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.

 

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.

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

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.

Palpitations

Brief H&P

48F with a history of Grave disease (off medications for 4 months), presenting with palpitations. Noted gradual onset of palpitations while at rest, describing a pounding sensation lasting 3-4 hours and persistent (though improved) on presentation. Symptoms not associated with chest pain, shortness of breath, loss of consciousness, nor triggered by exertion. She reported a history of 8-10 episodes in the past for which she did not seek medical attention. Review of systems notable only for heat intolerance.

On physical examination, vital signs were notable for tachycardia (HR 138bpm). No alteration in mental status, murmur, tremor or hyperreflexia appreciated.

Labs

  • Hb: 14.7
  • Urine hCG: negative
  • TSH: <0.01
  • Total T3: 311ng/dL
  • Free T4: 2.64ng/dL

ECG

Palpitations - Sinus Tachycardia

Sinus Tachycardia

Impression/Plan

Palpitations due to sinus tachycardia from symptomatic hyperthyroidism secondary to medication non-adherence. Improved with propranolol, discharged with methimazole and PMD follow-up.

Differential Diagnosis of Palpitations1, 2

Differential Diagnosis of Palpitations

Evaluation of Palpitations

History and Physical

Subjective description of symptom quality
Rapid and regular beating suggests paroxysmal SVT or VT. Rapid and irregular beating suggests atrial fibrillation, atrial flutter, or variable conduction block.
Stop/start sensation: PAC or PVC
Rapid fluttering: Sustained supraventricular or ventricular tachycardia
Pounding in neck: Produced by canon A waves from AV dissociation (VT, complete heart block, SVT)
Onset and offset
Random, episodic, lasting instants: Suggests PAC or PVC
Gradual onset and offset: Sinus tachycardia
Abrupt onset and offset: SVT or VT
Syncope
Suggests hemodynamically significant arrhythmia, often VT
Examination
Identify evidence of structural, valvular heart disease

ECG1

ECG Finding Presumed etiology
Short PR, Delta waves WPW, AVRT
LAA, LVH Atrial fibrillation
PVC, BBB Idiopathic VT
Q-waves Prior MI, VT
QT-prolongation VT (polymorphic)
LVH, septal Q-waves HCM
Blocks  

Algorithm for the Evaluation of Palpitations3

Algorithm for the Evaluation of Palpitations

References

  1. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med. 1998;338(19):1369-1373. doi:10.1056/NEJM199805073381907.
  2. Probst MA, Mower WR, Kanzaria HK, Hoffman JR, Buch EF, Sun BC. Analysis of emergency department visits for palpitations (from the National Hospital Ambulatory Medical Care Survey). The American Journal of Cardiology. 2014;113(10):1685-1690. doi:10.1016/j.amjcard.2014.02.020.
  3. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician. 2005;71(4):743-750.

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.

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)

Oncologic Emergencies

Overview

  •  Complications
    • Airway obstruction
    • PNA
    • Pleural effusion
    • Pericardial effusion
    • VTE
    • SVC syndrome
      • Symptoms: dyspnea (airway edema), chest fullness, blurred vision, headache (increased ICP)
    • Massive hemoptysis
      • Management: ETT (large-bore for bronschoscopy), affected side down
  • Brain Metastases
    • Cancers: melanoma, lung, breast, colorectal
    • Management: dexamethasone 10mg IV load, elevated HOB, hypertonic saline or mannitol, prophylactic anti-eplipetics
  • Meningitis
    • Pathogens: Listeria (ampicillin), Cryptococcus (amphotericin)
    • Evaluation: CSF sampling with cytology (diagnose leptomeningeal metastases)

Metabolic Disturbances

  • Hypercalcemia
    • Cancers: MM, RCC, lymphoma, bone metastases (breast, lung, prostate)
    • Mechanism: metastatic destruction, PTH-RP, tumor calcitriol
    • Prognosis: 50% 30-day mortality
    • Symptoms
      • Chronic: anorexia, nausea/vomiting, constipation, fatigue, memory loss
      • Acute: CNS (lethargy, somnolence)
    • Findings
      • Calcium: >13.0mg/dL
      • ECG: QT shortening
    • Treatment
      • Mild: IVF
      • Severe: IVF, loop diuretics, bisophosphanate (pamidronate 90mg IV infused over 4 hours), consider calcitriol, consider hemodialysis if cannot tolerate fluids or unlikely to respond to diuretics
  • Hyponatremia
    • Cancers: lung (small-cell), pancreatic, ovarian, lymphoma, thymoma, CNS
    • Mechanism: SIADH
    • Symptoms: muscle twitching, seizure, coma
    • Management: fluid restriction, if seizing administer 3% hypertonic saline at 100cc/hr until resolution
  • Hypernatremia
    • Mechanism: decreased intake, increased GI losses from chemotherapy
    • Management: cautious fluid resuscitation
  • Tumor Lysis Syndrome (TLS)
    • Cancers: hematologic, rapid-growth solid tumors
    • Mechanism: release of intracellular contents (uric acid, K, PO4, Ca)
    • Timing: 1-4 days after therapy (chemo, radiation)
    • Diagnosis
      • Uric acid >8mg/dL
      • Potassium >6mEq/L
      • Calcium <7mg/dL
      • PO4 >4.5mg/dL
      • Acute kidney injury
    • Management
      • IVF, allopurinol, rasburicase, urinary alkalinization
      • Consider hemodialysis if volume overloaded

Localized Complications

  • Musculoskeletal Complications
    • Spinal cord compression
      • Cancers: prostate, breast, lung, RCC, non-Hodgkin lymphoma, MM (5-10% of all cancer patients)
      • Sites: thoracic (60%), lumbosacral (30%), cervical (10%)
      • Symptoms: pain (worse lying flat, cough/sneeze, heavy lifting)
      • Evaluation: MRI (se 93%, sp 97%)
      • Management: dexamethasone 10mg IV load, 4mg q6h, neurosurgical consultation, radiation oncology consultation
    • Pathologic fracture
      • Features: sudden onset, low-force mechanism
  • Therapy Complications
    • Neutropenic fever
      • Definition: ANC <500 or ANC <1000 with expected nadir <500 (nadir typically occurs 5-10d after chemotherapy) with Tmax >38.3°C or >38.0°C for >1h
      • Examination: subtle signs of infection, thorough examination is critical (skin, catheter, perineum)
      • Treatment: carbapenem monotherapy, vancomycin if indwelling catheter, oncology consultation for colony stimulating factors
    • Chemotherapy-induced vomiting
      • Management: ondansetron with dexamethasone, consider NK-1 antagonist (aprepitant)

Hematologic Malignancies

  • Acute leukemia
    • Signs/Symptoms: leukopenia (infection), anemia (weakness/fatigue), thrombocytopenia (bleeding)
    • Diagnosis: >5% blasts
  • Thrombocytopenia
    • Management
      • No bleeding, goal >10,000
      • Fever, coagulopathy, hyperleukoctosis, goal >20,000
      • One unit of platelets increases count by 5,000
  • Hyperleukocytosis
    • Definition: WBC > 50-100k
    • Complications: microvascular congestion (pulmonary, cerebral, coronary)
    • Symptoms
      • CNS: confusion, somnolence, coma
      • Pulmonary: dyspnea, respiratory alkalosis
    • Management: cytoreduction (induction chemotherapy, increased risk TLS)
  • Hyperviscosity
    • Cancer: macroglobulinemia, MM
    • Symptoms: epistaxis, purpura, GIB, neuro deficits
    • Diagnosis: serum viscosity > 1.4-1.8
    • Management: emergent plasmapheresis
  • Polycythemia
    • Diagnosis: Hb >17
    • Differential: dehydration, hypoxia, smoking, altitude
    • Symptoms: HA, vertigo, angina, claudication, pruritus (after showering)
    • Complications: thrombosis (stroke), bleeding
    • Management: emergent phlebotomy (500cc if otherwise healthy)
  • Thrombocytosis
    • Diagnosis: platelet >1,000,000
    • Symptoms: vasomotor (HA, lightheadedness, syncope, chest pain, paresthesias)
    • Management: low-dose aspirin

Adrenal/Pituitary Emergencies

Adrenal Emergencies

  • Hormones: aldosterone, cortisol, androgens, catecholamines
  • Adrenal insufficiency
    • Primary
      • Causes
        • Autoimmune (associated with other endocrinopathies, PTH, DM)
        • Infection (TB, viral, meningococcemia)
        • Infiltration (sarcoidosis, amyloidosis)
        • Hemorrhage (trauma, anti-coagulation)
        • Malignancy (primary, metastatic)
      • Signs/Symptoms
        • AMS
        • Hypotension (refractory)
        • GI: anorexia, nausea/vomiting, diarrhea
        • Hyperpigmentation
      • Labs
        • Hyponatremia
        • Hyperkalemia
        • Hypercalcemia
        • Mild metabolic acidosis
        • Hypoglycemia
    • Secondary
      • Causes
        • Iatrogenic (>5mg prednisone/day for > 2 weeks)
        • Pituitary/sellar tumors
        • Hemorrhage (Sheehan)
        • Cranial radiation
      • Signs/Symptoms
        • RAAS function maintained, hypotension rare
        • Features of pituitary/hypothalamic dysfunction: menstrual disturbances, headache, vision changes, galactorrhea, acromegaly
    • Adrenal Crisis
      • Precipitated by physiologic stressor: sepsis, MI, trauma, surgery
      • Diagnosis
        • AM cortisol <3
        • ACTH stimulation peak cortisol <15
        • ACTH level
      • Management
        • Glucose management
        • Fluid resuscitation
        • Dexamethasone 10mg IV
        • Identify and treat precipitant

Cushing syndrome

  • Causes
    • Pituitary adenoma (Cushing disease)
    • Malignancy (ACTH-producing): SCLC, pancreatic, carcinoid
    • Adrenal neoplasm
  • Signs/Symptoms
    • Obesity, fat deposition in face, neck
    • Skin atrophy with striae
    • Proximal myopathy
    • Hypertension

Pheochromocytoma

  • Familial: MEN 2A/2B, NF, Von Hippel-Lindau
  • Signs/Symptoms
    • Refractory hypertension (paroxysmal)
    • Heat intolerance, sweating, weight loss
  • Diagnosis
    • 24h urine metanephrine, catecholamine
    • CT/MRI

Hypopituitarism

  • Adenoma
    • Symtoms/Signs
      • Headache
      • Vision changes (bitemporal hemianopsia)
      • Cavernous sinus involvement (CN III, IV, V1, V2, VI)
  • Ischemic necrosis
    • Sickle cell disease, vasculitis, cavernous sinus thrombosis, infection, TBI, post-partum (Sheehan)
  • Pituitary apoplexy
    • Acute loss of pituitary function from infection/hemorrhage, rarely tumor
    • Symptoms/Signs
      • Abrupt onset headache
      • Vision changes
      • Meningismus
      • ALOC

Thyroid Emergencies

Hyperthyroidism

Symptoms

Constitutional Weight loss, heat intolerance, perspiration
Cardiopulmonary Palpitations, chest pain, dyspnea
Neuropsychiatric Tremor, anxiety, double vision, muscle weakness
Neck Fullness, dysphagia, dysphonia
Musculoskeletal Extremity swelling
Reproductive Irregular menses, decreased libido, gynecomastia

Signs

Vital signs Tachycardia, widened pulse pressure, fever
Cardiovascular Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur
Ophthalmologic Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze
Neurologic Tremor, hyperreflexia, proximal muscle weakness
Dermatologic Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia
Neck Enlarged or nodular thyroid

Causes

  • Grave disease
    • Mechanism: thyroid-stimulating antibodies
    • Female > Male (10x)
    • Findings: ophthalmopathy (lid lag), infiltrative dermopathy (pretibial)
  • Toxic adenoma, toxic multinodular goiter
    • Mechanism: Excess thyroid hormone production
  • Thyroiditis
    • Mechanism: inflammation results in increased thyroid hormone release, typically followed by depletion and TSH suppression resulting in hypothyroidism
    • Signs/symptoms: tachycardia, weight loss, irritability, sweating, anxiety, heat intolerance
    • Subacute thyroiditis
      • Post-viral
      • Symptoms: hoarseness, dysphagia, painful thyroid
    • Hashimoto
      • Typically hypothyroidism
    • Drug-induced: Lithium, amiodarone
    • Trauma: surgical, direct

Thyroid Storm

  • Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).
  • Precipitants
    • Medical: Sepsis, MI, CVA, CHF, PE, visceral ischemia
    • Trauma: Surgery, blunt, penetrating
    • Endocrine: DKA, HHS, hypoglycemia
    • Drugs: Iodine, amiodarone, inhaled anesthetics
    • Pregnancy: post-partum, hyperemesis gravidarum
  • Scoring (Burch, Wartofsky)
  • Management
    • Supportive measures
      • Volume resuscitation (with MVI, Thiamine) and cooling
      • Benzodiazepines for agitation
    • Beta-blockade
      • Propranolol 60-80mg PO q4h
      • Propranolol 0.5-1.0mg IV, repeat q15min then 1-2mg q3h
      • Esmolol continuous infusion
    • MTZ/PTU 1-hour prior to iodine
      • Methimazole 20mg (except pregnancy)
      • Propylthiouracil 600mg (hepatotoxic)
    • Steroids: dexamethasone
    • Iodine
    • Endocrinology consultation

Hypothyroidism

Symptoms

Constitutional Weight gain, cold intolerance, fatigue
Cardiopulmonary Dyspnea, decreased exercise capacity
Neuropsychiatric Impaired concentration and attention
Musculoskeletal Extremity swelling
Gastrointestinal Constipation
Reproductive Irregular menses, erectile dysfunction, decreased libido
Integumentary Coarse hair, dry skin, alopecia, thin nails

Signs

Vital signs Bradycardia, hypothermia
Cardiovascular Prolonged QT, increased ventricular arrhythmia, accelerated CAD, diastolic heart failure, peripheral edema
Neurologic Lethargy, slowed speech, agitation, seizures, ataxia/dysmetria, mononeuropathy, delayed relaxation of reflexes
Musculoskeletal Proximal myopathy, pseudohypertrophy, polyarthralgia
Gastrointestinal Ileus

Causes

  • Hashimoto: auto-antiboids
  • Thyroidectomy
  • Radiation, radioactive iodine ablation

Myxedema Coma

  • Precipitants
    • Critical illness: sepsis (especially PNA), CVA, MI, CHF, trauma, burns
    • Endocrine: DKA, hypoglycemia
    • Drugs: amiodarone, lithium, phenytoin, rifampin, medication non-adherence
    • Environmental: cold exposure
  • Recognition
    • History: hypothyroidism, thyroidectomy scar and acute precipitating illness
    • Hypothermia: temp <95.9°F (or normal in presence of infection)
    • AMS: lethargy, confusion, coma, agitation, psychosis, seizures
    • Hypotension: refractory to volume resuscitation and pressors
    • Bradypnea: with hypercapnia and hypoxia
    • Skin: non-pitting edema of face and hands
    • Hyponatremia
  • Management
    • Airway protection
    • Fluid resuscitation
    • Thyroid hormone replacement
      • Young, otherwise healthy patients: T3 10ug IV q4h
      • Elderly, cardiac compromise: 300ug IV x1
      • Steroids: dexamethasone 1h prior to thyroid hormone
    • Treat precipitating illness

Interpretation of Thyroid Function Tests

Condition TSH T4
None Normal Normal
Hyperthyroidism Low High
Hypothyroidism High Low
Subclinical hyperthyroidism Low Normal
Subclinical hypothyroidism High Normal
Sick euthyroid Low Low

Acid-Base Disturbances

Method

  • Primary disturbance (acidemia/alkalemia)
  • Primary process (metabolic/respiratory)
  • Presence of mixed disorder
    • Increase PCO2 of 10, increases HCO3 by 1 (acute) or 3 (chronic)
    • Decreased PCO2 of 10, decreases HCO3 by 2 (acute) or 5 (chronic)
    • Increase HCO3 of 1, increases PCO2 by 0.7
    • Decreased HCO3, add 15, result should equal PCO2 and number after decimal of pH
  • Anion gap

Causes

  • Anion Gap
    • Methanol
    • Uremia
    • DKA/AKA
    • Paraldehyde, propylene glycol
    • INH
    • Lactate
    • Ethylene glycol
    • Salicylate
  • Non-Anion Gap
    • Fistulae
    • Ureteral fistulae
    • Saline
    • Diarrhea
    • Carbonic anhydrase inhibitors
    • Spironolactone
    • RTA
  • Metabolic Alkalosis
    • Vomiting
    • Volume depletion
    • Diuretics
    • Steroids
  • Respiratory Acidosis
    • CNS lesion
    • Myopathies
    • Chest wall abnormalities
    • Obstructive lung disease
  • Respiratory Alkalosis
    • Anxiety
    • Fever
    • Hyperthyroidism
    • Hypoxia
    • Sympathomimetic

See Also

Hypoglycemia

Case 1

In the medical intensive care unit, a patient who had sustained a cardiac arrest with return of spontaneous circulation but no recovery of neurological function develops septic shock complicated by end-stage renal disease, shock liver, and now refractory hypoglycemia.

Case 2

An approximately 60 year-old male with diabetes is brought in by ambulance after family called 911 for unresponsiveness. His initial glucose was 35mg/dL, his home medications are unknown.

Symptoms

  • Autonomic: tremor, palpitations, anxiety, diaphoresis
  • Neuroglycopenic: cognitive impairment, psychomotor, seizure, coma

Diagnosis

  • Serum glucose <60mg/dL
  • Generally symptomatic at <55mg/dL though threshold is variable depending on chronicity
  • Whipple Triad:
    • Symptoms suggestive of hypoglycemia
    • Low glucose
    • Resolution of symptoms after administration of glucose

Differential Diagnosis of Hypoglycemia

Differential Diagnosis of Hypoglycemia

Common Anti-hyperglycemic Drugs and Pharmacology

Drug Pharmacology
Onset Peak Duration
Rapid-acting insulin

  • Aspart (Novolog)
  • Lispro (Humalog)
15-30min 1-2h 3-5h
Short-acting insulin

  • Regular
30-60min 2-4h 6-10h
Intermediate-acting insulin

  • NPH
1-3h 4-12h 18-24h
Long-acting insulin

  • Glargine (Lantus)
2-4h None 24h
Sulfonylurea

  • Glimepiride
  • Glipizide (Glucotrol)
  • Glyburide (Glycron, Micronase)
2-6h 12-24h

Evaluation of Hypoglycemia

Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. In severely ill patients, consider:

  • BMP
  • LFT
  • EtOH
  • Infectious workup: CXR, UA, urine and blood cultures
  • ECG, troponin
  • Other studies: insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies

Management and Monitoring

Management and Monitoring of Hypoglycemia

Disposition

Admission or observation for oral anti-hyperglycemic agent or intermediate- to long-acting insulin. Consider discharge after 4h uneventful observation if:

  • Hypoglycemia fully and rapidly reversed without continuous infusion of dextrose
  • Tolerated a full meal in ED
  • Clear and innocuous cause identified with recurrence unlikely
  • Adequate patient understanding, home support/monitoring, and ability to detect/prevent recurrence with close primary care follow-up

References:

  1. Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.
  2. Service, FJ. Hypoglycemia in adults: Clinical manifestations, definition, and causes. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on March 18, 2016.)
  3. Service FJ. Hypoglycemic disorders. N Engl J Med. 1995;332(17):1144–1152. doi:10.1056/NEJM199504273321707.
  4. Krinsley JS, Grover A. Severe hypoglycemia in critically ill patients: risk factors and outcomes. Critical Care Medicine. 2007;35(10):2262–2267. doi:10.1097/01.CCM.0000282073.98414.4B.
  5. Lacherade J-C, Jacqueminet S, Preiser J-C. An overview of hypoglycemia in the critically ill. J Diabetes Sci Technol. 2009;3(6):1242–1249.

Portal Venous Gas

Brief HPI

Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.

Imaging

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CT Abdomen/Pelvis with Contrast

Inflammatory changes in the right lower quadrant concerning for ruptured appendicitis with approximately 9 cm abscess.
Gas in the liver likely representing portal venous gas which can be seen in the setting of appendicitis vs less likely secondary to bowel ischemia.

Differentiation between Portal Venous Gas and Pneumobilia

Portal venous gas vs. Pneumobilia

References

  1. Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia. http://radiopaedia.org/articles/pneumobilia.
  2. Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia. http://radiopaedia.org/articles/portal-venous-gas
  3. Sebastià C, Quiroga S, Espin E, Boyé R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):1213–24–discussion1224–6. doi:10.1148/radiographics.20.5.g00se011213.
  4. Sherman SC, Tran H. Pneumobilia: benign or life-threatening. J Emerg Med. 2006;30(2):147-153. doi:10.1016/j.jemermed.2005.05.016.

Epiglottitis

Brief H&P:

30 year-old male with no significant medical history presenting with 24 hours of progressively worsening throat pain, difficulty swallowing and voice hoarseness. He reports subjective fevers and chills.
Vital signs notable for Tmax 38.4°C. On physical examination, the patient was sitting upright, unable to swallow secretions with faint inspiratory stridor and dysphonia (though he was able to speak in full sentences and without apparent respiratory distress). Oropharyngeal examination showed minimal right parapharyngeal edema without uvular or palatal deviation and there was exquisite right lateral neck tenderness to palpation.

Labs

  • CBC: 24.2/14.4/43.4/202
  • Wound culture: MSSA
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CT Neck/Soft Tissue with Contrast

Edema of the oropharynx/hypopharynx, consistent with epiglottitis and early abscess formation.

ED/Hospital Course

The patient acutely decompensated prior to fiberoptic laryngoscopy and proceeded emergently to the operating room for controlled intubation. The operative report described the following findings: “The patient had diffuse edema of the posterior oropharyngeal wall. The epiglottis was severely thickened, Omega shaped, soft to palpation and with moderate pressure, it appeared to come to a head and pus was expressed from the lingual side of the epiglottis.” The patient was extubated on hospital day three and discharged soon thereafter, he was doing well on follow-up.

Evaluation of Sore Throat – Applied

Evaluation of Sore Throat - Applied

Spinal Epidural Abscess

Case Presentation

HPI:

34M with no PMH presenting with joint pain and rash. The patient was in his usual state of good health until 1 week prior to presentation, noting bilateral shoulder pain. Diagnosed with musculoskeletal process at outside hospital and discharged with analgesics. Presented with partner due to worsening pain involving multiple joints, a non-painful, non-pruritic rash on bilateral lower extremities, and apparent confusion/hallucinations. Social history was non-contributory, no recent procedures or instrumentation.

Objectively, vital signs were notable for tachycardia and elevated core temperature. The patient was ill-appearing, disoriented and unable to provide detailed history. Skin examination was notable for non-blanching petechial rash with areas of confluence most dense in anterior distal lower extremities, rarer proximally, and otherwise without palm/sole involvement. Mucous membranes were dry, neck was supple. There was tenderness to palpation and manipulation of bilateral shoulders. No back tenderness to palpation or percussion was identified. Neurological examination notable for disorientation, intact cranial nerve function, pain-limited weakness in bilateral upper extremities particularly shoulder abduction, and 4/5 hip flexion, knee flexion/extension in bilateral lower extremities.

Labs:

  • CBC: 34.0/11.8/35.7/216
  • Differential: 31 bands
  • INR: 1.94
  • BMP: 131/5.3/102/17/88/2.55/215
  • LFT: AST 93, ALT 57, AP 237, TB 2.9, DB 1.9, Alb 1.4
  • Lactate: 3.3
  • UA: 47WBC, 5RBC
  • Utox: Negative
  • ESR: 83, CRP: 11.9
  • HIV: Nonreactive

Radiology

  • CT head: Negative
  • CXR: Negative
  • XR Shoulder: Negative
  • CT Chest/Abdomen/Pelvis non-contrast: Mild bilateral hydrouereter/hyndronephrosis, L4-L5 grade 2 anterolisthesis.
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MRI Lumbar Spine w/contrast

Diffuse epidural enhancement posterior to the L4 and L5 vertebral bodies compressing the thecal sac and resulting in moderate severe spinal canal stenosis. Rim enhancement of the 1.5 cm left paraspinal fluid that may be within the L4 tendon sheath or simply paraspinal abscess.

Assessment/Plan:

Severe sepsis with end-organ dysfunction, unclear source (urinary tract involvement unlikely to account for severity of illness). Covered empirically with broad-spectrum anti-microbials including CNS infection given component of encephalitis. Admitted to the intensive care unit.

Hospital Course:

On hospital day 1, the patient underwent non-contrast MRI of the entire neuraxis with findings concerning for L4-L5 and L5-S1 epidural and paraspinal infection resulting in moderate-severe spinal canal stenosis. Blood and urine cultures grew gram-positive cocci in clusters.

On hospital day 2, the patient became increasingly somnolent. Repeat examination by consulting neurology service was concerning for evidence of meningeal irritation. Cultures speciated as methicillin-sensitive staphylococcus aureus and oxacillin was added. MRI was repeated with gadolinium, findings concerning for L4 epidural vs. paraspinal abscess.

On hospital day 3, the patient’s mental status continued to worsen and he was intubated for airway protection. Neurosurgical intervention was deferred due to deteriorating clinical status. Shoulder synovial fluid aspirate culture positive for MSSA, orthopedic surgery consulted for washout/serial arthrocentesis. TTE performed without evidence of valvular vegetation.

On hospital day 4, additional warm joints were aspirated by orthopedic surgery including knee, bilateral ankles, and shoulder each of which ultimately grew MSSA.

On hospital day 6, the patient underwent OR washout of affected joints with intraoperative findings of purulent fluid. TEE performed without evidence of valvular vegetation. The following day, underwent fluoroscopically-guided lumbar puncture, CSF studies inconclusive. Rifampin added for high-grade bacteremia with multiple seeded sites.

The patient was extubated on hospital day 9 and transferred out of the intensive care unit. The following day, he became increasingly tachypneic with evidence of volume overload on examination and was intubated and returned to the intensive care unit. Sustained PEA arrest post-intubation with ROSC, possibly secondary to pneumothorax vs. hypoxia from extensive mucous plugging. Required increasing vasopressor support over the subsequent 12 hours, emergent CVVHD for worsening academia and hypervolemia. The patient sustained another arrest and ultimately expired.

The final impression was that of high-grade bacteremia from unclear source (vague history of proximate hand laceration/infection) with resultant seeding of epidural/paraspinal space, urinary tract, multiple joints, and likely CNS/meninges. Review of abdominal ultrasonography with evidence of cirrhosis, suggesting that some component of initial hepatic synthetic dysfunction may have been chronic and this may have increased the patient’s risk for disseminated infection and SEA. Neurosurgical intervention was not pursued due to unstable clinical status and as the patient’s neurological findings were not consistent with the location of the identified lesion.

Spinal Epidural Abscess (SEA)1

Risk factors:

  • Immunocompromise: diabetes, cirrhosis, CKD, HIV/AIDS
  • Anatomic: DJD, trauma, prior surgery
  • Introduction: IVDA, epidural anesthesia, tattoo

Organism:

  • S. aureus, 2/3
  • S. epidermidis (associated with device, instrumentation)
  • E. coli (urine spread)
  • P. aeruginosa (IVDA)
  • Rare: anaerobes, mycobacteria, fungi

Staging:

  1. Back pain at affected site
  2. Nerve root pain from affected level
  3. Weakness, sensory deficit, bladder/bowel dysfunction
  4. Paralysis

Clinical features:

  • Back pain (75%)
  • Fever (50%)
  • Neuro deficit (33%)

Diagnosis:

  • Labs: Leukocytosis, ESR/CRP, blood cultures
  • Imaging: MRI with gadolinium, 90% sensitivity
  • Clinical findings and laboratory studies are insensitive and non-specific, in one study, approximately ½ of patients had >2 visits.

Prevalence of abnormal physical findings 2

Finding Prevalence
Fever (T>38°C) 19-32%
Focal spinal TTP 52-62%
Diffuse spinal TTP 63-65%
Positive SLR 11-13%
Abnormal sensation 17-27%
Weakness 29-40%
Abnormal reflexes 8-17%
Abnormal rectal tone 5-10%
Saddle anesthesia 2%

Clinical Decision Guideline 3

Spinal Epidural Abscess Clinical Decision Guideline

Management:

  • Neurosurgical evacuation/fusion
  • Antibiotics (vancomycin, oxacillin, cefepime)
  • Neurosurgical intervention may not result in neurological recovery if symptoms present for > 24-36 hours and may be impractical in the setting of panspinal infection.

References:

  1. Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012–2020. doi:10.1056/NEJMra055111.
  2. Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. 2004;26(3):285–291. doi:10.1016/j.jemermed.2003.11.013.
  3. Davis DP, Salazar A, Chan TC, Vilke GM. Prospective evaluation of a clinical decision guideline to diagnose spinal epidural abscess in patients who present to the emergency department with spine pain. J Neurosurg Spine. 2011;14(6):765–770. doi:10.3171/2011.1.SPINE1091.
  4. WikEM: Epidural abscess (spinal)

Nonsustained Ventricular Tachycardia

Case 1

64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.

In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.

Evaluation and Management:

  • NSVT with known (severe) ischemic heart disease
  • For repetitive monomorphic ventricular tachycardia: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)1

ECG’s

ECG 1
ECG 1

ECG 1

Non-specific IVCD, LAA, VPC

ECG 2
ECG 2

ECG 2

VT initiated by fusion complex

Case 2

31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.

In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.

Evaluation and Management:

  • NSVT progressing to VT
  • Initially attributed to electrolyte disturbances. However, serial ECG’s continued to show prolonged QTc (possibly acquired, home medications included metoclopramide and erythromycin). Early echocardiography demonstrated global hypokinesis with EF 30-35% attributed to severe sepsis and recurrent defibrillation. Cardiac CT after resolution of acute illness showed persistently depressed ejection fraction without coronary atherosclerosis. The presence of NICM associated with malignant dysrhythmias warranted ICD placement.
  • Cardioversion for hemodynamic compromise (I, B), B-blockade (I, B), amiodarone if no LQTS (I, C), urgent angiography if ischemia not excluded (I, C)1
  • Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.2

ECG’s

ECG 1
ECG 1

ECG 1

Ventricular bigeminy

ECG 2
ECG 2

ECG 2

Long-QT

VT on Telemetry
VT on Telemetry

VT on Telemetry

Non-sustained ventricular tachycardia noted on telemetry monitoring

Definition3,4

  • > 3-5 consecutive beats originating below the AV node
  • Rate > 100bpm
  • Duration <30s

Epidemiology3,5

  • Occurs in 0-4% of ambulatory patients
  • Increased frequency in males and with increasing age
  • In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.6,7,8

Evaluation

In all patients:
History: including arrhythmogenic medications/substances, pertinent family history
Physical examination
ECG/CXR
TTE
In selected patients:
Exercise testing
Advanced imaging (CT/C-MR)
Electrophysiologic studies
Genetic testing

NSVT in the absence of structural heart disease

NSVT in Idiopathic Ventricular Tachycardia

Ventricular outflow arrhythmias:
RVOT: 70-80%, LBBB pattern
LVOT: 20-30%, RBBB pattern
Mechanism:
Adrenergically mediated
Occur during exercise, resolve as heart-rate increases, recur during recovery
Management:
Exclude arrhythmogenic right ventricular cardiomyopathy (imaging, myocardial biopsy)
If symptomatic, beta-blockade, ± IC anti-arrhythmic, CCB (verapamil) for ILVT
Prognosis:
Good, rare tachycardia-induced cardiomyopathy, rare SCD

NSVT in Polymorphic Ventricular Tachycardia

Mechanism
LQTS (acquired or inherited)
Familial catecholaminergic polymorphic VT
Management
Symptomatic (ex. syncope, cardiac arrest): ICD
Asymptomatic QTc > 550ms: consider ICD
Prognosis
Increased risk SCD

Arrhythmogenic Right Ventricular Cardiomyopathy

Mechanism
Fibrosis, fibro-fatty replacement of myocardium in RVIT/RVOT/RV apex
May occur with only subtle structural abnormalities of the right ventricle
LBBB morphology
Management
Anti-arrhythmics of limited utility
Catheter ablation, ICD backup
Prognosis
Increased risk SCD

NSVT with apparent structural heart disease1

Hypertension and LVH

Mechanism
Stretch-induced abnormal automaticity
Fibrotic tissue
Presence of NSVT correlates with degree of hypertrophy and subendocardial fibrosis
Management
Evaluation for ischemic heart disease
Aggressive medical management of hypertension (including beta-blockade)
Prognosis
Unclear

Valvular Disease

Mechanism
High incidence in AS, severe MR (25%)
Mechanical stress from dysfunctional valvular apparatus
Management
Beta-blockade if symptomatic
Prognosis
No evidence that NSVT is an independent predictor of SCD.

Ischemic Heart Disease9-14

Mechanism
Monomorphic VT associated with re-entry at the borders of ventricular scars
Ischemia induces polymorphic NSVT/VF
Management
Revascularization, beta-blockade, statin, ACE/ARB
MADIT I, MUSTT: ICD for ICM LVEF <40%, NSVT, EPS inducible VT
MADIT II, SCD-HeFT: ICD for moderate-to-severe LV dysfunction irrespective of NSVT or EPS findings
Prognosis
NSTEMI with NSVT >48h after admission 2x risk SCD (MERLIN-TIMI 36)
STEMI with NSVT common, not as predictive of ACM or SCD as LVEF (CARISMA)
NSVT <24h after admission for NSTEMI/STEMI not of prognostic significance.

Hypertrophic Cardiomyopathy

Mechanism
Genetic myocardial disease
Myocyte disarray, fibrosis, ischemia result in arrhythmogenic substrate
Management
Restriction of physical activity
ICD (NSVT, LV thickness, FH SCD, syncope, abnormal BP response to exercise)
Beta-blockade, anti-arrhythmic for symptoms
Prognosis
Increased risk SCD (1% annual)

Other Conditions

  • Non-ischemic dilated cardiomyopathy
  • Giant-cell myocarditis
  • Repaired TOF
  • Amyloidosis
  • Sarcoidosis
  • Chagas cardiomyopathy

Algorithm for the Evaluation of NSVT1

Algorithm for the Evaluation of Nonsustained Ventricular Tachycardia

References

  1. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death–executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(17):2099–2140. doi:10.1093/eurheartj/ehl199.
  2. Higham PD, Adams PC, Murray A, Campbell RW. Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study. Q J Med. 1993;86(9):609–617.
  3. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol. 2012;60(20):1993–2004. doi:10.1016/j.jacc.2011.12.063.
  4. Katritsis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J. 2004;25(13):1093–1099. doi:10.1016/j.ehj.2004.03.022.
  5. Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.
  6. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890. doi:10.1056/NEJM199912163412503.
  7. Jouven X, Zureik M, Desnos M, Courbon D, Ducimetière P. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med. 2000;343(12):826–833. doi:10.1056/NEJM200009213431201.
  8. Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.
  9. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989;321(6):406–412. doi:10.1056/NEJM198908103210629.
  10. Goldstein S. Propranolol therapy in patients with acute myocardial infarction: the Beta-Blocker Heart Attack Trial. Circulation. 1983;67(6 Pt 2):I53–7.
  11. Moss AJ. MADIT-I and MADIT-II. J Cardiovasc Electrophysiol. 2003;14(9 Suppl):S96–8.
  12. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996;335(26):1933–1940. doi:10.1056/NEJM199612263352601.
  13. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890. doi:10.1056/NEJM199912163412503.
  14. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225–237. doi:10.1056/NEJMoa043399.
  15. WikEM: Nonsustained Ventricular Tachycardia

Low Voltage ECG

Definition

  • QRS in limb leads <5mm
  • QRS in precordial leads <10mm

General Causes

  • Fluid, fat or air attenuating signal
  • Myocardial infiltration
  • Loss of viable myocardium

Example

Low Voltage ECG
Low Voltage ECG

Low Voltage ECG

ECG of patient with pericardial effusion

Baseline ECG
Baseline ECG

Baseline ECG

Old ECG from same patient

Differential Diagnosis of Low Voltage ECG

Differential Diagnosis of Low Voltage ECG

References

  1. Madias JE. Low QRS voltage and its causes. J Electrocardiol. 2008;41(6):498–500. doi:10.1016/j.jelectrocard.2008.06.021.
  2. WikEM: Low ECG voltage