult to differentiate based on clinical signs alone)
- Treatment: leukocyte reducing filters for transfusion dependent patients. Only 15% of patients with 1 reaction have a repeat episode; if a 2nd reaction does occur, give leukocyte reduced RBC and platelets.

Urticaria

- Cause: soluble substances in donor plasma react with IgE which stimulates mast cell degranulation.
-Symptoms: rash, pruritus
- Treatment: monitor for anaphylaxis. Benadryl 50 mg IV. If rash or symptoms resolve within 30 minutes, may resume transfusion.

Infectious Disease

Infectious Disease

Antibiotic Recommendations/Dosing

General Principles

  1. Initiate empiric therapy based on severity of illness, likely pathogen, likelihood of drug resistance, host factors (allergy, poor renal function, immunocompromised)
  2. Initiate antibiotic therapy as soon as possible
  3. tailor antibiotic therapy based on culture results
  4. tailor antibiotic therapy once culture results are available (often 48-72 hours)
  5. Transition from IV to oral antibiotic as soon as feasible to decrease cost and reduce complications from IV access
  6. Consult ID for further assistance

Disease // Treatment with Dosing

Another useful app that you can access in phone (require fee) : Sanford Guide

*All drug dosing is based on immunocompetent patients with no renal or hepatic dysfunction and normal weight, not elderly and not in ICU

BONE/JOINT

Joint infections with hardware

Non-Vertebral Osteomyelitis

Septic Arthritis

CNS

Brain Abscess

Epidural Abscess

Meningitis (community-onset) 

INTRAABDOMINAL INFECTION

C. difficile (non-complicated) 

Community-Acquired Secondary Peritonitis

Diverticulitis

Liver Abscess 

Spontaneous Bacterial Peritonitis 

Traveler's Diarrhea

PNEUMONIA

Pneumonia, Community Acquired

Pneumonia, Healthcare Associated

RESPIRATORY, HEAD AND NECK INFECTIONS

Bacterial Exacerbation of COPD 

Acute Sinusitis // Watchful waiting first,

Peritonsillar Abscess

Pharyngitis

SEPSIS

Community Acquired Sepsis 

Fever in person who injects drugs

Healthcare Acquired Sepsis 

SEXUALLY TRANSMITTED INFECTIONS

Gonorrhea

Chlamydia

URINARY TRACT INFECTIONS

Uncomplicated Cystitis 

Acute Prostatitis

Community-Acquired Pyelonephritis/Complicated UTI


Reference:

Guidelines for Empiric Therapy: Adults | Infectious Diseases Management Program at UCSF

Adult Outpatient Treatment Recommendations | Antibiotic Use | CDC

Antibiotic Courses for Common Infections: Recommendations From the ACP - Practice Guidelines - American Family Physician (aafp.org)

Antimicrobial stewardship in hospital settings - UpToDate


Neurology

Neurology

Seizures

Objective

The primary objectives of the medical evaluation of the first seizure are to establish whether the event was a seizure, and if so, whether it resulted from a correctable systemic process or whether the patient is at risk for developing further unprovoked seizures 

Seizures are further categorized as either focal or generalized according to whether the onset of electrical activity involves a focal region of the brain or the entire cortex simultaneously. The clinical manifestations of seizures vary based on the location of the seizure in the brain and the amount of cortex that is involved.

Cause

Differential Diagnosis

Work-Up

Management

Antiseizure medications are not always indicated after a first seizure.

In criticaly ill patients, commonly used drugs in this setting include levetiracetam, fosphenytoin/phenytoin, and valproic acid

Hospitalization may be required for patients who have a first seizure associated with a prolonged postictal state or incomplete recovery. Other indications for hospitalization include status epilepticus, the presence of a systemic or neurologic illness or injury requiring additional evaluation and treatment, and questions regarding compliance

Seizure Disorders - American Family Physician (aafp.org)

Evaluation of First Nonfebrile Seizures - American Family Physician (aafp.org)

Evaluation and management of the first seizure in adults - UpToDate

Neurology

AMS

Causes

CNS insults, Systemic Infections, Metabolic Disturbances, Toxin Exposure, Medications, Chronic Systemic Diseases, Psychiatric conditions

Definition

Change in consciousness, appearance, behavior, mood, affect, motor activity or cognitive function

Best Practice

Do not assume a diagnosis of dementia in elderly patients with AMS without assessing for delirium

Do not use physical or chemical restraints, outside of emergency situations. Assess for unmet needs or environmental triggers

Evaluation:

As the differential is broad, history and physical exam is always the first step to determine diagnostic testing.

  1. Evaluate ABC's
  2. Vitals, glucose, H&P
  3. Diagnostic studies as indicated by H&P
  4. Neuroimaging
  5. MRI brain or EEG or LP
  6. If still unclear, specialty consultation

Treatment

Definitive treatment is removal of the underlying cause

However, if patients' behaviors threaten self or others, then attempt nonpharmacologic interventions are the treatment of choice. This includes reassurance, family, friends and environmental factors.

Medications are used only when nonpharmacologic treatments are ineffective and only when it is essential to control behavior. These include antipsychotics, benzodiazepines and ketamine, but they contraindications and FDA warnings.  

Recent-Onset Altered Mental Status: Evaluation and Management - American Family Physician (aafp.org)

Pulmonary

Pulmonary

CAP

Common causes

Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the most frequently detected pathogens in patients with CAP

Typical bacteria

Atypical bacteria ("atypical" refers to the intrinsic resistance of these organisms to beta-lactams and their inability to be visualized on Gram stain or cultured using traditional techniques)

Making the diagnosis

For most patients with moderate CAP admitted to the general medical ward, obtain the following:

DIFFERENTIAL DIAGNOSIS

Noninfectious illnesses that mimic CAP or co-occur with CAP and present with pulmonary infiltrate and cough include:

Inpatient antibiotic therapy

Without suspicion for MRSA or Pseudomonas

●Combination therapy with ceftriaxone (1 to 2 g IV daily), cefotaxime (1 to 2 g IV every 8 hours), ceftaroline (600 mg IV every 12 hours), ertapenem (1 g IV daily), or ampicillin-sulbactam (3 g IV every 6 hours) plus a macrolide (azithromycin [500 mg IV or orally daily] or clarithromycin [500 mg twice daily] or clarithromycin XL [two 500 mg tablets once daily]). Doxycycline (100 mg orally or IV twice daily) may be used as an alternative to a macrolide.

●Monotherapy with a respiratory fluoroquinolone (levofloxacin [750 mg IV or orally daily] or moxifloxacin [400 mg IV or orally daily] or gemifloxacin [320 mg orally daily]) is an appropriate alternative for patients who cannot receive a beta-lactam plus a macrolide.

With suspicion for Pseudomonas 

Acceptable regimens include combination therapy with an antipseudomonal/antipneumococcal beta-lactam antibiotic and an antipseudomonal fluoroquinolone, such as the following regimens:

●Piperacillin-tazobactam (4.5 g every 6 hours) or Imipenem (500 mg every 6 hours) or Meropenem (1 g every 8 hours) or Cefepime (2 g every 8 hours) or ●Ceftazidime (2 g every 8 hours; activity against pneumococcus more limited than agents listed above)

PLUS ●Ciprofloxacin (400 mg every 8 hours) or ●Levofloxacin (750 mg daily)

With suspicion for MRSA

Influenza therapy

Antibiotic Therapy for Adults Hospitalized With Community-Acquired PneumoniaThe Clinical Utility of Methicillin-Resistant Staphylococcus aureus (MRSA) Nasal Screening to Rule Out MRSA Pneumonia

Treatment of CAP

Pulmonary

Asthma/COPD Flare

Initial pharmacologic therapy

Beta adrenergic agonists

Ipratropium

also available in an MDI that can be used with a spacer, 2 to 4 inhalations every hour for two to three doses, and then every two to four hours as needed.

Systemic glucocorticoids

Antimicrobial therapy

Recommend antibiotics with at least two of these three symptoms – increased dyspnea, increased sputum volume, or increased sputum purulence.

Oxygen therapy

Supplemental oxygen be titrated to a target of 88 to 92 percent pulse oxygen saturation, rather than using high-flow, nontitrated oxygen

https://www.uptodate.com/contents/copd-exacerbations-management/abstract/1,17,

https://www.uptodate.com/contents/copd-exacerbations-management/abstract/33

https://www.uptodate.com/contents/copd-exacerbations-management/abstract/12,34,35

ttps://www.uptodate.com/contents/copd-exacerbations-management/abstract/1,12,39-41

Pulmonary

Oxygen Therapy

●Venturi masks permit a precise upper limit for the FiO2, preferable for patients at risk of hypercapnia. Venturi masks can deliver an FiO2 of 24, 28, 31, 35, 40, or 60%.

●Nasal cannula can provide flow rates up to 6 L per minute with an associated FiO2 of approximately 40%

●When a higher FiO2 is needed, simple facemasks can provide an FiO2 up to 55% using flow rates of 6 to 10 L.

●Non-rebreathing masks with a reservoir, one-way valves, and a tight face seal can deliver an inspired oxygen concentration up to 90%

●High-flow nasal cannula (HFNC) provide supplemental oxygen (adjustable FiO2) at a high flow rate (up to 60 L/min that results in a low level of continuous positive airway pressure).

Oxygen Therapy

Pulmonary

ARDS/Mechanical Ventilation

Pathophysiology:

Scattered, nonhomogeneous alveolar damage that leads to oxygenation (V/Q mismatch) problems

Diagnosis:

Etiology:

Management:

Indications for intubation

Initial ventilator settings


Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000; 342:1334-49.
https://www.uptodate.com/contents/acute-respiratory-distress-syndrome-clinical-features-diagnosis-and-complications-in-adults
https://www.uptodate.com/contents/ventilator-management-strategies-for-adults-with-acute-respiratory-distress-syndrome 

Pulmonary

Stepwise approach to managing Asthma

Intermittent (Step 1) — 
Symptoms — <2 days a week, <2x nighttime awakenings/month, SABA use <2 days/week
Preferred: SABA prn

Mild persistent (Step 2) —
Symptoms — >2 days a week, 3-4x nighttime awakenings/month, SABA use >2 days/week
 Preferred: Low dose ICS
Alternative: Cromolyn, LRTA, Nedocromil, Theophylline

Moderate persistent (Step 3) —
Symptoms — Daily, >1x nighttime awakenings/week, SABA use daily
Preferred: Low dose ICS + LABA OR Medium dose ICS
Alternative: Low-dose ICS + either LTRA, Theophylline, or Zileuton

Severe persistent (Step 4) — 
Symptoms — Throughout the day, Often 7x nighttime awakenings/week, SABA use several times daily
Preferred: Medium dose ICS + LABA
Alternative: Medium dose ICS + either LTRA, Theophylline, or Zileuton

Severe Persistent (Step 5) —
Preferred: High-dose ICS + LABA AND Consider Omalizumab for patients who have allergies

Severe Persistent (Step 6) —
Preferred: High-dose ICS + LABA + oral corticosteroid AND Consider Omalizumab for patients who have allergies

https://getasthmahelp.org/documents/GIST-Stepwise-Approach.pdf

Nephrology

Nephrology

Acute Renal Failure

What is AKI?

According to The Kidney Disease: Improving Global Outcomes (KDIGO), which it the most current and preferred definition, it is:

an increase in serum creatinine of ≥0.3 mg/dL within 48 hours OR an increase in serum creatinine of ≥50% within 7 days OR Urine output of <0.5 mL/kg/hour for >6 hours

Etiology:

1)Prerenal: Decreased renal perfusion (70% of causes)

a. Intravascular volume depletion: Dehydration, third-spacing

b. Decreased arterial pressure: CHF, sepsis, 

c. Extracellular fluid loss : Burns, diarrhea, vomiting, diuretics or hemorrhage

d. Decreased CO: CHF, shock

e. Medication changes to renal vasculature:  ACE-i, ARBs, NSAIDs, Tacrolimus, Cyclosporine

2)Intrinsic: classified according to the site of injury

a. Vascular Injury: afferent arteriolar vasoconstriction --> decreased GFR (Ex. TTP, Vasculitis, RAS, malignant HTN)

b. Glomerulonephritis:  Includes renal (PSGN, IgA, membranoproliferative GN), hematologic dz (HUS, TTP), systemic inflammation (SLE, HSP), and pulm-renal syndromes (Goodpasture, granulomatosis with polyangitis). +hematuria( RBC casts) and proteinuria.

c. Interstitial Nephritis: analogous to an allergic rxn in the kidney, may be associated with fever, arthralgia, and rash. Allergic rxns can be due to drugs (penicillin, cephalosporin, NSAIDs, Sulfas, PPIs), autoimmune disorders (ex. SLE), infections (diphtheria, GAS), or other dzs such as sarcoidosis. 

d. Acute Tubular Necrosis (ATN): cell death and necrosis from renal ischemia (prolonged hypoperfusion aka prolonged prerenal state), toxins( rhabdo, uric acid crystals, radiocontrast dye, hemolysis, amioglycosides)

3)Postrenal: Renal outflow obstruction

a. Intrarenal/tubular: crystals, nephrolithiasis

b. Ureteral: bilateral nephrolithiasis, thrombosis, edema from retrograde pyelography

c. Extra-ureteral: Bladder or cervical CA

d. Bladder neck: neurogenic bladder, autonomic neuropathy

e. Urethra: BPH, prostate CA, urethral stricture

-Evaluate for volume status, skin tenting LE edema, ascites, skin rash, purpura, bladder distension, prostate enlargement etc.

-Monitor urine output, sediment, UA, electrolytes

-Calculate FENa (collect urine sample prior to IV fluid or diuretic tx). If patient is on diuretics utilize FEUrea.

-FENa: (Una/Pna)/(Ucr/Pcr), FEUrea: (Uurea/Purea)/(Ucr/Pcr)

- Renal US to r/o obstruction or assess for hydronephrosis

-Serology for complement levels and renal biopsy if etiology is unclear. 






Nephrology

Chronic Renal Failure

Definition

GFR <60 for 3 months or more

AND/OR

presence of kidney damage (albuminuria, sediment or anatomic abnormalities or a hx of kidney transplantation).

Stages of CKD:

image-1649960548419.png

Etiology: 

Most common is DM. Others are HTN/RAS, glomerular, interstitial , drugs, congenital, myeloma and PKD.

Evaluation:

-Evaluate for uremic symptoms and signs

General Nausea, weight loss, hypothermia
Skin Pruritus, calciphylaxis(skin ulcers)
Metabolic

increased K and phosphorus, decreased Ca, 2 PTH, acidosis
Cardio HTN, CHF, LVH, pericarditis
Neuro seizures, neuropathy. decreased memory/attention/MS (encephalopathy)
Heme Anemia, bleeding(plt dysfunction)

Management:

-Consult Nephrology if proteinuria or GRF <30.  BP measurements, IVs for dialysis access planning.

-Restrict sodium, potassium, phosphorus and protein intake especially if HTN or hyperkalemic. 

-Treat/ risk reduction of co-morbidities (DM, HTN, CAD) with glucose control/ SGLTi, statin, ACEi/ARB ( reassess Cr and d/c if there is a 30% increase post ACEi/ARB).

-Sevelamer to control phosphorus levels, HCO3 replete if acidotic, Fe supplementation for anemia (goal Hb 10-11.5).

-Evaluate for transplant (GFR <20) 

Nephrology

Indications for Dialysis

Acute Indications:

Volume overload refractory to diuresis

Severe hyperkalemia (K >6.5 mEq/L) or rapidly rising K+ levels

Severe metabolic acidosis ( and pH <7.1)

Uremia (pericarditis, uremia, unexplained mental status decline)

Toxic overdose of a dialyzable drug (Barbiturates, Isoniazid, Salicylates, Methanol etc)

Chronic Indications:

CKD stage 5, GFR<15

Modalities:

Intermittent Hemodialysis (IHD): access-> AV fistula/graft

Peritoneal Dialysis (PD): access ->peritoneal catheter.

Timing:

3 times weekly, on alternate days, (MWF or TThSa) is the recommendation for intermittent hemodialysis (IHD).

Newborn Service

Newborn Service

FM Unassigned Newborn Service

Welcome to the Family Medicine newborn inpatient service! We admit most “unassigned” babies (no pediatrician selected, or one selected that does not have permissions at St. Agnes). We are working on a list for inclusion and exclusion criteria for our service. Remember, nothing is set in stone and this will all likely change as the rotation evolves.

Written by Arianna Crediford, MD (PGY1) 

Useful Tips

Admissions: .NBHPFAM (EPIC, if it doesn't auto populate, search Phillip Kim in Personalization and use the SHARE ICON for access)

Cap: 12 total notes or 6 total admissions for the day. No more than 12 INTERACTIONS/NOTES per day. So if you start the day with 12 babies on the list and you discharge 6, you don't have to admit 6 more.  This will likely change as the rotation evolves.

Progress Notes: .NBPNFAM
Discharges: .NBDCFAM

Toxicology

Toxicology

ETOH Intoxication

Management:

Symptoms:

1. Tremulousness (6-12 hours after last drink)

2. Seizures

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 approx. 5%

Other toxic alcohols:

References:
Kraut JA, Kurtz I. Toxic alcohol ingestions: Clinical features, diagnosis, and management. Clin J Am Soc Nephrol 2008 Jan;3(1!):208-25.
Goldfrank's Toxicology Emergencies, 9th ed 2010.
Poisoning and Drug overdose, 6th ed. 2012.
UpToDate. (2022). https://www.uptodate.com/contents/management-of-moderate-and-severe-alcohol-withdrawal-syndromes.



Toxicology

Acetaminophen Overdose

Check Acetaminophen levels and urine toxicology for co-ingestions

  1. Call poison control
  2. NGT, lavage with 2 L NS
  3. Activated charcoal: Give a single dose of activated charcoal at 1 g/kg p.o. via NG tube within 4 hours of ingestion
  4. N–Acetylcysteine: Passive given within 8 hours of ingestion and before ALT begins to rise, can give a charcoal
  5. Oral dosing of acetylcysteine: 140 mg/kg loading dose followed by 17 doses of 70 mg.kg every 4 hours.  If patient vomits within 1 hour administration give full dose again
  6. Give acetylcysteine based on the nomogram.  If unable to obtain level just treat.
  7. Follow acetaminophen levels q4h, LFT, PT/PTT
  8. Evaluate potential need for liver transplant; pH < 7.3, Cr > 3.4, INR >6.5

References:

1. Hospitalist Handbook, iPhone App

2. UpToDate -- Acetaminophen Overdose

3. NCBI

 

Toxicology

Salicylate Overdose

Check salicylate level and check urine toxicology for co-ingestions. Try to determine whether salicylate was regular or enteric-coated (Affects pharmacokinetics).

  1. Call poison control
  2. NGT, lavage with 2L NS
  3. Intubate for respiratory depression if indicated
  4. Activated charcoal, if indicated. 1g/kg po/per NGT q2-4h
  5. Alkalinize plasma/urine with a bolus of 1 to 2 Amps of sodium bicarb, then start 2 Amps of sodium bicarb per 1 L of D5 ¼ NS.  Run this at approximately 4 mL/kg/hr.  Do not use acetazolamide.  Caution in elderly and renal failure as aspirin can cause pulmonary edema
  6. Replete potassium to maintain normal serum levels otherwise alkalinization will be difficult to achieve
  7. Be sure to treat concurrent hypoglycemia and coagulopathy if present
  8. External cooling if febrile (no acetaminophen)
  9. Hemodialysis indicated if level > 100mg/dL - level checked 6 hours after ingestion, refractory acidosis, persistent CNS symptoms, and/or if renal failure.

References:

1. Hospitalist Handbook, iPhone App

2.UpToDate -- Salicylate Toxicity

Toxicology

TCA Overdose

Call poison control. 

References:

1. Hospitalist Handbook, iPhone App

2. UpToDate -- TCA

 

Toxicology

Cocaine Overdose


Diagnosis

Management

Source: Uptodate: Cocaine Overdose

Hospitalist Handbook



Toxicology

Opiate Overdose

Effects

Diagnosis

Treatment

Source: Uptodate: Opiate overdose


Toxicology

Carbon Monoxide Inhalation

Symptoms depend on CO level (carboxyhemoglobin)

Diagnosis

Management

Source: Uptodate: CO poisoning

OB/GYN

OB/GYN

Rotation expectations

Call group (only cover patients of the following):

Dr. Vishwanath

Dr. Dickinson

Dr. Marquez

Dr. Gade

Dr. Matharu

Any unassigned patients 

Door Codes:

Sleep Rm 4th floor 611#

6th floor doctors’ lounge 33115

From elevator on 6th floor 425#

From COVID area to 6th floor 425 

Expectations: 

Round on postpartum patients - 4th floor

Round on Antepartum patients - 6th floor 

Cover patients in L&D

See all patients in OB ED - 4th floor 

Assist for CSs (Surgery is on 2nd floor close to main elevator)

Read NSTs 

Cover GYN consults in ER or floors 

Postpartum Rounds

Post Op Fever: 

Wind - atelectasis 

Water - UTI

Wound - infection

Walk - DVT

Wonder drug - heparin

Woman - mastitis, breast engorgement

Womb - endometritis, pelvic vein thrombophlebitis, TOA

Postpartum Hemorrhage:

Can happen postpartum often!

Pre Delivery Hgb → Post Delivery Hgb

Significant drop is > 2

  1. Oxytocin 20-80 IU/500ml NS IV infused over 10 mins, then 250ml/hr 
  2. Methergine 0.2mg IM or PO (contraindication: HTN) 
  3. Hemabate 0.25mg IM (contraindication: asthma)
  4. Misoprostol 200 mcg (up to 3 tabs PR or 1 tab PO) 
  5. TXA 1gm/100ml NS IV over 10 minutes

Post-Partum Counseling

  1. Breastfeeding or Bottle Feeding? - Takes 3-5 days for milk letdown; longer in c/s patients
  2. Contraceptive Counseling 

         A) COC's - wait 3 wks postpartum (early Estrogen increases risk for DVT)

    - estrogen may cause decrease milk production if breastfeeding-would not start in house but should not wait for 6 week      check to do so

             B) Progestins- can give immediately post-partum if desired 

  1. Depo provera 150 mg IM q3 mo-same as above 

     2. IUD - at other institutions is placed immediately postpartum, but more likely can be placed ANYTIME after delivery 

      3. MIcronor 0.35 mg pill po qd

Post partum Vaccine

  1. Rubella - if nonimmune or equivocal, need vaccine]
  2. If Rh negative - check infant

If infant positive → Rhogam

If infant negative → none 

OB/GYN

Routine Visit Schedule

The first visit of prenatal care typically occurs in the first trimester. The frequency of follow up is based on the individual needs and assessment of risks. 

In General, this is what we follow:

Remember to always check fetal heart tone with doppler for every pregnant visit especially >12 weeks

Remember urine dip EVERY VISIT!

Start measure the fundal height of uterus after 20 weeks (expect approx 1cm fundal height growth per week of gestation)

Guidelines to Perinatal care Chapter 6

OB/GYN

Routine Testing Intervals/Schedules

Initial Visit or First trimester visit:

14 to 20 weeks:

20 to 32 weeks:

32 to 36 weeks:

36 to 40 weeks:


Perinatal Care Chp 6. Page 159

Prenatal Genetic Screening Test

OB/GYN

Pregnancy Dating

Step 1: Document First day of the last normal menstrual period then use Nigel's rule or use uptodate EDD calculator to estimate EDD

Step 2: Compare with EDD from first TM ultrasound. Look at Table 1 to see if we should use EDD based on LMP or US

Step 3: Determined EDD

Estimating due date

OB/GYN

Fetal Well-Being

These are ways used to establish fetal well being:

These test are used to follow:

ACOG Guidelines on Antepartum Fetal Surveillance

OB/GYN

Intrauterine Growth Restriction

Definition

Sonographic EFW <10th percentile

Etiology

Maternal factor: Behavioral (smoking, substance use, decrease nutritional intake), Medical (Diabetes, HTN, renal insufficiency, autoimmune), extreme of maternal age

Fetal factor: Chromosomal or genetic cause, fetal infection, multiple gestations

Physical examination

Suspect if fundal height < dates or poor maternal weight gain

Magagement

Pocket Obstetrics and gynecology by K Joeph Hurt 2nd edition

OB/GYN

Nonstress Testing

Contraindications:

Gestational age <24 weeks

Interpretation:

>32 weeks
Reactive NST: two fetal heart rate accelerations within a 20-minute interval, peaking at least 15 beats per minute above the base line and lasting 15 seconds 

<32 weeks

Reassuring for gestational age: two fetal heart rate accelerations 10 beats above the baseline and lasting for 10 seconds within a 20-minute interval.

NST

OB/GYN

Contraction Stress Test

The contraction stress test is interpreted by the presence or absence of late fetal heart rate decelerations.

Relative contraindications to the contraction stress test usually include conditions that are associated with an increased risk of preterm labor and delivery, uterine rupture or uterine bleeding. 

Contraction stress test

OB/GYN

Biophysical Profile

Scoring: The non stress test (2), fetal breathing movement (2), Fetal tone (2), Fetal movement (2), amiotic fluid (2)

The modified BPP combines the nonstress test and an evaluation of the amount of amniotic fluid called the amniotic fluid index (AFI).

The largest  pocket of amniotic fluid is measured in each of the four quadrants of the mother's abdomen using ultrasound. All four quadrants added together give the amniotic fluid index.

BPP

OB/GYN

Fetal Heart Rate Monitoring

BASELINE FHR

The normal FHR range is between 120 and 160 beats per minute (bpm). The baseline rate is interpreted as changed if the alteration persists for more than 15 minutes.

FHR VARIABILITY

Prematurity decreases variability therefore, there is little rate fluctuation before 28 weeks. Variability should be normal after 32 weeks.

Beat-to-beat or short-term variability is the oscillation of the FHR around the baseline in amplitude of 5 to 10 bpm.

Long-term variability is a somewhat slower oscillation in heart rate and has a frequency of 3 to 10 cycles per minute and an amplitude of 10 to 25 bpm. Clinically, loss of beat-to-beat variability is more significant than loss of long-term variability and may be ominous.

Decreased or absent variability should generally be confirmed by fetal scalp electrode monitoring when possible.

Increased variability in the baseline FHR is present when the oscillations exceed 25 bpm. This pattern is sometimes called a saltatory pattern and is usually caused by acute hypoxia or mechanical compression of the umbilical cord. 

FETAL TACHYCARDIA

Baseline heart rate greater than 160 bpm and is considered a non-reassuring pattern.  Mild when the heart rate is 160 to 180 bpm and severe when greater than 180 bpm.

FETAL BRADYCARDIA

Fetal bradycardia is defined as a baseline heart rate less than 110 bpm.

Bradycardia in the range of 100 to 110 bpm with normal variability is not associated with fetal acidosis. Bradycardia of this degree is common in post-date gestations and in fetuses with occiput posterior or transverse presentations.

Moderate bradycardia of 80 to 100 bpm is a nonreassuring pattern.

ACCELERATIONS

The presence of at least two accelerations, each lasting for 15 or more seconds above baseline and peaking at 15 or more bpm, in a 20-minute period is considered a reactive NST.

EARLY DECELERATIONS

Early decelerations are caused by fetal head compression during uterine contraction, resulting in vagal stimulation and slowing of the heart rate. This type of deceleration has a uniform shape, with a slow onset that coincides with the start of the contraction and a slow return to the baseline that coincides with the end of the contraction.

LATE DECELERATIONS

Late decelerations are associated with uteroplacental insufficiency and are provoked by uterine contractions. Any decrease in uterine blood flow or placental dysfunction can cause late decelerations. 

A late deceleration is a symmetric fall in the fetal heart rate, beginning at or after the peak of the uterine contraction and returning to baseline only after the contraction has ended

VARIABLE DECELERATIONS

Variable decelerations are shown by an acute fall in the FHR with a rapid downslope and a variable recovery phase.

 

https://www.aafp.org/pubs/afp/issues/1999/0501/p2487.html

OB/GYN

Laboratory Values in Pregnancy

Lab values in Pregnancy

pregnancy value 1.pngpregnancy value 2.png

OB/GYN

Bishop Score

The Bishop score may be used to rate the readiness of the cervix for labor. 

bishop score.png

MDCalc Bishop score

OB/GYN

Recurrent Pregnancy Loss

Definition

3 or more consecutive preg losses before 20wk gest or after 2 consecutive losses, esp if age >35 y.o

Evaluation

Diagnostic Workup

Pocket Obstetric and Gynecology by K Joseph Hurt, 2nd edition



OB/GYN

Hyperemesis Gravidarum

Definition

Nausea and vomiting in pregnancy that significant enough to cause dehydration, metabolic alkalosis, ketonuria, weight loss (>5%), hypokalemia

Risk Factors

Multi gestation, Family history or personal hx in prior pregnancy

Labs

CBC, lytes, UA, TSH, LFT

Therapy

IV hydration with dextrose +/- thiamine

hospitalization for monitoring

Pharmacotherapy

Diglecis 

Ondansetron 4 to 8 mg q8hr

Promethazine 12.5 to 25 q4-6hr

Metoclopromide 5 to 10mg q8hr

Diet

Usually begin with a diet consisting of bananas, rice, applesauce and toast (BRAT diet) and then advance the diet as tolerated. 


UpToDate

OB/GYN

Hypertension in Pregnancy

Definition

Chronic HTN: SBP greater equal to 140 or DBP greater equal to 90 prior to 20 weeks or persisting longer than 12w post partum

Gestational HTN: SBP greater equal to 140 or DBP greater equal to 90 after 20 weeks with or without proteinuria

Pre-eclampsia: New onset HTN (SBP >140 or DBP >90 x2 greater than 4hrs apart) with proteinuria more than 20 weeks. Proteinuria defined as >300mg/24hr (or 1+ urine dip or urine protein:creatinine ration of >0.3). If severe features are present, proteinuria is NOT needed for the diagnosis.

Severe features: SBP >160 or DBP >110; thrombocytopenia <100,000; elevated liver enzyme test more than 2x upper limit of normal, severe RUQ pain, renal insufficiency (cr >1.1 or doubling of baseline value); pulmonary edema; new onset cerebral/visual sympmtoms

Eclampsia: Pre-eclampsia with seizures

Diagnostic work up

CBC. CMP (evaluate liver and renal function), assessment of proteinuria (by urine spot prot to creatinine ratio, UA, or 24h urine collection)

Treatment and Medication

Acute HTN

Labetalol: 20mg IV, rpt at 10 min intervals, double dose with max dose of 80mg at 1 given time; total max dose of 300mg 

Hydralazine: 5-10mg IV over 1-2 min, rpt a 20 mins interval. Max dose of 30mg

Nifedipine: 10mg PO, rpt at 20 min interval. If next BP severe, can give 20mg PO

Nitroprusside: 0.20-4mcg.kg.min IV drip, titrate to effect. Only in critical illness

Nicardipine: 2.5mg/h IV titrating, do not exceed 15mg/h

DO NOT USE: ACEI or ARB

Oral treatment

Labetalol: 100-800mg PO BID-TID (Max dose 2400mg/24hr)

Methyldopa: 250 mg PO BID (Max dose 3g/24hr)

Nifedipine XR: 30-90 mg PO daily (Max dose 120mg/24h)

Pre-Eclampsia with severe features or chronic HTN with superimposed pre-Eclampsia with severe features

Magnesium sulfate for seizure prevention: Given during stabilization prior to expectant management, during delivery, and 24h postpartum. Bolus 4-6g IV with maintenance of 1-2g/h for seizure prevention, titrate and consider no bolus if pt has renal failure. Monitor closely for pulm edema as MgSo4 is a smooth muscle relaxer

Timing for delivery:

Chronic HTN: No earlier than 38w if well controlled

Gestation HTN: 37weeks

Pre-Eclampsia

Chronic HTN with superimposed preeclampsia: at 37 week if no severe features. Otherwise same as preeclampsia with severe feature

Pocket Obstetric and Gynecology by K Joseph Hurt, 2nd edition

OB/GYN

Vaginal birth after Cesarean

Appropriate candidates

Hx 1-2 C-section via low transverse hysterotomy. 

Inappropriate candidates

Previous classical or T-incision, prior uterine rupture, extensive transfundal uterine surgery (ex: myomectomy), and patient with any contraindication to vaginal delivery.

Online NICHD VBAC success rate calculator

Delivery Considerations

Pocket Obstetrics and gynecology by K Joeph Hurt 2nd edition

OB/GYN

Post Dates Management

  1. Review gestational dating
  2. AFI/BPP and NST at 41 weeks and repeat once to twice a week
  3. Consider membrane stripping at 39 weeks
  4. Consider induction at 41 weeks and cervical ripening agents
OB/GYN

Gestational Diabetes

Universal screening start at 24-248 weeks.

Consider screening earlier in all women with BMI >25 and one or more risk factors:

Screening test:

1hr OGTT (50g): serum >130-140 , Positive screening test -->3hr OGTT (100g)

3hr OGTT (100g): Fasting plus 1hr, 2hr, 3hr. 2 or more abnormal values = GDMGDM.png

Management

Pocket Obstetrics and gynecology by K Joeph Hurt 2nd edition




OB/GYN

Twins

At risk for hyperemesis, GDM, HTN, hemorrhage, cesaeran, postpartum depression, preeclampsia, preterm delivery, IUGR, birth/genetic defects

Management 

Pocket Obstetrics and gynecology by K Joeph Hurt 2nd edition

https://www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2021/06/indications-for-outpatient-antenatal-fetal-surveillance

OB/GYN

ER precautions in Term Pregnancy

  1. Regular painful contraction every 5 minutes (nulliparous) or every 10 minutes (multiparous), or sooner if long distance to hospital or history of precipitous delivery
  2. Rupture of membrane
  3. Vaginal bleeding
  4. No or decreased fetal movement (<10 kicks in 2hrs)
OB/GYN

Medication in Obstetrics

Minimize all medication use during pregnancy (especially in 1st TM), unless clearly indicated!

FDA pregnancy categories

A: No risk in controlled human studies

B: No risk in controlled animal studies and no risk seen in humans

C: Small risk in controlled animal studies, but not seen or not studied in humans

D: Strong evidence of risk in humans but benefit may outweigh tisk

X: High risk - never to be used in pregnant humans

Analgesics

Antibiotics

Anticoagulation

Antiemetics

Diabetes medication

Hypertension or preeclampsia treatment

Psychiatric / substance abuse medications

https://www.aafp.org/afp/2003/0615/p2517.html

Pocket Obstetric and Gynecology by K Joseph Hurt, 2nd edition

 

OB/GYN

PAP Smear Referral Guideline

Algorithm 2013 Univ Washington

PEDS

PEDS

Peds Inpatient Expectation

PEDS

Developmental Milestones

Newborn

Social Language and Self-help:

Verbal Language:

Gross Motor:

Fine Motor:

1 month

Social Language and Self-help:

Verbal Language:

Gross Motor:

Fine Motor:

2 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

4 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones

Movement/Physical Development Milestones

6 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones

Movement/Physical Development Milestones

9 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones

Movement/Physical Development Milestones

12 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

15 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

18 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

24 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

30 months

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

3 years

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

4 years

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

5 years

Social/Emotional Milestones

Language/Communication Milestones

Cognitive Milestones 

Movement/Physical Development Milestones

 

CDC’s Developmental Milestones

Immunization Schedule

Immunization Schedule

Peds Immunization

Can also download cdc vaccination schedule app via your phone store

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Child and Adolescents Immunization

Immunization Schedule

Adult Immunization

Download CDC vaccination schedule via your phone app

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Adult Immunization Schedule

ACLS Protocols

ACLS Protocols

VFib/Pulseless VT/Asystole/PEA

AHA

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ACLS Protocols

Bradycardia

AHA

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ACLS Protocols

Tachycardia

AHA

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Outpatient Service

Outpatient Service

Expectations

You have 24hrs to submit all chart notes to be signed off by your preceptor attending unless there's a valid excuse

Outpatient Service

Morning Report

Mon and Tue from 8-8:30AM

Location:  NW Clinic Back Conference Room

Mon
Board Review Questions 

Tue

Attendance will be taken during your AMB rotation

Outpatient Service

Stanford Diabetes ECHO

GME SAMC IM and FP have signed a collaborative agreement with Stanford University's Diabetes ECHO project providing the latest guidelines and management of Type 1 and 2 Diabetes. 

All Residents on AMB rotation are expected to attend the Zoom conference on Thur 12:15-1:15 PM as posted in the Didactics Calendar.  Lecture topics and Case presentation will be given. 

Case presentation if requested by Stanford will be assigned or voluntarily chosen.  Any resident who presents a patient case will be given Scholarly Activity credit 
Attendance will be taken, please use Stanford's Zoom Chat box with your [name], St. Agnes Medical Center

 

Screening Schedule

Screening Schedule

USPSTF screening

Abdominal Aortic Aneurysm: Screening:

Asymptomatic Bacteriuria in Adults: Screening: pregnant persons

Breast Cancer: Screening: women aged 50 to 74 years

Cervical Cancer: Screening: women aged 21 to 65 years

Chlamydia and Gonorrhea: Screening: sexually active women, including pregnant persons

Colorectal Cancer:

Depression screening:

Gestational Diabetes: Screening:

Hepatitis B Virus Infection in Adolescents and Adults:

Hepatitis C Virus Infection in Adolescents and Adults

Human Immunodeficiency Virus (HIV) Infection:

Hypertension in Adults: Screening: adults 18 years or older without known hypertension

Intimate Partner Violence, Elder Abuse, and Abuse of Vulnerable Adults: Screening: women of reproductive age

Lung Cancer: Screening:

Osteoporosis to Prevent Fractures: Screening: women 65 years and older

Prediabetes and Type 2 Diabetes: