Causes of Renal Failure

Causes of Renal Failure broken down by pre-renal, renal, and post-renal.

Source: Clinical Survival Guide for PA Students by G.Broughton, MD, PhD

Atrial Fibrillation

AFib, The Basics

Characteristics

1. irregularly iregular
2. irregular RR intervals
3. not a P wave in front of every QRS
4. atrial rate = 400-600bpm, ventricular rate = 80-160bpm

Etiologies = PIRATES

P = pulmonary (COPD, PE)/pheo/pericarditis

I = ischemic heart dz +/- HTN

R = rheumatic heart dz

A= anemia/atrial myxoma

T = throtoxicosis

E = ethanol ("holiday heart)/cocaine

S = sepsis (post-operative)

Signs/Symptoms

1. fatigue (most common)
2. tachypnea
3. palpitations
4. lightheaded

Work Up

(Test yourself... why would you order each of these? what are you looking for?) - answers below

1. EKG
2. ECHO
3. TSH (?)
4. Baseline coags

1. EKG = narrow complex QRS (<120msec), variable RR, irregular or absent P waves
2. ECHO = maybe thrombi, maybe dilated L atrium
3. TSH (?) = hyperthyroidism can cause AF
4. Baseline coags = getting baseline prior to starting anticoagulation

Of note: if you are looking for THROMBI..."normal" ECHOs (transthoracic) has low sensitivity - transesophageal ECHOs allow for better visualization of L atrial appendage (location where most thrombi form) 

source: First Aid for the Wards by Le, Bhushan, Skapik

pic source: http://www.saintvincenthealth.com/Services/Heart/Heart-Resource-Library/Atrial-Fibrillation/default.aspx

Family Practice Notebook

The FPNotebook site is a wealth of information - unfortunately- much of it is buried. They have changed their site a bit and added more advertisements which makes everything a little harder to find, but on there is still a lot of great info (especially under the tabs such as Derm and Nephrology).

Free Ophthalmoscope App

"The Virtual Ophthalmoscope is a free, educational resource for the clinical ophthalmologist. The Virtual Ophthalmoscope features a library of more than 50 clinical cases with high-quality, zoomable images and commentary from a leading consultant ophthalmologist.  Available on iPad and iPhone

This app is provided as an educational service by Alcon UK. It is intended for healthcare professionals only. Not for patient use."

iTunes Link

Asthma Charts

Every PACK-RAT I've taken has had at least 1-2 questions on asthma. During my primary care, pediatrics, and emergency medicine rotations I keep these charts with me because I used them daily.

Source: http://www.rtmagazine.com/issues/articles/2009-05_01.asp, http://www.uspharmacist.com/content/c/10133/?t=men%27s_health,otc_medications

Reading a Chest Xray

You should feel confident reading a chest x-ray (CXR). It is one of the few films that will follow you from rotation to rotation. It doesn't matter if it is pediatrics, internal medicine, or surgery - You need to know how to read a CXR. Below are a couple sources to choose from because not everyone teaches or learns this in the same way. Here are a couple tips that I learned during my rotations from studying, my preceptors, or just plain screwing up!

• The first thing you should check is the name/date/type of film! (On one of my rotations, an intern (1st yr resident) was asked to read a chest X-ray for one of our patients who had just gotten a chest tube placed. He did a great job with lung pathology and describing the fluid - and he was also able to pick out that the chest tube was perfectly placed. I was impressed until the chief resident said "great job, you just harmed your patient." The chief had purposefully put up a CXR from 2 years ago when the pt had rec'd another chest tube. He then pulled up the current CXR to reveal that the tube was improperly placed. )
• Read every film in the same order every time. 
• Learn the anatomy of what you are reading. 

Step by Step Tip for reading CXRs

University of Washington's Method

1. PA or AP, supine or upright

2. Pt rotated? Check for vertebral and clavicle symmetry.

3. Lung volumes

4. Tube & line placement

- ETT 3-5 cm above carina

- NGT in stomach

- FT in stomach/duodenum

- Central line in SVC/R atrium

- Swan in PA

5. Pneumothorax: check apices on upright film, deep sulcus sign at bases

6. Pleural effusion, pleural thickening

7. Mediastinum: normal contour, wide

8. Heart: normal size, cardiomegaly

9. Lung parenchyma: masses, opacites, look for silhouette sign

10. Soft tissues: foreign bodies, SQ air, breast shadows

11. Bones: fractures, osteopenia, abnormalities

Silhouette Sign = obscuring of normal borders on radiograph caused by intrathoracic lesion.

Obscured R heart border = R middle lobe

Obscured L heart border = Lingula

Obscured diaphragm = Lower lobe

PANCE REVIEW: Thyroiditis

So today's topic hits close to home because I was diagnosed with Hashimoto's thyroiditis this year after complaining of incredible fatigue. It was getting to the point that I was having difficulty getting through the day past 2p without napping. I was wiped out. So for today's PANCE review we will discuss Hashimoto's specifically - but you should also be familiar with the other forms such as subacute, post-partum, and infectious.

Hashimoto's Thyroiditis, Noteworthy Stuff Only

• Most common form
• Autoimmune or polyglandular syndrome
• More common in women than me
• Familial
• Frequency increases with 1) iodine supp and 2) certain meds
• Diffuse, enlarged, firm nodules (often asymmetric)
• NOT painful*
• Can see depression/chronic fatigue
• Tests: serum antithyroid peroxidase and antithyroid globulin antibodies
• Tx: lifelong thyroid hormone replacement (levothyroxine) for hypothyroidism, watchful waiting if goiter is present

*In contrast to subacute which is PAINFUL!

NOTE: Don't forget - for the PANCE... the single best screening test for thyroid dz is TSH!

Source: AAPA, PAEA Exam Review Book
Pic: http://www.nature.com/nm/journal/v10/n9/fig_tab/nm0904-895_F1.html

PANCE REVIEW: Spirochetal infections

Those pesky spirochetal infections:

	LYME	ROCKY MNT SPOTTED FEVER
General	Borrelia burgdorferi, deer tick must feed for 24-36hrs to pass dz, *Most common vector born-dz	Rickettsia rickettsii (wood tick), common in eastern US
Clinical	Stage 1:local infx (7-10d after bite) - erythema migrans "bull's eye", flu-like sx in 50% pts, Stage 2: early dissemination - HA, stiff neck, malaise, fatigue, MS sx, cardiac sx in 20% cases, Stage 3:late persistent infx, MSD, central/perip NS	fever/chills/ N/V, insomnia can develop in 2-14 days, face is flushed and conjunctiva injected, small rash develops on extremities
Lab	antibody detection (immunoflu assay or ELISA), western blot to confirm, Ig M wanes after 6-8 wks, IgG can be indefinite, high likelihood of false+	leukocytosis, thrombocytopenia, hypONa+, proteinuria, hematuria, transient rise in bili, rise in antibody titers in 2nd wk, CSF = pleocytosis, hypocorrhachia
Tx	doxy for erythma migrans or lyme, NSAIDS, prevention	mild, untx cases wane in 2wks, doxy or chloramphenicol hasten recovery, poor outcome for advanced age

ANKLE-BRACHIAL INDICES

ANKLE-BRACHIAL INDICES (ABI)
Indications: Presence of peripheral arterial disease
Technique
1. Have patient in supine position so arms, legs and heart are at same level.
2. Use blood pressure cuff and Doppler to measure systolic BP in both arms and record.
3. Use Doppler to identify location of dorsalis pedis and/or posterior tibialis pulses, mark location bilaterally.
4. Wrap BP cuff around lower leg. Using Doppler to listen to signal, inflate cuff until signal disappears, then slowly deflate until pulse signal returns. Record pressure at which pulse is heard (systolic) by Doppler at DP and PT in both ankles.
5. To calculate the AAI divide the highest SBP from each ankle (either DP or PT) by the highest SBP reading from the upper extremities.
6. ABI = ankle / arm systolic pressure
> 1.3 = suggests noncompressible, calcified vessels
0.91-1.3 = normal
0.41-0.9 = mild to mod peripheral arterial dz (range for claudication)
<0.4 = Severe peripheral arterial dz. (range for critical leg ischemia and rest pain)





Source: http://students.washington.edu/aomega/procedures.shtml#chestTube

Lobar Collapse Tutorial

In the ED you see tons of chest films and you approach them with a "worst first" mentality. I recently found a tutorial on collapsed lungs and radiography. It is pretty straight forward and basic - but at times, that is just what I need - a basic knowledge base to build on. The site if definitely worth a look. You could probably go through the entire page in under an hour and learn a good deal in the process.

Lobar Collapse Tutorial

Wound Closure Series

This site provides 12 great videos on wound closure. Check it out:

• Chapter 1: Equipment (1:54 min)
• Chapter 2: Anesthesia (3:09 min)
• Chapter 3: Irrigation (1:11 min)
• Chapter 4: Starting the Procedure (2:30 min)
• Chapter 5: Simple Interrupted (3:45 min)
• Chapter 6: Horizontal Mattress (3:11 min)
• Chapter 7: Vertical Mattress (1:10 min)
• Chapter 8: Corner Suture (1:30 min)
• Chapter 9: Buried Suture (1:51 min)
• Chapter 10: Dermabond (1:56 min)
• Chapter 11: Steristrips (0:39 min)
• Chapter 12: Staples (0:47 min)

Wound Closure Series: Academic Life in the Emergency Room

Basic Suturing Technique

There are a ton of suturing tutorial videos online, but I often find that it is tough to see exactly what they are doing in the videos. SIM SUTURE is a company that makes an at-home practice kit so they came up with a 7 part suturing tutorial that has great lighting, instructions, and visuals. Happy sewing!

SIM SUTURE TUTORIALS

Causes of Hearing Loss

Ambulatory Topic #2: Causes of Hearing Loss

At my present clinic, my attending does the annual physical exam for the state-employed divers. Many of them have exostoses, which are bony outgrowth of the external auditory canal related to repetitive exposures to cold water. They are common in divers and swimmers. This led us into a conversation about hearing loss and thus my topic of the day.

There are 2 types of hearing loss: Conductive vs Sensorineural

Conductive = caused by lesion in external or middle ear

Sensorineural = lesions in cochlea or CN VIII

Conductive

1.     External canal

a.     WAX! (Cerumen impaction)

b.     Otitis externa (TIP: Don’t forget to palpate external ear before introducing otoscope!)

c.      Exostoses

2.     TM performation

a.     Trauma

b.     Secondary to middle ear infection

3.     Middle ear

a.     Middle ear effusion (Otitis media, allergic rhinitis)

b.     Otosclerosis (bony fusion between stapes and ova = immobilization)

c.      Neoplasm

d.     Congenital malformation

Sensorineural

1.     Old Age (Presbycusis)

a.     Degeneration of sensory cells

b.     MOST COMMON

2.     Too many concerts (Noise-induced hearing loss)

a.     >85 dB for prolonged time

b.     Damaged hair cells

3.     Infection

a.     Viral or bacterial

4.     Drug-induced hearing loss

a.     Aminoglycosides

b.     Cisplatin

c.      Furosemide

d.     Aspirin can cause tinnitus (usually reversible)

5.     Inner ear injury

a.     Skull fx

6.     Meniere’s Dz

a.     Fluctuating, unilateral hearing loss

b.     Ear feels “full”

c.      Vertigo

7.     CNS cause

a.     Acoustic neuroma

b.     Meningitis

c.      Neuritis of auditory nerve

8.     Congenital

a.     TORCH infections

Tips on Hearing Tests:

RINNE vs WEBER

CONDUCTION LOSS	Finding:
Rinne Test (Abnl)	Bone conduction (BC) > Air conduction (AC)
Weber Test	Sound lateralizes to AFFECTED side*
SENSORINEURAL LOSS
Rinne Test (Nl)	AC > BC
Weber Test	Sound lateralizes to UNAFFECTED side

*This means that the tuning fork is heard louder in the ear with the conductive hearing loss.

I remember it as the Rinne test is Abnormal and sound lateralizes to the Affected side. Both start with “A”.



Source: Step Up to Medicine 2nd Ed.

Atypical vs. Typical CAP - Clinical Signs/Sx

Definition of CAP: Community Acquired Pneumonia is acquired in the community or within the first 72hrs of hospitalization

Typical

Bugs: 

S. pneumo (most common)

H. Flu

Staph aureus

Klebsiella

Clinical Symptoms:

Quick onset with fever/chills

Pleuritic chest pain

Productive (thick) cough

Signs:

Tachycardia

late inspiration crackles

CXR:

Lobar consolidation

Tx:

Doxycycline, Azithromycin, Clarithromycin, Flouroquinolones

Atypical

Bugs: 

Mycoplasma pneumoniae (most common)

Chlamydia pneumoniae

Chlamydia psittaci 

Coxiella burnetii

Legionella

Viruses

Clinical Symptoms:

Slow onset

HA, sore throat, fatigue, myalgias

Dry cough

Fever

Signs:

normal pulse with high fever

wheezing/rhonci

CXR:

Diffuse infiltrates

No/minimum consolidation

Tx:

start empiric tx with:
 erythromycin (for Mycoplasma pneumoniae and Legionella)
tetracycline (for Chlamydia pneumoniae)

Pic: http://emedicalppt.blogspot.com/2011/02/community-acquired-pneumonia-cap.html

Source: Step Up to Medicine 2nd Ed Agabegi and Agabegi

Paracentesis Video

NEJM Paracentesis Procedure Video

I am in my Ambulatory clinical rotation and I was able to do 2 paracentesis procedures in one day. One was therapeutic (drained 13L) and one was diagnostic. It was awesome! I love doing procedures.

Ambulatory Topic #3: QT Intervals

Ambulatory Topic #3: QT Intervals

Normal QT Interval:
less than 1/2 of the R-R interval (approx <0.42s)


Causes of Prolonged QT:
1-Meds:
2-Electrodisturbances (hypOCa+ and hypOK+)
3-Congenital
4-Ischemia
5-CNS lesion
6-Bradyarrhythmia

How to get the corrected QT interval (QTc):

What is it "correcting" for? The heart rate. The length of the QT interval is obviously dependent on the rate the heart is pumping so the QTc adjusts for this.



Pic: http://www.mayoclinic.com/health/medical/IM02677
Pic: http://heart.bmj.com/content/93/9/1051.abstract

Causes of Secondary Hypertension

I am currently on my Ambulatory Medicine rotation at a hospital that sees a patient population primarily comprised of the homeless, imprisoned, and uninsured. The staff is incredibly nice and I'm loving my time there. Every week I am assigned a couple of topics to look up and present orally to the attending. I thought I would share my findings on each topic.

Ambulatory Topic #1: Causes of Secondary Hypertension

1.     Primary renal disease — Both acute and chronic kidney disease, particularly with glomerular or vascular disorders.

*You see elevated serum Cr concentration and/or an abnormal urinalysis.

2.     Oral contraceptives — Oral contraceptives typically raise the BP within the normal range but can also induce overt hypertension.

3.     Drug-induced — Long term use of NSAIDs + many antidepressants can induce HTN. Chronic ETOH intake and ETOH abuse can also raise blood pressure.

4.     Pheochromocytoma — About 1/2 of patients with a "pheo" have paroxysmal HTN, most of the rest have what appears to be primary HTN.

* You see:

-paroxysmal elevations in blood pressure (which may be superimposed upon stable chronic hypertension)

-triad of headache (usually pounding), palpitations, and sweating

-drug-resistant hypertension and those with an adrenal incidentaloma should be evaluated for pheochromocytoma. Patients identified with pheochromocytoma are rarely asymptomatic.

5.     Primary aldosteronism — The presence of primary mineralocorticoid excess, primarily aldosterone, should be suspected in any patient with the

*You see:

-triad of hypertension, unexplained hypokalemia, and metabolic alkalosis. However, some patients have a normal plasma K+ concentration.

-otherwise unexplained or easily provoked hypokalemia due to urinary potassium wasting.

->1/2 pts =normal serum K+ concentration.

-suspected in the presence of slight hypernatremia, drug-resistant hypertension, and/or hypertension with an adrenal incidentaloma

6.     Renovascular disease — Renovascular disease = common disorder, occurring primarily in patients with generalized atherosclerosis.

7.     Cushing's syndrome — HTN is a major cause of morbidity + death in pts with Cushing's syndrome.

-Cushing's syndrome (including that due to glucocorticoid administration) is usually suggested by the classic physical findings of cushingoid facies, central obesity, proximal muscle weakness, and ecchymoses.

-Cushing’s or subclinical Cushing’s syndrome should also be suspected in patients with drug-resistant hypertension and in those with an adrenal incidentaloma.

8.     Other endocrine disorders — Hypothyroidism, hyperthyroidism, and hyperparathyroidism

-HTN may be associated with both hypothyroidism, which may be suspected because of suggestive symptoms or an elevated serum TSH level, and primary hyperparathyroidism. The latter is most often suspected because of otherwise unexplained hypercalcemia, which may affect vascular reactivity, day-night blood pressure regulation, and renal function

9.     Obstructive sleep apnea — Disordered breathing during sleep appears to be an independent risk factor for systemic hypertension.

-sleep apnea syndrome is most commonly identified in obese men who snore loudly while asleep. These patients have repeated apneic episodes at night due to passive collapse of the pharyngeal muscles during inspiration, such that the airway becomes occluded from the apposition of the tongue and soft palate against the posterior oropharynx.

-A variety of other symptoms may be seen including headache, daytime somnolence and fatigue, morning confusion with difficulty in concentration, personality changes, depression, persistent systemic hypertension, and potentially life-threatening cardiac arrhythmias.

-Patients with obstructive sleep apnea often retain sodium and fail to respond optimally to antihypertensive drug therapy

  10.  Coarctation of the aorta — Coarctation of the aorta is one of the major causes of secondary hypertension in young children

               -Coarctation of the aorta is one of the major causes of secondary hypertension in young children but may first be detected in adulthood (picture 1A-B). The classic findings are HTN in the upper extremities, diminished or delayed femoral pulses ("brachial-femoral delay"), and low or unobtainable arterial blood pressure in the lower extremities. In addition, a prominent “to-and-fro machinery murmur” from the aorta may be heard over the posterior chest.

Source: uptodate.com

Pic:http://www.aakp.org/aakp-library/ped-hypertension/

Pic: http://www.angiologist.com/secondary-hypertension/

Nephrolithiasis - When Should I Admit?

I recently had a patient who came in complaining of severe flank pain radiating to his groin with nausea and vomiting… it was determined that he had nephrolithiasis (kidney stones). My attending asked me whether or not we should admit the patient… Good question, I thought. I was able to rattle off the text book treatments, but I wasn’t clear on the guidelines for admission vs. out-patient treatment. Below is an overview of treatment including some clear indications for admission.

General Treatment (for all types of stones):

1-PAIN CONTROL!

a-PO analgesic or IV morphine, situation dependent

b-Parenteral NSAID (Ketorolac)

2-Hydration (vigorous)

3-Antibx, if UTI present

Additional treatment measures based on pain severity:

MILD-MOD pain = high fluid intake, oral analgesics, wait for stones to pass (Give pt a urine strainer because you want to know what “kind” of stone the patient has.)

SEVERE pain = IV fluids and pain control, KUB, IVP to find site of obstruction, consult urology (surgery) if stones do not pass in 3 days

ONGOING pain w/o relief from narcotics = Surgery

Types of Surgery (10,000 foot view):

Shock wave lithotripsy: most common, it breaks apart the larger stones so they can be passed spontaneously, typically used for stone >5mm and < 2cm

Percutaneous nephrolithotomy: used if the above fails, if stones are > 2cm, for struvite stones

Admission is indicated if:

1-Oral analgesics are insufficient to manage the pain.

2-Ureteral obstruction from a stone occurs in a solitary or transplanted kidney.

3-Ureteral obstruction from a stone occurs in the presence of a urinary tract infection (UTI), fever, sepsis, or pyonephrosis.

4-Large stones (>1cm)

*The above indications were found in a couple of sources, but more say that the ultimate decision is made on a clinical basis, not solely on guidelines.

Parting suggestion: brush up on the different kinds of kidney stones

Sources:

Medscape: Nephrolithiasis and Treatment, http://emedicine.medscape.com/article/437096-treatment

Step Up to Medicine 2^nd Ed. by Agabegi and Agabegi

Picture: http://knol.google.com/k/kidney-stones#

Treating Hyponatremia in the ED

After reading this blog entry from EM CRIT BLOG I felt better regarding the treatment of hyponatremia so I thought I would share. This blog has some great information and most blogs have a podcast option.

"In this podcast, I discuss the management of hyponatremia in the ED. After reading countless articles from the nephrology literature…I can still attest that I have not a friggin’ clue about renal physiology. But I think I have found a simpler path to the work-up and treatment of low sodium in the ED."

Click here for rest of entry...

I have a headache.

I have a headache and, of course, my natural instinct is to run a differential in my head – an unfortunate side effect of PA school. Since headaches are a common patient complaint I thought I’d share my thought process…

Is it primary or secondary? (Note: Primary HA are non-life threatening.)

Primary = migraines, cluster, or tension

Secondary = think VOMIT

V = vascular (SAH, subdural hematoma, epidural hematoma, intraparenchymal hemorrhage, temporal arteritis)

O = other causes (malignant HTN, pseudomotor cerebri, post-LP, pheochromocytoma)

M = medication (drug related – nitrates, ETOH withdrawal, chronic analgesic use/abuse)

I = infection (meningitis, encephalitis, cerebral abscess, sinusitis, herpes zoster, fever)

T = tumor

Great Article and DDx Chart on Headaches (includes tests/treatments): 

Pitfalls in Management of Headaches in the Emergency Department

I may even add an “S”to the end – it will stand for studying student. I think I’m going to live.

Source: Step Up to Medicine  2^nd Ed.