]]> http://www.sinaiem.org/wellness/2013/05/16/yoga-524/feed/ 0 http://www.sinaiem.org/pearls/2013/05/13/1939/ http://www.sinaiem.org/pearls/2013/05/13/1939/#comments Mon, 13 May 2013 13:19:29 +0000 tali http://8.1939 22 y/o F 35 weeks gestation being treated with magnesium sulfate for preeclampsia in your ED awaiting transfer to nearby hospital for definitive care. You go to re-evaluate the patient and find her somnolent, decreased respiratory drive and decreased deep tendon reflexes. After managing the airway what is the next step in management:

1. Dexamethasone
2. Lidocaine
3. Labetolol
4. Calcium gluconate
5. Atropine

Answer:  Calcium gluconate. This patient has signs and symptoms of magnesium toxicity. Although uncommon in women with good renal function toxicity is related to serum magnesium levels. Symptoms include loss of deep tendon reflexes, respiratory paralysis and cardiac arrest at higher doses. Calcium gluconate (1gm IV over 5-10 minutes) antagonizes the affects of magnesium and can counteract these life threatening side effects.

Less concerning but other side affects of Magnesium infusion at rapid rates include diaphoresis, flushing and warmth (likely due to peripheral dilation) nausea, vomiting, HA and palpitations.

Pre-eclampsia as a reminder is new onset HTN and proteinuria after 20 weeks gestation in a previously normotensive woman. Magnesium is used to prevent eclampsia (seizures) intrapartum. The mechanism of how it prevents seizures is not well understood. Recommendation is to begin infusion at onset of labor or prior to c-section.

Bethamethasone, not Dexamethasone, is administered to women to promote fetal lung maturation in prematurity (unrelated to pre-eclampsia but possibly a complicating factor).

Labetolol along with Hydralazine are 1^st line therapies in hypertensive women during pregnancy that might present to the ED (Nifedipine, Nicardipine and nitroglycerin are also safe to use). Remember though that treating hypertension does not alter the pre-eclampsia disease process nor does it reduce morbidity or mortality surrounding pre-eclampsia.

Source of question: www.1000emergencymedicinequestions.com

56 y/o F with acute organophosphate overdose, severe bronchorrhea, bradycardia and coma. She is intubated for airway protection and atropine therapy initiated. After 10 mg Atropine her HR is 130, BP 160/90 and secretions are still copious. Which of the following is the most appropriate next step in management?

1. Stop Atropine, start Epinephrine
2. Stop Atropine, start Vasopressin
3. Stop Atropine, Start Pralidoxime
4. Continue Atropine therapy alone
5. Continue Atropine therapy and add Pralidoxime

Answer: E

Organophosphates bind to and inhibit Acetylcholinesterase causing a cholinergic syndrome (Sludge- Salivation, lacrimation, Urination, Defecation, GI distress and Emesis – as well as Bronchorrhea with variable effects on HR). Mortality from organophosphate OD is usually attributed to hypoxia from bronchorrhea. Treatment includes high doses of Atropine (endpoint being reduction of bronchial secretions, not HR or BP control). Over time the bond between Acetylcholinesterase and organophosphates becomes irreversible (aging) so Pralidoxime has to be given as it acts to break the complex bond between the two and reverse symptoms further.

Source:  www.1000emergencymedicinequestions.com

Labs: alcohol (271), ASA (wnl), Tylenol (wnl)

Initial VBG: pH 7.34, PCO2 55, PO2 40 lactate 1.5

Carboxyhemoglobin 0.9

EKG- NSR 79, no STT changes. Incomplete RBBB. Flattening T waves laterally

CO poisoning

CO – colorless, odorless gas formed from hydrocarbon combustion that binds to Hgb at much higher affinity (240x) than O2 forming COHb à results in impaired oxygen transportation and utilization

-          Once it binds to the heme moiety it changes the heme so that it cant unload the three oxygen binding sites to the peripheral tissue and also interferes with cytochrome oxidase

Symptoms depend on duration of exposure and CO levels.

-          Cardiac: myocardial ischemia, MI , dysrhythmias, cardiac arrest

-          Brain: Stroke like symtpoms , Seizures Syncope,  Leukoencephalopathy, DNS

• DNS (delayed neuro sequlea)- not well understood  – theorized that involved lipid peroxidation by toxic oxygen species- when you recover from CO exposure you have a similar phenomenom to ischemia-reperfusion injury and exposure to hyperoxia may exacerbate oxidvative damage

-          Skin- cherry red skin – usually only present in excessive exposure (fatal levels)- also can see cutaneous bullae but uncommon as well

Workup

A+B – hypoventilation, high flow O2 via NRB With resevor – remember SPO2 wont change much

ECG (MI, dysrhythmia), cardiac monitor, volume resuscitation

Mental status / mini mental

Get an exposure history—duration, soursc, other exposures, other people exposed…

VBG- Initial respiratory alkalosis (compensation for reduced delivery); later anion gap metabolic acidosis  due to elevated lactate

CO-oximetry – levels correlate poorly with degree of poisoning and do not predict DNS (normal CO levels in a non-smoker up to 3%; smoker 10-15%)

-          Children are more likely to be affected cause they have a higher RR so they get higher doses of the poison;

Treatment: supplemental oxygen (NRB) or hyperbaric oxygen (JACOBI hospital)

-          Hyperbaric oxygen – 100% oxygen pressurized –not used to expedite removal of blood CO but to stop tissue level destruction

-           Indications for HBO (recommendations, not criteria): Syncope, Coma, Sz, AMS/confusion, COHb > 25% (even if asymptomatic), pregnant woman and children, abnormal cerebellar exam

-          Should be considered up to 24 hours after exposure

Hyperbaric fellow consulted on this patient but determined due to other causes of AMS (alcohol) and low levels not a candidate for hyperbaric at that time.

Thanks to Dr. Hernandez for this case!

Initial venous blood gas revealed pH of 7.21, pco2 40, lactate 2.1 and glucose of 20.

Initial ER venous revealed Na of 140, K 5.1, Cl 109, CO2 23, Bun 19, Cr 1.1 and glu 20.

Patient has a non-anion gap acidosis. Helpful mnemonic for differential in this category is HARDUP.

• Hyperalimentation
• Acetazolamide or other carbonic anhydrase inhibitors
• Renal Tubular Acidosis
• Diarrhea
• Ureteroenteric fistula
• Pancreaticoduodenal fistula

Of these, RTA is most likely given her history and physical. Which RTA however?

RTA type 1

• Affects distal tubules
• Hypokalemia 2/2 H+ secretion

RTA type 2

• Affects proximal tubules
• Hypokalemia 2/2 failed hco3 reabsorption from the urine by the proximal tubular cells

RTA type 4

• Affects adrenal glands
• Hyperkalemia 2/2 aldosterone deficiency

So this patient has RTA type 4, treat with dextrose for the hypoglycemia, hydrocortisone for glucocorticoid and fludrocortisone for the mineralcorticoid activity.

Thanks to Jake Isserman for his informative morning report.

What is the next initial management after starting IV TMP-SMX?

A. Corticosteroids

B. Intubate

C. Continue supportive care

D. Start antiretroviral therapy

Severe PCP is defined as arterial PaO2<60 mmHg on air. Moderate PCP is defined as: PaO₂ between 60 and 80 mmHg on air. Corticosteroid therapy should be considered in patients with paO2 below 70 mmHg. ART should be initiated after two weeks of initial dose of TMP-SMX for ART naive patients. ART in patients already on their course should continue.

To those further interested, below is the link to ‘The One Fund Boston’ to help those most affected by this tragedy. 

The One Fund Boston 2013

Please see below for today’s pearl.

44 yo female presenting with nausea, vomiting and abdominal pain. Patient is a chronic alcoholic with no other drug use admitted. Patient is tachycardic to 116 and hypotensive 90/68. She is alert and oriented x 3 but actively vomiting clear non-bilious and non-bloody vomit. She is tender in the epigastric and ruq. No tremors, jaundice or significant findings on exam. She has a Na 139, K 4.5, Cl 91, Co2 5, Bun 16, Cr 1.1. Her pH and lacate is 7.08 and 8.5, respectively, her urine dipstick contains ketones. There is no osmolality gap. What is your next best step in management after starting normal saline fluids?

A. CT scan of the abdomen

B. Thiamine and glucose infusion

C. Phosphate level

D. Abdominal x-ray

In this patient with a gap acidosis most likely relating to her chronic use of alcohol, the typical treatment of fluids and most importantly fluids with glucose and thiamine to help the nutrition depleted patient to improve their acid-base imbalance.

Alcoholic ketoacidosis usually develops in chronic alcoholics given their pan-nutritional deficiency status, causing the body to make ketones from the fasting state of alcohol only intake combined with low to none normal dietary food sources.

Patients, however, who develop marked hypophosphatemia are in significant risk for life-threatening sequelae including myocardial dysfunction or encephalopathy. Therefore, it is very important to ascertain the phosphate levels in such individuals to replet such a deficiency. Levels in a patient can be normal, but once treatment starts the insulin the body starts producing can drive extracellular phosphate intracellularly causing a drop in the level.

Although this occurs 12-36 hours after treatment, depending on where the level of phosphate is or how long the patient has been in the emergency department for, it is important to keep that in mind in the treatment of AKA.

Thanks to Dr. Hansen for his morning report.

Let’s try to brighten up our day with another wonderful pearl by yours truly!

55 year old Caucasian male, presents with right shoulder pain after bicycle accident. Helmeted, patient fell off after hitting a rock with his bike, landing on his right shoulder. Although wanting to go home and sleep it off, like most men who like to stay married, patient listened to his wife and came to ED to get checked out and go home quickly. He denies any other issues, signs, symptoms, or complaints.

Vital signs are stable.

Exam is unremarkable except for right shoulder abrasions and large ecchymoses at the AC joint. Range of motion is intact, significant tenderness to AC joint area with no deformity or step-offs noted. X-ray of shoulder is below. And of course, we will expect to find something in our AC joint area.

So what do we have?

Yes! Its a lateral clavicular fracture. Low grade, minimal to non displacement. So you call ortho and have the patient get setup for a follow up appointment and sling and we are done. On to our next patient!

But wait! What else is that?!

So you, the ortho team, your attending are so quick to want to discharge this otherwise very well appearing patient that we don’t notice the diffuse subcutaneous air in this man’s chest.

Even the radiology resident didn’t notice it on their first read. It wasn’t until the attending radiologist, who was present because it was during the daytime morning, supplemented the read two hours later, that we were notified about the subcutaneous air.

And then here’s the dedicated PA x-ray of the chest.

So, to make a long post short, this gentleman started having a throat tightening sensation 4 hours later. ENT noticed ‘bubbling’ in the posterior wall area near the vocal cords. He was awake, nasal-tracheo intubated, was given a chest tube to relieve the pneumothorax.

He eventually healed on his own and was eventually discharged after an inpatient stay of a few days upstairs.

So always, always, look for the forest! And especially the ENTS!!!

I love summer!! Its a beautiful, gorgeous day in the big bad city! Beware the T-storms later tonight!

Thanks to Dr. Elizabeth Weinstein from Indiana University School of Medicine for a riveting and wonderful lecture on potentially lethal diseases with easy-to-miss signs and symptoms.

In the same vein, I would like to present a bonus pediatrics pearl. Given that it is so beautiful outside, I’m going to be lazy and provide a link to a pediatrics case that was presented recently in the New York Times Health section in the ‘Think Like a Doctor’ series authored by Lisa Sanders, M.D.

Please, despite my laziness, I am sure you will not be disappointed in reading this article and besides, I think most of us can always use all the pediatric knowledge that we can get. And if you don’t think you do, then you should have a little something called Humble Pie.

It is titled, ‘The Baby Who Won’t Eat.’

http://well.blogs.nytimes.com/2013/04/04/think-like-a-doctor-the-baby-who-wont-eat/?smid=pl-share

PS

For those in our senior core didactics today, the following is to clarify pulsus paradoxus.

Normally, during the inspiratory phase of breathing, blood pressure falls <10 mmHg due to the drop in intrathoracic pressure. This drop in pressure causes increased venous return, causing increased right heart filling, increasing right heart pressure, increasing pulmonary venous pooling. This in turn causes decreased left heart filling, decreased left heart filling, increased heart rate in response and thereby decrease in output and blood pressure.

This all becomes exacerbated in the setting of cardiac tamponade and voila! Pulsus paradoxus.