Category Archives: FOAMed

TOXCARD: Hyperthermia in the toxicological setting

Author: Jenna Otter, MD (EM Resident Physician, Temple University Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) 

toxcard

Case Presentation:

A 32 year-old man presents to the emergency department with altered mental status. The patient is agitated but sleepy-appearing. He appears to be uncomfortable, shifting on the stretcher and unable to lie still. An empty bottle of cough syrup is found in his pocket. His vitals are HR 141, rectal temperature 103.6F, BP 214/110, RR 22, SpO2 98% in room air.

Question:

What is the differential diagnosis for hyperpyrexia with altered mental status? How is hyperthermia secondary to drug ingestion and toxic syndromes treated?

Pearl:

Drug-related hyperthermia is difficult to distinguish but may be differentiated based on components of history and physical exam. Hyperthermia secondary to toxic syndromes and drug ingestion will not respond to antipyretics like ibuprofen or acetaminophen and external cooling measures are key.

  • Fever is defined as a physiologic elevation in the hypothalamic set-point for body temperature induced by inflammatory cytokines in response to a stressor.
  • Hyperthermia in the toxicological setting differs from fever in that it results from an unregulated increase in body temperature either from increased heat production or decreased heat dissipation, usually resulting from increased skeletal muscle metabolism or activity.
  • Toxicological causes of increased heat production include serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia, alcohol withdrawal, sedative-hypnotic withdrawal, and ingestions of sympathomimetics, anticholinergics, and ecstasy. Decreased heat dissipation through poor sweat production also occurs in anticholinergic ingestions.
  • Initially, fever and hyperthermia are difficult to distinguish but may be differentiated based on components of history and physical exam.

Hyperthermia Differential Diagnosis2

Toxic Syndrome CNS Other
Serotonin Syndrome Meningitis Sepsis
Neuroleptic Malignant Syndrome ICH Heat Stroke
Malignant Hyperthermia Hypothalamic stroke Pheochromocytoma
Alcohol/Sedative-Hypnotic Withdrawal Encephalitis Thyrotoxicosis
Sympathomimetic Syndrome (e.g. cocaine, amphetamines, PCP, MDMA, cathinones, etc.)

 

Status epilepticus Infection (Tetanus, malaria, etc)
Alcohol/Benzodiazepine Withdrawal
Anticholinergic Syndrome
Salicylate Toxicity

 

Some toxicological causes of hyperthermia and their differentiations:

HYPERTHERM

Table Source: Boyer E and Shannon M. The Serotonin Syndrome. N Engl J Med. 2005; 352:1112-1120. DOI: 10.1056/NEJMra041867.

  • Antipyretics have no role in the management of hyperthermia in the toxicological setting since the fever usually results from muscular hyperactivity, not an alteration in hypothalamic homeostasis.
  • Hyperthermia should be addressed promptly by using external cooling blankets, ice water submersion, evaporative cooling techniques, or cool IV fluids. Benzodiazepines should also be used to reduce excess heat production from muscle hyperactivity.
  • To prevent end-organ damage, the goal should be to reduce rectal temperature to below 40°C within 30 minutes of beginning cooling therapy.
  • In severe cases, internal cooling catheters can be used for more regulated cooling, using thermal regulation devices such as CoolLineR or CoolGardR. If necessary, cold fluids can be given through a NG or OG tube in intubated patients. Also the bladder can be irrigated with cool fluids using a foley catheter.

Main point:

Hyperthermia secondary to drug ingestion differs from infection-related fevers in that it results from an unregulated increase in body temperature, usually from increased skeletal muscle activity. Drug-related hyperthermia is difficult to distinguish but may be differentiated based on components of history and physical exam. Hyperthermia secondary to toxic syndromes and drug ingestion will not respond to antipyretics like ibuprofen or acetaminophen and external cooling measures are key.

References:

  1. Simon H. Hyperthermia. N Engl J Med. 1993; 329:483-487. DOI: 10.1056/NEJM199308123290708.
  2. LoVecchio F. Chapter 210: Heat Emergencies. In: Tintinalli J, ed. Tintinalli’s Emergency Medicine. 8th ed. McGraw Hill; 2016: 1365-1370.
  3. Boyer E and Shannon M. The Serotonin Syndrome. N Engl J Med. 2005; 352:1112-1120. DOI: 10.1056/NEJMra041867.

The Hand: An Expedited Examination and Key Points Regarding ED Diagnoses

Authors: Alin Gragossian, DO (EM Resident Physician, Drexel University), Matthew A. Varacallo, MD (Orthopedics Resident Physician, Drexel University), and Richard J. Hamilton, MD (EM Professor and Chair, Drexel University) // Edited by: Erica Simon, DO (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital)

A 31-year-old male, the victim in a low-speed MVC versus pedestrian, arrives to the trauma bay via EMS. As the stretcher rolls by you see an alert patient, yelling in pain. A c-collar is in place, and a splint supports what appears to be a mangled right hand and an open right forearm fracture. As your trauma team hurriedly connects monitors, you note initial VS: HR 110, BP 132/96, RR 14, SpO2 98% RA.

You’re reassured by your primary survey: ABCs are intact; the radial and ulnar pulses of both upper extremities are palpable. Your secondary survey is significant for what appears to be a serious injury to the dorsal aspect of the distal right upper extremity: a large skin avulsion revealing extensor tendons of the hand and an open distal radius fracture.

CT imaging and radiographs demonstrate that the patient is without additional injuries, save those identified on your exam. After administering analgesia, cefazolin, and updating a tetanus, the patient wheels off to the OR for washout, re-approximation, and repair. As you complete the trauma paperwork, you replay the hand examination in your mind.  Was there anything that your team overlooked?

If it’s been a while since you’ve treated a patient with a hand complaint, let’s review some high-yield material.

Epidemiology

Hand complaints represent nearly 12% of injury-related visits to ED setting.1,2 Trauma involving the hands imparts a significant burden on healthcare systems given the frequent requirement for referral, and potential necessity for surgical intervention. According to a 2009 study of 134 patients presenting for the evaluation of hand lacerations secondary to electric saws, mean treatment costs per injury (including hospitalization) were $30,704, with an average loss of 64 productive work days.3 As limitations in dexterity can significantly impact activities of daily living and quality of life, the early identification and treatment of neurovascular, tendon, and bone injuries of the hand are paramount.4

History & Physical

History
When obtaining a history, question patients regarding the type of injury (burn, laceration, injection injury, etc.), the mechanism, time elapsed between injury and evaluation, and the possibility of occupational exposures. Hand dominance, prior hand injury, and prior hand surgeries should be documented.5

Physical Exam
Table 1 offers a quick reference guide for use when performing muscle and tendon function evaluation of the hand and wrist.6,7

Table 1. Muscle and Tendon Function of the Hand and Wrist
Table 1. Muscle and Tendon Function of the Hand and Wrist

Nerves
Examination of the hand should include an assessment of nerve function:

Median Nerve

  • Motor: thumb abduction and opposition => test by asking the patient to place his hands in anatomic position.  Apply resistance to the thumbs while prompting the patient to move them towards the ceiling.
  • Sensory: innervates the central aspect of the palm and terminates distally in the radial 3.5 digits of the hand => test sensation by assessing two-point discrimination. Normal two-point discrimination is 5mm at the volar fingertips. Sensory testing should be repeated 2-4 times on each side of each digit.5,6

Radial Nerve

  • Motor: thumb extension => test the patient’s thumb extension against resistance.
  • Sensory: the superficial branch of the radial nerve and its terminal branches provide sensation to the central and radial aspects of the dorsum of the hand, and the dorsal-radial aspect of the thumb => test sensation by performing two-point discrimination on the dorsum of the thumb.5,6

Ulnar Nerve

  • Motor: innervates the adductor pollicis muscles and controls thumb adduction => test by asking the patient to cross her fingers, or abduct her fingers against resistance.
  • Sensory: provides sensation to the dorsal-ulnar aspect of the hand and into the fingertips of the fourth and fifth digits => test ulnar nerve sensation by assessing two-point discrimination of the fourth and fifth digits.5,6
Figure 1. Cutaneous Nerve Supply of the Hand O’Rahilly R. Basic Human Anatomy: Chapter 10: The Hand. 2008. Available from: https://www.dartmouth.edu/~humananatomy/about/credits.html
Figure 1. Cutaneous Nerve Supply of the Hand
O’Rahilly R. Basic Human Anatomy: Chapter 10: The Hand. 2008. Available from: https://www.dartmouth.edu/~humananatomy/about/credits.html

Vascularity

The radial and ulnar arteries perfuse the hand. The radial artery forms the deep palmar arch, and the ulnar artery forms the superficial palmar arch.5,7 Vascularity may be evaluated through palpation (temperature and pulses), Doppler (if required), and capillary refill. While some advocate the use of the Allen’s test during the vascular examination, it is important to note that this test lacks sensitivity and specificity as findings vary according to the time employed (e.g. – injury transecting the radial artery may initially present with a normal Allen’s test, however subsequent radial artery vasospasm and thrombosis may result in an later abnormal Allen’s test), and operator experience.8

Alignment

When it comes to hand injuries, malrotation resulting from fracture is an indication for ED reduction. When the fingers are flexed, a cascade directed towards the scaphoid tubercle should be observed (Figure 2). If abnormalities in alignment are identified, radiographs and consultation are advised.

Figure 2. Assessment of Malrotation Steinman S. Seattle Children’s Hospital Finger Fractures: Don’t Forget the Malrotation. 2017. Available from: http://www.seattlechildrens.org/healthcare-professionals/resources/case-studies/finger-fractures-dont-forget-rotation/
Figure 2. Assessment of Malrotation
Steinman S. Seattle Children’s Hospital Finger Fractures: Don’t Forget the Malrotation. 2017. Available from: http://www.seattlechildrens.org/healthcare-professionals/resources/case-studies/finger-fractures-dont-forget-rotation/

Special Examinations

Carpal Tunnel

Tinel’s and Phalen’s tests may be utilized to assess for the presence of carpal tunnel syndrome. A positive Tinel’s sign is elicited when the examiner taps the median nerve as it passes through the carpal tunnel, eliciting a report of paresthesias in median nerve distribution. A positive Phalen’s test occurs when paresthesias are experienced in median nerve distribution after > 60 seconds of maximum wrist flexion.8

Ulnar Motor Weakness

Froment’s test identifies ulnar nerve motor dysfunction (specifically, a weakness of the adductor pollicis). The patient is instructed to grasp a thin object between the thumb and radial aspect of the index finger.   If the examiner is able to remove the thin object, or the patient flexes the IP joint (flexing the flexor pollicis longus, innervated by the anterior interosseous nerve) to increase the grasping force, the test is said to be positive. If the patient simultaneously hyperextends the first metacarpophalangeal joint, this is said to be a positive Jeanne’s test, again indicating ulnar motor weakness.9

Figure 3. Froment's Test Ujash S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand#
Figure 3. Froment’s Test
Ujash S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand
Figure 4. Positive Jeanne's Test Ujesh, S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand
Figure 4. Positive Jeanne’s Test
Ujesh, S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand

Imaging

In the ABCs of Emergency Radiology, Chan and Touquet offer a number of excellent recommendations on the basics of ED radiographs:

The Rules of Two:1

  • Two views: one view is one too few
  • Two joints: image the joint above and below a long bone
  • Two sides: compare the other side if unsure of pathology
  • Two abnormalities: look for a second abnormality
  • Two occasions: compare current films and old films (if available)
  • Two visits: repeat films before and after procedures
  • Two specialists: if possible, obtain a formal radiology report
  • Two examination modalities: US, CT, or MRI should be considered as appropriate to the clinical scenario

Speaking of imaging, ultrasound is quickly becoming a popular mechanism for identifying foreign bodies. Prior to the employment of US, epidemiological studies estimate that nearly 38% of non-radiopaque foreign bodies went unidentified during initial ED encounters (1982 publication).11 A recent study by Saboo and colleagues demonstrated sensitivities of 94–98% for ultrasound detection of both radiolucent and radiopaque foreign bodies (n =123 patients, 7.5 MHz transducer).12 As US may be difficult to perform on the small surfaces of the hands, a water bath may be utilized with a high frequency linear transducer to generate high resolution images.

Figure 5. Water Bath for Hand US Lin, Michelle. Tricks of the Trade: Underwater Ultrasonography. 2011. Available from: https://www.aliem.com/2011/tricks-of-trade-underwater/
Figure 5. Water Bath for Hand US
Lin, Michelle. Tricks of the Trade: Underwater Ultrasonography. 2011. Available from: https://www.aliem.com/2011/tricks-of-trade-underwater/

Urgent or Emergent  Surgical Intervention

The following offers a review of hand conditions requiring urgent or emergent ED attention.

 Acute Compartment Syndrome

Compartment syndrome of the hand is relatively uncommon, but may occur secondary to trauma, insect bites, snake bites (2-8%13), high-pressure injection, contrast infusion, and crush injuries.12 The hand is anatomically separated into ten compartments; those most commonly at risk for the development of elevated intra-compartmental pressures include: the interossei (dorsal and palmar), the thenar and hypothenar, the adductor, and the finger compartments.14 Symptoms associated with acute compartment syndrome are classically characterized as the “six Ps” – pain, pallor, paresthesias, poikilothermia, pulselessness, and paralysis. The most reliable indicator is pain out of proportion to physical examination findings.12 It is paramount that fasciotomy be performed within 8 hours of the onset of symptoms as axonal and myocyte damage may be irreversible outside of this time frame.15-17

Replantation

Replantation, the surgical reattachment of a finger, hand, or arm that has been severed, is a topic best discussed with the orthopedic/hand specialist –  patient outcomes depend upon the skill of the surgical team, patient co-morbidities, and the extent of the injury.18 Primary indications for replantation after trauma include amputations to the thumb at any level, involvement of multiple digits, amputations through the palm, amputations at or proximal to the wrist, and almost all amputated parts in the pediatric patient.18 Consideration for replantation should be given for individual digit amputations distal to the insertion of flexor digitorum superficialis, ring avulsion injuries, and amputations through or above the elbow.18

Primary contraindications to replantation include patients with severe vascular disorders, crush injuries, or injuries with mangling of the severed limb.18

Flexor tenosynovitis

 Flexor tenosynovitis is an infection of the flexor tendon sheath that is characterized by Kanavel’s Signs: finger held in flexion, pain with passive extension, pain with palpation of the flexor tendon sheath, and fusiform swelling.19 Flexor tenosynovitis may result from minor trauma as the distance from the volar dermis to the flexor sheath is 1-2 millimeters.19 If suspected, initiate broad-spectrum antibiotic therapy, and consult for surgical intervention.19

High-Pressure Injection Injuries

Patients utilizing high-pressure injection equipment often present to the ED for the evaluation of an injury to the non-dominant hand (equipment most commonly held in the dominant hand).20,21 Injury severity is dependent upon the force of injection, volume of material injected, and the composition of the material injected.20 While injuries may initially appear relatively benign, specialty consultation is a must as tracking of the injected material may ultimately result in gross contamination of subcutaneous tissue and deep muscle. Upon ED arrival, imaging should be performed to assess for the presence of foreign bodies, and parenteral antibiotic therapy initiated.20,21 In terms of morbiditiy, as compared to all other finger injuries, those due to high-pressure injection are three times as likely to require amputation.19

Pearls:

  • A rapid hand exam can be performed in the following manner:
    • As the patient make an “OKAY” sign with thumb and first finger (median nerve). Spread the fingers apart maximally (ulnar nerve). Dorsiflex the wrist fully (radial nerve). These can be combined into an OKAY sign with remaining fingers spread apart and the wrist dorsiflexed to get an all-in-one motor exam.
    • Check sensation of the median and ulnar nerve by testing two-point discrimination at the index and small finger pads respectively. Radial nerve sensation can be tested over the dorsum of the thumb.
  • For carpal tunnel syndrome, perform Tinel’s and Phalen’s tests. Remember, a positive test occurs when the patient reports paresthesias in median nerve distribution.
  • Acute compartment syndrome must go to the OR within 8 hours of onset.
  • Kanavel’s Signs are key physical exam findings for flexor tenosynovitis: finger held in flexion, pain with passive extension, pain with palpation of the flexor tendon sheath, and fusiform swelling.
  • Beware of high-pressure injection injuries. They look more benign than they truly are, and warrant a careful physical examination of the hand and consultation.


References / Further Reading:

  1. Niska R, Bhuiya F, Xu J. National Hospital Ambulatory Medical Care Survey: 2007 emergency department summary. Natl Health Stat Report. 2010;(26):1-31.
  2. Maroukis BS, Chung KC, MacEachern M, Mahmoudi E. Hand trauma care in the United States: a literature review. Plastic and Recon Surg. 2016 Jan; 137(1): 100e-111e.
  3. Hoxie SC, Capo JA, Dennison DG, Shin AY. The economic impact of electric saw injuries to the hand. J. Hand Surg. 2009 Jun; 34A: 886-889.
  4. Soucacos P. Indications and selection for digital amputation and replantation. J Hand Surg Br. 2001;26(6):572–581.
  5. Tintinalli J, Stapczynski J, Cline D, Ma OJ et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th edition. McGraw-Hill Education / Medical; 2015.
  6. Chung KC. Hand and Wrist Surgery. Elsevier Health Sciences; 2012.
  7. Morton DA, Foreman K, Albertine KH. eds. The Big Picture: Gross Anatomy New York, NY: McGraw-Hill; 2011.
  8. Jarvis MA, Jarvis CL, Jones PR, Spyt TJ. Reliability of Allen’s test in selection of patients for radial artery harvest. Ann Thorac Surg. 2000;70(4):1362-5.
  9. Ujash S. Physical Exam of the Hand. 2017. Accessed 15 March 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand#
  10. Chan O and Touquet R. General Principles: How to Interpret Radiographs. In ABC of Emergency Radiology. 3rd 2013. West Sussex, UK. Wiley-Blackwell Publishing.
  11. Lewis D, Jivraj A, Atkinson P, Jarman R. My patient is injured: identifying foreign bodies with ultrasound. Ultrasound. 2015;23(3):174-80.
  12. Saboo S, Saboo SH, Soni SS, et al. High-resolution sonography is effective in detection of soft tissue foreign bodies. J Ultrasound Med 2009; 28: 1245–9.
  13. Anz A, Schweppe M, Halvorson J, Bushnell B, Sternberg M, Andrew Koman L. Management of venomous snakebite injury to the extremities. J Am Acad Orthop Surg. 2010 Dec; 18(12): 749-59.
  14. Chandraprakasam T and Kumar R. Acute compartment syndrome of forearm and hand. Indian J Plast Surg. 2011; 44(2):212-218.
  15. Oak NR, Abrams RA. Compartment Syndrome of the Hand. Orthop Clin North Am. 2016;47(3):609-16.
  16. Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996;4(4):209–18. 21.
  17. Von keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis and treatment of acute extremity compartment syndrome. Lancet. 2015;386(10000):1299-310.
  18. Sabapathy SR, Venkatramani H, Bharathi RR, Bhardwaj P. Replantation surgery. J Hand Surg Am. 2011;36(6):1104-10.
  19. Ong YS, Levin LS. Hand infections. Plast Reconstr Surg. 2009;124(4):225e-233e.
  20. Eroglu O, Sari E, Vural S, Coskun F. Warning: This may be as dangerous as firearm injuries; “grease-gun injury”: A case report. The Pan African Medical Journal. 2015;20:40. doi:10.11604/pamj.2015.20.40.5892.
  21. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20(7):503-11.

EM@3AM – Acute Coronary Syndrome

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 69 year-old male with a history of hypertension, hyperlipidemia, and smoking presents with pre-cordial chest pain radiating to his right upper extremity, associated with shortness of breath. The patient reports the onset of his symptoms one hour prior to arrival, while mowing his lawn. He characterizes his chest pain as an 8/10 “tightness” and notes nausea that “comes in waves.” ROS is negative for recent illness, travel, and hospitalization within the previous 90 days. The patient denies personal or familial history of DVT/PE.

 Triage VS: BP 157/98, HR 102, RR 22, T99.8°F Oral, SpO2 98% on room air

What diagnosis do you suspect? What’s the next step in your evaluation and treatment?


Answer: Acute Coronary Syndrome (ACS)1-4

  • ACS: Consists of unstable angina, NSTEMI, and STEMI
  • Risk Factors: Hypertension, diabetes, dyslipidemia, tobacco use, family history of CAD (i.e. – CAD in a male primary relative younger than 55 years of age, or CAD in a female primary relative younger than 65 years of age), HIV/AIDS, SLE, cocaine use.1 
  • Presentation: Chest pain or pressure radiating to the neck, jaw, or upper extremities; mid-epigastric pain, diaphoresis, nausea with or without emesis.2
    • Increased likelihood of acute MI:3
      • Chest pain with radiation to right arm or shoulder: positive likelihood ratio (+LR) 4.7; 95% CI 1.9-12
      • Chest pain with radiation to both arms or shoulders: +LR 4.1; 95% CI 2.5-6.5
      • Chest pain associated with exertion: +LR 2.4; 95% CI 1.5-3.8
  •  Evaluation:
    • Focused H&P, serial EKGs, cardiac biomarkers, chest radiograph
      • Troponin I most sensitive marker of cardiac myocyte damage (positive in NSTEMI and STEMI).1
  •  Treatment:1
    • Administer non-enteric coated, chewable ASA.
    • Antithrombotic therapy and/or anti-platelet therapy as appropriate per the diagnosis.
    • Nitrates to relieve chest discomfort (caution in the setting of inferior STEMI => perform R-sided EKG to rule out RV infarct,  a pre-load dependent condition).
    • Supplemental oxygen therapy for patients with shortness of breath, signs of acute heart failure, or cardiogenic shock.
  •  Pearls:
    • Females, diabetics, and the elderly often present atypically.
    • Keep in mind there are numerous ACS mimics: aortic dissection, PE, pneumonia, pericarditis, myocarditis, pleurisy, PUD, etc.
    • Previous non-invasive cardiac stress testing does not rule out coronary artery disease.4 

References:

  1. Qazi M and Patel P. Acute Coronary Syndrome. In: Ferri’s Clinical Advisor 2017. Philadelphia: Saunders Elsevier, 2017: 25-29.e1.
  2. Kumar A and Cannon C. Acute Coronary Syndromes: Diagnosis and Management, Part I. Mayo Clin Proc. 2009; 84(10): 917-938.
  3. Swap C and Nagurney J. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005; 294(20): 2623-2629.
  4. Walker J, Galuska M, Vega D. Coronary disease in emergency department chest pain patients with recent negative stress testing. West J Emerg Med. 2010; 11(4): 384-388.

For Additional Reading:

EKG Findings in ACS:
http://www.emdocs.net/leftmainstemi/
http://www.emdocs.net/hyperacute-t-waves/
http://www.emdocs.net/ber-vs-anterior-stemi/

ST Elevation in aVR:
http://www.emdocs.net/r-e-b-e-l-em-st-segment-elevation-lead-avr-getting-much-respect-amal-mattu/

Risk Stratification:
http://www.emdocs.net/chest-pain-controversies-risk-stratification-stress-test-utility-part-1/
http://www.emdocs.net/chest-pain-controversies-coronary-cta-use-part-2/

Management of Low-Risk Chest Pain:
http://www.emdocs.net/r-e-b-e-l-em-management-and-disposition-of-low-risk-chest-pain/

EM@3AM – Acute Cholecystitis

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 41-year-old obese female presents for evaluation of severe right upper quadrant pain and nausea without emesis. The patient reports post-prandial pain of one months duration, acutely worsening prior to presentation following the consumption of a bacon cheeseburger. ROS is negative for sick contacts, foreign travel, and changes in bowel habits. The patient denies a surgical history.

Triage VS: T101.6°F Oral, HR 134, BP 147/99, RR 24, SpO2 98% on room air

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?


Answer: Acute Cholecystitis1-4

  • Risk Factors: oral contraceptives or estrogen replacement therapy (alters cholesterol and bile salt metabolism leading to gallstone formation and gallbladder hypomotility1), diseases of the terminal ileum (e.g. Crohns; secondary to poor bile salt reabsorption), cirrhosis (decreased bile acid secretion), hemolytic diseases (pigmented gallstones), pregnancy, obesity, TPN
  • Presentation: RUQ or epigastric pain, postprandial pain, nausea +/- emesis, +Murphy’s sign (+LR: 2.8; 95% CI, 0.8-8.62), +/- fever
  • Evaluation:
    • US (Sensitivity 95%, Specificity 98%3): sonographic Murphy’s, pericholecystic fluid, gallstones/biliary sludge, gallbladder wall thickening > 3mm.
    • CBC, LFTs
      • CBC: often demonstrates leukocytosis
      • LFTs: transaminitis; allows for evaluation of choledocolithiasis
  • Treatment:
    • Antimicrobials:
      • Mildly ill: ciprofloxacin 400 mg IV + metronidazole 500 mg IV
      • Critically ill: vancomycin 20 mg/kg (up to 2 g) IV + piperacillin/tazobactam 4.5 g IV
    • Fluid Resuscitation
    • Pain control
    • Anti-emetic PRN
    • Surgical Consultation – cholecystectomy
  • Pearls:
    • Diabetes is a risk factor for emphysematous cholecystitis:3 initiate antibiotic therapy directed against Gram-negative rods and anaerobes, and consult surgery.
    • Include acalculous cholecystitis in your differential diagnosis of the critically ill: RUQ pain, epigastric pain, and nausea are absent upon initial evaluation in up to 75% of these patients.1

 

References:

  1. Welch J, Chike V, Bowens N, Arnell T, Ferri F. Acute Cholecystitis. First Consult. 2011. Elsevier, Philadelphia, PA.
  2. Trowbridge R, Rutkowski N, Shojania K. Does this patient have acute cholecystitis? JAMA. 2003; 289(1): 80-86.
  3. Glasgow R, Mulvihill S. Treatment of Gallstone Disease. In: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Philadelphia: Saunders Elsevier, 2016:1134-1151.e5.
  4. Senturk S, Miroglu T, Cilici A, Gumua H, Tekin R, et al. Diameters of the common bile duct in adults and postcholecystectomy patients: a study with 64-slice CT. Eur J Radiol. 2012; 81(1): 39-42.

EM@3AM – Acute Limb Ischemia

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 62-year-old male with a history of paroxysmal a.fib (CHADS2: 0; daily ASA1) presents for evaluation of left lower extremity (LLE) numbness and weakness. The patient reports the onset of his symptoms five hours prior to arrival, during his granddaughter’s dance recital. He denies slurred speech, visual changes, facial and upper extremity sensory and motor deficit. He denies right lower extremity symptoms.  HPI is negative for back pain, recent trauma, joint pain, and joint redness prior to symptom onset. ROS is unremarkable. Surgical history is significant only for remote inguinal hernia repair.

 Triage VS: T99.7°F Oral, HR 82, BP 129/76, RR 24, SpO2 98% on room air

Physical exam:

Neuro: LLE: weakness of plantarflexion and dorsiflexion; decreased sensation L4-S2 dermatomes below the knee

Cardiac: irregularly irregular

Vascular: Cool, mottled LLE; femoral pulse palpable, popliteal pulse non-palpable, dorsalis pedis and posterior tibial pulses non-palpable. Doppler confirms the absence of popliteal, dorsalis pedis, and posterior tibial pulses.

EKG: NSR, 82 bmp, axis WNL, no ST-T wave changes, QT WNL

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?


Answer: Acute Limb Ischemia1-4

  • Risk Factors: Conditions that pre-dispose to thrombosis (hypercoagulable state, arterial aneurysms, peripheral arterial disease (atherosclerotic plaque rupture), etc.) or embolism (atrial fibrillation, post MI, left ventricular dysfunction, mechanical cardiac valve with sub therapeutic anticoagulation, etc.).
    • Trauma is an uncommon etiology: limb ischemia may occur secondary to direct vessel injury and subsequent thrombosis.2
  • Clinical Presentation: Classically taught as the six Ps: pain, paresthesia, pallor, poikilothermia, pulselessness, and paralysis. Patients may also report claudication.
    • Considered to be acute in onset if symptoms began within 2 weeks of presentation 2
  • Evaluation:
    • Assess limb: appearance, temperature, pulses (including by Doppler), sensation, and strength
    • Lower extremities: ABI < 0.3 = subcritical acute ischemia2
  • Treatment:
    • Consult vascular surgery:
      • The Society for Vascular Surgery publishes classification standards based upon clinical and Doppler findings (limb viable vs. threatened vs. irreversibly damaged) which direct management and treatment.4
    • Discuss initiation of heparin bolus 80 U/kg, then 18 U/kg/hr + ASA PO.2
  • Pearls:
    • Palpable pulses in the contralateral extremity suggests embolism as the underlying etiology.3
    • Morbidity and mortality rates are high in patients with acute limb ischemia: 10-15% undergo limb amputation during hospitalization.2

 

References:

  1. Hart R, Pearce L, Rothbart R, McAnulty J, Asinger R, et al. Stroke with intermittent atrial fibrillation: incidence and predictors during aspirin therapy. Stroke prevention in atrial fibrillation investigators. J Am Coll Cardiol. 35(1):183-187.
  2. Creager M, Kaufman H, Conte M. Clinical Practice. Acute limb ischemia. N Engl J Med. 2012; 366(23):2198-2206.
  3. Earnshaw J. Acute Ischemia: Evaluation and Decision Making. In: Rutherford’s Vascular Surgery. 8th ed. Philadelphia: Saunders Elsevier, 2014: 2518-2527.e1.
  4. Rutherford D, Baker J, Ernst C, Johnston K, Porter J, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg. 1997; 26(3): 517-538.

Toxcards: Alcohol Ketoacidosis

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Case Presentation:

A 45 year old male presents intoxicated, smelling of alcohol and appears disheveled with vomit on his clothes. He is sleepy but arousable to noxious stimuli. His serum ethanol level is 143 mg/dL. Na 135, K 3.9, Cl 97, CO2 20, BUN 33, Cr 1.1. Lactate 3.1. pH 7.35, CO2 28, HCO3 15. His urine is negative for ketones. His vitals are HR 103, RR 30, BP 115/65, O2 98% RA.

toxcard

Question:

Could these laboratory results be consistent with alcohol ketoacidosis (AKA)?

Pearl:

The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis and an elevated lactate. Early in AKA patients may be negative for ketones when the nitroprusside test is used because it does not detect beta-hydroxybutyrate. As patients recover, the nitroprusside test will become positive as beta-hydroxybutyrate gets converted to acetone and acetate.

Acid/base status:

  • Patients with AKA typically have elevated anion gap metabolic acidosis. However, vomiting may cause a primary metabolic alkalosis and a compensatory respiratory alkalosis which may result in a normal or even elevated pH.
  • AKA patients, as compared to DKA patients, typically have higher pH, lower K and Cl, and higher HCO3 in their blood tests.

High Redox State (Excess NADH):

  • As ethanol is metabolized by ADH and ALDH to acetaldehyde and acetate, respectively, an increased amount of NADH forms which causes a high redox state and excess of reducing potential (increased NADH:NAD+ ratio).

ethanol pathway

Increased lactate due to pyruvate shunting:

  • Reduced caloric intake, decreased glycogen stores, and thiamine depletion results in amino acids being converted to pyruvate. The excess pyruvate that forms can then be diverted to gluconeogenesis, be converted to acetyl-CoA, which can enter the Kreb’s cycle, or can enter various biosynthetic pathways (e.g. fatty acids, ketones, etc.). Pyruvate can be diverted to these pathways if there is sufficient NAD+.
  • However ethanol causes a high redox state (excess NADH). In the setting of a high redox state ethanol results in increased lactate due to the conversion of pyruvate to lactate and diverts pyruvate from gluconeogenesis.
pyruvate to lactate

Figure source: Shull P, & Rapoport J.

Anion gap primarily due to beta-hydroxybutyrate:

  • The primary anion contributor in patients with AKA and diabetic ketoacidosis (DKA) is beta-hydroxybutyrate with lactate having less of a role.
  • Decreased caloric intake and glycogen stores results in increased fatty acid mobilization and oxidation resulting in increased acetyl-CoA. In normal states (when there is sufficient NAD+) acetyl-CoA can then enter the Kreb’s cycle or be used in fatty acid synthesis. Thiamine also facilitates the entry of acetyl-CoA into the Kreb’s cycle.
  • However, when there is a high redox state (excess NADH) and thiamine deficiency acetyl-CoA gets converted to acetoacetate which then gets converted to beta-hydroxybutyrate.

ketone production

Ketone production:

  • Early the main anion contributor is beta-hydroxybutyrate, which is not detected well by the nitroprusside test (used to detect ketones in serum and urine). The nitroprusside test does not detect beta-hydroxybutyrate, although it is good for detecting acetoacetate and acetone.
  • It is common for early AKA to have a falsely negative ketone test if the nitroprusside test is used because of the test’s inability to detect beta-hydroxybutyrate. If available, specific assays for beta-hydroxybutyrate should be done.
  • As patients recover and receive glucose and thiamine supplementation, ATP is made which reverses the pyruvate-to- lactate and NAD+-to-NADH ratios.  This allows beta-hydroxybutyrate to be converted to acetoacetate and as patients recover the nitroprusside test will actually become more positive due to the increased production of acetoacetate.

ketone body ratio in alcoholic ketoacidosis

Figure Source:  www.derangedphysiology.com

Main Point:

The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis, and elevated lactate that is insufficient to account for the gap. The main anion contributor early in AKA is beta-hydroxybutyrate, but it will not be detected when evaluating for ketones using the nitroprusside test. As patients recover and are given glucose and thiamine supplementation, the lactate will decrease as pyruvate is no longer shunted to lactate and instead enters the Kreb’s cycle and other biosynthetic pathways. The anion gap decreases as beta-hydroxybutyrate gets converted to acetone and acetate. The nitroprusside test then becomes positive for ketones later as patients recover.

Resources:
  1. Yip L. Ethanol, Chapter in Goldfrank’s Toxicological Emergencies. Tenth Edition. Editors: Hoffman R, Howland M, Lewin N, Nelson L, Goldfrank L. McGraw Hill (2015); New York.
  2. Woods W, Perrina D. Alcohol Ketoacidosis, Chapter in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Edition. Editors: Tintinalli JE, et al. McGraw Hill (2011); New York.
  3. Shull P, & Rapoport J. Life-threatening reversible acidosis caused by alcohol abuse. Nature Reviews Nephrology (2010) 6, 555-559
  4. Diabetic, Alcoholic, and Starvation Ketoacidosis. Chapter 6.17. Available at:  http://www.derangedphysiology.com/main/core-topics-intensive-care/acid-base-disturbances/Chapter%206.1.7/diabetic-alcoholic-and-starvation-ketoacidosis

EM@3AM – Acute Angle Closure Glaucoma

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 62 year-old female with a PMHx of hypertension presents for evaluation of severe left eye pain associated with blurred vision, headache, and nausea.  The patient reports the sudden onset of her symptoms as occurring 30 minutes prior to arrival while entering a movie theater. ROS is negative for sick contacts, ocular discharge, and foreign body sensation. The patient wears glasses that she is “unable to see without.”

Triage VS: HR 122, BP 132/91, RR 18, SpO2 98% RA
Corrected: OD 20/20, OS 20/200, OU 20/40

Ocular examination:
 OD:
-EOMI, PERRLA (3mm)
-No evidence of foreign body
-Fluorescein stain without uptake
-IOP 15 mmHg

OS:
-EOMI, pupil (5mm) mid-position and fixed, conjunctival injection, hazy cornea
-No evidence of foreign body
-Fluorescein stain without uptake
-IOP 34 mmHg

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?


Answer: Acute Angle Closure Glaucoma1-3

  • Risk Factors: hyperopia, age >60, female sex
  • Presentation: sudden onset, severe eye pain +/- blurred vision, +/- nausea or emesis, +/- headache, pupil mid-positioned +/- fixed or sluggish, IOP >20mmHg
  • Precipitating factors:
    • Transition to dim lighting
    • Medications
      • Anticholinergics (topicals: cyclopentolate, tropicamide, etc., or systemic: antihistamines, antipsychotics, anticonvulsants, anti-parkinsonian medications, atropine, etc.)
      • Adrenergic agents (vasoconstrictors, bronchodilators, appetite depressants, etc.)
    • Emotional stress/pain (mydriasis secondary to increased sympathetic tone)
  •  Treatment:
    • Consult ophthalmology
    • Decrease production of aqueous humor:
      • Beta blockade: timolol 0.5% gtt
      • Alpha-2 agonists: apraclonidine 1% gtt or brimonidine 0.2% gtt
      • Carbonic anhydrase inhibitors:
        • Acetazolamide gtt or dorzolamide 2% gtt + 500 mg PO or IV acetazolamide
    •   Improve outflow of aqueous humor:
      • Cholinergic agent: pilocarpine 2% gtt
    • Decrease volume of aqueous humor:
      • Osmotic diuretic: mannitol 1-2g/kg IV
  •  Pearls:  
    • Obtain a thorough medical history:
      • B-blockade: caution with heart blocks, history of severe bronchospasm
    • Carbonic anhydrase inhibitors: avoid in sickle cell patients
    • Pilocarpine therapy should not be initiated until one hour following the instillation of an aqueous humor reducing agent:
      • Pilocarpine constricts the ciliary muscle causing miosis and increasing the axial thickness of the lens. While this allows for increased outflow of aqueous humor, it may also paradoxically worsen the condition by reducing the depth of the anterior chamber.2
    •  Suspect medication induced acute angle closure glaucoma if elevated IOP is present bilaterally.4


References:

  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 60, Aneurysmal Disease.
  2. Jovina S, Aquino M, Chew P. Angle-Closure Glaucoma. In Ophthalmology. 4th ed. Philadelphia, Elsevier 2014; 10.12: 1060-1069.e2.
  3. Day A, Nolan W, Malik A, Viswanathan A, Foster P. Pilocarpine induced acute angle closure. BMJ Case Rep. 2012; 2012.
  4. Aminlari A, East M, Wei W, Quillen D. Topiramate induced acute angle closure glaucoma. Open Ophthalmol J. 2008; 2:46-47.

EM@3AM – Acute Chest Syndrome

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


 A 4-year old male with a history of sickle cell anemia presents to the ED for evaluation of fever of two days duration (Tmax 103.2) and progressively worsening shortness of breath. The patient’s parents report 48-hour hospitalization 6 months prior secondary to a vaso-occlusive crisis (pain localized to the extremities). ROS is negative for sick contacts. Medications include penicillin prophylaxis. Immunizations are up to date.

VS: HR 127, BP 97/64, RR 32, SpO2 91% on room air.

Physical examination:
Neuro: GCS 15
HEENT: PERRLA, TMs clear bilaterally, nasal mucosa unremarkable, oropharynx clear and moist, no lymphadenopathy
CV: Tachycardia, cap refill 2 secs
Pulm: End-expiratory wheezing
Abdomen: ND, NT, no guarding or rebound
GU: Without findings
MSK: No TTP
Derm: No rashes

CXR demonstrates multi-lobar infiltrate.

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?


Answer: Acute Chest Syndrome (ACS)1-3

  • Presentation: fever (>38.5°C or 101.3°F), tachypnea, cough, +/-chest pain, +/- wheezing and new infiltrate on CXR
  • Evaluation:
    • CXR, CBC, reticulocyte count, VBG, blood cultures, sputum culture2
    • Consider underlying etiologies and evaluate as appropriate:
      • Sepsis
      • PNA
      • PE
      • Fat embolism
  •  Treatment:
    • Bronchodilators – improve peak expiratory flow2
    • Incentive spirometry and analgesia – prevent development/worsening of atelectasis
    • Empiric antibiotic therapy following procurement of culture samples (target Chlamydia, Mycoplasma, and Streptococcus)
    • Oxygen therapy to maintain SpO2 >92%
    • Fluid resuscitation targeting euvolemia (avoid iatrogenic pulmonary edema)
    • Exchange transfusion (in consultation with heme/onc) for:
      • Severe hypoxemia
      • Multi-lobar involvement
      • Worsening course
  •  Pearls:
    • Acute chest syndrome is the leading cause of death in sickle cell patients in the U.S. (12% mortality).2
    • Infection is most common cause of ACS ( C. Pneumoniae and RSV).
    • A normal pulmonary exam is most frequently associated with ACS.2
    • ACS rapidly progresses to ARDS = admit to ICU level care


References:

  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 236, Sickle Cell Disease and Hereditary Hemolytic Anemias.
  2. Vichinsky E, Neumayr L, Earles A, Williams R, Lennette E, et al. Causes and outcomes of the acute chest syndrome in sickle cell disease. N Engl J Med. 2000; 342:1855-1865.
  3. Traill L and Barton M. Focus On: Acute Chest Syndrome – The Critical Cough. American College of Emergency Physicians Clinical and Practice Management. 2008. Available from: https://www.acep.org/Clinical—Practice-Management/Focus-On–Acute-Chest-Syndrome—The-Critical-Cough/