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

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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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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

Radiation Exposure

Physics

  • Units
    • Gray (amount of radiation absorbed by body)
    • Sievert (toxicity associated with radiation exposure)
  • Types
    • Alpha: 0.1mm penetration, injury through ingestion
    • Beta: 1cm penetration, injury through skin or ingestion
    • Gamma: deep penetration
  • Factors
    • Time and distance (1/d2)
    • Shielding
    • Radiosensitive cells (rapidly dividing such as hematopoetic, GI)

Injury

  • Localized: epilation or burns, delayed by days
  • Internal (inhaled, ingestion)
    • Radioactive iodine: high dose results in thyroid ablation, low dose increases risk of thyroid malignancy
  • External: managed by removing clothing, soap/water shower
  • Whole body (gamma)
System Dose Time of onset Signs/Symptoms
Hematopoetic 2G 2d Pancytopenia, increased risk of infection
GI 6G Hours Nausea/vomiting, diarrhea, GI bleeding
CV/CNS 10G Minutes Shock, seizure

Key clinical features

  • Multiple affected individuals with nausea/vomiting suggests radiation exposure
  • Rapidity of onset of symptoms suggests increased dose/exposure
  • LD505G
  • Prognosis by lymphocyte count
    • ALC >1000 at 48h suggests good prognosis
    • ALC <300 at 48h suggests poor prognosis

Neurosyphilis

Brief H&P

A young male with a history of HIV (untreated for the last year, with unknown CD4 count), and syphilis (reportedly treated with an intramuscular injection 1 year ago), presents with 4 months of a painful rash on the palms and soles and diplopia. Examination revealed the rash pictured below, ocular examination with minimal papilledema and anterior chamber inflammation.

Labs were unremarkable. CSF sampling was notable for 34 WBC’s with lymphocyte predominance (92%), and elevated protein (56mg/dL). The patient was admitted for syphilis with presumed neurosyphilis. Serum RPR titer was elevated at 1:64,  FTA-ABS and CSF VDRL were reactive. The patient was treated with intravenous penicillin and anti-retroviral therapy was reinitiated.

Epidemiology1

  • Transmission
    • Sexual contact (estimated transmission probability 60% per partner)
    • Trans-placental
  • Race/Sex
    •  African-American, Hispanic
    • Male > Female
    • Male (primary syphilis), female (secondary syphilis) – lesion visibility
    • Urban > rural

Natural History1

Stage Signs/Symptoms Incubation Period
Primary Chancre, reginal lymphadenopathy 3 weeks
Secondary Rash, fever, malaise, generalized lymphadenopathy, mucous membrane lesions, condyloma lata, headache, meningitis 2-12 weeks
Latent Asymptomatic Early (<1 year)

Late (>1 year)

Tertiary Cardiovascular:

Aortic aneurysm, aortic insufficiency, coronary artery ostial stenosis

<2 years
CNS:
Acute syphilitic meningitis: headache, confusion, meningeal irritation <2 years
Meningovascular: cranial nerve palsy 5-7 years
General paresis: headache, vertigo, personality changes, vascular event 5-7 years
Tabes dorsalis: dementia, ataxia, Argyl-Robertson, [arrow-down] proprioception 10-20 years
Gumma:

Local tissue destruction

1-46 years

Diagnosis1

  • Serologic
    • Non-treponemal (screening)
      • RPR, VDRL
      • Limitations:  sensitivity, false positive (age, pregnancy, drugs, malignancy, autoimmune, viral infections)
    • Treponemal (confirmatory)
      • FTA-ABS
    • Neurosyphilis
      • Indications for CSF sampling: neurologic/ophthalmologic symptoms, tertiary syphilis (aortitis, gumma, iritis), HIV coinfection with elevated RPR titer (> 1:32)
      • CSF: leukocytosis (predominantly lymphocytes),  protein
      • CSF VDRL reactive
      • Negative CSF FTA-ABS may rule out neurosyphilis

Syphilis in HIV-infected Individuals2

  • Primary: larger and more lesion, multiple ulcers
  • Secondary: genital ulcers more common, higher RPR/VDRL titers
  • Tertiary: possibly more rapid progression to neurosyphilis

References

  1. Singh AE, Romanowski B. Syphilis: review with emphasis on clinical, epidemiologic, and some biologic features. Clin Microbiol Rev. 1999;12(2):187-209.
  2. French P. Syphilis. BMJ. 2007;334(7585):143-147. doi:10.1136/bmj.39085.518148.BE.

Submersion Injury

Pathophysiology

  • Breath-holding until eventual involuntary gasp which triggers reflexive laryngospasm. Resultant loss of consciousness may cause laryngeal relaxation and aspiration.
  • Fluid aspiration results in decreased surfactant activity and atelectasis. This is complicated by V/Q mismatch and atelectrauma which can lead to ARDS.

Symptoms

  • Progressive respiratory distress
  • AMS: due to cerebral hypoxia
  • Shock: uncommon, consider trauma

Management

  • Albuterol
  • BiPAP
  • Endotracheal intubation
  • ECMO

Disposition

  • Asymptomatic or minor event: observe 2-3 hours
  • Mildly symptomatic: observe 4-6 hours
  • Hypoxia: admit
  • PPV: ICU

Hematologic Emergencies

Sickle Cell Crises

  • Triggers: infection, acidosis, dehydration, cold-exposure, hypoxia, pregnancy
  • Presentation: exclude alternative more serious pathology prior to ascribing pain to vaso-occlusive crisis

Effects by Organ System

System Symptom
CNS Focal or generalized neurological symptoms, stroke, seizure
Pulmonary Acute chest syndrome (fever, chest pain, cough, hypoxia, pulmonary infiltrates), pulmonary embolism
GI Abdominal pain, nausea/vomiting
Renal Papillary necrosis
GU Priapism, testicular/ovarian ischemia
Muskuloskeletal Bone pain (back, proximal extremities), exclude osteomyelitis, avascular necrosis
ID Infection, functional asplenia (streptococcus, haemophilus)
OB Preterm labor, placental abruptions, SAB
Ophthalmology Acute retinal ischemia, hyphema (with intra-ocular hypertension)
Hematology
  • Sequestration crisis: acute anemia, often post-viral
  • Hemolytic crisis: acute anemia, reticulocytosis, hyperbilirubinemia
  • Megaloblastic crisis: folate deficiency
  • Aplastic crisis: inadequate reticulocytosis

Evaluation

  • CBC with reticulocyte count
    •  Hemoglobin: suggests sequestration or hemolytic crisis
    • Reticulocyte index: suggests aplastic or megaloblastic crisis
  • LDH/haptoglobin: evaluate for hemolysis
  • UA: evaluate for infection/infarction
  • CXR: evaluate for acute chest syndrome

Management

  • Rehydration (hypotonic fluids)
  • Analgesia
  • Supplemental oxygen if hypoxic
  • Exchange transfusion for priapism, neurologic symptoms, aplastic/sequestration/hemolytic crises

Transfusion Reactions

  • Epidemiology: overall 0.25%, 0.09% severe
  • Management: stop transfusion

Management by Presumed Etiology

Reaction Mechanism Signs/symptoms Management
Acute, Severe
Acute hemolysis Incompatibility Fevers, HR, BP, vomiting, back pain IVF, vasopressors if needed, furosemide
Anaphylaxis IgA-mediated 1min: flushing laryngospasm, bronchospasm, BP Epinephrine, steroids, diphenhydramine, IVF
Sepsis Bacterial contamination (Y. entercolitica), increased risk in platelet transfusion Fevers, BP IVF, vasopressors if needed, broad-spectrum antibiotics
TRALI (transfusion-related acute lung injury) Non-cardiogenic pulmonary edema, increased risk in FFP transfusion Hypoxia, respiratory distress, XR bilateral infiltrates Supplemental oxygen, PPV/ETT
TACO (transfusion-associated circulatory overload) Hypervolemia in patients with history of CHF Hypoxia, respiratory distress, heart failure Supplemental oxygen, PPV/ETT, furosemide
Acute, Minor
Simple febrile reaction Cytokine-mediated Isolated fever Acetaminophen
Minor allergic reaction Response to transfused plasma proteins Urticaria, pruritus, flushing Diphenhydramine
Delayed
Delayed hemolysis Minor RBC antigens 5-10d, low-grade hemolysis  
GVHD Immunocompromised host Fever, rash, N/V, transaminitis, pancytopenia  
Massive Transfusion
Massive transfusion Large-volume, refrigerated products Coagulopathy, hypothermia, hypocalcemia, hyperkalemia, lactic acidosis

Bleeding Disorders

Overview

  • Disorders of primary hemostasis
    • General: present with mucocutaneous, post-operative bleeding
    • vWD
    • Platelet disorders
      • Medication-induced: NSAID, valproate, B-lactam, SSRI
      • Systemic disease: hepatic, renal failure
    • ITP: antibody-mediated platelet destruction
  • Disorders of secondary hemostasis
    • General: present with bleeding into soft-tissue, joints
    • Hemophilia A (VIII)
    • Hemophilia B (IX)
  • Disorders of both primary and secondary hemostasis
    • DIC
    • Liver disease
    • Severe vWD
  • Evaluation
    • PT: VII, vitamin K
    • PTT: VIII, IX, XI, XIII, vWD, heparin
    • Increased PT/PTT: XI, V, vitamin K, heparin, DIC
    • CBC: degree of anemia, platelet count, differential (hematopoetic disorders)
  • Management
    • Thrombocytopenia
      • Prophylactic transfusion for avoidance of spontaneous hemorrhage for platelet count <10,000
      • Transfusion for active bleeding at platelet count <50,000
      • Dosing
        • Adults: one RDP increases platelet count by 7-10,000
        • Pediatrics: 5-10ml/kg
      • ITP
        • Transfuse platelets for active bleeding
        • High-dose steroids (prednisone 1mg/kg)
        • IVIG (1g/kg/d)
      • Uremia
        • Hemodialysis
        • DDAVP (0.3ug/kg IV)
      • vWD
        • DDAVP (0.3ug/kg IV)
        • Severe: VWF (Humate-P) 40-80IU/kg
        • Tranexamic acid
      • Hemophilia A
        • Minor: 20IU/kg
        • Major: 50IU/kg
      • Hemophilia B
        • Minor: 40IU/kg
        • Major: 100IU/kg

DIC/TTP/HUS

  • Disseminated Intravascular Coagulation
    • Etiology: severe systemic illness/injury
      • Trauma, burn, crush
      • Sepsis
      • Malignancy
      • Obstetric complication: abruption, amniotic fluid embolism
      • Hemolytic anemia
    • Exam: petechiae/purpura, hemorrhage (puncture site, GI, GU, pulmonary)
    • Labs:
      • PT/PTT
      • Fibrinogen
      • CBC: schistocytes, thrombocytopenia
      • FDP/D-Dimer
    • Management
      • Treat underlying illness
      • Transfuse (PRBC, FFP for INR > 2, cryoprecipitate for fibrinogen < 100)
      • Heparin if apparent embolic events
      • Consult hematology
  • TTP/HUS
    • Presentation
      • Thrombocytopenia
      • Altered mental status
      • Renal dysfunction
      • Fever
      • MAHA
    • TTP: more commonly associated with altered mental status
      • Etiology: drugs, pregnancy, infection (HIV)
      • Mechanism: ULvWF uncleaved by dysfunctional ADAMTS-13
    • HUS: more commonly associated with renal dysfunction
      • Mechanism: toxin from E. coli, Shigella
      • Timing: 1-2wks after diarrheal illness
    • Evaluation
      • CBC: anemia, schistocytes, thrombocytopenia
      • PT/PTT (normal)
      • BUN/Creatinine
      • LDH
    • Management
      • Platelets contraindicated except as stopgap measure in ICH (can worsen process)
      • Plasma exchange with FFP (replaces functional ADAMTS-13)
      • Steroids (prednisone 1mg/kg daily)
      • Hematology consultation

Complications of anti-thrombotic therapy

  • Agents
    • Anti-platelet
      • TXA: Aspirin
      • ADP: clopidogrel, ticagrelor, prasugrel
      • GPIIb/IIIa: abciximab, eptifibatide, tirofiban
    • Anti-coagulants
      • Anti-thrombin: heparin, LMWH (enoxaparin, dalteparin)
      • Vitamin K antagonist: warfarn (anti-II, VII, IX, X)
      • Direct thrombin inhibitor: bivalirudin, argatroban, dabigatran
      • Xa inhibitor: rivaroxaban, apixaban
    • Fibrinolytics
      • Alteplase, tenectaplase
  • Complications
    • HIT: platelet count decrease >50% at 5 days

Summary of Management

Agent Reversal
Aspirin, clopidogrel 5-10U platelets

DDAVP 0.3ug/kg

GPIIb/IIIa Abciximab: 5-10U platelets

Eptifibatide/tirofiban: none

Heparin Protamine 1mg/100mg heparin in last 2-3 hours
LMWH Enoxaparin: 1mg/1mg

Dalteparin: 1mg/100U

Warfarin See supratherapeutic INR algorithm
DTI Dabigatran: Praxbind, hemodialysis, consider Factor VIIa
Xa PCC
Fibrinolytics 10U cryoprecipitate, 2U FFP, consider platelets and aminocaproic acid (4-5g IV)