Dermatologic Emergencies

Brief H&P

A 68 year-old male with hypertension and gout presents with rash for 2-3 weeks. He note some subjective fevers but is otherwise asymptomatic. He denies recent travel or sick contacts. When asked about his medications, he reports that his primary care provider started him on allopurinol approximately two months ago.

He first noted the rash on his face, characterizing it as “pimples” which were slightly pruritic. The lesions subsequently spread to his trunk and extremities and have been growing in size.

Objectively, vital signs were notable for fever (38.2°C) and tachycardia (108bpm). Examination demonstrated diffuse blanching erythema most prominent on the trunk and extremities. The remainder of the physical examination was normal. Laboratory studies were obtained and notable for a complete blood count (CBC) with peripheral eosinophilia, as well as mildly elevated serum transaminases.

The patient was diagnosed with Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), likely owing to the initiation of a xanthine oxidase inhibitor. He improved after withdrawal of the drug and a brief course of systemic corticosteroids.


Principles of Dermatologic Emergencies

Critical dermatologic processes can be broadly divided into two categories:

1. Cutaneous manifestation of critical illness

The presence of a dermatologic abnormality does not itself represent a life-threat. Instead, the skin lesion is a signal suggestive of the presence of an underlying critical process. The prototypical example would be the petechiae/purpura in meningococcemia.

2. Acute Skin Failure

As with any other organ system failure, Acute Skin Failure carries significant morbidity and mortality and is characterized by derangements in normal skin function.

Critical functions of skin
Temperature regulation
Protection against excess fluid loss
Mechanical barrier to prevent penetration of foreign materials
Important pathophysiologic changes in ASF
Increased peripheral vasodilation (dramatic increase in cardiac output to low-resistance circuits) and increased vascular permeability resulting in relative hypovolemia and shock.
Increased blood flow and dysfunction of eccrine sweat glands results in altered temperature regulation (usually hypothermia)
Fluid imbalances occur, similar to burns (transepidermal water loss) which varies in quality somewhat between “dry” (erythroderma) and “wet” (vesiculobullous) diseases
Electrolytes: increased basal metabolic rate, hyperglycemia (insulin resistance), hypophosphatemia, protein depletion
Barrier dysfunction: increased risk of infection
Management
Intensive Care Unit: Dermatologic (DICU) or Burn Center preferred
Treatment: Temperature management, early enteral nutrition, fluid/electrolyte management, local wound care, disease-specific management
Complications: Sepsis/shock, ARDS, high-output CHF, known complications of critical illness (multi-organ failure, GI ulcers, VTE)
Long-term complications: occular (ectropion, keratitis, ulcer), esophageal (stricture), GU (urethral stricture, phimosis, vaginal stenosis), Integumentary (scarring, alopecia)

Skin Lesions and their Pathophysiology

The objective of this algorithm is to develop a systematic approach to the evaluation of dermatologic processes with a focus on the identification of dermatologic emergencies. The foundation of this approach is an understanding of the underlying pathophysiologic mechanisms for each of four broad categories of dermatologic processes which guide the resultant differential diagnosis.

Erythroderma

Pathophysiology
Extensive cutaneous capillary dilation, results in widespread exfoliation of the epidermis
Inflammatory mediators result in dramatic increase of epidermal turnover rate, accelerated mitotic rate, increased number of germinative skin cells.
Causes
Exfoliative toxin
Eosinophils
Basophils/Histamine
Skin-homing T-cells

View Erythroderma Algorithm

Petechiae/Purpura

Pathophysiology
Represent the passage of erythrocytes from the intravascular to extravascular compartment
May be the result of disruption of vascular integrity (trauma, infection, vasculitis) or disorders of primary or secondary hemostasis
Palpable
If lesions are palpable, this may suggest a more prominent underlying inflammatory process such as vasculiitis.
When cutaneous manifestations are identified, other small vessels may be affected (commonly renal and pulmonary

View Petechiae/Purpura Algorithm

Fluid-filled

Pustule
Pustules more commonly suggest an infectious process (bacterial, fungal)
Vesiculobullous
Vesiculobullous lesions are generally more concerning
Loss of basic structural elements maintaining cohesion between keratinocytes in the epidermis, or between the epidermal layer and the dermis (near basement membrane zone).
Intraepidermal blisters tend to be flaccid, fragile and thin-roofed.
Subepidermal blisters have a thick roof and can remain intact when compressed
Often due to autoantibodies targeting structural proteins in the skin.

View Fluid-filled Algorithm

Maculopapular

Pathophysiology
Catch-all term with a wide range of potential pathophysiologic mechanisms and causative etiologies.
Any process that results in erythroderma, petechiae, or fluid-filled lesions may start as a macule or papule.
Pathophysiology is of little guidance in this category where we must instead rely on the patient’s history and identification of red-flags to exclude dermatologic emergencies.
High-risk Features (Identified by dermatologists to stratify urgency of inpatient consultations):
Ill-appearing, vital sign instability
New-onset fever with rash
Mucocutaneous or ocular lesions
Recent introduction of anti-convulsant or sulfa-drug
Skin pain
Immunocompromised

View Maculopapular Algorithm

Algorithm for the Evaluation of Dermatologic Processes

Algorithm for the Evaluation of Dermatologic Processes
An algorithm for the evaluation of dermatologic processes was developed initially by Lynch in 1984. Since then, several modified Lynch algorithms have emerged. The concept of an algorithmic approach to dermatologic diagnosis was further expanded with the development of VisualDx, a decision-support application. There is evidence to suggest that the use of algorithms and decision support tools like VisualDx (and by extension this algorithm) may aid with the development of more thorough differential diagnoses and improve diagnostic accuracy.


References

Reviews

  1. Wolf R, Parish LC, Parish JL. Emergency Dermatology, Second Edition. August 2017:1-369.
  2. Usatine RP, Sandy N. Dermatologic emergencies. Am Fam Physician. 2010;82(7):773-780.
  3. Shilpi Khetarpal MD, Anthony Fernandez MP. Dermatological Emergencies. Cleveland Clinic. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/dermatological-emergencies/. Published August 2014. Accessed August 5, 2017.
  4. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  5. Browne BJ, Edwards B, Rogers RL. Dermatologic emergencies. Prim Care. 2006;33(3):685–95–vi. doi:10.1016/j.pop.2006.06.002.
  6. Drage LA. Life-threatening rashes: dermatologic signs of four infectious diseases. Mayo Clinic Proceedings. 1999;74(1):68-72. doi:10.4065/74.1.68.
  7. Baibergenova A, Shear NH. Skin conditions that bring patients to emergency departments. Arch Dermatol. 2011;147(1):118-120. doi:10.1001/archdermatol.2010.246.

Erythroderma

  1. Tan TL, Chung WM. A case series of dermatological emergencies – Erythroderma. Med J Malaysia. 2017;72(2):141-143.
  2. Karakayli G, Beckham G, Orengo I, Rosen T. Exfoliative dermatitis. Am Fam Physician. 1999;59(3):625-630.

Petechiae/Purpura

  1. Stevens GL, Adelman HM, Wallach PM. Palpable purpura: an algorithmic approach. Am Fam Physician. 1995;52(5):1355-1362.

Algorithms

  1. Lynch PJ, Edminster SC. Dermatology for the nondermatologist: a problem-oriented system. YMEM. 1984;13(8):603-606.
  2. Nguyen T, Freedman J. Dermatologic Emergencies: Diagnosing And Managing Life-Threatening Rashes. Emergency Medicine Practice. 2002;4(9):1-28.
  3. Murphy-Lavoie H, LeGros TL. Emergent Diagnosis of the Unknown Rash: an Algorithmic Approach-Rash Is Among the Top 20 Reasons for ED Visits in the United States. Certain Rashes …. Emergency Medicine; 2010.
  4. Dean S. Emergency Medicine Dermatology. 2017:1-20. doi:10.21980/J8DW21.
  5. Talley NJ, O’Connor S. Clinical Examination. Elsevier Health Sciences; 2013.
  6. Jack AR, Spence AA, Nichols BJ, Peng DH. A simple algorithm for evaluating dermatologic disease in critically ill patients: a study based on retrospective review of medical intensive care unit consults. J Am Acad Dermatol. 2009;61(4):728-730. doi:10.1016/j.jaad.2008.12.025.

DRESS

  1. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  2. Cardoso CS, Vieira AM, Oliveira AP. DRESS syndrome: a case report and literature review. BMJ Case Rep. 2011;2011. doi:10.1136/bcr.02.2011.3898.

Evidence-Based Algorithms

  1. David CV, Chira S, Eells SJ, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011;17(3):1.
  2. Chou W-Y, Tien P-T, Lin F-Y, Chiu P-C. Application of visually based, computerised diagnostic decision support system in dermatological medical education: a pilot study. Postgrad Med J. 2017;93(1099):256-259. doi:10.1136/postgradmedj-2016-134328.

Pediatric Foreign Body Ingestion

Brief H&P

XR Chest: Circular radioopaque foreign body likely in the antrum of the stomach.

A healthy 5 year-old boy is brought to the pediatric emergency department after he informed his parents that he accidentally swallowed a coin just prior to presentation. He has no complaints and on evaluation appears to be breathing comfortably and is tolerating secretions normally. A plain radiograph was obtained and is shown below.

The patient remained well-appearing and was discharged with primary care follow-up.


Indications for Emergent Endoscopy

  • Esophageal button battery
  • Severe symptoms
  • Sharp foreign body in esophagus
  • Multiple magnets in esophagus or stomach

Radiographic Findings


Esophageal foreign bodies typically orient coronally. For example, a coin will appear as a circle on an anteroposterior projection.

Tracheal foreign bodies typically orient sagitally. For example a coin will appear as a line on an anteroposterior projection.

Algorithm for the Evaluation and Management of Pediatric Foreign Body Aspiration

Algorithm for the Management of Pediatric Foreign Body Ingestion

References

  1. Sahn, B, et al. Foreign Body Ingestion Clinical Pathway. 1 Aug. 2016, www.chop.edu/clinical-pathway/foreign-body-ingestion-clinical-pathway. Accessed 26 Aug. 2017.
  2. Wyllie R. Foreign bodies in the gastrointestinal tract. Current Opinion in Pediatrics. 2006;18 N2 -(5).
  3. Uyemura MC. Foreign body ingestion in children. Am Fam Physician. 2005;72(2):287-291.
  4. Chung S, Forte V, Campisi P. A Review of Pediatric Foreign Body Ingestion and Management. Vol 11. 2010:225-230.
  5. Louie MC, Bradin S. Foreign Body Ingestion and Aspiration. Pediatrics in Review. 2009;30(8):295-301. doi:10.1542/pir.30-8-295.
  6. Green SS. Ingested and Aspirated Foreign Bodies. Pediatrics in Review. 2015;36(10):430-437. doi:10.1542/pir.36-10-430.

Penetrating Neck Trauma

Brief H&P

A young male presents to the emergency department after a self-inflicted stab wound to the neck. Examination revealed a knife handle protruding from the left lateral neck. A plain radiograph is shown below.

CXR: Radiopaque foreign body in left neck.

The patient was initially stable but developed shortness of breath upon attempting to lie flat for advanced imaging and was taken emergently to the operating room. Neck exploration showed no obvious neurovascular injuries, and the course of the 6cm blade was posterior to the trachea and esophagus. The knife was removed with “considerable force” as it was likely lodged within a portion of vertebral bone. The patient underwent esophagoscopy and bronchoscopy without identified tracheoesophageal injuries. The patient did well post-operatively and was discharged home.

Zones of Injury1-3

Previously, the evaluation and management of hemodynamically stable patients with penetrating neck injury was guided by the anatomic “zone” of injury. The affected zone guided the performance of additional diagnostic procedures including potentially morbid neck explorations.

Neck Zones of Injury

Understanding zone definitions remains important for the emergency physician to appreciate potentially implicated underlying structures. However, the advent of modern imaging modalities, specifically computed tomography with angiography, provides appropriate sensitivity for vascular and tracheoesophageal injuries when combined with detailed physical examination and maintenance of an appropriate threshold for the performance of additional studies if warranted by the clinical presentation (suboptimal imaging, concerning projectile trajectory, etc).

Zone Definition
I Clavicles/sternum to cricoid cartilage
II Cricoid cartilage to the angle of mandible
III Superior to the angle of mandible to the skull base

 

Algorithm for the Evaluation of Penetrating Neck Trauma

 

References

  1. Sperry JL, Moore EE, Coimbra R, et al. Western Trauma Association critical decisions in trauma: penetrating neck trauma. J Trauma Acute Care Surg. 2013;75(6):936-940. doi:10.1097/TA.0b013e31829e20e3.
  2. Brywczynski JJ, Barrett TW, Lyon JA, Cotton BA. Management of penetrating neck injury in the emergency department: a structured literature review. Emerg Med J. 2008;25(11):711-715. doi:10.1136/emj.2008.058792.
  3. Shiroff AM, Gale SC, Martin ND, et al. Penetrating neck trauma: a review of management strategies and discussion of the “No Zone” approach. Am Surg. 2013;79(1):23-29. doi:10.1007/978-3-662-49859-0_29.

 

Principles of Neonatal Resuscitation

The following resource for neonatal resuscitation and neonatal critical care was developed with the guidance of Dr. Agrawal (Neonatology) while on rotation at the White Memorial Medical Center Neonatal Intensive Care Unit.

Endotracheal Tube Size1-3

Simplified Formula
Estimated gestational age in weeks ÷ 10 = round to nearest half-size uncuffed tube

NRP Recommendation

Gestation age (weeks) Weight (kg) ETT Size (ID, mm) Depth (cm from lip)
<28 <1.0 2.5 6-7
28-34 1.0-2.0 3.0 7-8
34-38 2.0-3.0 3.5 8-9
>38 >3.0 3.5-4.0 9-10

Laryngoscope Blade Size

Age Blade
Preterm 0
Term 1

Umbilical Vein Catheter Placement4

ED Indications
Unstable neonate
Contraindications
Omphalocele
Gastroschisis
Necrotizing enterocolitis
Depth
4-5cm or until blood return (for emergent placement)

Umbilical artery/vein catheter position on plain radiograph.

Umbilical catheter size

Weight (kg) Size (F)
<1.5 3.5
1.5-3.5 5
>3.5 8

Umbilical catheter positioning on plain radiographs

Umbilical venous catheter position can be verified with a plain radiograph. Positioning within the umbilical vein can be confirmed by tracing a cephalad trajectory from the insertion point at the umbilicus. An umbilical artery catheter will first pass caudally into the internal iliac artery before travelling cephalad into a common iliac artery and the abdominal aorta.

Medications5

Medication Dose
Epinephrine 0.1mL/kg (1:10,000) IV, 0.01mg/kg
Volume Expansion 10mL/kg (normal saline, blood)
Naloxone 0.1-0.2mg/kg
Dopamine 5-20mcg/kg/min IV infusion

Neonatal Physiology and Transition to Extrauterine Life6

An important principle in neonatal resuscitation is supporting the appropriate transition from intra- to extra-uterine life which is dependent on several key anatomic and physiologic changes occurring in an optimal environment.

Anatomy7

Fetal Circulation
Neonatal Circulation

Fetal Circulation

In the fetal circulatory system, oxygenated blood is delivered via the umbilical vein, entering the inferior vena cava via the ductus venosus. The majority of this oxygenated blood passes through the right atrium and into the left atrium through the foramen ovale to enter the systemic circulation.

Meanwhile, high pulmonary pulmonary vascular resistance (due to hypoxic vasoconstriction in fluid-filled alveoli) means that most of the deoxygenated right ventricular output is routed through the ductus arteriosus and enters into the systemic circulation – mixing with oxygenated blood distal to the highest priority end-organs (brain and heart), to be reoxygenated at the placenta.

Post-transition Circulation

The transition to extra-uterine life involves several key steps detailed below and is supported by appropriate ventilation, oxygenation and temperature regulation.

  1. Alveolar Fluid Clearance
    Catecholamine and hormone changes (predominantly corticosteroids) during the process of labor induce changes in enzymatic expression that result in the resorption of alveolar fluid into the interstitial space. At the time of delivery, negative intra-thoracic pressure from inspiration further promotes the resorption of alveolar fluid. Mechanical thoracic compression from delivery may also contribute.
  2. Respiration and Breathing
    Disconnection from the placenta ceases the transfer of placenta-derived factors including prostaglandins. The withdrawal of tonic inhibition of central respiratory drive from prostaglandins with cord clamping stimulates rhythmic breathing. The infant’s initial breaths and resultant lung expansion promotes alveolar expansion and stimulates surfactant production – this decreases alveolar surface tension, increases lung compliance and further facilitates breathing.
  3. Circulatory Changes
    At delivery, clamping the umbilical cord removes a large bed of low-resistance circulation, increasing systemic vascular resistance and systemic blood pressure. At the same time, lung expansion and alveolar aeration decreases pulmonary vascular resistance and pulmonary arterial pressures. At the ductus arteriosus, increased systemic vascular resistance combined with decreased pulmonary vascular resistance decreases shunting and contributes to closure. Similarly, as left atrial pressure approaches and exceeds right atrial pressure, right-to-left flow across the foramen ovale ceases. Collectively, these changes serve to effectively separate the left- and right-sided circulations.

NRP Resuscitation Algorithm5,8

Neonatal Resuscitation Algorithm

References

  1. Luten R, Kahn N, Wears R, Kissoon N. Predicting Endotracheal Tube Size by Length in Newborns. J Emerg Med. 2007;32(4):343-347. doi:10.1016/j.jemermed.2007.02.035.
  2. Peterson J, Johnson N, Deakins K, Wilson-Costello D, Jelovsek JE, Chatburn R. Accuracy of the 7-8-9 Rule for endotracheal tube placement in the neonate. J Perinatol. 2006;26(6):333-336. doi:10.1038/sj.jp.7211503.
  3. Kempley ST, Moreiras JW, Petrone FL. Endotracheal tube length for neonatal intubation. Resuscitation. 2008;77(3):369-373. doi:10.1016/j.resuscitation.2008.02.002.
  4. Anderson J, Leonard D, Braner DAV, Lai S, Tegtmeyer K. Videos in Clinical Medicine. Umbilical Vascular Catheterization. Vol 359. 2008:e18. doi:10.1056/NEJMvcm0800666.
  5. Association AAOPAAH. Textbook of Neonatal Resuscitation. 2016.
  6. Caraciolo J Fernandes MD. Physiologic transition from intrauterine to extrauterine life. UpToDate.
  7. Sadler TW. Langman’s Medical Embryology. Lippincott Williams & Wilkins; 2011.
  8. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 7: Neonatal Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. In: Vol 132. American Heart Association, Inc.; 2015:S204-S241. doi:10.1161/CIR.0000000000000276.

Diplopia Applied

Brief H&P:

A young male with no past medical history presents to the emergency department after assault. He was punched multiple times in the face and has since noted double vision, worse with upward gaze. Examination revealed right peri-orbital edema with associated limitation to upward gaze.

Imaging:

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CT Maxillofacial Non-contrast

Inferior orbital wall fracture with herniation of the inferior rectus muscle.

Extraocular Muscle Actions:

Extra-ocular movement actions.

Affected Anatomic Sites in Diplopia:

Coordinated eye positioning is affected by voluntary movements (requiring cranial nerve control for conjugate eye movements), vergence (for depth adjustments), as well as reflexive adjustments for head movement (requiring vestibular input). As with any motor activity, neuromuscular control must be normal with unrestricted movement of the globe within the orbit.

Sites causing diplopia

Algorithm for the Evaluation of Diplopia:

Diplopia has been explored previously on ddxof. The earlier algorithm was focused on identifying the paretic nerve. This algorithm uses features of the history and physical examination to identify potential etiologic causes of diplopia.

Algorithm for the Evaluation of Diplopia

References:

  1. Rucker JC, Tomsak RL. Binocular diplopia. A practical approach. Neurologist. 2005;11(2):98-110. doi:10.1097/01.nrl.0000156318.80903.b1.
  2. Friedman DI. Pearls: diplopia. Semin Neurol. 2010;30(1):54-65. doi:10.1055/s-0029-1244995.
  3. Alves M, Miranda A, Narciso MR, Mieiro L, Fonseca T. Diplopia: a diagnostic challenge with common and rare etiologies. Am J Case Rep. 2015;16:220-223. doi:10.12659/AJCR.893134.
  4. Dinkin M. Diagnostic approach to diplopia. Continuum (Minneap Minn). 2014;20(4 Neuro-ophthalmology):942-965. doi:10.1212/01.CON.0000453310.52390.58.
  5. Marx J, Walls R, Hockberger R. Rosen’s Emergency Medicine – Concepts and Clinical Practice. 8 ed. Elsevier Health Sciences; 2013:176-183.
  6. Nazerian P, Vanni S, Tarocchi C, et al. Causes of diplopia in the emergency department: diagnostic accuracy of clinical assessment and of head computed tomography. Eur J Emerg Med. 2014;21(2):118-124. doi:10.1097/MEJ.0b013e3283636120.
  7. Low L, Shah W, MacEwen CJ. Double vision. BMJ. 2015;351:h5385. doi:10.1136/bmj.h5385.
  8. Danchaivijitr C, Kennard C. Diplopia and eye movement disorders. J Neurol Neurosurg Psychiatry. 2004;75 Suppl 4:iv24-iv31. doi:10.1136/jnnp.2004.053413.
  9. Huff JS, Austin EW. Neuro-Ophthalmology in Emergency Medicine. Emerg Med Clin North Am. 2016;34(4):967-986. doi:10.1016/j.emc.2016.06.016.

Cervical Spine Injuries

Brief H&P

A young patient with no past medical history is brought in by ambulance after a high-speed motor vehicle accident. Trauma survey demonstrates absent motor/sensation in bilateral lower extremities with sensory level at T3-T4. Computed tomography of the cervical spine was obtained and is shown below.

Imaging

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CT C-Spine

Fracture-dislocation at C6-C7 and C7-T1 with comminuted burst fracture to C7 and locked facet joint with resultant anterior migration of C6 over C7, unstable cervical spine fracture.

Anatomy

Atlas and Axis
Axis (C2 vertebra)
C-spine Lateral View
C-spine Radiographs
Skull base and C1/C2
Vertebral Columns

Flexion

C1/C2

Wedge fracture

  • Stretch on strong nuchal ligament transmits force to vertebral body.
  • Stability: Generally stable unless >50% compression or multiple contiguous.

Flexion-teardrop fracture

  • Severe flexion force, avulsion of fragment of anterior/inferior portion of vertebral body.
  • Stability: Unstable, involves anterior/posterior ligamentous disruptions.

Clay shoveler’s fracture

  • Oblique fracture of spinous process of lower cervical spine.
  • Stability: Stable

Subluxation

  • Pure ligamentous injury without associated fracture.
  • Imaging: Widening of interspinous and intervertebral spaces on lateral.
  • Stability: Potentially unstable.

Bilateral facet dislocation

  • Anterior displacement of spine above level of injury caused by dislocation of upper inferior facet from lower superior facet.
  • Imaging: Anterior displacement greater than ½ AP diameter of vertebral body.
  • Stability: Unstable

Odontoid process fracture

  • Head trauma with shear force directed at odontoid.
  • Sub-classification: Type I (above transverse ligament), type II (odontoid base), type III (extension to body of C2)
  • Stability: Types II, III unstable.

Flexion/Rotation

Rotary atlantoaxial dislocation

  • Imaging: Open-mouth odontoid, asymmetric lateral masses of C1.
  • Stability: Unstable

Unilateral facet dislocation

  • Flexion and rotation centered around single facet results in contralateral facet dislocation.
  • Imaging: AP radiograph shows spinous processes above dislocation displaced from midline, lateral radiograph shows anterior displacement of lower vertebra (less than ½ AP diameter of vertebral body).

Extension

Posterior neural arch fracture (C1)

  • Forced extension causes compressive force on posterior elements of C1 between occiput and C2.
  • Stability: Unstable

Hangman’s fracture (spondylolysis C2)

  • Abrupt deceleration causes fracture of bilateral pedicles of C2, potentially with associated subluxation. Rarely associated with SCI due to large diameter of neural canal at C2.
  • Imaging: May be associated with retropharyngeal space edema.
  • Stability: Unstable

Extension-teardrop fracture

  • Abrupt extension (ex. diving) results in stretch along anterior longitudinal ligament with avulsion of anterior/inferior fragment of vertebral body (usually C5-C7).
  • Imaging: May be radiographically similar to flexion-teardrop fracture.
  • Complications: Central cord syndrome
  • Stability: Unstable in extension

Vertical compression

Burst fracture

  • Force applied from above or below causes transmission of force to intervertebral disc and vertebral body.
  • Imaging: Comminuted vertebral body, >40% compression of anterior vertebral body.
  • Complications: Fracture fragments may impinge on spinal cord.
  • Stability: Stable

Jefferson fracture (C1)

  • Vertical force transmitted from occipital condyles to superior articular facets of atlas, resulting in fractures of anterior and posterior arches.
  • Imaging: Widening of predental space. Open-mouth odontoid view may reveal bilateral offset distance of >7mm between lateral masses of C1/C2.
  • Stability: Unstable

Cervical Spine Imaging Decision Rule (Canadian)

Algorithm for the Evaluation of Cervical Spine Trauma (Canadian)

References:

  1. MD RK, MD BED, CAQ-SM KHM, MD WF. Emergency Department Evaluation and Treatment of Cervical Spine Injuries. Emergency Medicine Clinics of NA. 2015;33(2):241-282. doi:10.1016/j.emc.2014.12.002.
  2. Denis F. Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res. 1984;(189):65-76.
  3. Munera F, Rivas LA, Nunez DB, Quencer RM. Imaging evaluation of adult spinal injuries: emphasis on multidetector CT in cervical spine trauma. Radiology. 2012;263(3):645-660. doi:10.1148/radiol.12110526.

Dysphagia

Brief H&P

A 47-year-old male with no known medical history presents with dysphagia. He reports 3 weeks of symptoms, describing difficulty predominantly with swallowing solid foods which is aided by the concomitant ingestion of liquids. He points to his throat as the area of discomfort, but has not noted any choking or coughing after attempts at swallowing. He occasionally suffers from “heartburn”, describing a burning sensation in his chest provoked by certain foods and was previously prescribed omeprazole which he has not taken for several years. He denies any prior surgeries, tobacco or alcohol use, relevant family history or similar symptoms in the past.

Physical examination was unrevealing, demonstrating a normal neurological examination, normal phonation, normal oropharynx and no appreciable neck masses. The patient was observed to comfortably swallow water.

He was discharged with gastroenterology follow-up and ultimately underwent esophagogastroduodenoscopy which demonstrated narrowing of the distal esophagus suggestive of a peptic stricture. Dilation was deferred in favor of resumption of proton pump inhibitor therapy.


Types of Dysphagia1,2

Oropharyngeal3
Characterized by difficulty initiating swallowing and accompanied by choking/coughing, nasopharyngeal regurgitation or aspiration.
Involved anatomy: Tongue, muscles of mastication, soft palate (elevation to close nasopharynx), suprahyoid muscles (elevate larynx), epiglottis (occlude airway), cricopharyngeus muscle (release upper esophageal sphincter). Neurological control predominantly coordinated by cranial nerves (V, VII, IX, X, XII)
Esophageal4
Delayed after initiating swallowing and characterized by a sensation of food bolus arresting in transit.
Involved anatomy: Skeletal and smooth muscle along the esophagus and lower esophageal sphincter. Neurological control predominantly coordinated by medulla

Important Historical Features5,6

  • Difficulty with liquids suggests motility problem
  • Difficulty with solids only or solids progressing to liquids suggests mechanical obstruction
  • Identify a history of head and neck surgery or radiation therapy
  • Identify a personal or family history of connective tissue disorder (scleroderma, RA, SLE) which may be associated with esophageal dysmotility
  • Review home medications (NSAID, bisphosphonate, potassium chloride, ferrous sulfate)
  • Immunocompromised patients are at risk for infectious esophagitis (Candida, CMV, HSV) which are generally associated with odynophagia
  • A history of heartburn may be associated with reflux-mediated complications such as erosive esophagitis, peptic stricture, and adenocarcinoma of the esophagus
  • Young patients are more likely to be affected by eosinophilic esophagitis
  • Patient localization of site of obstruction is generally accurate, patients are more accurate at localizing proximal than distal obstructions7

Algorithm for the Evaluation of Dysphagia8

Algorithm for the Evaluation of Dysphagia

Management9-11

Patients who are safely tolerating oral intake can be referred for outpatient gastroenterology evaluation. Admission should be considered for patients at high-risk for aspiration.

References

  1. Spieker MR. Evaluating dysphagia. Am Fam Physician. 2000;61(12):3639-3648.
  2. Abdel Jalil AA, Katzka DA, Castell DO. Approach to the patient with dysphagia. Am J Med. 2015;128(10):1138.e17-.e23. doi:10.1016/j.amjmed.2015.04.026.
  3. Shaker R. Oropharyngeal Dysphagia. Gastroenterol Hepatol (N Y). 2006;2(9):633-634.
  4. Galmiche JP, Clouse RE, Bálint A, et al. Functional esophageal disorders. Gastroenterology. 2006;130(5):1459-1465. doi:10.1053/j.gastro.2005.08.060.
  5. McCullough GH, Martino R. Clinical Evaluation of Patients with Dysphagia: Importance of History Taking and Physical Exam. In: Manual of Diagnostic and Therapeutic Techniques for Disorders of Deglutition. New York, NY: Springer New York; 2012:11-30. doi:10.1007/978-1-4614-3779-6_2.
  6. Cook IJ. Diagnostic evaluation of dysphagia. Nat Clin Pract Gastroenterol Hepatol. 2008;5(7):393-403. doi:10.1038/ncpgasthep1153.
  7. Wilcox CM, Alexander LN, Clark WS. Localization of an obstructing esophageal lesion. Is the patient accurate? Dig Dis Sci. 1995;40(10):2192-2196.
  8. Trate DM, Parkman HP, Fisher RS. Dysphagia. Evaluation, diagnosis, and treatment. Prim Care. 1996;23(3):417-432.
  9. American Gastroenterological Association medical position statement on management of oropharyngeal dysphagia. Gastroenterology. 1999;116(2):452-454. doi:10.1016/S0016-5085(99)70143-5.
  10. Spechler SJ. American Gastroenterological Association medical position statement on treatment of patients with dysphagia caused by benign disorders of the distal esophagus. Gastroenterology. 1999;117(1):229-232. doi:10.1016/S0016-5085(99)70572-X.
  11. Varadarajulu S, Eloubeidi MA, Patel RS, et al. The yield and the predictors of esophageal pathology when upper endoscopy is used for the initial evaluation of dysphagia. Gastrointest Endosc. 2005;61(7):804-808.

 

Kawasaki Disease

Brief H&P:

An 8-month old male is brought to the emergency department with fever. He has had four days of fever (temperature ranging from 37-40°C), rash on trunk and extremities, white-colored tongue discoloration, and irritability with decreased oral intake. Temperature on presentation was 39.4°C, examination revealed an erythematous maculopapular rash on the extremities and trunk including soles of the feet. Mucous membrane involvement was noted with oropharyngeal erythema and bilateral conjunctival injection. Neck examination demonstrated right-sided cervical adenopathy.

Labs:

  • WBC: 23.4 (N: 59%, B: 21%)
  • ESR: 100mm/hr
  • CRP: 7.59mg/dL
  • Albumin: 3.3g/dL
  • AST/ALT: 78U/L, 65U/L
  • UA: 7WBC, no bacteria

Hospital Course

The patient was admitted with a diagnosis of Kawasaki Disease and was treated with IVIG and high-dose aspirin. The patient demonstrated marked improvement with treatment and had a normal echocardiogram. He was discharged on hospital day three.

Epidemiology1,2

  • Age: 6 months to 5 years
  • Northeast Asian
  • Possible heritable component
  • Seasonal (winter/spring)

Course

  • Acute febrile (T > 39°C refractory to anti-pyretics)
  • Subacute (coronary vasculitis)
  • Convalescent

Diagnosis

  • Fever >5d
  • Criteria (4/5)
    • Conjunctivitis (bilateral, non-exudative)
    • Oropharynx changes (strawberry tongue, erythema, perioral)
    • Cervical lymphadenopathy (unilateral, >1.5cm)
    • Rash
    • Extremity changes (erythema, edema, palm/sole involvement)
  • Incomplete (2-3 criteria)

Labs

  • CBC: Elevated WBC (neutrophil predominant)
  • Urinalysis: Sterile pyuria
  • Acute phase reactants: Elevated ESR (>40-60mm/hr), CRP (>3.0-3.5mg/dL)
  • CMP: Hyponatremia, hypoalbuminemia, hypoproteinemia, elevated transaminases
  • ECG: AV block, ischemia/infarction (aneurysm/thrombosis)
  • Echocardiography: Decreased LVEF, MR, pericardial effusion

Management

  • Hospital admission
  • IVIG (2g/kg)
  • Aspirin (80mg/kg/day)

Algorithm for the Evaluation of Kawasaki and Incomplete Kawasaki Disease3,4

Algorithm for the Evaluation of Kawasaki and Incomplete Kawasaki Disease

References:

  1. Shiari R. Kawasaki Disease; A Review Article. Arch Pediatr Infect Dis. 2014;2(1 SP 154-159).
  2. Yu JJ. Diagnosis of incomplete Kawasaki disease. Korean J Pediatr. 2012;55(3):83-87. doi:10.3345/kjp.2012.55.3.83.
  3. Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Pediatrics. 2004;114(6):1708-1733. doi:10.1542/peds.2004-2182.
  4. Yellen ES, Gauvreau K, Takahashi M, et al. Performance of 2004 American Heart Association recommendations for treatment of Kawasaki disease. Pediatrics. 2010;125(2):e234-e241. doi:10.1542/peds.2009-0606.

Bradycardia

Brief H&P:

A 38 year-old male with no medical history presents to the emergency department with abdominal pain. He had one episode each of non-bloody emesis followed by watery, non-bloody diarrhea and cited several sick contacts at home with similar symptoms. Vital signs were notable for bradycardia with a heart rate ranging from 38-46bpm though he was normotensive. The examination including abdominal examination was benign. A 12-lead electrocardiogram was obtained which demonstrated sinus bradycardia. The patient was asymptomatic during episodes of bradycardia and his heart rate responded appropriately during activity and on further history reported that he was an endurance athlete and runs multiple marathons each year. He was discharged after symptomatic improvement with anti-emetics.

Bradycardia 1

  • Definition: heart rate <60bpm
  • Sinus rhythm: upright P-wave in I, II, aV; inverted P-wave in aVR

Electrocardiographic Findings 1-4

  • Sinus bradycardia
    • Potentially asymptomatic and present in healthy individuals
  • Sinoatrial node dysfunction (sick sinus syndrome, SSS) 5,6
    • Sinus bradycardia
    • Sinus arrest
    • Tachy-brady syndrome (sinus bradycardia/arrest interspersed with SVT)
  • Atrioventricular block
    • 1st degree: PR prolongation, rarely symptomatic
    • 2nd degree: Intermittent interruption of conduction of atrial impulses to ventricles
      • Type 1: progressive PR prolongation leading to interrupted conduction
      • Type 2: fixed PR interval with interrupted conduction
    • 3rd degree: atrioventricular dissociation
  • Slow atrial fibrillation
    • Irregular RR interval without recognizable P-wave

Epidemiology7

  • Analysis of 277 patients presenting to the emergency department with “compromising” bradycardia.
  • Symptoms
    • Syncope (33%)
    • Dizziness (22%)
    • Angina (17%)
    • Dyspnea/Heart Failure (11%)
  • ECG
    • High-grade AV block (48%)
    • Sinus bradycardia (17%)
    • Sinus arrest (15%)
    • Slow atrial fibrillation (14%)
  • Cause
    • Primary (49%)
    • Drug (21%)
    • Ischemia/Infarction (14%)
    • Pacemaker failure (6%)
    • Intoxication (6%)
    • Electrolyte disorder (4%)

Important Historical Features8,9

  • Fever/travel
  • Chest pain
  • Cold intolerance, weight gain
  • Headache, AMS, trauma
  • Abdominal pain/distension
  • Medication changes

Important Examination Findings8,9

  • Perfusion (temperature, capillary refill)
  • Presence of fistula or hemodialysis catheter
  • Existing device (malfunction)

Workup8,9

  • ECG
  • Continuous telemetry monitoring
  • Labs
    • Potassium
    • Digoxin level
    • TFT
    • Infection titers (RPR, Lyme)
    • Cardiac enzymes

Management8,10

  • Unstable
    • Airway
    • Atropine 0.5mg IV q3-5min (maximum 3mg)
    • Dopamine/epinephrine infusion
    • Temporary pacemaker (transcutaneous, transvenous) with blood-pressure preserving sedation
    • Admission and evaluation for permanent pacemaker placement
  • Stable (outpatient evaluation)
    • Event monitor
    • Stress test (chronotropic incompetence)

Algorithm for the Evaluation and Management of Bradycardia

Algorithm for the evaluation and management of bradycardia

References

  1. Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342(10):703-709. doi:10.1056/NEJM200003093421006.
  2. Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emergency Medicine Clinics of NA. 2006;24(1):1–9–v. doi:10.1016/j.emc.2005.08.006.
  3. Hayden GE, Brady WJ, Pollack M, Harrigan RA. Electrocardiographic manifestations: diagnosis of atrioventricular block in the Emergency Department. J Emerg Med. 2004;26(1):95-106. doi:10.1016/j.jemermed.2003.10.001.
  4. Da Costa D, Brady WJ, Edhouse J. Bradycardias and atrioventricular conduction block. BMJ. 2002;324(7336):535-538.
  5. Semelka M, Gera J, Usman S. Sick sinus syndrome: a review. Am Fam Physician. 2013;87(10):691-696.
  6. Ewy GA. Sick sinus syndrome: synopsis. J Am Coll Cardiol. 2014;64(6):539-540. doi:10.1016/j.jacc.2014.05.029.
  7. Sodeck GH, Domanovits H, Meron G, et al. Compromising bradycardia: management in the emergency department. Resuscitation. 2007;73(1):96-102. doi:10.1016/j.resuscitation.2006.08.006.
  8. Deal N. Evaluation and management of bradydysrhythmias in the emergency department. Emergency Medicine Practice. 2013;15(9):1–15–quiz15–6.
  9. Demla V, Rohra A. Emergency Department Evaluation and Management of Bradyarrhythmia. Hospital Medicine Clinics. 2015;4(4):526-539. doi:https://doi.org/10.1016/j.ehmc.2015.06.009.
  10. Brady WJ, Harrigan RA. Evaluation and management of bradyarrhythmias in the emergency department. Emergency Medicine Clinics of NA. 1998;16(2):361-388.

Pediatric Head Trauma

Brief H&P:

A young child, otherwise healthy, is brought to the pediatric emergency department after a fall. The parents report a fall from approximately 2 feet after which the patient cried immediately and without apparent loss of consciousness. Over the course of the day, the patient developed an enlarging area of swelling over the left head. The parents were concerned about a progressive decrease in activity and interest in oral intake by the child, and they were brought to the emergency department for evaluation. Examination demonstrated a well-appearing and interactive child – appropriate for age. Head examination was notable for a 5x5cm hematoma over the left temporoparietal skull with an underlying palpable skull irregularity not present on the contralateral side. Non-contrast head computed tomography was obtained.

Imaging

ct_head_0007_Screen-Shot-2017-06-05-at-4.18.59-PM
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ct_head_0000_Screen-Shot-2017-06-05-at-4.19.22-PM

CT Head

Fracture of the left temporal and parietal bone with overlying scalp hematoma.

Algorithm for the Evaluation of Pediatric Head Trauma (PECARN)1,2,3

Algorithm for the evaluation of pediatric head trauma

References

  1. Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374(9696):1160-1170. doi:10.1016/S0140-6736(09)61558-0.
  2. Brenner D, Elliston C, Hall E, Berdon W. Estimated risks of radiation-induced fatal cancer from pediatric CT. American Journal of Roentgenology. 2001;176(2):289-296. doi:10.2214/ajr.176.2.1760289.
  3. Schonfeld D, Bressan S, Da Dalt L, Henien MN, Winnett JA, Nigrovic LE. Pediatric Emergency Care Applied Research Network head injury clinical prediction rules are reliable in practice. Archives of Disease in Childhood. 2014;99(5):427-431. doi:10.1136/archdischild-2013-305004.

Acute Urinary Retention

Brief H&P:

A 62 year-old male with no significant medical history, presented to the emergency department with several days of vomiting. Examination showed suprapubic fullness with tenderness to palpation and a bedside ultrasound was performed:

RUQ
RUQ

RUQ

Right upper quadrant ultrasound with moderate hydronephrosis.

LUQ
LUQ

LUQ

Left upper quadrant ultrasound with moderate hydronephrosis.

Bladder
Bladder

Bladder

Relatively non-distended bladder.

Bladder Volume
Bladder Volume

Bladder Volume

Post-void bladder volume.

Ultrasound revealed moderate bilateral hydronephrosis with a relatively non-distended bladder. Labs were notable for new renal failure and the patient was admitted for continued evaluation. He was ultimately diagnosed with idiopathic retroperitoneal fibrosis with bilateral distal ureteral obstruction requiring stenting.

Anatomy of Acute Urinary Retention:

Differential Diagnosis of Acute Urinary Retention:1,2,3

Algorithm for the Evaluation of Acute Urinary Retention

Hypotension

Brief H&P:

A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.

Imaging

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IM-0001-0040
IM-0001-0041
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IM-0001-0042
IM-0001-0043
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IM-0001-0046
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IM-0001-0047
IM-0001-0048
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IM-0001-0049
IM-0001-0050
IM-0001-0050

CT Abdomen/Pelvis

Free air is seen diffusely in the non-dependent portions of the abdomen: in the anterior abdomen and pelvis, inferior to the diaphragm, and in the perisplenic region. There is complex free fluid in the abdomen.

Algorithm for the Evaluation of Hypotension1

This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.

  1. The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
  2. The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
  3. If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
  4. Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
  5. Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.

Algorithm for the Evaluation of Hypotension

Guided Lecture

EM Ed
Watch “The Transiently Hypotensive Patient: Who Cares?” from EM Ed. In this lecture Dr. Basrai reviews the diagnostic pathway for a patient who presents with transient hypotension.

References

  1. Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.

Wellens Syndrome

Case Presentation

49M with a history of hypertension who presented to his primary physician for routine follow-up and was referred to the ED for an abnormal ECG. He denied chest pain, shortness of breath, or any limitation to baseline exercise tolerance. His vital signs were notable for systolic hypertension and his examination was unremarkable. A chest x-ray showed no acute cardiopulmonary findings. His initial ECG demonstrated a biphasic T-wave in V2 and deep, symmetric T-wave inversions in V3-V6. His initial serum troponin was markedly elevated at 3.499. He was admitted and urgent coronary angiography revealed proximal LAD stenosis (70%), mid-LAD stenosis (85%) and 1st right posterolateral stenosis (85%) which were stented. He was discharged on post-procedure day one and has remained asymptomatic at outpatient follow-up.

Presentation ECG
Presentation ECG

Presentation ECG

Biphasic T-wave in V2, deep and symmetric T-wave inversions in V3-V4

Post-Catheterization ECG
Post-Catheterization ECG

Post-Catheterization ECG

Resolution of biphasic T-wave and T-wave inversions

History1

Initially described in 1982 where a subset of patients who did poorly with medical management of “impending myocardial infarction” (essentialy unstable angina) were found to have characteristic ECG changes. These patients were noted to be at increased risk for extensive anterior wall myocardial infarctions due to proximal LAD stenosis.

Wellens ECG patterns

Criteria2,3

  1. History of chest pain
  2. Normal or slightly-elevated cardiac enzymes
  3. No precordial Q-waves
  4. Isoelectric or <1mm ST-segment elevation
  5. Pattern present in pain-free state
  6. Type A (25%): Biphasic T-wave in V2/V3
  7. Type B (75%): Deep, symmetrically inverted T-waves in V2/V3

Clinical Significance3

Wellens Syndrome (or LAD coronary T-wave syndrome) represents a “pre-infarction” stage of coronary artery disease manifested by critical LAD stenosis. The natural history includes progression to extensive anterior wall myocardial infarction, often associated with severe left ventricular systolic dysfunction, cardiogenic shock and death. These changes may be mistaken for “non-specific” T-wave changes (which in the presence of a non-concerning history and typically non-elevated cardiac markers) may lead providers to inappropriate dispositions such a stress testing which is contraindicated. Recognition of this pattern and its appropriate management (urgent coronary angiography) is critical.

Case Summary

The case presented above is atypical. The patient had no history of chest pain and cardiac enzymes were significantly elevated – two features which are uncommon in Wellens Syndrome. However, the patient’s elevated cardiac biomarkers led to admission and angiography with identification of the characteristic proximal LAD stenosis (and other disease).

References:

  1. de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982;103(4 Pt 2):730-736.
  2. Tandy TK, Bottomy DP, Lewis JG. Wellens’ syndrome. YMEM. 1999;33(3):347-351.
  3. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. American Journal of Emergency Medicine. 2002;20(7):638-643. doi:10.1053/ajem.2002.34800.
  4. Mead N, O Keefe K. Wellen′s Syndrome: An Ominous EKG pattern. J Emerg Trauma Shock. 2009;2(3):206– doi:10.4103/0974-2700.55347.
  5. Kannan L, Figueredo VM. Images in clinical medicine. Wellens’ syndrome. N Engl J Med. 2015;372(1):66. doi:10.1056/NEJMicm1400946.

Hypocalcemia

Brief H&P:

34M with a history of HTN, polysubstance abuse, presenting with muscle cramps. He reported onset of diffuse muscle cramping 1-hour prior to presentation while showering. Symptoms involved bilateral upper and lower extremities and resolved spontaneously.

On initial evaluation, the patient was tachycardic and hypertensive. Examination was notable for tremors in bilateral upper extremities with outstretched hands, as well as of extended tongue. Other notable findings included spasm of the upper extremity during blood pressure measurement, hyperreflexia and clonus.

Laboratory evaluation was notable for normal total calcium level, low ionized calcium level, primary respiratory alkalosis, and elevated anion gap metabolic acidosis.

The patient was treated with intravenous fluids, benzodiazepines for alcohol withdrawal, and calcium gluconate 4g IV and was admitted.

Calcium Homeostasis1

  • Fraction
    • 15% bound to anions (phosphate, lactate, citrate)
    • 40% bound to albumin
    • 45% free (regulated by PTH, Vit-D)
  • Conditions causing changes in total calcium (without affecting ionized calcium)
    • Low albumin causes hypocalcemia. Corrected = measured + [0.8 x (4-albumin)]
    • Elevated albumin causes hypercalcemia
    • Multiple myeloma causes hypercalcemia
  • Conditions causing changes in ionized calcium (without affecting total calcium)
    • Alkalemia causes increased ionized calcium binding to albumin and decreases ionized calcium levels
    • Hyperphosphatemia causes increased ionized calcium binding to phosphate and decreases ionized calcium levels
    • Hyperparathyroidism causes decreased ionized calcium binding to albumin and increases ionized calcium levels

Causes of Hypocalcemia1,2,3

Algorithm for the Evaluation of Hypocalcemia

Symptoms1

Acute Chronic

Neuromuscular

  • Paresthesia
  • Tetany
  • Carpopedal spasm
  • Trousseau
  • Chvostek
  • Seizure
  • Laryngospasm

Cardiac

  • QT prolongation
  • Hypotension
  • Heart failure
  • Arrhythmia

CNS

  • Basal ganglia calcifications
  • EPS
  • Parkinsonism
  • Dementia

Ophthalmologic

  • Cataracts

Management

  • Severe (symptomatic, QT prolongation)
    • Calcium gluconate 1-2g IV in 50mL of D5W over 10-20min followed by slow infusion of additional 2g over 2 hours.
  • Asymptomatic
    • Calcium gluconate 1g PO q6h
    • Calcitriol 0.2mcg PO BID

References:

  1. Yu, AS. Relation between total and ionized serum calcium concentrations. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on October 6th, 2016.)
  2. Cooper MS, Gittoes NJL. Diagnosis and management of hypocalcaemia. BMJ. 2008;336(7656):1298-1302. doi:10.1136/bmj.39582.589433.BE.
  3. Hannan FM, Thakker RV. Investigating hypocalcaemia. BMJ. 2013;346(may09 1):f2213-f2213. doi:10.1136/bmj.f2213.

Pediatric Emergencies

Diseases by Age

  • 1 week – 1 month: Ductal dependent cardiac lesions
  • 1st month: Malrotation with volvulus
  • 1 – 2 months: Pyloric Stenosis
  • 2 – 6 months: CHF
  • 3 months – 2 years: Intussusception
  • 6 months – 2 years: Croup
  • <2 years: Bronchiolitis
  • 2 years: Meckel’s
  • 2 years – 6 years: Epiglottitis

Cardiology

Ductal Dependent Lesions

  • Present 1st week to 1st month
  • Normal duct seals by 3 weeks
  • If dependent on shunt for pulmonary flow  cyanosis
  • If dependent on shunt for systemic flow cold shock (may be worse w/ fluids)
  • Prostaglandin E1
    • 1 mg/kg/min
    • Side effects include apnea, bradycardia, hypotension, seizure
      • Consider intubating prior to administration
    • IVF, cover for sepsis

Congestive Heart Failure

  • Present 2nd to 6th month
  • Presents with respiratory symptoms (wheezing, retractions, tachypnea)
  • Difficulty with feeding (the infant stress test)
  • Treatment: Supportive

 Tetrology of Fallot

  1. Calm the child, knee to chest
  2. O2 = reduction in PVR
  3. Analgesia: morphine 0.1mg/kg, fentanyl 1.5 mcg/kg, ketamine 0.25 mg/kg
  4. Establish Access: 10-20cc/kg bolus
  5. Phenylephrine 0.2 mg/kg IV (to increase SVR)
  6. +/- HCO3 1mmol/kg (if acidosis)
  7. +/- beta blocker (with cardiology consultation)
  8. PGE1 0.05mcg/kg/min titrating to 0.1mcg/kg/min

Dermatology

Slapped Cheek/5th Disease

  • Parvo B19
  • Slapped cheeks, lacy reticular pattern of rash on body
  • Complications:
    • Pregnancy hydrops
    • Sickle Cell Disease  aplastic crisis

Measles

  • Koplik spots, conjunctivitis, fever
  • Can cause blindness

VZV

  • Different stages of development
  • Treat with acyclovir if > 12 years old
  • Give VZIG in neonates and immunocompromised

Scarlet Fever

  • Erythematous rash, palatal petechiae, pastia’s lines
  • Strawberry tongue
  • Trunk to periphery
  • Treat with Pen VK: 50mg/kg BID x10d or Amox 20mg/kg BID x10d
  • Pen allergic: Azithro 10mg/kg day 1 then 5mg/kg 2-5

Staphylococcal Scalded Skin Syndrome

  • Toxin mediated, negative Nikolsky, good prognosis
  • Treatment: Anti-staphylococcal antibiotics
    • Nafcillin 25mg/kg/d IV
    • Augmentin 45mg/kg/d PO in 2 divdied doses 7-10d
    • Keflex 10mg/kg/d QID x7-10d

Henoch-Schonlein Purpura

  • Palpable purpura in dependent areas
  • Arthralgia/Arthritis (50-84%)
  • Abdominal pain (50%): vascular lesions in bowel, may be intussusception lead point
  • Renal Disease (20-50%) may develop within 2 months
  • Treatment: Supportive, NSAIDs

Kawasaki Disease

  • 5 days of fever + 4/5 of criteria
    • Diffuse polymorphous diffuse rash
    • Conjunctivitis
    • Mucous membrane change (strawberry tongue)
    • Cervical LAD (usually unilateral)
    • Extremity changes
  • Incomplete and atypical forms more common in infants
  • Treatment (drop complications from 25% to 4-5%)
    • Aspirin 20mg/kg/dose Q6H
    • IVIG 2gm/kg over 12H

Gastroenterology

Bilious Vomiting

  • Bilious vomiting malrotation with volvulus until proven otherwise  surgical emergency
  • 1st month of life “pre-verbal child’s disease”
  • Dx: Upper GI Series (10-15%) false positive rate

Necrotizing Enterocolitis

  • 10% of cases full term
  • XR w/ pneumatosis intestinalis

Hirschsprung’s

  • No meconium, slightly distended abdomen
  • Less severe  later presentation, p/w constipation

Pyloric Stenosis

  • Presents around 6 wks: vomiting but very hungry
  • Diagnosis
    • US pylorus > 4mm thick, >15mm long
    • NGT aspiration 5cc is abnormal
  • Treatment
    • Resuscitate
    • Correct metabolic abnormalities
    • Consult surgery

Intussusception

  • Most common infant emergency
    • 3 months – 2 years
  • Abdominal pain, currant jelly, palpable mass (30% only)
  • Typical presentation
    • Lethargy (may be only sign)
    • Vomiting
    • Paroxysms of pain
    • SBO
    • PO intolerance
  • Diagnosis: US
  • Treatment: Enema (80-95% successful), 10% recurrence

Meckel’s Diverticulum

  • Around 2 years of age, boys > girls
  • Obstruction, intussusception
  • Diagnose with technetium scan

Appendicitis

  • 1/3rd with vomiting and diarrhea (AGE-type syndrome)

Hemolytic Uremic Syndrome

  • Watery/bloody diarrhea
  • Three components
    • Acute renal failure
    • Thrombocytopenia
    • Microangiopathic hemolytic anemia (MAHA)
  • Signs
    • Pallor
    • Abdominal Pain
    • Decreased urine output
    • Low energy/AMS
    • Hypertension
    • Edema
    • Petechiae
    • Icterus
  • Treatment: Supportive vs. Dialysis (50%)

GI Bleed by Age

Age Well-Appearing Ill-Appearing
Neonate Allergic Proctocolitis Malrotation with Volvulus
Anal Fissure Necrotizing Enterocolitis
Swallowed Maternal Blood Coagulopathy
Infant/Young Child Allergic Proctocolitis Meckel’s
Gastritis Intussusception
Infectious Colitis Vascular Malformation
Older Child/Adolescent Gastritis IBD
Esophageal Bleeding Cryptic Liver Disease
Juvenile Polyps Intestinal Ulceration

Congenital Disorders

Congenital Adrenal Hyperplasia

  • Presents in first two weeks of life
  • Chief complaint may be vomiting
  • Lyte: HyperK, HypoNa, Hypoglycemia  dysrhythmias, seizures
  • Treatment
    • IVF (usual dose)
    • Glucose (usual dose)
    • Hydrocortisone: 25mg (neonate/infant), 50mg child, adolescent/adult 100mg

Inborn Errors of Metabolism

  • Possible CC: Vomiting, Lethargy, Seizures, Hepatomegaly, Metab Acidosis, Odor
  • May have normal labs and imaging
  • Life-threatening: Metabolic acidosis, Hypoglycemia, Hyperammonemia, Sepsis
  • Labs
    • VBG (acidosis),
    • CMP (liver, kidney, anion gap)
    • Ammonia, lactate, urine (ketones, reducing substance)
    • Bunch of extra tubes for labs later
  • Treatment
    • NPO
    • IVF bolus
    • D10 at 1.5x maintenance
    • Treat Sepsis
    • Control seizures PRN, correct hyperammonemia/acid/lyte (may need dialysis)

Pulmonary

Croup

  • Toddlers (6-24 months), 5% of all children, boys > girls
    • PIV #1
    • Rhinovirus, Metapneumovirus, PIV II-IV, RSV, Flu A/B
    • Frequent co-infections with one or more viruses
  • Sx: 1-3 days of URI Sx  Abrupt cough/stridor worse for one day, then better
  • Signs: Nontoxic, if wheezing likely RSV
  • Studies: XR to r/o FB (steeple sign if positive)
  • Treatment: Racemic Epi: 0.25-0.75 cc in 3 cc Q 20 minutes, lasts < 2 hours
  • Disposition: If stridor at rest then treat if no improvement, then admit
Stridor Steroids Racemic Epi Dispo
Mild 0.15 mg/kg No Home
At rest with WOB 0.30 mg/kg Yes Admit
Severe at rest 0.60 mg/kg Yes ICU

Bronchiolitis

  • Children < 2 years old, November through April (peak Jan/Feb)
    • Apnea in neonates and ex-premies < 2 months
    • Bacterial superinfection is very rare
  • Presentation: Desat, tachypnea, nasal flaring, intercostal retractions, secretions
  • Exam: Fine rales, diffuse/fine wheezing
  • Treatment: Suction, O2 (if < 90%), NPPV
  • Maybe albuterol, but no steroids/epi/abx

Epiglottitis

  • Bimodal (2-6, 20-40y), < 1% URI with stridor, boys = girls, al year
    • Non-typable H.flu, staph/strep, Moraxella
    • Candida, HSV, VZV, crack cocaine
  • Symptoms: Muffled voice, drooling rapid progression in hours
  • Signs: No pharyngeal findings with severely tender anterior neck
  • Studies: XR w/ thumb sign
  • Treatment: Laryngoscopy, airway management

Bacterial Tracheitis

  • Preschool (1-10y), boys = girls, Downs
  • Symptoms: Several days’ URI  toxic in hours, rapid progression
  • Signs: Subglottic diffuse inflammation, edema with exudates and pseudomembranes
  • Studies: CXR demonstrates narrow trachea
  • Treatment: Emergent intubation, 3rd generation cephalosporin

Altitude and Dysbarism

Altitude Illness

  • Risk factors: altitude, rapidity of ascent, sleeping altitude
  • Pathophysiology
    • Hypobaric hypoxia
      • Pulmonary: vasoconstriction  pulmonary hypertension capillary leak
      • Cerebral: vasodilation edema
    • Acclimatization
      • Hyperventilation primary respiratory alkalosis compensatory metabolic acidosis
      • Acetazolamide promotes renal bicarbonate excretion and accelerates acclimatization
  • Management: oxygen and descent

Acute mountain sickness (2000m)

  • Mild cerebral edema
  • Symptoms: headache, nausea/vomiting, fatigue (hangover)
  • Management: acetazolamide 250mg PO BID, dexamethasone 4mg q6h

High-altitude pulmonary edema (HAPE, 3000m)

  • Non-cardiogenic pulmonary edema
  • Symptoms: dyspnea at rest, cough, fever
  • Signs: hypoxia, crackles
  • CXR: patchy infiltrates
  • Management: nifedipine, PDEi (sildenafil), HBO

High-altitude cerebral edema (HACE, 4500m)

  • Cerebral edema
  • Symptoms: ataxia, altered mental status
  • Management: acetazolamide 250mg PO BID, dexamethasone 10mg then 4mg q6h, HBO
  • Gamow bag: portable HBO

Dysbarism (diving pathology)

  • Principles
    • Boyle’s Law: volume = 1/pressure
      • Volume changes greatest near surface
    • Henry’s Law: increased pressure increases proportion of dissolved gas

Barotrauma

  • Localized (descent)
    • Barotitis media
      • Mechanism: unequal pressure between external and middle ear.
      • Symptoms: pain, vertigo if ruptured
    • Barotitis externa
      • EAC edema/hemorrhage
    • Barotitis interna
      • Bleeding/rupture of round window
      • Symptoms: vertigo, tinnitus, hearing loss
      • Management: ENT referral
    • Sinus squeeze: pain and epistaxis
    • Mask squeeze: periorbital petechiae
  • Localized (ascent)
    • Barodontalgia
      • Air trapped in filling
      • Symptoms: pain, fracture
    • Alternobaric vertigo: Unequal ear pressure causing vertigo
    • GI barotrauma: belching, flatulence
  • Pulmonary overpressurization (ascent)
    • Mechanism: rapid ascent without exhalation, focal alveolar rupture leading to pneumomediastinum, rarely pneumothorax
    • CXR: continuous diaphragm sign
    • Symptoms: dysphonia, neck fullness, chest pain
    • Management: supportive
  • Air gas embolism (ascent)
    • Mechanism: similar to POP, air enters pulmonary venous circulation
    • Symptoms: MI, arrest, stroke, seizure within 10 minutes
    • Management: IVF, oxygen, HBO

Dissolved Gas Problems

  • Nitrogen narcosis
    • At >100ft, nitrogen enters nervous system and acts similarly to general anesthetic
    • Symptoms: similar to alcohol intoxication, complications arise from poor judgement
    • Management: ascent
  • Oxygen toxicity
    • Setting: industrial dives, deep
    • Symptoms: seizure, nausea, muscle twitching
  • Decompression sickness
    • Mechanism: nitrogen gas dissolves poorly in solution, with ascent forms bubbles, occurs 1-2 hours after ascent
    • Types
      • Musculoskeletal, integumentary (“bends”)
        • Symptoms: arthralgia, cutis marmorata
      • Neurological
        • Lower spinal cord (thoracic/lumbar/sacral)
          • Symptoms: paraplegia, paresthesia, bladder dysfunction
        • Cerebellum (“staggers”)
          • Symptoms: ataxia
        • Pulmonary (“chokes”)
          • Symptoms: similar to pulmonary embolus
        • Management: IVF, oxygen, HBO

Bites

Mammalian

  • Human: Eikenella corrodens
  • Dog/Cat: Pasteurella multocida

Athropod

  • Hymenoptra (bee, wasp, hornet, ant)
    • Venom: histamine reaction, anaphylaxis
    • Symptoms
      • Local: pain, swelling, pruritus
      • Toxic (<48h): multiple bits, N/V, syncope, HA
      • Anaphylaxis: minutes
      • Delayed (10-14d): serum sickness, fever, arthralgia, malaise
    • Management
      • Remove stinger
      • Wash, ice, anti-histamine, analgesia
  • Brown recluse (violin pattern)
    • Location: Midwest, wood pile
    • Symptoms: initially painless, cytotoxic venom may cause necrosis
    • Management: supportive, Tdap, delayed debridement if necrotic
  • Black widow (red hourglass)
    • Venom: neurotoxic, ACh, NE
    • Symptoms: painful, erythema, muscle contractions (“acute abdomen”), localized diaphoresis from ACh release
    • Management: analgesia, benzodiazepines, antivenom for refractory pain (may cause anaphylaxis)

Snake

  • Crotalid (rattlesnake, copperhead, cottonmouth, collectively “pit vipers”)
    • Venom: cytotoxic, hemorrhagic
    • Symptoms: erythema/edema (ecchymoisis/bullae), nausea/vomiting, metallic taste
    • Labs: DIC
    • Management
      • Immobilization (no tourniquet)
      • Local wound care, Tdap
      • CBC, INR, fibrinogen (q2h)
      • Antivenom (Crofab 4-6 vials): given until symptoms or laboratory abnormalities arrest
      • Compartment syndrome: avoid surgery
  • Elapidae (coral snake, “red on yellow”)
    • Venom: neurotoxic, delayed 10-12h
    • Symptoms: no significant local reaction, bulbar palsies, respiratory depression
    • Management: no antivenom, supportive care, intubation

Cnidaria (jellyfish)

  • Symptoms: local pain, erythema, pruritus
  • Management: 5% acetic acid, alcohol, remove stinger
    • Antivenom for box jellyfish

Stingray

    • Symptoms: local pain, edema
    • Management: Local wound care, Tdap, hot water immersion, antibiotics for Vibrio (cephalexin with doxycycline)

Vibrio vulnificus

  • Symptoms: necrotizing fasciitis, in cirrhotic primary septicemia after ingesting shellfish

Electrical Injuries

 

Physics

  • High-voltage defined as >1,000V
  • Voltage related to injuries current via resistance (V=IR)
  • AC is 3x more lethal than DC
    • Fluctuation at 60Hz causes tetany, maintained grasp on source

Effects

  • Dysrhythmia
    • DC: asystole
    • AC: ventricular fibrillation
    • Delayed dysrhythmia uncommon
  • Burn
  • Tissue ischemia: vascular spasm or thrombosis
  • CNS: AMS, seizure, ICH, neuropathy
  • MSK: posterior shoulder dislocation

Management

  • Asymptomatic: None
  • Mild (i.e. small burn): ECG, UA (rhabdo)
  • High voltage: Labs, CT, admit for observation
  • Pediatrics: oral commissure burn, discharge with plastic surgery follow-up if no LOC, normal ECG, tolerating PO. Risk of delayed labial artery bleeding.

Complications

  • Keraunoparalysis: current travels up and down lower extremities causing transient paresthesia and paralysis.
  • Trauma: TM rupture, other mechanical injuries

 

Heat Emergencies

Overview

  •  Spectrum
    • Cramps
    • Syncope
    • Exhaustion
    • Stroke
  • Physiology of cooling
    • Radiation: body warmer than environment, heat radiates away
    • Evaporation: environment warmer than body, sweat promotes heat exchange, affected by ambient humidity

Heat cramps

  • Mechanism: fluid/electrolyte depletion resulting in muscle cramps
  • Management: IVF, electrolyte repletion, cooling

Heat syncope

  • Mechanism: vasodilation resulting in hypotension
  • Management: IVF, cooling, rule out alternative etiologies

Heat exhaustion

  • Mechanism: similar to heat cramps
  • Symptoms: influenza-like, headache, fatigue, dizziness, nausea, normal mental status distinguishes from heat stroke
  • Findings: temperature <40°C
  • Management: IVF, cooling

Heat stroke

  • Mechanism: similar to heat cramps
  • Symptoms: prodrome of heat exhaustion
  • Signs: AMS, ataxia, seizure
  • Findings: temperature >40°C
  • Mortality: 30-80%
  • Labs: AST/ALT, coagulopathy, DIC, rhabdomyolysis, ATN/AKI
  • CXR: pulmonary edema
  • Types
    • Classical: elderly, dry skin, mild dehydration, increased mortality
    • Exertional: young athlete, diaphoretic, increased morbidity (organ failure)
  • Management
    • Evaporative cooling
    • Ice packs to large vessels
    • GI lavage
    • Liberal intubation
    • Benzodiazepines or thorazine for inappropriate thermogenesis (shivering)
    • Halt cooling at 40°C

Hypothermia

Overview

  • Risk factors
    • Extremes of age
    • Behavioral: psychosis, intoxication
  • Types
    • Chillblains
    • Immersion foot
    • Frostnip
    • Frostbite
    • Generalized

Hypothermia

Chilblains

  • Findings: red/white plaques on extremities
  • Symptoms: pruritus, pain
  • Management: supportive (gentle warming), topical corticosteroids, consider nifedipine

Immersion foot (trench)

  • Mechanism: prolonged immersion in non-freezing water, vasoconstriction leads to ischemia/necrosis
  • Findings: pale, mottled skin, paresthesia
  • Management: supportive, drying and rewarming
  • Complications: gangrene

Frostnip

  • Retrospective distinction from frostbite after rewarming if no tissue loss

Frostbite

  • Mechanism: extracellular then intracellular crystal formation (mechanistically similar to crush injury)
  • Reperfusion: cellular injury triggers cytokine release upon reperfusion, results in microvascular thrombosis and tissue ischemia/necrosis
  • Classification: grades I-II superficial to dermis, grades III-IV involve subcutaneous tissue to bone
  • Management
    • Rapid rewarming (immersion in warm water at 41°C)
    • Tdap
    • Debridement of clear blisters

Generalized

  • Causes
    • Exposure
    • Metabolic (adrenal, thyroid, hypoglycemia)
    • Sepsis
  • Grading
    • Mild (32.2-35°C)
      • Findings: excitation, tachycardia, hypertension, shivering thermogenesis
    • Moderate (30-32.2°C)
      • Findings: ataxia, AMS, bradycardia, hypotension, bradypnea
      • ECG:  Osborn wave
    • Severe (<30°C)
      • Complications
        • Increased risk of arrhythmia (bradycardia, slow atrial fibrillation, ventricular fibrillation, asystole)
        • Irritable myocardium
        • Decreased enzymatic activity
          • Renal: cold diuresis
          • Heme: coagulopathy (hidden on labs as blood rewarmed prior to testing)
          • Metabolic: hyperglycemia as insulin ineffective
      • Management
        • Ventricular fibrillation: attempt one shock, then focus on rewarming if ineffective
        • Goal >30°C