Episode 29 – Hyperglycemia

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The Free Open Access Medical Education (FOAM)

We review a post on Pediatric DKA from Dr. Anton Helman’s Emergency Medicine Cases.

Pearls from this episode:

  • Fluids come first in DKA but you may not need as much as you think. They recommend only using fluid boluses, and even then a baby bolus of 5-10 cc/kg, in the hypotensive decompensated patients, coupled with frequent re-assessments. Other patients can get up to twice maintenance of 0.9% NaCl.
  • No insulin bolus for pediatric patients, ever.
  • Cerebral edema is the most dreaded complication of DKA and seems to be associated with severe presentations, young children (<5), or DKA as the presentation of diabetes. Treatment related factors such as administration of an insulin bolus or sodium bicarbonate may also contribute. The role of fluids (particularly over-aggressive fluids) is less clear [1-3].
  • Management of cerebral edema: ABCs, Elevate head of the bed 30 degrees, Mannitol 0.5-1g/kg IV over 20min AND/OR hypertonic (3%) NaCl 5-10cc/kg IV over 30min

The Bread and Butter

We cover hyperglycemia including diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). We do this based on osen’s Emergency Medicine, Chapter 126 (8th ed) and Tintinalli, Chapter 222 (7th ed). But, don’t just take our word for it. Go enrich your fundamental understanding yourself.

Diabetic Ketoacidosis

Diagnosis – glucose >250 mg/dL, pH <7.3, bicarbonate <18, anion gap >10

Workup – evaluate electrolytes (particularly potassium) and potential triggers for DKA.

Treatment – fluid resuscitation is initial intervention as these patients are typically 4-6 L down. In adults we hold insulin treatment until we know the patient’s serum potassium, as these patient’s are depleted secondary to osmotic diuresis. Further, the patient’s serum potassium may be falsely elevated by acidosis. Insulin may be started once the potassium is >3.5 (with potassium replacement if <5.3). We do not bolus pediatric patients but the ADA guidelines and Rosenalli state we do not need the insulin bolus in adults either [4-6]. The use of subcutaneous insulin in DKA is popular amongst pediatric patients and growing in popularity in adults [7,8].

Screen Shot 2015-06-02 at 11.19.08 AM

Hyperosmolar Hyperglycemic State (HHS)

Diagnosis – elevated serum glucose (often >600 mg/dL), serum osmolar >315-320 mOsm/kg. Patient’s may have a concomitant acidosis or ketosis, but this is often less profound than in DKA.

Workup – ascertain why the patient ended up in HHS – whether it was a mobility issue or polypharmacy (diuretic, lithium, etc). Check osmolality and for DKA.

Treatment – these patients are often severely dehydrated (>8 Liters). Start with volume resuscitation and add an insulin infusion (0.1 units/kg/hr).

 

Generously Donated Rosh Review Questions

1. A 43-year-old man presents with altered mental status. His vital signs are HR 113, BP 143/63, T 98.9°F and blood glucose of 750 mg/dl. During your evaluation he has a brief generalized tonic-clonic seizure. [polldaddy poll=8904849]

Answers

1. This patient presents with signs and symptoms consistent with hyperglycemic hyperosmolar state (HHS) and intravenous fluids should be given aggressively early in management. HHS is a syndrome characterized by dehydration, hyperglycemia, hyperosmolarity and altered mental status. Patients may present with confusion, lethargy, seizures, focal neurologic deficits or frank coma. Pathophysiologically, decreased insulin (or insulin action) leads to gluconeogenesis and increased circulating glucose levels. This in turn draws fluid from the intracellular space into the intravascular space. The resultant osmotic diuresis leads to profound intravascular dehydration, electrolyte abnormalities and hyperosmolarity. Typically, patients will have a blood glucose >600 mg/dl and an osmolarity >350 mOsm/L. Blood urea nitrogen and creatinine are usually elevated. Initial management focuses on supportive care and aggressive fluid resuscitation. Patients with HHS are estimated to be 5-10 liters behind. In addition to fluid administration, electrolyte repletion is paramount.

2. A 45-year-old man presents with altered mental status. On arrival, his finger stick is 35 mg/dL. He is given dextrose leading to the return of a normal mental status. On history, he reports he may have accidentally taken extra medication. Which of the following medications requires prolonged observation in the hospital?

  • Glipizide
  • Metformin
  • Novolog
  • Sitagliptin

In most adults, symptomatic hypoglycemia occurs when glucose levels reach 40 to 50 mg/dL. Glipizide is a sulfonyurea oral hypoglycemic drug. This class of medication is associated with hypoglycemic episodes through their action as an insulin secretagogue. In a sulfonylurea overdose, patients should be observed for 24 hours. When the etiology is unclear, laboratory testing including renal function is indicated. In situations without large ingestions, patients may be discharged if no additional episodes of hypoglycemia occur after an observation period. In cases of severe, prolonged or recurrent episodes of hypoglycemia from sulfonylureas, additional therapy with octreotide as an inhibitor of insulin release is indicated.

References:

  1. Glaser NS, Wootton-Gorges SL, Buonocore MH, et al. Subclinical cerebral edema in children with diabetic ketoacidosis randomized to 2 different rehydration protocols. Pediatrics. 2013;131(1):e73–80. doi:10.1542/peds.2012-1049.
  2. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344(4):264–9. doi:10.1056/NEJM200101253440404.
  3. Lawrence SE, Cummings E a, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):688–92. doi:10.1016/j.jpeds.2004.12.041.
  4. Diabetic Emergencies : New Strategies For An Old Disease.
  5. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335–43. doi:10.2337/dc09-9032.
  6. Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010;38(4):422–7. doi:10.1016/j.jemermed.2007.11.033.
  7. Umpierrez GE, Cuervo R, Karabell A, Latif K, Freire AX, Kitabchi AE. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care. 2004;27(8):1873–8. Available at: http://www.ncbi.nlm.nih.gov/pubmed/15277410. Accessed July 17, 2014.
  8. Umpierrez GE, Latif K, Stoever J, et al. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis. Am J Med. 2004;117(5):291–6. doi:10.1016/j.amjmed.2004.05.010.

FOAMcastini – One Year Anniversary

 We enjoy contributing to the Free Open Access Medical education (FOAM) community.  Creating FOAM is not free and requires significant costs in time and money.  Yet, we find this investment invaluable and appreciate everyone who listens, as well as those who champion our endeavor (including the supportive people in our life that tolerate “FOAMcast dates” and tiptoe around whilst recording). We would also like to thank everyone who has contributed by means of post-publication peer review (Brett Schupack, Dr. Marc Probst, Dr. Gabriel Cade, Dr. Iain Beardsell, and countless others).  Please continue to not only let us know when we get it right, but also when we get it wrong.  We appreciate the suggestions, praise, feedback, and corrections.

Given our love of spaced repetition,  we review our favorite pearls and mnemonics from the past year.

Favorite Mnemonics:

Causes of atrial fibrillation = ATRIAL FIB

Screen Shot 2014-09-16 at 3.57.07 PM

Causes of intestinal obstruction from the episode on Small Bowel Obstruction

  • HANG IV: hernia, adhesions, neoplasm, gallstone (ileus), intussception,

Heart failure episodetreatment for right ventricular heart failure.

  • Optimize OHCRAP – Oxygenation, Hemodynamics, Contractility, Rate/rhythm, Afterload, and Preload

Headaches – Likelihood of migraine diagnosis (comes from the outpatient literature) = POUND.  4 criteria  very indicative of migraine (+LR 24), 3 criteria also likely (+LR 3)

  • Pounding headache
  • hOurs: headache lasts 4-72 h without medication
  • Unilateral headaches
  • Nausea
  • Disabling: disrupts daily activities

Our most frequently used clinical pearl:

The hand exam, in one movement:

Motor Exam of the Hand
Motor Exam of the Hand

Our favorite visual aid:

Burns – Grading the burn according to the Egyptian flag (because we all knew what that looked like).

Burn Degree
Burn Degree

Worst visual aid:  the Knee volcano (we won’t go there again)

Time is….

Pee/Urethra – Infected obstructing kidney stones require urgent urologic intervention for source control.

Cord – complete cord syndrome that persists longer than 24 hours is highly unlikely to have any motor recovery. These patients need urgent intervention. This is we must differentiate between the complete and incomplete cord syndromes. Complete = “total loss of motor power and sensation distal to the site of the spinal injury.”

Knee/Leg – Beware knee dislocations.  Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.

Knee Dislocation Algorithm
Knee Dislocation Algorithm

Time is skin?

FOAMcastini – ACEP tPA Clinical Policy Update

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The Free Open Access Medical Education (FOAM)

Comment on the 2015 ACEP tPA Clinical Policy Draft here

ACEP tPA Clinical Policy 2012 – This policy has been entrenched in controversy since it was published.  Why?  Well, largely because the evidence was given a stronger level recommendation than the data supported, conflicts of interest abounded, and the data (mostly from NINDS (The SGEM review), ECASS, and IST-3) were problematic.  This has been well covered by these reviews of the clinical policy:

What changed in the 2015 draft?

Screen Shot 2015-01-13 at 10.22.04 AM

FOAMcastini – ACEP Wednesday

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FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Weekend review, Monday review, Tuesday review

Scientific Assembly Wednesday Pearls

(there’s too much to choose from, so follow #ACEP14)

Debating Clinical Policies: Implications for tPA and Beyond – Drs. David Newman, David Seaberg, and Edward Sloan

  • The ACEP clinical policy on TPA is hotly debated, as it gives Level A evidence to TPA in acute ischemic stroke.  This policy is being reconsidered and big props to ACEP for doing this, most professional organizations aren’t that responsive.
  • TPA has a NNT of 8 and a NNH of 16.  The TPA supporters typically reference NINDS, ignoring the other RCTs.  They also reference large sets of registry data.
TPA in Stroke courtesy of Dr. Andy Neill
TPA in Stroke courtesy of Dr. Andy Neill
  • Check out his SMART EM podcast on the topic

Evidence-Based Approach to the “Other” Stroke – Dr. Jon Edlow

  • Prothrombin complex concentrate (PCCs) are all the rage, particularly since the 4 factor PCC was approved last year in the United States.  It improves patients numbers of coagulopathy, but not necessarily patient outcomes (Dr. Rory Spiegel on the topic).
  • Fresh frozen plasma, dosing is based on INR and the patient’s weight, it’s not an empiric “2 units.”
  • Blood pressure control may be safe in Intracerebral hemorrhage, but the studies such as INTERACT don’t show that it benefits patients (The SGEM).

Chest Pain in the ED: Is One Troponin Enough? – Dr. David Newman

  • The miss rate for MI is often quoted as 2%, but it’s more like 0.2% per the Pope et al study.  So, we’re pretty good at this.
  • ACEP has a policy stating that a single troponin after 8 hours of chest pain is sufficient
  • States that have tort reform have shown fewer lawsuits and less money without compromising patient outcomes.
  • See the SMART EM talk on this

Clinical Pearls From the Recent Medical Literature – Drs. Jerome Hoffman and Richard Bukata (#hofkata)

  • Topical analgesia for corneal abrasions – the FOAM world has been buzzing with the notion of using tetracaine for corneal abrasions (Rebel EM, The SGEM).  Hofkata reviewed this paper by Waldman et al that showed no difference in visual analog scores for normal saline compared with tetracaine for corneal abrasions.  Tetracaine was perceived more effective so there may be a role for dilute proparacaine but we’ll need some more studies.
  • Cough medicines don’t work, as demonstrated by Smith et al but honey might per Cohen et al (The SGEM)
EMRA award!
EMRA award! Thanks, y’all!

FOAMcastini – ACEP Tuesday

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FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  Weekend review, Day 1 review.

Scientific Assembly Day 2 Pearls

(there’s too much to choose from, so follow #ACEP14)

Simple Complaints in Patients with HIV – Dr. John Perkins

  • HIV is a risk factor for coronary artery disease (CAD) and these patients are prone to thrombotic complications [Boccara et al]
  • Dr. Amal Mattu has really championed this point, as in this videocast

Resuscitation Pearls – Dr. Scott Weingart 

  • REBOA and ECMO are exciting and coming…but most of us don’t have them.  Watch the literature.
  • “Normal” vital signs shouldn’t reassure us in trauma. Don’t wait for patients to become hypotensive (this is a danger of euboxia)
  • The Shock Index (Heart Rate/Systolic Blood Pressure) is one way to help detect badness amongst “normal” vital signs in these patients (See this post)
  • ACLS algorithms, they’re helpful for people who don’t specialize in resuscitation.  Think about the individual patient and target interventions accordingly.  Oh, and do good CPR.
    • The AHA supports this, for example, they recommend against the routine use of calcium and sodium bicarbonate [2010 Guidelines].

End of Life/Palliative Care – Dr. James Adams

  • Hospice and palliative care are INTENSIVE. Listen to Dr. Ashley Shreves on the EMCrit podcast if you’re not convinced of this (actually, listen regardless, it’s worth it).
  • A Do Not Resuscitate (DNR) order only speaks to whether or not a patient wants CPR if they die.  No more, no less.  But, for more on this, check out this blog post.
  • In general, physicians don’t broach end-of-life topics with patients. Dr. Adams quoted a statistic “Approximately 50% of doctors don’t know their patient’s resuscitation wishes.”  The consensus in the room was that it really doesn’t take that much time to initiate these conversations but brief questions asking about a patient’s wishes, checking in to see if they have sufficient resources, or.  (Lauren’s take on the topic).

ACEP’s New Additions to Choosing Wisely

The cliff notes, courtesy of Dr. Seth Trueger

Screen Shot 2014-10-28 at 3.48.17 PM

Also, the first 5 from 2013:

Screen Shot 2014-10-28 at 3.48.55 PM

FOAMcastini – ACEP Round Up 1

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FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.  However, Jeremy and I both worked overnights so we got into town a little late.  Our friends and ACEP luminaries, Drs. Justin Hensley, Howie Mell, and Todd Slesinger.

For updates, follow #ACEP14

A Few Council Pearls:

Opiates are a huge problem in the United States.  A Town Council met and discussed this issue and the role of emergency physicians in this “epidemic.”  There were a lot of opinions about how emergency departments may contribute to this problem and can possibly play a role in the solution. Further reading on this topic below and, look out for the December ALiEM Journal Club on this paper Lack of Association Between Press Ganey Emergency Department Patient Satisfaction Scores and Emergency Department Administration of Analgesic Medications.

Naloxone (Narcan) – The council approved resolutions in support of naloxone for everyone.  There was also a resolution on developing a clinical policy for emergency physicians prescriptions of naloxone. Watch out for it.

Medical Marijuana – Apparently http://www.mindanews.com/buy-inderal/ every year brings some bickering about medical marijuana….and every year, the council defeats the resolutions.  This year was no different…no support for medical marijuana from ACEP.

 Emergency Department Pharmacists – These folks are indispensable in the ED (and in the FOAM world), and ACEP recognized this with the passing of Resolution 44 (what this means, clinically, not sure).  And if you haven’t work with them – you’re missing out.  We’re huge fans of EMPharmD and, naturally, Bryan Hayes (@PharmERToxGuy)

There’s also a lot of politics that goes into these bills, for that part, we got Dr. Kevin Klauer, Council Speaker on FOAMcast to explain.

But the real news… Dr. Kevin Klauer’s haircut.

Dr. Kevin Klauer
Dr. Kevin Klauer’s former look

 

 

Also, congratulations to the new ACEP president-elect, Dr. Jay Kaplan and all others elected to new ACEP board positions.

And, of course, the conference is fun (and, it turns out, Dr. Seth Trueger (@MDaware) is actually the nice one).

FOAMcastini 3 – All About the Pearls

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In this tiny episode, Jeremy reviews his favorite pearl from each episode, loooking at episodes 4-14.  Why the repetition?  Well, it turns out we learn better when information is spaced in small aliquots over time (spaced repetition).

Episode 4 – Transfusions and Ingested Foreign Bodies.

  • Most common infection from blood transfusion – Parvovirus B19

Episode 5 – Psychiatry and Increased ICP.

  • If re-initiating medications in the emergency department, some need to be titrated up slowly, such as quetiapine (Seroquel) and risperidone.
  • Figure out why patients stopped taking their medications.

Episode 6 – Hepatic Emergencies.

  • INR peaks after about 24-36 h in acute liver failure
  • AST>3000 suggests toxic or ischemic injury
  • ALT OR AST>300: Alk phos is useful.

Episode 7 – Heart Failure.

  • Right Ventricle MI: ST elevation in lead III greater than lead II – you know what to do (cath lab).  ST elevation in II greater than III – think pericarditee (pericarditis).
  • Right sided leads: elevation in V4R most specific but elevation in V3R-6R are indicative of RVMI.

Episode 8 – Acid-Base and Hyponatremia.

  • Strong Ion Difference (SID), which is the difference between the sums of concentrations of the strong cations and strong ions (typically Sodium minus Chloride). Small SID = acidic (example SID of 0.9% NaCl = 0)

Episode 9 – Pregnancy Emergencies.

  • The discriminatory zone is out.  Get ultrasounds in pregnant patients, regardless of the quantitative beta-hCG. A certain beta-hCG level can not be used to rule in or rule out ectopic pregnancy or viable intrauterine pregnancy (IUP), get the ultrasound and ensure you identify the uterus.

Episode 10 – Pediatric GI Emergencies.

  • Jaundice in the first 24 hours is NOT normal and is bad.

Episode 11 – Ebola and Transmission Precautions.

  • Airborne precautions recommended for: Measles (rubeola), Varicella, Tuberculosis.  Ebola is not airborne, but often we treat it as such.

Episode 12 – Anaphylaxis and Angioedema.

  • Biphasic anaphylaxis is extremely rare and prolonged ED observation does not really help as these reactions can occur up to 6 days later.  Rosenalli recommend observation 2-4 hours.

Episode 13  Tricyclic Antidepressants and Sodium Channel Blockade.

  • Tricyclic antidepressants can cause a rightward axis, in addition to prolonged QRS on an ECG.  This can resolve with treatment with sodium bicarbonate.

Episode 14 – Hand.

  • Flexor TenosynovitisKanavel’s Cardinal Signs (look for words that start with “F”).
    • Pain on passive extension -happens early
    • Finger held in flexion – see above point..extension hurts!
    • Fusiform (uniform) swelling of finger – most common
    • Tenderness along flexor tendon sheath – happens later

Episode 14 – Hand

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

This week we review EM in 5’s episode on the Neuro Exam of the Hand.

All 3 motor nerves (median, ulnar, radial) in one motion:

  • Make the “ok sign” and try to break the ring formed by the thumb and index finger – median
    • Memory aid: The median is “ok.”
  • Spread 3-5 fingers apart and adduct against resistance – ulnar
    • Memory aid: The intertriginous areas between abducted fingers make a “U” for ulnar
  • Dorsiflex wrist – radial
    • Memory aid…if you look really hard, the the dorsiflexed hand and arm appear to be a sideways, lower case “r”

…all in one

Motor Exam of the Hand
Motor Exam of the Hand

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 280, 295 ; Rosen’s 8(e) Chapter  50 – a well written chapter, but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Flexor Tenosynovitis

Kanavel’s Cardinal Signs (look for words that start with “F”).

  • Pain on passive extension -happens early
  • Finger held in flexion – see above point..extension hurts!
  • Fusiform (uniform) swelling of finger – most common
  • Tenderness along flexor tendon sheath – happens later [3]

Treatment – serious surgical emergency and failure to treat adequately can result in necrosis, proximal spread, and loss of use of hand.

  • IV Antibiotics – penicillinase resistant penicillin (ampicillin-sulbactam, piperacillin-tazobactam) + vancomycin (if suspect MRSA)
  • Consult hand surgery
  • Admit

Hand Pearls

Mallet Finger:  Disruption of the distal extensor tendons, often caused by a jamming injury, hyperextension, or crush.  Look for bruising at the distal interphalangeal joint. Closed injury –  immobilization. Open- extensor tendon repair.

High pressure injection injuries (paint gun, on the job stuff): Worse than they look.  Tetanus, IV antibiotics, consult hand.

Digit amputation storage: Cover the stump with saline gauze and wrap amputated digit in saline soaked gauze.  Put the saline soaked gauze covered digit in airtight plastic bag and place that bag in a bag on ice.

Amputations have best success of reimplantation if they are:

  • Clean cut (saw, etc) versus a crush injury
  • Distal (distal finger > proximal finger > hand)

Learn to Splint Like a Pro (via ERCast) and document a thorough neurovascular exam pre and post-splinting.

Bonus Rosenalli Myth Buster:  Common teaching prevails that epinephrine should not be used with anesthesia of the fingers, nose, toes, penis, etc.  FOAM has debunked this (SMART EM podcast), as well as peer reviewed literature: Waterbrook et alTruth, and epinephrine, at our fingertips: unveiling the pseudoaxioms.

  • Use of epinephrine in finger, nose, etc IS Rosenalli approved [Ch 40, Tintinalli 7e; Ch 3 Rosen’s 8e].

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  Which of the following is classically seen in flexor tenosynovitis?

A. Extended position of the involved digit

B. Fusiform swelling of the digit

C. Tenderness over the extensor sheath

D. Vesicular eruption over the flexor surface

Question 2. A 42-year-old man presents to the ED with an amputation of his left thumb just proximal to the interphalangeal joint. The injury occurred 1 hour ago at a rural construction site while the patient was operating a power miter saw. The thumb is brought in, in a sandwich bag, along with the patient. Which of the following is true regarding predictors of successful replantation?

A. Crush injuries have a high success rate of replantation

B. Digits have better tolerance for ischemia than limbs have

C. The amputated part should be kept cold and dry

D. The patient’s social history adds little value to the success rate of replantation

References

1. Chapters 3, 50.  Rosen’s Emergency Medicine, 8e.

2.Chapters 40, 280, 295.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

3. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am Acad Orthop Surg. 2012 Jun;20(6):373-82. doi: 10.5435/JAAOS-20-06-373.

Answers.

1. B.  The flexor tendons of the fingers are covered by a double layer of synovium to promote gliding of the tendon underneath. Infections in the synovial spaces in the hand tend to spread along the course of the flexor tendon sheaths and may extend proximally to the hand. Infections are usually due to penetrating trauma involving the sheath but occasionally from hematogenous spread. Four cardinal signs of acute flexor tenosynovitis are usually present to help distinguish tenosynovitis from other hand infections. These criteria are referred to as the Kanavel’s signs. Flexor tenosynovitis is a surgical emergency. Consultation with a hand surgeon is warranted along with intravenous antibiotics. The affected digit is held in a flexed (A), not extended, posture. The tenderness is over the flexor (C) sheath, not extensor. Vesicles (D) are not commonly associated with flexor tenosynovitis. A localized herpes simplex infection may cause vesicles to form on a digit

2. B.  Ischemia time is one of the most important predictors of successful replantation. Digits have less muscle mass to oxygenate and tolerate ischemia better than amputations more proximally along the limb. Replantation of limbs must be completed within 4–6 hours, but digits can tolerate an ischemic time of up to 8 hours, given proper preservation.  Crush injuries (A) have a low success rate for replantation due to the significant destruction of neurovascular structures. The amputated body part should be irrigated with normal saline to remove gross contamination, wrapped insterile gauze moistened with saline (C), and placed in a sterile, watertight container. This container should be placed in ice water, but the digit itself should not be submerged. Research has repeatedly shown that tobacco use (D), especially smoking after surgery, will worsen the chance of successful replantation. Obtaining a social history is important in these cases.

Episode 13 – Tricyclic Antidepressants and Sodium Channel Blockade

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The Free Open Access Medical Education (FOAM)

We review Dr. Amal Mattu’s episode, Why You Should Care When Things are Totally RAD, on his fabulous weekly ECG video series. This week’s episode reviews Rightward Axis Deviation (RAD) and the two “can’t miss” causes in the Emergency Department (ED): Sodium channel blocker toxicity (tricyclic antidepressants and cocaine) and pulmonary hypertension (pulmonary embolism).

Causes of Rightward Axis Deviation – Lead misplacement, Hyperkalemia (can do anything on the ECG)
Ventricular ectopy (VT), Lateral MI (Q-waves in lead I), Left posterior fascicular block, Right ventricular hypertrophy, Dextrocardia

Sodium Channel Blocker Toxicity ECG clues:

  • Tachycardia (most common)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1
  • Prolonged QRS
  • Prolonged QTc

EMCrit Episode 98 – Dr. Scott Weingart reviews the treatment of tricyclic antidepressant (TCA) toxicity. Top pearls

  • When using sodium bicarbonate (NaHCO3) to treat TCA toxicity, the pH doesn’t seem to rise above 7.5 (but you still have to check it). Ventilate these patients appropriately (given breakdown of NaHCO3 to CO2).
  • When infusing NaHCO3, check a VBG every hour to follow the pH and the potassium.
  • Calcium can be critically low in these patients, replete and check accordingly.

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 171 ; Rosen’s 8(e) Chapter 151, Goldfrank’s Toxicology Chapter 73 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

Tricyclic Antidepressants

Includes drugs like amitriptyline, nortriptyline and work on a variety of receptors. Other drugs, such as carbemazepine and cyclobenzaprine demonstrate TCA-like properties, albeit with different toxicologic properties (ALiEM post) Properties include anticholinergic, antihistamine, and alpha-1 adrenergic blockade in addition to sodium channel blockade and inhibition of the reuptake of norepinephrine and serotonin.

Clinical Presentation

  • Anticholinergic Symptoms predominate early on – tachycardia, flushed/dry skin, mydriasis, altered mental status, urinary retention (Mad as a Hatter, Hot as a Hare, Dry as a Bone, Blind as a Bat)
  • Mumbling speech
  • Seizures and ventricular dysrhythmias typically occur within the first few hours after ingestion.

Diagnosis – serum TCA levels and urine drug screens have no value in acute treatment (that’s per Rosen) [2]. In addition to history and physical examination, the ECG may be helpful:

  • QRS >100 ms*
  • Tall R wave in lead aVR (>3mm), R/S(avr) > 0.7
  • T40-ms axis between 120° and 270° (difficult to measure)

*It is widely taught, included in Rosen’s, Tintinalli, and Goldfrank, that seizures occur with a QRS >100 ms and ventricular dysrhythmias occur with a QRS >160 ms [1-3]. A 2004 meta-analysis demonstrated operating characteristics that were less than favorable, with the following characteristics:

  • QRS duration >100 ms to predict seizure: Sensitivity 69% (CI 57-78), +LR 3.18, -LR 0.38
  • QRS duration to predict ventricular dysrhythmia: Sensitivity 79% (CI 58-91), +LR 1.77, – LR 0.39
    • Note: It appears the studies in this analysis used a QRS of 100 ms whereas traditional teaching references 160 ms as the threshold for most ventricular dysrhythmias
  • Most predictive of ventricular dysrhythmia: R/S waves ratio (+LR 15.67) but this was evaluated in only one study (Sensitivity 47%)

[4]

Treatment

In acute overdose with an ingestion < 1 hour prior, activated charcoal may be given if no contraindications exist.

Symptomatic treatment and observation for at least six hours.

Hypotension – crystalloid intravenous fluids, vasopressors if needed (norepinephrine)

Seizure – Most seizures are self-limiting and spontaneously terminate within 3 minutes but benzodiazepines and standard seizure treatment can be used .

Prolonged QRS (>100 ms) or Dysrhythmia

Sodium Bicarbonate – 1-2 mEq/kg bolus. Each amp of NaHCO3 has 50 mEq so the average 70 kg patient can get 1.5-2.5 amps. An infusion of NaHCO3 may be used (3 amps of NaHCO3 in 1 L of D5W).

  • Caution: must follow pH (can titrate as high as 7.5-7.55) as well as potassium.

If the NaHCO3 pushes the patient’s pH to the 7.5-7.55 limit and the QRS remains wide, 200 mL of hypertonic saline (3%) can be used.

Lidocaine, a class IB sodium channel blocker/antiarrhythmic can also be used although it may seem counterintuitive.

Magnesium may also be used

Disposition:

Asymptomatic patients six hours after ingestion (no sinus tachycardia) can be medically cleared.

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1. A 24-year-old man presents to the ED via the police because of altered mental status and violent behavior. The patient reportedly had been on a drug binge, using amphetamines and cocaine for the last 2 days. On arrival, he is afebrile, his heart rate is 140 beats per minute, blood pressure is 180/110 mm Hg, and he is respiring at 22 breaths per minute. He is agitated and combative, but there is no evidence of traumatic injury. His pupils are dilated, and he is diaphoretic. Which of the following statements is true regarding the treatment of amphetamine and cocaine toxicity?

A. Antipsychotics are the preferred initial therapy for agitation and psychosis

B. Beta-adrenergic blockers are safe for managing tachycardia and dysrhythmias

C. Body packers with leaking packets should receive whole-bowel irrigation

D. Vasodilators are first-line therapy for treating amphetamine-induced hypertension

E. Wide-complex tachydysrhythmias should be treated initially with sodium bicarbonate

Question 2. A 27-year-old man is brought to the ED by EMS after being found wandering in the street. His BP is 155/70, HR 115, T 37.5°C, RR 16, pulse ox 99% on room air, and finger stick glucose 98. On exam, the patient is confused with mumbling speech. His pupils are 7 mm and reactive. His face is flushed. Mucous membranes and skin are dry. Which of the following toxidromes is this patient exhibiting?

A. Anticholinergic

B. Cholinergic

C. Sedative-hypnotic

D. Sympathomimetic

More FOAM:

Life in the Fast Lane TCA case

Life in the Fast Lane TCA ECG

References:

1. Chapter 151. Rosen’s Emergency Medicine, 8e.

2.Chapter 171. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

3.Chapter 73. Goldfrank’s Toxicologic Emergencies, 9e, 2010

4. Bailey B, Sc M. A Meta-Analysis of Prognostic Indicators to Predict Seizures , Arrhythmias or Death After Tricyclic Antidepressant Overdose . 2004;42(6):877–888. doi:10.1081/CLT-200035286.

Episode 12 – Back to Biphasics

(iTunes or listen here)

The Free Open Access Medical education (FOAM)

We review Episode 1 of Dr. Salim Rezaie’s REBEL Cast covering exposing the dogma behind biphasic anaphylaxis reactions.

Traditionally, we’re taught to observe patients in the Emergency Department (ED) for 4-6 hours to watch out for biphasic reactions, as the rate of biphasic reactions can approach 20%.

Grunau BE et al. Incidence of Clinically Important Biphasic Reactions in Emergency Department Patients with Allergic Reactions or Anaphylaxis. Ann of EM 2014; 63(6): 736 – 44.

  • Retrospective chart review of 430,000 visits
  • Anaphylaxis n=496 (2 had biphasic reactions, Allergic reactions n=2323 (3 had biphasic reactions)
  • No deaths, biphasic reactions occurred anywhere from 16 minutes into the ED stay to 6 days later

Rohacek M et al. Biphasic Anaphylactic Reactions: Occurrence and Mortality. Eur J All Clin Imm 2014; 69(6): 791 – 7.

  • Retrospective study in Europe of presentations to one hospital from 2001-2013 of n=1334 allergic reactions, n=524 anaphylaxis reactions
  • 2.3% (n=12) met criteria for clinically important biphasic reactions

Additional FOAM on the topic: The SGEM

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 27 ; Rosen’s 8(e) Chapter 119 but, the point isn’t to just take our word for it. Go enrich your fundamental understanding yourself!

Anaphylaxis

Diagnosis

Two or more systems involved after likely allergen exposure (within hours):

  • Skin – generalized hives, itch-flush, swollen lips-tongue-uvula
  • Pulmonary – dyspnea, wheezing, bronchospasm, stridor
  • Cardiovascular -hypotension or associated symptoms (syncope, incontinence)
  • Gastrointestinal symptoms- crampy abdominal pain, vomiting

Hypotension after exposure to known allergen for that patient (minutes to several hours)also qualifies

Differential Diagnosis -vasovagal (most common mimicker), myocardial ischemia, status asthmaticus, epiglottitis, angioedema, foreign body, carcinoid, vocal cord dysfunction, drug reactions, psychogenic

Treatment

Epinephrine. Commit the dose to memory and look up if, needed as this is a huge source of medication errors [Gaeta et al, Benklefat ].

  • Adults: 0.3mg, Pediatrics 0.01mg/kg of 1:1000 epinephrine intramuscular (IM) to lateral thigh (pediatric patients >30kg get the adult dose).
  • If repeated doses of IM epinephrine required and patient continues to remain hypotensive, start intravenous epinephrine. ALiEM’s post on making the dirty epi drip.

Adjuncts:

  • IV fluids for blood pressure/shock
  • Corticosteroids may help prevent recurrence although they take 4-6 hours to work, so are unhelpful in acute attacks [Choo et al]. Rosen recommends either prednisone 0.5-1mg/kg orally or methylprednisolone 80-125 mg IV. (You don’t have to give IV in all cases)
  • Histamine blockers (H1 and H2 such as diphenhydramine and famotidine, respectively) may help with the dermatologic symptoms and pruritis.
  • Glucagon in patients that aren’t responding or are on beta-blockers. ALiEM post.
  • Give patients that are going home a prescription for an EpiPen (for pediatric patients, have one parent go fill the script during the observation period) and show them how to use the autoinjector. These things are expensive and do expire, and there are some coupons out there to help out.

Disposition – Clearly patients with ongoing symptoms and/or shock should stay in the hospital. However, most patients can be discharged home once they are improved and the effects of the epinephrine have worn off. Tintinalli recommends about 4 hours, referencing a study by Brady et al from 2007. Interestingly, in this study there were 2 biphasic reactions that occurred at 20 hours and 46 hours after the initial ED visit. So, not sure how they came up with 4 hours.

FOAM Pearls Supported by the Literature and Rosenalli –

Iodine Allergy is not a thing.

Shellfish allergy does NOT put a patient at increased risk of contrast allergy more than any other allergen [Kaufman et al].

Cross-reactivity between penicillin and cephalosporins is often quoted at 10-20% but, in reality, is far less and a review demonstrates cross reactivity of 1% in patients reporting a penicillin allergy [Campagna et al]. Rosen’s agrees with this assessment and states that the overall cross reactivity is minimal. ALiEM post on this myth

ACE-Inhibitor Induced Angioedema

Cause: The vasodilation and non-pitting edema of the mucosal, dermal, and subcutaneous tissues thought to be mediated by the build up of bradykinin and substance P. Non-allergic, often asymmetric.

Presentation: Swelling of the lips, tongue, airway most often although it can also involve the genitals and viscera.

Treatment:

  • Stop the ACE-Inhibitor.
  • Active, anticipatory airway management. Perhaps, even an awake airway (The EMCrit Way, The Strayer Way).
  • Epinephrine, corticosteroids, and histamine blockers do not work. While fresh frozen plasma may work for hereditary angioedema, but it doesn’t really work in ACE-inhibitor angioedema and there’s no proven therapy [Winters et al].
  • Investigations underway for icatibant (bradykinin 2 receptor antagonist) Bas et al, Schmidt et al and Ecallantide (reversible kallikrein inhibitor)

Question 1. A 55-year old man who is taking several antihypertensive medications presents to the ED with nausea, vomiting, shortness of breath, and a rash after eating a home-cooked Thai meal at a friend’s house about 1 hour ago. The symptoms began within seconds of the first bite of his meal. Despite the patient being administered 2 doses of intramuscular epinephrine, diphenhydramine, dexamethasone, and crystalloid fluids, his blood pressure remains at 75/38 mm Hg.Which other medication should be considered in this patient?

  • A. Cimetidine
  • B. Glucagon
  • C. Norepinephrine
  • D. Octreotide

Question 2. A 55-year-old woman presents to the ED for swelling of her tongue and lips.

Photo: Rosh Review
Photo: Rosh Review

She recently started a new antihypertensive medication. Which of the following is the direct mediator for her condition?

  • A. Angiotensin
  • B. Bradykinin
  • C. C1-esterase inhibitor
  • D. Histamine

Answers.

1. B. The patient is experiencing an acute anaphylactic reaction, most likely to peanuts that are commonly found in Thai cooking. Although uncommon, patients taking beta-blocking agents for hypertension may exhibit refractory hypotension despite being administered fluids and epinephrine. This is because epinephrine acts by binding to adrenergic receptors, which includes beta-receptors. To circumvent the beta-receptor, glucagon can be administered, which will bypass the beta-adrenergic second messenger system, potentiate the circulating epinephrine, and help restore vasomotor tone.

Cimetidine (A) is an antihistamine. Although it may help in mild allergic reactions, it will not treat hypotension in severe anaphylaxis. In addition, cimetidine prolongs the metabolism of beta-blockers. Octreotide (D) may be used in management of esophageal variceal bleeding control, treatment of carcinoid syndrome, and refractory hypoglycemia after sulfonylurea-induced hypoglycemia. There is no role in anaphylaxis. Norepinephrine (C) also binds adrenergic receptors that may be inhibited in patients who take beta-blocking medications.
2. B. Angioedema is the clinical manifestation of transient, localized, nonpitting swelling of the subcutaneous layer of the skin or submucosal layer of the respiratory or gastrointestinal tracts. There are many cases of angioedema, but the condition is usually divided into hereditary, acquired, and drug-induced causes. Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1-esterase inhibitor and is usually precipitated by stress or trauma. Acquired angioedema is also due to deficiency or dysfunction of C1-esterase inhibitor, but is not due to a genetic cause; rather, it appears later in life. The exact etiology is unknown, but the condition is exceedingly rare. The most common cause of drug-induced angioedema is due to an adverse reaction from ACE inhibitors. When ACE is inhibited by medications, angiotensin I is not converted to angiotensin II, and bradykinin is not metabolized. It is thought that the increased level of bradykinin is responsible for angioedema induced by ACE inhibitors. Angioedema can result in severe airway compromise or, less commonly, compromise in the GI tract that is associated with abdominal pain. Evaluation should focus on ruling out laryngeal edema and airway compromise. Although direct visualization is best, asking the patient to phonate a high-pitched “E” is one quick way of assessing for laryngeal edema. If the patient is able to phonate a high-pitched “E,” then the presence of laryngeal edema is unlikely. Treatment is mainly supportive with special attention to airway protection. Angioedema caused by deficiency or dysfunction of C1-esterase inhibitor can be treated by replacing C1-esterase inhibitor with fresh frozen plasma or other recombinant agents.

Angiotensin (A) is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs (ACE inhibitors) that lower blood pressure. An elevated level of angiotensin is not responsible for angioedema. C1-esterase inhibitor (C) serves as the main regulator of the kallikrein-kinin system. As a result of decreased amounts of functional C1-INH, when the kallikrein-kinin system is activated, it is not kept in check. This leads to increased formation of bradykinin and the resultant increased vascular permeability and edema formation and is the cause of hereditary angioedema, not ACE-inhibitor induced angioedema. Histamine (D) has many roles in the body, but its primary role is within the immune system. Mast cells release histamine through a process known as degranulation when they have been sensitized with IgE antibodies and then come in contact with an appropriate antigen leading to the development of urticaria and pruritus.