Hyponatremia

HPI:

A 62 year-old male with a history of hepatitis C cirrhosis complicated by hepatocellular carcinoma s/p radiofrequency ablation presenting after referral from hepatology clinic for hyponatremia. One week ago, the patient developed abdominal distension and shortness of breath that resolved after large-volume paracentesis and was started on furosemide 40mg p.o. daily and aldactone 100mg p.o. daily. After initiating diuretics, the patient noted worsening lower extremity edema, and increased thirst/fluid intake.

He reports two days of fatigue and intermittent confusion supported by family members who reported slowed speech. He otherwise denies abdominal pain, distension, nausea/vomiting, diarrhea/constipation, chest pain or shortness of breath. In the ED, the patient received 1L NS bolus.

PMH:

  • Hepatitis C cirrhosis c/b HCC s/p RFA
  • Rheumatoid arthritis

PSH:

  • None

Family History:

  • Non-contributory.

Social History:

  • Lives with partner, denies current or prior t/e/d abuse
  • HepC contracted from blood transfusions

Medications:

  • Furosemide 40mg p.o. daily
  • Spironolactone 100mg p.o. daily
  • Rifaximin 550mg p.o. b.i.d.

Allergies:

  • NKDA

Physical Exam:

VS: T 98.2 HR 80 RR 14 BP 95/70 O2 98% RA
Gen: Elderly male in no acute distress, alert and answering questions appropriately.
HEENT: NC/AT, PERRL, EOMI, faint scleral icterus, MMM.
CV: RRR, normal S1/S2, no murmurs. JVP 8cm.
Lungs: Faint basilar crackles on bilateral lung bases.
Abd: Normoactive bowel sounds, mildly distended but non-tender, without rebound/guarding.
Ext: 2+ pitting edema in lower extremities to knees bilaterally. 2+ peripheral pulses, warm and well perfused.
Neuro: AAOx3. CN II-XII intact. No asterixis. Normal gait. Normal FTN/RAM.

Labs/Studies:

  • BMP (admission): 112/5.6/88/22/28/1.1/97
  • BMP (+10h): 118/5.4/93/23/26/1.0/133
  • sOsm: 264
  • Urine: Na <20, K 26, Osm 453
  • BNP: 40
  • AST/ALT/AP/TB/Alb: 74/57/91/2.4/2.2

Assessment/Plan:

62M with HepC cirrhosis, with e/o decompensation (new-onset ascites) and hyponatremia.

  1. #Hyponatremia: Sodium 114, likely chronic, patient currently asymptomatic without concerning findings on neurological exam. Clinical findings suggestive of hypervolemic hyponatremia 2/2 decompensated cirrhosis resulting in decreased effective arterial blood volume and volume retention. However, the recent initiation of diuretics, mild AKI and early response to isotonic fluids in the ED suggests possible hypovolemic component.
    • 1L fluid restriction
    • q.4.h. sodium check, goal increase of 8mEq per 24h
    • hold diuretics
  2. #Hyperkalemia: Potassium 5.6, asymptomatic, AKI vs. medication-induced (aldactone). Continue monitoring.
  3. #AKI: Elevated creatinine 1.1 from baseline 0.7. Likely pre-renal given recent initiation of diuretics. Consider hepatorenal syndrome given decompensated cirrhosis. Follow-up repeat creatinine after 1L NS bolus in ED.
  4. #Hepatitis C: decompensated with new-onset ascites. No e/o encephalopathy, continue home rifaximin.

Physiology of Hyponatremia: 1,2,3,4

Physiology of Hyponatremia

Differential Diagnosis of Hyponatremia: 5

Differential Diagnosis of Hyponatremia

Evaluation of Hyponatremia: 2

  1. Identification of onset (acute vs. chronic)
  2. Presence of symptoms (HA, nausea, confusion, seizures)
  3. Assessment of volume status (edema, JVD, skin turgor, postural BP)
  4. Medical history (cardiac, liver, renal disease), drug history

References:

  1. Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatremia: a little physiology goes a long way. Cleve Clin J Med. 2004;71(8):639–650.
  2. Biswas M, Davies JS. Hyponatraemia in clinical practice. Postgrad Med J. 2007;83(980):373–378. doi:10.1136/pgmj.2006.056515.
  3. Adrogué HJ, Madias NE. Hyponatremia. N. Engl. J. Med. 2000;342(21):1581–1589. doi:10.1056/NEJM200005253422107.
  4. Marx JA, Hockberger RS, Walls RM, Adams JG. Rosen’s emergency medicine: concepts and clinical practice. 2010;1.
  5. Milionis HJ, Liamis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ. 2002;166(8):1056–1062.

Transfusion Reactions

Brief HPI:

A 28 year-old female with a history of systemic lupus erythematosus and end-stage renal disease without access to scheduled hemodialysis presents to the emergency department with 1 week of worsening dyspnea, fatigue and leg swelling. Her symptoms are reminiscent of prior episodes resolving with hemodialysis. On evaluation, vital signs are normal and laboratory tests demonstrate microcytic anemia (Hb 5.9g/dL) but no hyperkalemia. A plain chest radiograph is normal and the patient ambulates without hypoxia.

The patient was deemed to not meet any requirements for emergent hemodialysis. One unit of packed red blood cells was ordered for transfusion for symptomatic anemia. During transfusion, the patient developed worsening dyspnea and was found to be hypertensive and hypoxic. A chest radiograph was obtained and is shown below.

Chest x-ray with pulmonary edema

Pulmonary vascular congestion and bilateral pleural effusions.


The transfusion was discontinued, the patient was placed on non-invasive positive pressure ventilation, and emergent hemodialysis was initiated with subsequent resolution of presumed transfusion associated circulatory overload.

Algorithm for the Evaluation and Management of Transfusion Reactions

Algorithm for the Evaluation and Management of Transfusion Reactions

This algorithm was developed by Dr. Eric Madden, chief resident in emergency medicine at McGovern Med EM.

References

  1. Carson JL, Triulzi DJ, Ness PM. Indications for and Adverse Effects of Red-Cell Transfusion. N Engl J Med. 2017;377(13):1261-1272. doi:10.1056/NEJMra1612789.
  2. Delaney M, Wendel S, Bercovitz RS, et al. Transfusion reactions: prevention, diagnosis, and treatment. Lancet. 2016;388(10061):2825-2836. doi:10.1016/S0140-6736(15)01313-6.
  3. Goel R, Tobian AAR, Shaz BH. Noninfectious transfusion-associated adverse events and their mitigation strategies. Blood. 2019;133(17):1831-1839. doi:10.1182/blood-2018-10-833988.
  4. Osterman JL, Arora S. Blood product transfusions and reactions. Emerg Med Clin North Am. 2014;32(3):727-738. doi:10.1016/j.emc.2014.04.012.
  5. Silvergleid AJ. Approach to the patient with a suspected acute transfusion reaction. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on September 01, 2019.)
  6. Suddock JT, Crookston KP. Transfusion Reactions. January 2019.

Hypertensive Emergency

Brief HPI:

A 62 year-old female with a history of hypertension, diabetes and coronary artery disease is brought to the emergency department with altered mental status. The patient is confused and unable to provide history. Her family note that symptoms have been gradually worsening for the past one day and she had previously been in her usual state of good health. There was no history of recent illness, medication changes, recreational substance use, sick contacts, or travel.

On evaluation, vital signs were notable for hypertension (224/120mmHg, comparable on all extremities) though otherwise normal including afebrile core temperature – capillary glucose was 114mg/dL. On examination, the patient was awake and alert, making coordinated movements symmetrically in all four extremities without hyperreflexia or increased tone. Speech was unintelligible and the patient was unable to follow simple commands.

Labs/Imaging

Laboratory tests were notable for a serum creatinine of 1.2mg/dL (baseline unknown) but otherwise normal including CBC, troponin, TSH, and UA. ECG demonstrated left ventricular hypertrophy without acute ischemic changes. Imaging including chest radiograph and CT head non-contrast and CTA brain/neck were normal. Lumbar puncture was performed and CSF was normal.

Hospital Course

The patient was initiated on a continuous infusion of nicardipine for presumed hypertensive encephalopathy and admitted to the medical intensive care unit. An MRI was performed on hospital day 1 and demonstrated chronic microvascular ischemic changes. The patient’s mental status gradually improved over the course of her hospitalization and she was discharged home on hospital day 4.

An Algorithm for the Evaluation and Management of Hypertensive Emergencies

An Algorithm for the Evaluation and Management of Hypertensive Emergencies

References

General

  1. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2017 Focused Update of the 2016 ACC Expert Consensus Decision Pathway on the Role of Non-Statin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. In: Vol 70. 2017:1785-1822. doi:10.1016/j.jacc.2017.07.745.
  2. Janke AT, McNaughton CD, Brody AM, Welch RD, Levy PD. Trends in the Incidence of Hypertensive Emergencies in US Emergency Departments From 2006 to 2013. J Am Heart Assoc. 2016;5(12). doi:10.1161/JAHA.116.004511.
  3. Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiology in Review. 2010;18(2):102-107. doi:10.1097/CRD.0b013e3181c307b7.
  4. Katz JN, Gore JM, Amin A, et al. Practice patterns, outcomes, and end-organ dysfunction for patients with acute severe hypertension: the Studying the Treatment of Acute hyperTension (STAT) registry. Am Heart J. 2009;158(4):599–606.e1. doi:10.1016/j.ahj.2009.07.020.
  5. Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48(5):316-325. doi:10.1016/j.pcad.2006.02.004.
  6. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. 2006;24(1):135-146. doi:10.1016/j.ccl.2005.09.002.
  7. Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003;7(5):374-384. doi:10.1186/cc2351.
  8. Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. YMEM. 2003;41(4):513-529. doi:10.1067/mem.2003.114.
  9. Vaughan CJ, Delanty N. Hypertensive emergencies. The Lancet. 2000;356(9227):411-417. doi:10.1016/S0140-6736(00)02539-3.

Ischemic Stroke

  1. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2018;49(3):e46-e110. doi:10.1161/STR.0000000000000158.

Hemorrhagic Stroke

  1. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060. doi:10.1161/STR.0000000000000069.

Subarachnoid Hemorrhage

  1. Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737. doi:10.1161/STR.0b013e3182587839.

Renal

  1. Gillies MA, Kakar V, Parker RJ, Honoré PM, Ostermann M. Fenoldopam to prevent acute kidney injury after major surgery-a systematic review and meta-analysis. Crit Care. 2015;19(1):449. doi:10.1186/s13054-015-1166-4.
  2. Tumlin JA, Dunbar LM, Oparil S, et al. Fenoldopam, a dopamine agonist, for hypertensive emergency: a multicenter randomized trial. Fenoldopam Study Group. Academic Emergency Medicine. 2000;7(6):653-662.
  3. Shusterman NH, Elliott WJ, White WB. Fenoldopam, but not nitroprusside, improves renal function in severely hypertensive patients with impaired renal function. Am J Med. 1993;95(2):161-168.

Aortic Disease

  1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13):e266-e369. doi:10.1161/CIR.0b013e3181d4739e.

Pregnancy

  1. Townsend R, O’Brien P, Khalil A. Current best practice in the management of hypertensive disorders in pregnancy. Integr Blood Press Control. 2016;9:79-94. doi:10.2147/IBPC.S77344.
  2. Al-Safi Z, Imudia AN, Filetti LC, Hobson DT, Bahado-Singh RO, Awonuga AO. Delayed Postpartum Preeclampsia and Eclampsia. Obstet Gynecol. 2011;118(5):1102-1107. doi:10.1097/AOG.0b013e318231934c.
  3. Hypertension in pregnancy: diagnosis and management. National Institute for Health and Care Excellence. https://www.nice.org.uk/guidance/cg107. Published August 1, 2010. Accessed May 20, 2019.

Cerebrospinal Fluid

Brief HPI:

An approximately 70 year-old male with unknown medical history is brought to the emergency department with altered mental status. A community member contacted police after not seeing the patient for the past three days which was unusual. Upon entering the patient’s home, EMS found the patient on the ground, unresponsive. Capillary glucose was normal and naloxone was administered without appreciable effect.

On arrival in the emergency department, the patient remained unresponsive to verbal and noxious stimulation and was intubated for airway protection. Vital signs were notable for hypotension (BP 88/45mmHg) and a core temperature of 96.5°F. Physical examination demonstrated cool extremities and ecchymosis and edema involving the right upper and lower extremities. The patient’s blood pressure improved with fluid resuscitation and empiric broad-spectrum antibiotics were administered due to concern for infection in the setting of hypothermia.

Laboratory/Imaging Results

Laboratory tests were notable for leukocytosis and creatine kinase above the threshold for detection. Radiology preliminary interpretation of non-contrast head imaging was normal. A lumbar puncture was performed with grossly purulent cerebrospinal fluid.

00_ventriculitis
00_ventriculitis
01_ventriculitis
01_ventriculitis
02_ventriculitis
02_ventriculitis
03_ventriculitis
03_ventriculitis
04_ventriculitis
04_ventriculitis
05_ventriculitis
05_ventriculitis
06_ventriculitis
06_ventriculitis
07_ventriculitis
07_ventriculitis
08_ventriculitis
08_ventriculitis
09_ventriculitis
09_ventriculitis

MRI Brain

Dependent material within the occipital horns of the lateral ventricles consistent with ventriculitis.

Hospital Course

The patient was admitted for the treatment of presumed meningitis. Radiology final interpretation of non-contrast head computed tomography commented on ventricular debris suggestive of ventriculitis which was later confirmed on magnetic resonance imaging1,2. Due to poor response to systemic antibiotics, neurosurgery was consulted, a ventricular drain was placed with administration of intrathecal antibiotics. The patient’s condition continued to deteriorate and family members elected to allow his natural death.

An Algorithm for the Analysis of Cerebrospinal Fluid (CSF)3-14

An Algorithm for the Analysis of Cerebrospinal Fluid (CSF)

References

  1. Lesourd A, Magne N, Soares A, et al. Primary bacterial ventriculitis in adults, an emergent diagnosis challenge: report of a meningoccal case and review of the literature. BMC Infect Dis. 2018;18(1):226. doi:10.1186/s12879-018-3119-4.
  2. Gofman N, To K, Whitman M, Garcia-Morales E. Successful treatment of ventriculitis caused by Pseudomonas aeruginosa and carbapenem-resistant Klebsiella pneumoniae with i.v. ceftazidime-avibactam and intrathecal amikacin. Am J Health Syst Pharm. 2018;75(13):953-957. doi:10.2146/ajhp170632.
  3. Dorsett M, Liang SY. Diagnosis and Treatment of Central Nervous System Infections in the Emergency Department. Emerg Med Clin North Am. 2016;34(4):917-942. doi:10.1016/j.emc.2016.06.013.
  4. Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ. 2015;350:h568. doi:10.1136/bmj.h568.
  5. Lee SCM, Lueck CJ. Cerebrospinal fluid pressure in adults. J Neuroophthalmol. 2014;34(3):278-283. doi:10.1097/WNO.0000000000000155.
  6. Brouwer MC, Thwaites GE, Tunkel AR, van de Beek D. Dilemmas in the diagnosis of acute community-acquired bacterial meningitis. Lancet. 2012;380(9854):1684-1692. doi:10.1016/S0140-6736(12)61185-4.
  7. Wright BLC, Lai JTF, Sinclair AJ. Cerebrospinal fluid and lumbar puncture: a practical review. J Neurol. 2012;259(8):1530-1545. doi:10.1007/s00415-012-6413-x.
  8. Gorchynski J, Oman J, Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007;8(1):3-7.
  9. Deisenhammer F, Bartos A, Egg R, et al. Guidelines on routine cerebrospinal fluid analysis. Report from an EFNS task force. Eur J Neurol. 2006;13(9):913-922. doi:10.1111/j.1468-1331.2006.01493.x.
  10. Seehusen DA, Reeves MM, Fomin DA. Cerebrospinal fluid analysis. Am Fam Physician. 2003;68(6):1103-1108.
  11. Shah KH, Edlow JA. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. J Emerg Med. 2002;23(1):67-74.
  12. Walker HK, Hall WD, Hurst JW. Clinical Methods: The History, Physical, and Laboratory Examinations. 1990.
  13. Mayefsky JH, Roghmann KJ. Determination of leukocytosis in traumatic spinal tap specimens. Am J Med. 1987;82(6):1175-1181.
  14. Geiseler PJ, Nelson KE, Levin S, Reddi KT, Moses VK. Community-acquired purulent meningitis: a review of 1,316 cases during the antibiotic era, 1954-1976. Rev Infect Dis. 1980;2(5):725-745.

Pleural Fluid

Brief HPI:

A 43 year-old female with no reported medical history presents with shortness of breath. She notes 2 months of gradually worsening symptoms associated with unproductive cough and intermittent subjective fevers. Symptoms are worsened with activity and when laying flat. She has no history of similar symptoms in the past.

Vital signs are notable for tachycardia, tachypnea and hypoxia. Examination demonstrates absent breath sounds in the entire right lung field. A plain chest radiograph is obtained and shown below. The patient was placed on non-invasive positive pressure with minimal improvement and an emergent therapeutic thoracentesis was performed. Pleural fluid was exudative and a large volume was submitted for cytology.

Whiteout right lung field Whiteout right lung field

An Algorithm for the Analysis of Pleural Fluid

An Algorithm for the Analysis of Pleural Fluid

References

  1. Light RW, Girard WM, Jenkinson SG, George RB. Parapneumonic effusions. Am J Med. 1980;69(4):507-512.
  2. Heffner JE, Brown LK, Barbieri CA. Diagnostic value of tests that discriminate between exudative and transudative pleural effusions. Primary Study Investigators. Chest. 1997;111(4):970-980. doi:10.1378/chest.111.4.970.
  3. Romero S, Martinez A, Hernandez L, et al. Light’s criteria revisited: consistency and comparison with new proposed alternative criteria for separating pleural transudates from exudates. Respiration. 2000;67(1):18-23. doi:10.1159/000029457.
  4. Light RW. Clinical practice. Pleural effusion. N Engl J Med. 2002;346(25):1971-1977. doi:10.1056/NEJMcp010731.
  5. Sahn SA, Huggins JT, San Jose E, Alvarez-Dobano JM, Valdes L. The Art of Pleural Fluid Analysis. Clinical Pulmonary Medicine. 2013;20(2):77-96. doi:10.1097/CPM.0b013e318285ba37.
  6. Light RW. The Light criteria: the beginning and why they are useful 40 years later. Clinics in Chest Medicine. 2013;34(1):21-26. doi:10.1016/j.ccm.2012.11.006.
  7. Aggarwal AN, Agarwal R, Sehgal IS, Dhooria S, Behera D. Meta-analysis of Indian studies evaluating adenosine deaminase for diagnosing tuberculous pleural effusion. Int J Tuberc Lung Dis. 2016;20(10):1386-1391. doi:10.5588/ijtld.16.0298.

Synovial Fluid

Brief HPI:

A 38 year-old female with a history of obesity and obstructive sleep apnea presents with right knee pain. She cannot identify a clear precipitant for her symptoms which she first noted 2 weeks ago. Her pain is worsened with ambulation and while previously tolerable, has grown more severe despite over-the-counter analgesics over the past two days. She denies fevers, intravenous drug use, recent travel or instrumentation.

On evaluation, vital signs are normal. Physical examination demonstrates a moderate-sized right knee effusion with overlying warmth though no edema. There is minimal pain with range of motion, no pain with heel percussion, and she is ambulatory independently with a mildly antalgic gait. Clinical suspicion for septic arthritis was low. A diagnostic arthrocentesis was performed without complication. Synovial fluid was less-viscous than normal with slight debris. Laboratory analysis revealed 14,230 white blood cells with 85% neutrophils and no crystals visualized. The patient was discharged with supportive care and outpatient follow-up – cultures were ultimately negative.

An Algorithm for the Analysis of Synovial Fluid

An Algorithm for the Analysis of Synovial Fluid

References

  1. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA. 2007;297(13):1478-1488. doi:10.1001/jama.297.13.1478.
  2. Brannan SR, Jerrard DA. Synovial fluid analysis. J Emerg Med. 2006;30(3):331-339. doi:10.1016/j.jemermed.2005.05.029.
  3. Couderc M, Pereira B, Mathieu S, et al. Predictive value of the usual clinical signs and laboratory tests in the diagnosis of septic arthritis. CJEM. 2015;17(4):403-410. doi:10.1017/cem.2014.56.
  4. MD HJC, MD LAB, MD ML. Septic Arthritis. Hospital Medicine Clinics. 2014;3(4):494-503. doi:10.1016/j.ehmc.2014.06.009.

Ascitic Fluid

Brief HPI:

A 56 year-old male with a history of alcoholic cirrhosis complicated by esophageal varices presents to the emergency department with abdominal distension. He notes gradually worsening symptoms over the past 2 weeks – roughly correlating with the timing of his last paracentesis. He has limited access to medical care and typically presents to emergency departments for palliative paracenteses. He is otherwise in his usual state of health and denies fevers, chills, abdominal pain, vomiting blood, or dark/bloody stools.

Vital signs are notable for a heart rate of 97bpm and blood pressure of 110/65mmHg – otherwise normal. Examination demonstrates a distended abdomen which is non-tender, dull to percussion and with a palpable fluid wave. Bedside ultrasonography shows large, homogenous-appearing ascites with readily-accessible pockets for drainage in the bilateral lower quadrants. A palliative paracentesis is performed with uncomplicated extraction of 4 liters of translucent, straw-colored fluid. Ascitic fluid analysis shows 90 white blood cells of which 10% are polymorphonuclear. The patient is observed briefly in the emergency department, noted symptomatic improvement and was discharged with a plan for telephone follow-up of fluid culture results.

An Algorithm for the Analysis of Ascitic Fluid

Algorithm for the Analysis of Ascitic Fluid

References

  1. Runyon BA. Care of patients with ascites. N Engl J Med. 1994;330(5):337-342. doi:10.1056/NEJM199402033300508.
  2. Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA. 2008;299(10):1166-1178. doi:10.1001/jama.299.10.1166.
  3. Tarn AC, Lapworth R. Biochemical analysis of ascitic (peritoneal) fluid: what should we measure? Ann Clin Biochem. 2010;47(Pt 5):397-407. doi:10.1258/acb.2010.010048.
  4. Li PK-T, Szeto CC, Piraino B, et al. ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment. Perit Dial Int. 2016;36(5):481-508. doi:10.3747/pdi.2016.00078.
  5. MacIntosh T. Emergency Management of Spontaneous Bacterial Peritonitis – A Clinical Review. Cureus. 2018;10(3):e2253. doi:10.7759/cureus.2253.

Pericardial Effusion

HPI:

43F with a history of HTN and diastolic heart failure presenting with two days of shortness of breath. Reports that symptoms are worse at night when lying down to sleep and associated with a cough productive of white sputum. She also reports intermittent left-sided chest pain, described as sharp and exacerbated by cough or deep inspiration. She denies fevers/chills, nausea/vomiting, sick contacts or recent travel.
m

PMH:

  • Hypertension
  • Diabetes Mellitus (Type II)
  • Hyperlipidemia
  • Diastolic heart failure

PSH:

  • Cesarean section

FH:

  • Father with MI at 76 years-old

SHx:

  • Lives at home.
  • Denies tobacco, alcohol or drug abuse.

Meds:

  • Lasix 40mg p.o. daily
  • Lisinopril 20mg p.o. daily
  • Atenolol 50mg p.o. daily
  • Omeprazole 20mg p.o. daily
  • Lantus 14 units daily
  • Novolin 6 units t.i.d

Allergies:

NKDA

Physical Exam:

VS: T 98.2 HR 81 RR 19 BP 219/91 O2 95% RA
Gen: Adult female in no acute distress, alert and responding appropriately to questions.
HEENT: PERRL, EOMI, mucous membranes moist.
CV: RRR, no murmurs appreciated, no JVD.
Lungs: Crackles at right lung base.
Abd: Soft, non-tender, non-distended, without rebound/guarding.
Ext: 1+ pitting edema in bilateral lower extremities to knee.
Neuro: AAOx4, grossly normal peripheral sensation and motor strength.

Labs/Studies:

  • Troponin: 0.15
  • Procalcitonin: 0.15
  • CBC: 10.9/9.1/26.4/296
  • BMP: 134/4.6/104/22/56/2.87/214

Imaging:

Pericardial Effusion

Pericardial Effusion

Measured in the largest dimension, suggestive of a moderate to large pericardial effusion.

E-Point Septal Separation

E-Point Septal Separation

E-Point Septal Separation (EPSS), estimated here is the smallest distance between the anterior leaflet of the mitral valve and intraventricular septum. Values > 12mm are suggestive of depressed ejection fraction.

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy

Thickened left ventricular wall.

Pericardial Effusion - Subxiphoid

Pericardial Effusion - Subxiphoid

Pericardial Effusion - Parasternal Long

Pericardial Effusion - Parasternal Long

Pericardial Effusion - Parasternal Short

Pericardial Effusion - Parasternal Short

  • CXR: Consolidation involving the majority of the right lung, cardiomegaly.
  • Bedside Echo: LVEF 55%, concentric LVH, no wall motion abnormality, moderate pericardial effusion noted, RV not collapsed.

Assessment/Plan:

43F with a history of HTN, diastolic heart failure presenting with SOB.

#SOB: CXR finding of right-sided consolidation with history of productive cough, evidence of leukocytosis with neutrophil predominance, and relative hypoxemia suggestive of community-acquired pneumonia. No evidence of systemic inflammatory response. PE unlikely, patient is not bed-bound and alternative diagnosis more likely.
– Start empiric antimicrobial therapy ceftriaxone 1g IV q24h, azithromycin 500mg IV q24h.

#Pericardial Effusion: Noted on bedside echo, no evidence of RV collapse to suggest cardiac tamponade. Also, no JVD and pulsus paradoxus measured at 8mmHg.
– Obtain formal transthoracic echocardiogram to evaluate effusion.
– Consult cardiology if worsening hemodynamics

#Elevated Troponin: No ECG changes suggestive of acute ST-elevation MI. May represent NSTEMI though historical features not consistent with ACS.
– Trend troponin/EKG q.8.h. x3
– Give aspirin 325mg, consider anti-coagulation.
– Consider stress echo prior to discharge

#Elevated Creatinine: Baseline unknown, likely acute component with or without chronic kidney disease.
– Volume resuscitation as tolerated, follow repeat chemistry.

#Hypertension: Asymptomatic, resume home medications.

Physiology of Cardiac Tamponade 1

  • Intrapericardial pressure (IPP) normally reflects intrathoracic pressure (ITP).
  • Inspiration: low ITP → low RAP → increased RA filling.
  • Expiration: high ITP → low LAP → increased LA filling.
  • Increased pericardial fluid → increased IPP → increased LA/RA filling pressures (diastolic dysfunction) → increased variation with respiration.
  • Earliest hemodynamic change in cardiac tamponade is JVD or IVC dilation.

IVC variation as marker for RAP 1

IVC Diameter (cm) Change with Respiration (%) RAP (mmHg)
<2.1 >50% 0-5
<2.1 <50% 5-10
>2.1 >50% 5-10
>2.1 <50% >15

Grading Pericardial Effusions 1

Grade Echo-free space (mm) Size (mL)
Small <10 100
Moderate 10-20 100-500
Large >20 >500

History and Physical Exam in Patients with Acute Pericarditis 2,3

Symptom/Sign ACS Pericarditis PE
Quality Pressure Sharp Sharp
Pleuritic No Yes Yes
Positional No Yes (worse when supine) No
Duration Minutes to hours Hours to days Hours to days
Improves with NG Yes No No
Friction Rub No Yes No
S3 Maybe No No

Differential Diagnosis of Pericardial Effusion 2-8

Differential Diagnosis of Pericardial Effusion

References:

  1. Schairer, J. R., Biswas, S., Keteyian, S. J., & Ananthasubramaniam, K. (2011). A Systematic Approach to Evaluation of Pericardial Effusion and Cardiac Tamponade. Cardiology in Review, 19(5), 233–238. doi:10.1097/CRD.0b013e31821e202c
  2. Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial Disease: Diagnosis and Management. Mayo Clinic Proceedings. 2010;85(6):572-593. doi:10.4065/mcp.2010.0046.
  3. Lange, RA, Hillis, LD. Clinical practice. Acute pericarditis. The New England journal of medicine. 2004;351(21), 2195–2202. doi:10.1056/NEJMcp041997
  4. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 2013;34(16):1186-1197. doi:10.1093/eurheartj/ehs372.
  5. LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med. 2014;371(25):2410-2416. doi:10.1056/NEJMcp1404070.
  6. Vakamudi S, Ho N, Cremer PC. Pericardial Effusions: Causes, Diagnosis, and Management. Prog Cardiovasc Dis. 2017;59(4):380-388. doi:10.1016/j.pcad.2016.12.009.
  7. Imazio M, Mayosi BM, Brucato A, et al. Triage and management of pericardial effusion. J Cardiovasc Med (Hagerstown). 2010;11(12):928-935. doi:10.2459/JCM.0b013e32833e5788.
  8. Maisch B, Seferović PM, Ristić AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; The Task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J. 2004;25(7):587-610. doi:10.1016/j.ehj.2004.02.002.

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

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.

Algorithm for the Evaluation and Management of Palpitations1, 2

Algorithm for the Evaluation and Management 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  

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.

Cardiac Arrest

Brief HPI:

An overhead page alerts you to an arriving patient with cardiac arrest. An approximately 35-year-old male was running away from police officers and collapsed after being shot with a stun gun. The patient was found to be pulseless, CPR was started by police officers and the patient is en route.

An Algorithm for the Evaluation and Management of Cardiac Arrest with Ultrasonography

An Algorithm for the Evaluation and Management of Cardiac Arrest with Ultrasonography

Causes of Cardiac (and non-cardiac) Arrest

Sudden cardiac arrest (SCA) leading to sudden cardiac death (SCD) if not successfully resuscitated, refers to the unexpected collapse of circulatory function. Available epidemiologic data for in-hospital and out-of-hospital cardiac arrest (OHCA) point appropriately to cardiac processes as the most common cause, though extra-cardiac processes (most frequently respiratory), comprise up to 40% of cases1-3.

Identifying the underlying cause is critical as several reversible precipitants require rapid identification. However, the usual diagnostic techniques may be challenging, limited or absent – including patient history, detailed examination, and diagnostic studies.

The initial rhythm detected upon evaluation is most suggestive of the etiologic precipitant. Pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) is suggestive of a cardiac process – most commonly an acute coronary syndrome although heart failure or other structural and non-structural heart defects associated with dysrhythmias may be at fault4.

Pulseless electrical activity (PEA) presents a broader differential diagnosis as it essentially represents severe shock. The most common extra-cardiac cause is hypoxia – commonly secondary to pulmonary processes including small and large airway obstruction (bronchospasm, aspiration, foreign body, edema). Other causes include substance intoxication, medication adverse effect5,6, or electrolyte disturbances7. Finally, any precipitant of shock may ultimately lead to PEA, including hypovolemia/hemorrhage, obstruction (massive pulmonary embolus8, tamponade, tension pneumothorax), and distribution (sepsis).

Asystole is the absence of even disorganized electrical discharge and is the terminal degeneration of any of the previously-mentioned rhythms if left untreated.

Management of Cardiac Arrest

Optimizing survival outcomes in patients with cardiac arrest is dependent on early resuscitation with the prioritization of interventions demonstrated to have survival benefit. When advanced notice is available, prepare the resuscitation area including airway equipment (with adjuncts to assist ventilation and waveform capnography devices). Adopt the leadership position and assign roles for chest compressions, airway support, application of monitor/defibrillator, and establishment of peripheral access.

High-quality chest compressions with minimal interruptions are the foundation of successful resuscitation – and guideline changes prioritizing compressions have demonstrated detectable improvements in rates of successful resuscitation9,10. Measurement of quantitative end-tidal capnography can guide adequacy of chest compressions11,12 and an abrupt increase may signal restoration of circulation without necessitating interruptions of chest compressions13,14. Sustained, low measures of end-tidal CO2 despite appropriate resuscitation may signal futility and (alongside other factors) guides termination of resuscitation11,12.

The next critical step in restoring circulation is prompt defibrillation of eligible rhythms (pVT/VF) when detected. The immediate delivery of 200J (uptitrated to the device maximum for subsequent shocks) of biphasic energy and restoration of a perfusing rhythm is one of few interventions with clear benefits. For pVT/VF that persists despite multiple countershocks (more than three), the addition of an intravenous antiarrhythmic appears to improve survival to hospital admission. The ARREST trial was a randomized controlled study comparing amiodarone to its diluent as placebo for OHCA with refractory pVT/VF showing significant improvement in survival to hospital admission for the amiodarone group15. This was followed by the ALIVE trial comparing amiodarone and lidocaine which showed significantly higher rates of survival to hospital admission in the amiodarone group16. However, a more recent randomized trial comparing amiodarone (in a novel diluent less likely to cause hypotension), lidocaine, and placebo in a similar patient population showed less convincing results, with no detected difference in survival or the secondary outcome of favorable neurological outcome for either amiodarone or lidocaine compared with placebo17. The heterogeneity of available data contributed to current guidelines which recommend that either amiodarone or lidocaine may be used for shock-refractory pVT/VF18.

Current guidelines also recommend the administration of vasopressors (epinephrine 1mg every 3-5 minutes). In one randomized controlled trial exploring the long-standing guideline recommendations, epinephrine was associated with increased rates of restoration of spontaneous circulation, though no significant impact on the primary outcome of survival to hospital discharge was identified19. Physiologically, increased systemic vascular resistance combined with positive beta-adrenergic impact on cardiac output would be expected to complement resuscitative efforts. However, more recent studies have suggested that arrest physiology and unanticipated pharmacologic effects may complicate this simplistic interpretation – particularly when patient-centered outcomes are emphasized. Research exploring the timing and amount of epinephrine suggest that earlier administration and higher cumulative doses are associated with negative impacts on survival to hospital discharge and favorable neurological outcomes20-22.

Ultimately, treatment should focus on optimal execution of measures with clear benefits (namely chest compressions and early defibrillation of eligible rhythms). Other management considerations with which the emergency physician is familiar with including establishing peripheral access and definitive airway management can be delayed.

Rapid Diagnostic Measures for the Identification of Reversible Processes

Traditional diagnostic measures are generally unavailable during an ongoing cardiac arrest resuscitation. The emergency medicine physician must rely on the physical examination and point-of-care tests with the objective of identifying potentially reversible processes. Measurement of capillary blood glucose can exclude hypoglycemia as a contributor. Point-of-care chemistry and blood gas analyzers can identify important electrolyte derangements, as well as clarifying the primary impulse in acid-base disturbances.

End-tidal capnography was discussed previously for the guidance of ongoing resuscitation, but it may have diagnostic utility in patients with SCD. In one study the initial EtCO2 was noted to be significantly higher for primary pulmonary processes (with PEA/asystole as presenting rhythm) compared to primary cardiac processes (with pVT/VF as presenting rhythm)23.

The use of point-of-care ultrasonography, particularly in PEA arrest where non-cardiac etiologies dominate, may help identify the etiology of arrest and direct therapy. Bedside ultrasonography should be directed first at assessment of cardiac function – examining the pericardial sac and gross abnormalities in chamber size. A pericardial effusion may suggest cardiac tamponade, ventricular collapse can be seen with hypovolemia, and asymmetric right-ventricular dilation points to pulmonary embolus where thrombolysis should be considered8. If cardiac ultrasound is unrevealing, thoracic ultrasound can identify pneumothorax24-27.

In the absence of ultrasonographic abnormalities, attention turns to other rapidly reversible precipitants first. If opioid toxicity is a consideration, an attempt at reversal with naloxone has few adverse effects. If any detected rhythm is a polymorphic ventricular tachycardia characteristic of torsades de pointes – rapid infusion of magnesium sulfate should follow defibrillation. Other potentially reversible medications or toxins should be managed as appropriate.

Post-Resuscitation Steps

After successful restoration of circulation, the next management steps are critical to the patient’s long-term outcomes. A definitive airway should be established if not already secured (and if restoration of circulation was not associated with neurological recovery sufficient for independent airway protection). Circulatory support should continue with fluid resuscitation and vasopressors to maintain end-organ perfusion.

An immediate ECG should be performed to identify infarction, ischemia or precipitants of dysrhythmia. ST-segment elevation after return of spontaneous circulation (ROSC) warrants emergent angiography and possible intervention. However, given the prevalence of cardiac causes (of which coronary disease is most common) for patients with pVT/VF arrest, the presence of ST elevations is likely of insufficient sensitivity to identify all patients who would benefit from angiography. Several studies and meta-analyses have explored a more inclusive selection strategy for angiography (patients without obvious non-cardiac causes for arrest), all of which identified survival benefits with angiography and successful angioplasty when possible28-30.

Finally, the induction of hypothermia (or targeted temperature management) has significant benefits in survivors of cardiac arrest and can be instituted in the emergency department. Studies first targeted a core temperature of 32-24°C, with a randomized controlled trial demonstrating higher rates of favorable neurological outcome and reduced mortality31. More recent studies suggest that a more liberal temperature target does not diffuse the positive effects of induced hypothermia. A randomized trial of 939 patients with OHCA comparing a targeted temperature of 33°C vs 36°C suggested that a lower temperature target did not confer higher benefit to mortality or recovery of neurological function32. The more liberal temperature target may alleviate adverse effects associated with hypothermia which include cardiovascular effects (bradycardia), electrolyte derangements (during induction and rewarming), and possible increased risk of infections33. Targeted temperature management is achieved with external cooling measures or infusion of cooled fluids, rarely requiring more invasive measures34. Aggregate review of available data in a recent meta-analysis further supports the use of targeted temperature management after cardiac arrest as standard-of-care35.

References

  1. Bergum D, Nordseth T, Mjølstad OC, Skogvoll E, Haugen BO. Causes of in-hospital cardiac arrest – Incidences and rate of recognition. Resuscitation. 2015;87:63-68. doi:10.1016/j.resuscitation.2014.11.007.
  2. Wallmuller C, Meron G, Kurkciyan I, Schober A, Stratil P, Sterz F. Causes of in-hospital cardiac arrest and influence on outcome. Resuscitation. 2012;83(10):1206-1211. doi:10.1016/j.resuscitation.2012.05.001.
  3. Vaartjes I, Hendrix A, Hertogh EM, et al. Sudden death in persons younger than 40 years of age: incidence and causes. European Journal of Cardiovascular Prevention & Rehabilitation. 2009;16(5):592-596. doi:10.1097/HJR.0b013e32832d555b.
  4. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001;104(18):2158-2163.
  5. Hoes AW, Grobbee DE, Lubsen J, Man in ‘t Veld AJ, van der Does E, Hofman A. Diuretics, beta-blockers, and the risk for sudden cardiac death in hypertensive patients. Ann Intern Med. 1995;123(7):481-487.
  6. Siscovick DS, Raghunathan TE, Psaty BM, et al. Diuretic therapy for hypertension and the risk of primary cardiac arrest. N Engl J Med. 1994;330(26):1852-1857. doi:10.1056/NEJM199406303302603.
  7. Gettes LS. Electrolyte abnormalities underlying lethal and ventricular arrhythmias. Circulation. 1992;85(1 Suppl):I70-I76.
  8. Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535.
  9. Callaway CW, Soar J, Aibiki M, et al. Part 4: Advanced Life Support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. In: Vol 132. American Heart Association, Inc.; 2015:S84-S145. doi:10.1161/CIR.0000000000000273.
  10. Kudenchuk PJ, Redshaw JD, Stubbs BA, et al. Impact of changes in resuscitation practice on survival and neurological outcome after out-of-hospital cardiac arrest resulting from nonshockable arrhythmias. Circulation. 2012;125(14):1787-1794. doi:10.1161/CIRCULATIONAHA.111.064873.
  11. Touma O, Davies M. The prognostic value of end tidal carbon dioxide during cardiac arrest: a systematic review. Resuscitation. 2013;84(11):1470-1479. doi:10.1016/j.resuscitation.2013.07.011.
  12. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997;337(5):301-306. doi:10.1056/NEJM199707313370503.
  13. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987;257(4):512-515.
  14. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318(10):607-611. doi:10.1056/NEJM198803103181005.
  15. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341(12):871-878. doi:10.1056/NEJM199909163411203.
  16. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346(12):884-890. doi:10.1056/NEJMoa013029.
  17. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2016;374(18):1711-1722. doi:10.1056/NEJMoa1514204.
  18. Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. In: Vol 132. American Heart Association, Inc.; 2015:S315-S367. doi:10.1161/CIR.0000000000000252.
  19. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82(9):1138-1143. doi:10.1016/j.resuscitation.2011.06.029.
  20. Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012;307(11):1161-1168. doi:10.1001/jama.2012.294.
  21. Dumas F, Bougouin W, Geri G, et al. Is epinephrine during cardiac arrest associated with worse outcomes in resuscitated patients? J Am Coll Cardiol. 2014;64(22):2360-2367. doi:10.1016/j.jacc.2014.09.036.
  22. Andersen LW, Kurth T, Chase M, et al. Early administration of epinephrine (adrenaline) in patients with cardiac arrest with initial shockable rhythm in hospital: propensity score matched analysis. BMJ. 2016;353:i1577. doi:10.1136/bmj.i1577.
  23. Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting. Crit Care. 2003;7(6):R139-R144. doi:10.1186/cc2369.
  24. Rose JS, Bair AE, Mandavia D, Kinser DJ. The UHP ultrasound protocol: a novel ultrasound approach to the empiric evaluation of the undifferentiated hypotensive patient. American Journal of Emergency Medicine. 2001;19(4):299-302. doi:10.1053/ajem.2001.24481.
  25. Hernandez C, Shuler K, Hannan H, Sonyika C, Likourezos A, Marshall J. C.A.U.S.E.: Cardiac arrest ultra-sound exam—A better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation. 2008;76(2):198-206. doi:10.1016/j.resuscitation.2007.06.033.
  26. Chardoli M, Heidari F, Shuang-ming S, et al. Echocardiography integrated ACLS protocol versus con- ventional cardiopulmonary resuscitation in patients with pulseless electrical activity cardiac arrest. Chinese Journal of Traumatology. 2012;15(5):284-287. doi:10.3760/cma.j.issn.1008-1275.2012.05.005.
  27. Zengin S, Yavuz E, Al B, et al. Benefits of cardiac sonography performed by a non-expert sonographer in patients with non-traumatic cardiopulmonary arrest. Resuscitation. 2016;102:105-109. doi:10.1016/j.resuscitation.2016.02.025.
  28. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. N Engl J Med. 1997;336(23):1629-1633. doi:10.1056/NEJM199706053362302.
  29. Dumas F, Cariou A, Manzo-Silberman S, et al. Immediate Percutaneous Coronary Intervention Is Associated With Better Survival After Out-of-Hospital Cardiac Arrest: Insights From the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) Registry. Circulation: Cardiovascular Interventions. 2010;3(3):200-207. doi:10.1161/CIRCINTERVENTIONS.109.913665.
  30. Millin MG, Comer AC, Nable JV, et al. Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis. Resuscitation. 2016;108:54-60. doi:10.1016/j.resuscitation.2016.09.004.
  31. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549-556. doi:10.1056/NEJMoa012689.
  32. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. N Engl J Med. 2013;369(23):2197-2206. doi:10.1056/NEJMoa1310519.
  33. Polderman KH, Peerdeman SM, Girbes AR. Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg. 2001;94(5):697-705. doi:10.3171/jns.2001.94.5.0697.
  34. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods*. Critical Care Medicine. 2009;37(3):1101-1120. doi:10.1097/CCM.0b013e3181962ad5.
  35. Schenone AL, Cohen A, Patarroyo G, et al. Therapeutic hypothermia after cardiac arrest: A systematic review/meta-analysis exploring the impact of expanded criteria and targeted temperature. Resuscitation. 2016;108:102-110. doi:10.1016/j.resuscitation.2016.07.238.

Atrial Fibrillation

A 64-year-old male with a history of hypertension and hyperlipidemia presents with palpitations. He reports intermittent symptoms over the past 3 days, associated with dyspnea on exertion, but no chest pain, dizziness or syncope. His vital signs are notable for tachycardia (HR 129bpm) without hypotension or hypoxia. An ECG shows atrial fibrillation with rapid ventricular response.

Evaluation and Management

While the patient’s tachyarrhythmia is not yet associated with hypotension or evidence of malperfusion, preparation is key and includes continuous telemetry and vital sign monitoring, establishment of intravenous access, and application of cardioversion pads 1.

The presence of atrial fibrillation is new and the rapid ventricular response (RVR) may be symptomatic of more serious and potentially reversible pathology. A thorough history and physical examination may elucidate a precipitant and should precede attempts at rate- or rhythm-control. RVR may be provoked by any of the processes that would otherwise induce a sinus tachycardia, including bleeding, infection, toxic/metabolic etiologies and endocrinopathies 2, 3

Candidacy for Cardioversion

In hemodynamically stable patients with new-onset atrial fibrillation, candidacy for cardioversion includes:4-6

  • Stable without ischemia, hypotension or acute CHF
  • Clear onset of <48 hours
  • Non-severe symptoms
  • Few prior episodes/treatments
  • Existing anti-coagulation with warfarin and therapeutic INR (at least 3 weeks)
  • Absence of high-risk features: rheumatic/valvular disease, severe left-ventricular dysfunction, prosthetic valves, or history of thromboembolism

Cardioversion may be pharmacologic (with procainamide, or amiodarone), or electrical (synchronized at 100-200J). Electrical cardioversion for acute atrial fibrillation is both more effective and results in shorter lengths-of-stay in the emergency department – though stable patients should participate in shared decision-making7. Another important consideration when cardioversion is pursued is the prevention of systemic embolization. While atrial fibrillation of duration less than 48-hours is rarely associated with systemic embolization, certain populations are at higher risk8. One retrospective study of 3143 patients with atrial fibrillation for less than 48-hours demonstrated an overall risk of 0.7% for thromboembolic events – though the rate was significantly higher in patients older than 60 years or with other comorbidities (heart failure, diabetes)9. The risk of embolic events should be weighed against the risk of bleeding.

CHA2DS2VASc10-12

C Congestive Heart Failure 1
H Hypertension 1
A2 Age >75 2
D Diabetes Mellitus 1
S2 Stroke, TIA, Thromboembolism 2
V Vascular disease 1
A Age >65 1
Sc Sex Category Female 1

 

  • 0: low risk (may not require anti-coagulation)
  • 1: low-moderate risk (consider anti-platelet or anti-coagulation)
  • ≥ 2: moderate-high risk (anti-coagulation recommended)

HAS-BLED13,14

H Uncontrolled hypertension 1
A Abnormal renal/liver function
Renal (renal replacement therapy, creatinine >2.3mg/dL) 1
Liver (cirrhosis, bilirubin >2x, AST/ALT >3x) 1
S Stroke 1
B Bleeding history/anemia 1
L Labile INR 1
E Elderly (>65) 1
D Drugs
Anti-platelet agent, NSAID 1
Alcohol (>8 drinks/week) 1

 

  • 0: low risk (0.6-1.13% annual risk of major bleeding)
  • 1-2: intermediate risk (1.02-3.2% annual risk of major bleeding)
  • ≥ 3: high risk (4.9-19.6% annual risk of major bleeding)

Pharmacologic Management

For patients who are not candidates for cardioversion, rate-control should be pursued. Options include AV nodal blocking agents such as calcium channel blockers and beta-blockers15. The most frequently studied agents of each category are metoprolol and diltiazem. Both classes show comparable efficacy and safety profiles with trends favoring diltiazem16, 17.

Algorithm for the management of atrial fibrillation with rapid ventricular response:

Algorithm for the management of atrial fibrillation with rapid ventricular response

References

  1. Atzema, C.L. and T.W. Barrett, Managing atrial fibrillation. Ann Emerg Med, 2015. 65(5): p. 532-9.
  2. January, C.T., et al., 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society, 2014. 64(21): p. 2246-2280.
  3. Scheuermeyer, F.X., et al., Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying Medical Illness May Not Benefit From Attempts to Control Rate or Rhythm. Ann Emerg Med, 2015. 65(5): p. 511-522 e2.
  4. Stiell, I.G., et al., Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM, 2010. 12(3): p. 181-91.
  5. von Besser, K. and A.M. Mills, Is discharge to home after emergency department cardioversion safe for the treatment of recent-onset atrial fibrillation? Ann Emerg Med, 2011. 58(6): p. 517-20.
  6. Cohn, B.G., S.M. Keim, and D.M. Yealy, Is emergency department cardioversion of recent-onset atrial fibrillation safe and effective? J Emerg Med, 2013. 45(1): p. 117-27.
  7. Bellone, A., et al., Cardioversion of acute atrial fibrillation in the emergency department: a prospective randomised trial. Emerg Med J, 2012. 29(3): p. 188-91.
  8. Weigner, M.J., et al., Risk for clinical thromboembolism associated with conversion to sinus rhythm in patients with atrial fibrillation lasting less than 48 hours. Ann Intern Med, 1997. 126(8): p. 615-20.
  9. Airaksinen, K.E., et al., Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study. J Am Coll Cardiol, 2013. 62(13): p. 1187-92.
  10. Friberg, L., M. Rosenqvist, and G.Y. Lip, Evaluation of risk stratification schemes for ischaemic stroke and bleeding in 182 678 patients with atrial fibrillation: the Swedish Atrial Fibrillation cohort study. Eur Heart J, 2012. 33(12): p. 1500-10.
  11. Lip, G.Y., et al., Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest, 2010. 137(2): p. 263-72.
  12. Ntaios, G., et al., CHADS(2), CHA(2)S(2)DS(2)-VASc, and long-term stroke outcome in patients without atrial fibrillation. Neurology, 2013. 80(11): p. 1009-17.
  13. Lip, G.Y., et al., Comparative validation of a novel risk score for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the HAS-BLED (Hypertension, Abnormal Renal/Liver Function, Stroke, Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score. J Am Coll Cardiol, 2011. 57(2): p. 173-80.
  14. Pisters, R., et al., A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest, 2010. 138(5): p. 1093-100.
  15. Goralnick, E. and L.J. Bontempo, Atrial Fibrillation. Emerg Med Clin North Am, 2015. 33(3): p. 597-612.
  16. Demircan, C., et al., Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J, 2005. 22(6): p. 411-4.
  17. Fromm, C., et al., Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med, 2015. 49(2): p. 175-82.
  18. DiMarco, J.P., Atrial fibrillation and acute decompensated heart failure. Circ Heart Fail, 2009. 2(1): p. 72-3.

Febrile Seizure

Brief HPI:

An 8-month old female, fully-immunized, otherwise healthy is brought in by paramedics after 1 minute of witnessed generalized tonic-clonic shaking. The patient had otherwise been well, eating and behaving normally earlier that day. On EMS arrival, the patient was post-ictal but grew increasingly responsive en-route and upon presentation to the pediatric emergency department she was crying and appeared normal to her parents. Capillary glucose was 118g/dL. On examination the patient was noted to be febrile with a rectal temperature of 39.4°C. The remainder of the physical examination was normal.

ED Course:

The patient received anti-pyretics and a urinalysis was obtained which was not suggestive of urinary tract infection. During the 3-hour period of observation in the emergency department the patient remained at her normal baseline, had no further seizure activity, and tolerated oral intake with difficulty. The patient was suspected to have a simple febrile seizure and was discharged home.

Algorithm for the Diagnosis of Febrile Seizure

Algorithm for the Evaluation of Febrile Seizure

References

  1. Syndi Seinfeld DO, Pellock JM. Recent Research on Febrile Seizures: A Review. J Neurol Neurophysiol. 2013;4(165). doi:10.4172/2155-9562.1000165.
  2. Whelan H, Harmelink M, Chou E, et al. Complex febrile seizures-A systematic review. Dis Mon. 2017;63(1):5-23. doi:10.1016/j.disamonth.2016.12.001.
  3. Millichap JJ, Gordon Millichap J. Methods of investigation and management of infections causing febrile seizures. Pediatr Neurol. 2008;39(6):381-386. doi:10.1016/j.pediatrneurol.2008.07.017.
  4. Subcommittee on Febrile Seizures, American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-394. doi:10.1542/peds.2010-3318.

Leukemoid Reaction

Brief HPI:

An approximately 80-year-old male with unknown medical history is brought to the emergency department from a skilled nursing facility after unwitnessed arrest – EMS providers established return of spontaneous circulation after chest compressions and epinephrine. On arrival, the patient was hypotensive (MAP 40mmHg) and hypoxic (SpO2 85%) with mask ventilation. The patient was intubated, resuscitated with intravenous fluids and started on vasopressors. Imaging demonstrated lung consolidation consistent with multifocal pneumonia versus aspiration. Laboratory studies were obtained:

  • CBC: WBC: 49.2 (N: 64%, Bands: 20%)
  • ABG: pH: 7.07, pCO2: 73mmHg
  • Lactate: 9.1mmol/L
leukemoid_ct_01
leukemoid_ct_01
leukemoid_ct_02
leukemoid_ct_02
leukemoid_ct_03
leukemoid_ct_03
leukemoid_ct_04
leukemoid_ct_04
leukemoid_ct_05
leukemoid_ct_05
leukemoid_ct_06
leukemoid_ct_06
leukemoid_ct_07
leukemoid_ct_07
leukemoid_ct_08
leukemoid_ct_08
leukemoid_ct_09
leukemoid_ct_09
leukemoid_ct_10
leukemoid_ct_10
leukemoid_ct_11
leukemoid_ct_11
leukemoid_ct_12
leukemoid_ct_12

CT Pulmonary Angiography

Peribronchial opacities and patchy consolidation in the lungs which may represent multifocal pneumonia and/or aspiration in the appropriate clinical setting.
Mildly dilated main pulmonary artery suggestive of pulmonary arterial hypertension.

ED Course:

The patient was admitted to the medical intensive care unit for cardiopulmonary arrest presumed secondary to hypoxia and septic shock from healthcare-associated pneumonia or aspiration. The markedly elevated white blood cell count was attributed to a combination of infection and tissue ischemia from transient global hypoperfusion.


Definition: 1

  • Markedly elevated leukocyte (particularly neutrophil) count without hematologic malignancy
  • Cutoff is variable, 25-50k

Review of Available Literature

Retrospective review of 135 patients with WBC >25k 2
48% infection
15% malignancy
9% hemorrhage
12% glucocorticoid or granulocyte colony stimulating therapy
Retrospective review of 173 patients with WBC >30k 3
48% infection (7% C. difficile)
28% tissue ischemia
7% obstetric process (vaginal or cesarean delivery)
5% malignancy
Observational study of 54 patients with WBC >25k 4
Consecutive patients presenting to the emergency department
Compared to age-matched controls with moderate leukocytosis (12-24k)
Patients with leukemoid reaction were more likely to have an infection, be hospitalized and die.

Differential Diagnosis of Leukemoid Reaction 1,5-8

Differential Diagnosis of Leukemoid Reaction

References

  1. Sakka V, Tsiodras S, Giamarellos-Bourboulis EJ, Giamarellou H. An update on the etiology and diagnostic evaluation of a leukemoid reaction. Eur J Intern Med. 2006;17(6):394-398. doi:10.1016/j.ejim.2006.04.004.
  2. Reding MT, Hibbs JR, Morrison VA, Swaim WR, Filice GA. Diagnosis and outcome of 100 consecutive patients with extreme granulocytic leukocytosis. Am J Med. 1998;104(1):12-16.
  3. Potasman I, Grupper M. Leukemoid reaction: spectrum and prognosis of 173 adult patients. Clin Infect Dis. 2013;57(11):e177-e181. doi:10.1093/cid/cit562.
  4. Lawrence YR, Raveh D, Rudensky B, Munter G. Extreme leukocytosis in the emergency department. QJM. 2007;100(4):217-223. doi:10.1093/qjmed/hcm006.
  5. Marinella MA, Burdette SD, Bedimo R, Markert RJ. Leukemoid reactions complicating colitis due to Clostridium difficile. South Med J. 2004;97(10):959-963. doi:10.1097/01.SMJ.0000054537.20978.D4.
  6. Okun DB, Tanaka KR. Profound leukemoid reaction in cytomegalovirus mononucleosis. JAMA. 1978;240(17):1888-1889.
  7. Halkes CJM, Dijstelbloem HM, Eelkman Rooda SJ, Kramer MHH. Extreme leucocytosis: not always leukaemia. Neth J Med. 2007;65(7):248-251.
  8. Granger JM, Kontoyiannis DP. Etiology and outcome of extreme leukocytosis in 758 nonhematologic cancer patients: a retrospective, single-institution study. Cancer. 2009;115(17):3919-3923. doi:10.1002/cncr.24480.

Thrombocytopenia

Brief HPI:

A middle-aged female with no known medical history is brought to the emergency department with altered mental status. Her family notes worsening confusion over the past 2-3 days associated with vomiting and yellow discoloration of skin and eyes.

Initial vital signs were normal, though with borderline hypotension (99/64mmHg). Examination demonstrated an alert, but lethargic patient with jaundice and scleral icterus, no skin lesions were appreciated. Laboratory studies were obtained:

CBC

  • WBC: 21.3 (N: 83%, Bands: 11%)
  • Hb: 5.5
  • Plt: 6k
  • Marked schistocytes

Coagulation Panel

  • INR: 1.26
  • PTT: Normal
  • Fibrinogen: Normal
  • FDP: Normal
  • D-dimer: >9,000 (normal 250)
  • Haptoglobin: Undetectable
  • LDH: 1493

CMP

  • Creatinine: 1.1
  • AST/ALT: Normal
  • TB: 4.3, DB: 0.8

Imaging:

CT Head: No acute intracranial process.

ttp_ct_01
ttp_ct_01
ttp_ct_02
ttp_ct_02
ttp_ct_03
ttp_ct_03
ttp_ct_04
ttp_ct_04
ttp_ct_05
ttp_ct_05
ttp_ct_06
ttp_ct_06
ttp_ct_07
ttp_ct_07
ttp_ct_08
ttp_ct_08
ttp_ct_09
ttp_ct_09
ttp_ct_10
ttp_ct_10
ttp_ct_11
ttp_ct_11
ttp_ct_12
ttp_ct_12
ttp_ct_13
ttp_ct_13
ttp_ct_14
ttp_ct_14
ttp_ct_15
ttp_ct_15
ttp_ct_16
ttp_ct_16
ttp_ct_17
ttp_ct_17
ttp_ct_18
ttp_ct_18
ttp_ct_19
ttp_ct_19

CT Abdomen/Pelvis with Contrast

Moderate free intra-abdominal fluid, heterogeneous liver with periportal edema, dense right middle lobe consolidation.

ED Course:

The patient developed worsening respiratory failure with hypoxia and tachypnea requiring endotracheal intubation. Thrombotic thrombocytopenic purpura was suspected and while awaiting emergent plasma exchange transfusion, the patient arrested and resuscitation efforts were unsuccessful.

The patient’s ADAMTS13 activity level was <3%. Autopsy demonstrated consolidation of the right middle lobe with possible lymphoproliferative mass, and lung petechial hemorrhages from microvascular thrombi.

Differential Diagnosis of Thrombocytopenia 1-7

Differential Diagnosis of Thrombocytopenia

Algorithm for the Evaluation of Thrombocytopenia 8

Algorithm for the Evaluation of Thrombocytopenia

Definition 9

  • Mild: <150k
  • Moderate: 100-150k
  • Severe: <50k
    • 10-30k: bleeding with minimal trauma
    • <10k: increased risk spontaneous bleeding

History 9,10

  • Prior platelet count
  • Family history bleeding disorders
  • Medications
    • Heparin
    • Quinine, quinidine
    • Rifampin
    • Trimethoprim-sulfamethoxazole
    • Vancomycin
  • Alcohol use
  • Travel-related infections

Physical Examination 9,10

  • Splenomegaly (liver disease)
  • Lymphadenopathy (infection, malignancy)

Workup 10,11

Schistocytes

Red blood cell fragments (schistocytes) 11

  • hCG
  • Repeat CBC
    • Detect spurious measure
    • Neutrophil-predominant leukocytosis: bacterial infection
    • Immature leukocytes (blasts): leukemia, myelodysplasia
  • Peripheral smear
    • Schistocytes: microangiopathic process (DIC, TTP, HUS)
    • Atypical lymphocytes: viral infection
    • Intracellular parasites: malaria
    • Hypersegmented neutrophils: nutritional deficiency
  • Infectious features: HIV, HCV, EBV, H.pylori, blood cultures
  • Autoimmune features: ANA, APL-Ab
  • Suspected occult liver disease: LFT, PT/PTT/INR
  • Suspected thrombotic microangiopathy: PT/PTT/INR, haptoglobin, LDH, fibrinogen, FDP, d-dimer

Specific Conditions 2-6,9,12-20

Disease Cause Presentation Laboratory Findings Treatment
DIC Sepsis
Trauma
Burn
Malignancy
Bleeding
Multi-organ failure
Shock
INR
Fibrinogen
FDP
D-dimer
Directed at underlying cause
Transfusion thresholds for hemorrhage:
FFP for INR >1.5
Platelets if <50k
Cryoprecipitate of fibrinogen <100mg/dL
TTP Insufficient ADAMTS-13 activity Non-specific constitutional symptoms (ex. weakness)
Neuro: headache, AMS, focal neuro deficit
GI: abdominal pain, nausea/vomiting
LDH
Reticulocyte
Unconjugated bilirubin
Haptoglobin
Plasma exchange
HUS Shiga-toxin-producing bacteria, E. coli O157:H7 Bloody diarrhea, anuria, oliguria, and hypertension Aggressive supportive care
HELLP Spectrum of eclampsia Hypertension
Visual symptoms
Headache
RUQ abdominal pain
AST/ALT
Uric acid
Unconjugated bilirubin
LDH
Reticulocyte
Haptoglobin
Delivery, MgSO4
ITP Primary ITP

Secondary ITP
– Drug
– Autoimmune
– Infection
– Malignancy

Usually asymptomatic, may have petechiae or easy bruising Isolated thrombocytopenia Steroids
HIT Exposure to heparin or LMWH Thrombocytopenia or a 50 percent reduction in platelet count between 5-10d exposure
New thrombosis or skin necrosis
4 T’s score
Platelet factor 4 antibodies Withdraw heparin

References

  1. Greinacher A, Selleng S. How I evaluate and treat thrombocytopenia in the intensive care unit patient. Blood. 2016;128(26):3032-3042. doi:10.1182/blood-2016-09-693655.
  2. Joly BS, Coppo P, Veyradier A. Thrombotic thrombocytopenic purpura. Blood. 2017;129(21):2836-2846. doi:10.1182/blood-2016-10-709857.
  3. Leslie SD, Toy PT. Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid. Am J Clin Pathol. 1991;96(6):770-773.
  4. Neunert C, Lim W, Crowther M, et al. The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia. Blood. 2011;117(16):4190-4207. doi:10.1182/blood-2010-08-302984.
  5. Kappler S, Ronan-Bentle S, Graham A. Thrombotic microangiopathies (TTP, HUS, HELLP). Emerg Med Clin North Am. 2014;32(3):649-671. doi:10.1016/j.emc.2014.04.008.
  6. Greinacher A. Heparin-Induced Thrombocytopenia. Solomon CG, ed. N Engl J Med. 2015;373(3):252-261. doi:10.1056/NEJMcp1411910.
  7. Reardon JE Jr., Marques MB. Evaluation of Thrombocytopenia. Lab Med. 2006;37(4):248-250. doi:10.1309/R7P79KERAJHPRHLT.
  8. Stasi R. How to approach thrombocytopenia. Hematology Am Soc Hematol Educ Program. 2012;2012:191-197. doi:10.1182/asheducation-2012.1.191.
  9. Gauer RL, Braun MM. Thrombocytopenia. Am Fam Physician. 2012;85(6):612-622.
  10. Abrams CS. 172 – Thrombocytopenia. Twenty Fifth Edition. Elsevier Inc.; 2016:1159–1167.e2. doi:10.1016/B978-1-4557-5017-7.00172-0.
  11. Wilson CS, Vergara-Lluri ME, Brynes RK. Chapter 11 – Evaluation of Anemia, Leukopenia, and Thrombocytopenia. Second Edition. Elsevier Inc.; 2017:195-234.e195. doi:10.1016/B978-0-323-29613-7.00011-9.
  12. Hui P, Cook DJ, Lim W, Fraser GA, Arnold DM. The frequency and clinical significance of thrombocytopenia complicating critical illness: a systematic review. Chest. 2011;139(2):271-278. doi:10.1378/chest.10-2243.
  13. Jokiranta TS. HUS and atypical HUS. Blood. 2017;129(21):2847-2856. doi:10.1182/blood-2016-11-709865.
  14. Neunert CE. Management of newly diagnosed immune thrombocytopenia: can we change outcomes? Hematology Am Soc Hematol Educ Program. 2017;2017(1):400-405. doi:10.1182/asheducation-2017.1.400.
  15. Lambert MP, Gernsheimer TB. Clinical updates in adult immune thrombocytopenia. Blood. 2017;129(21):2829-2835. doi:10.1182/blood-2017-03-754119.
  16. Arepally GM. Heparin-induced thrombocytopenia. Blood. 2017;129(21):2864-2872. doi:10.1182/blood-2016-11-709873.
  17. Aster RH, Bougie DW. Drug-induced immune thrombocytopenia. N Engl J Med. 2007;357(6):580-587. doi:10.1056/NEJMra066469.
  18. Boral BM, Williams DJ, Boral LI. Disseminated Intravascular Coagulation. Am J Clin Pathol. 2016;146(6):670-680. doi:10.1093/ajcp/aqw195.
  19. Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haematol. 2012;158(3):323-335. doi:10.1111/j.1365-2141.2012.09167.x.
  20. Levine RL, Hursting MJ, Drexler A, Lewis BE, Francis JL. Heparin-induced thrombocytopenia in the emergency department. Ann Emerg Med. 2004;44(5):511-515. doi:10.1016/j.annemergmed.2004.06.004.

Hepatobiliary Ultrasound

Brief H&P:

A 43-year-old female with a history of hypertension, diabetes and obesity presents with right-upper quadrant abdominal pain for the past 1 week. The pain is characterized as burning, non-radiating, intermittent (with episodes lasting 10-30 minutes), resolving spontaneously and without apparent provoking features. She notes nausea but no vomiting, no changes in bowel or urinary habits. She similarly denies fevers, chest pain or shortness of breath. Vital signs were normal, and physical examination was notable only for right upper quadrant tenderness to palpation without rigidity or guarding.

An ECG demonstrates normal sinus rhythm, laboratory tests including liver function tests and lipase were normal and a bedside ultrasound of the right upper quadrant was performed demonstrating gallstones and a positive sonographic Murphy sign. The patient was diagnosed with acute cholecystitis, antibiotics were initiated, the patient was maintained NPO while general surgery was consulted.

Evaluation of Right-Upper Quadrant Abdominal Pain

The initial evaluation of a patient presenting with right-upper quadrant (or adjacent) abdominal pain typically includes laboratory tests such as a complete blood count, chemistry panel, liver function tests and serum lipase. In patients at risk for atypical presentations for an acute coronary syndrome or with other concerning symptoms, electrocardiography and cardiac enzymes may be indicated.

The differential diagnosis is broad. A systematic approach proceeds anatomically from superficial to deeper structures centered around the site of maximal pain.

Skin

Skin

Herpes zoster, erysipelas, or cellulitis

Connective Tissue

Connective Tissue

Intercostal muscle strain, myositis, fasciitis

Bone

Bone

Rib contusion or fracture

Hepatobiliary

Hepatobiliary

Hepatitis (infectious, toxin-mediated), perihepatitis (Fitz-Hugh-Curtis), hepatic abscess, symptomatic cholelithiasis, acute cholecystitis, ascending cholangitis, pancreatitis

Gastric

Gastric

Peptic ulcer disease, gastroesophageal reflux, gastritis, gastroparesis

Small Bowel

Small Bowel

Duodenal ulcer, small bowel obstruction

Large Bowel

Large Bowel

Retrocecal appendicitis, inflammatory bowel disease

Genitourinary

Genitourinary

Pyelonephritis, ureterolithiasis

Referred

Referred

Acute coronary syndrome, lower-lobe pneumonia, pulmonary embolus

Ultrasound in the Evaluation of Right Upper Quadrant Abdominal Pain

The diagnosis is unlikely to be made based on laboratory tests alone 1. However, the addition of bedside ultrasound, particularly for the evaluation of gallbladder pathology, is both rapid and reliable 2-8. The algorithm below provides a pathway for the incorporation of bedside ultrasound of the right upper quadrant in the evaluation of suspected gallbladder disease.

Algorithm for the Use of Ultrasound in the Evaluation of Right Upper Quadrant Abdominal Pain

A normal-appearing gallbladder absent gallstones should prompt a traversal of the anatomic approach to the differential diagnosis detailed above. If gallstones are identified, the association with a positive sonographic Murphy sign is highly predictive of acute cholecystitis 2,5,6,9. Acute cholecystitis may be associated with inflammatory gallbladder changes such as wall-thickening (>3mm) or pericholecystic fluid 3,5,6,10-13. However, in the absence of cholelithiasis or a positive sonographic Murphy sign, these features are non-specific and may be the result of generalized edematous states such as congestive heart failure, renal failure, or hepatic failure and critically-ill patients may develop acalculous cholecystitis 7,11,14. Finally, common bile duct dilation may be due to intra-luminal obstruction as in choledocholithiasis, luminal abnormalities such as strictures, or extra-luminal compression from masses or malignancy.  Dilation is generally described as a diameter >6mm – allowing an additional 1mm for every decade over 60 years-old as well as more vague accommodations for patients with prior cholecystectomy 3,5,7,15.

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas

Gallstones

Many gallstones

Gallbladder wall thickening

Pericholecystic fluid

Choledocholithiasis

Common bile duct dilation

All illustrations are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

Downloads Page License

References

  1. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289(1):80-86.
  2. Scruggs W, Fox JC, Potts B, et al. Accuracy of ED Bedside Ultrasound for Identification of gallstones: retrospective analysis of 575 studies. West J Emerg Med. 2008;9(1):1-5.
  3. Ross M, Brown M, McLaughlin K, et al. Emergency physician-performed ultrasound to diagnose cholelithiasis: a systematic review. Acad Emerg Med. 2011;18(3):227-235. doi:10.1111/j.1553-2712.2011.01012.x.
  4. Jang T, Chauhan V, Cundiff C, Kaji AH. Assessment of emergency physician-performed ultrasound in evaluating nonspecific abdominal pain. Am J Emerg Med. 2014;32(5):457-460. doi:10.1016/j.ajem.2014.01.004.
  5. Kendall JL, Shimp RJ. Performance and interpretation of focused right upper quadrant ultrasound by emergency physicians. J Emerg Med. 2001;21(1):7-13.
  6. Summers SM, Scruggs W, Menchine MD, et al. A prospective evaluation of emergency department bedside ultrasonography for the detection of acute cholecystitis. Ann Emerg Med. 2010;56(2):114-122. doi:10.1016/j.annemergmed.2010.01.014.
  7. Rubens DJ. Ultrasound Imaging of the Biliary Tract. Ultrasound Clinics. 2007;2(3):391-413. doi:10.1016/j.cult.2007.08.007.
  8. Rosen CL, Brown DF, Chang Y, et al. Ultrasonography by emergency physicians in patients with suspected cholecystitis. American Journal of Emergency Medicine. 2001;19(1):32-36. doi:10.1053/ajem.2001.20028.
  9. Shea JA. Revised Estimates of Diagnostic Test Sensitivity and Specificity in Suspected Biliary Tract Disease. Arch Intern Med. 1994;154(22):2573-2581. doi:10.1001/archinte.1994.00420220069008.
  10. Miller AH, Pepe PE, Brockman CR, Delaney KA. ED ultrasound in hepatobiliary disease. J Emerg Med. 2006;30(1):69-74. doi:10.1016/j.jemermed.2005.03.017.
  11. Shah K, Wolfe RE. Hepatobiliary ultrasound. Emergency Medicine Clinics of NA. 2004;22(3):661–73–viii. doi:10.1016/j.emc.2004.04.015.
  12. Matcuk GR, Grant EG, Ralls PW. Ultrasound measurements of the bile ducts and gallbladder: normal ranges and effects of age, sex, cholecystectomy, and pathologic states. Ultrasound Q. 2014;30(1):41-48. doi:10.1097/RUQ.0b013e3182a80c98.
  13. Engel JM, Deitch EA, Sikkema W. Gallbladder wall thickness: sonographic accuracy and relation to disease. American Journal of Roentgenology. 1980;134(5):907-909. doi:10.2214/ajr.134.5.907.
  14. Gerstenmaier JF, Hoang KN, Gibson RN. Contrast-enhanced ultrasound in gallbladder disease: a pictorial review. Abdom Radiol (NY). 2016;41(8):1640-1652. doi:10.1007/s00261-016-0729-4.
  15. Becker BA, Chin E, Mervis E, Anderson CL, Oshita MH, Fox JC. Emergency biliary sonography: utility of common bile duct measurement in the diagnosis of cholecystitis and choledocholithiasis. J Emerg Med. 2014;46(1):54-60. doi:10.1016/j.jemermed.2013.03.024.

Wide-complex Tachycardia

Several algorithms exist for the electrocardigraphic evaluation of regular, wide-complex tachycardias with the objective of distinguishing ventricular tachycardia (VT) from a supraventricular tachycardia (SVT) with aberrant conduction. The algorithm detailed below, developed by Dr. James Niemann, presents an ED-centric approach favoring the diagnosis of the more life-threatening dysrhythmia. This approach recognizes that SVT with aberrancy is rare, particularly in patients with a history of cardiac disease where the likelihood of ventricular tachycardia exceeds 90%. The algorithm requires the use of only the most simple and easily-recalled criteria, and any point of failure along the algorithm lends to the universally-appropriate management as ventricular tachycardia.

Algorithm for the Evaluation of Regular, Wide-Complex Tachycardia

Algorithm for the Evaluation of Wide-Complex Tachycardia

  1. aVR: Is the initial deflection in aVR positive? If yes, then VT.
  2. Concordance: Is there concordance (monophasic with same polarity) in all of the precordial leads? If yes, then VT.
  3. AV Dissociation: Is there evidence of AV dissociation (fusion or capture beats)? If yes, then VT.
  4. Bundle-branch morphology: Is the QRS morphology in V1 and V6 consistent with either LBBB or RBBB? If no, then VT.

References

  1. Neimann J. Wide QRS Complex Tachycardias. Lecture. Harbor-UCLA Department of Emergency Medicine. 2014:1-19.
  2. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. 2008;5(1):89-98. doi:10.1016/j.hrthm.2007.09.020.
  3. Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med. 2013;20(11):1121-1130. doi:10.1111/acem.12247.
  4. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659.
  5. Lau EW, Pathamanathan RK, Ng GA, Cooper J, Skehan JD, Griffith MJ. The Bayesian approach improves the electrocardiographic diagnosis of broad complex tachycardia. Pacing Clin Electrophysiol. 2000;23(10 Pt 1):1519-1526.
  6. B Garner J, M Miller J. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythm Electrophysiol Rev. 2013;2(1):23-29. doi:10.15420/aer.2013.2.1.23.
  7. Vereckei A. Current algorithms for the diagnosis of wide QRS complex tachycardias. Curr Cardiol Rev. 2014;10(3):262-276.
  8. Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition: Part 1 – Epidemiology and Electrophysiology. West J Emerg Med. 2008;9(1):28-39.
  9. Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition Part 2 – Management, Miscellaneous Causes, and Pitfalls. West J Emerg Med. 2008;9(2):97-103.
  10. Griffith MJ, Garratt CJ, Mounsey P, Camm AJ. Ventricular tachycardia as default diagnosis in broad complex tachycardia. The Lancet. 1994;343(8894):386-388.

Sinus Tachycardia

Brief History and Physical:

A young female with a history of schizophrenia presents to the emergency department reporting hallucinations. She had been diagnosed with schizophrenia one year previously and was briefly admitted to a psychiatric hospital. She discontinued her anti-psychotic (risperidone) two months ago, and over the past week she reports increasingly prominent auditory and visual hallucinations.

She denies recent illness, vomiting/diarrhea, changes in urinary habits, new medications, alcohol or illicit substance use. She also denies chest pain, palpitations or shortness of breath.

Vital signs are notable for a heart rate of 148bpm and are otherwise normal (including core temperature). Detailed physical examination is normal except for a rapid, regular heart rate. Mental status examination demonstrated normal level of alertness and orientation, linear and cogent responses and occasional response to internal stimuli during which she appeared anxious.

Initial evaluation and management included a 12-lead ECG which showed sinus tachycardia. Multiple boluses of normal saline were initiated while awaiting laboratory workup.

ECG: Sinus Tachycardia

Presentation ECG demonstrates sinus tachycardia.

Update:

Laboratory studies were reviewed and unremarkable. Normal hemoglobin, normal chemistry panel, negative hCG, and negative toxicology screen. The patient remained persistently tachycardic with a heart rate ranging from 140-160bpm (again sinus tachycardia on 12-lead ECG). An atypical antipsychotic and anxiolytic were administered and additional studies were obtained. Serum TSH, troponin and D-dimer were normal and bedside ultrasound did not identify a pericardial effusion. The patient remained asymptomatic, reporting subjective improvement in anxiety and hallucinations. Psychiatry was consulted and the patient was placed in observation for monitoring of sinus tachycardia. Observation course was uneventful as the patient remained asymptomatic. Transthoracic echocardiography was normal. Psychiatry consultation recommended resumption of home anti-psychotic and outpatient follow-up. Tachycardia had improved but not resolved at the time of discharge (heart rate 109bpm) and the patient was instructed to follow-up with her primary care provider.


Algorithm for the Evaluation of Sinus Tachycardia

Algorithm for the Evaluation of Sinus Tachycardia

Any vital sign derangement is concerning and tachycardia may be associated with unanticipated death after discharge home1. The presence of tachycardia suggests one of several categories of hemodynamic, autonomic, or endocrine/metabolic derangement.

Demand for increased cardiac output

A perceived demand for increased cardiac output will prompt chronotropic (and inotropic) amplification before hypotension develops. Causative etiologies include: volume depletion (from hemorrhage, gastrointestinal or renal losses), distributive processes (such as infection), obstruction (pulmonary embolus, or pericardial effusion with impending tamponade), or tissue hypoxia (anemia or lung disease).

Autonomic nervous system

Autonomic nervous system disturbances induced by stimulant, sympathomimetic or anti-cholinergic use, or withdrawal of certain agents such as ethanol or beta-blockers may be at fault.

Endocrine and other causes

Hyperthyroidism and pheochromocytoma should be considered, and as diagnoses of exclusion: anxiety, pain, or inappropriate sinus tachycardia2.

Evaluation:
Core temperature
CBC
Troponin
D-dimer
Bedside cardiac ultrasound
Urine toxicology screen
Ethanol level
TSH/T4

Algorithm for the Evaluation of Narrow-Complex Tachycardia3,4,5,6

Algorithm for the Evaluation of Narrow-Complex Tachycardia

References:

  1. Sklar DP, Crandall CS, Loeliger E, Edmunds K, Paul I, Helitzer DL. Unanticipated Death After Discharge Home From the Emergency Department. Ann Emerg Med. 2007;49(6):735-745. doi:10.1016/j.annemergmed.2006.11.018.
  2. Olshansky B, Sullivan RM. Inappropriate sinus tachycardia. J Am Coll Cardiol. 2013;61(8):793-801. doi:10.1016/j.jacc.2012.07.074.
  3. Yusuf S, Camm AJ. Deciphering the sinus tachycardias. Clin Cardiol. 2005;28(6):267-276.
  4. Katritsis DG, Josephson ME. Differential diagnosis of regular, narrow-QRS tachycardias. Heart Rhythm. 2015;12(7):1667-1676. doi:10.1016/j.hrthm.2015.03.046.
  5. Bibas L, Levi M, Essebag V. Diagnosis and management of supraventricular tachycardias. CMAJ. 2016;188(17-18):E466-E473. doi:10.1503/cmaj.160079.
  6. Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012;367(15):1438-1448. doi:10.1056/NEJMcp1111259.

Tetanus Prophylaxis

An Algorithm for Tetanus Prophylaxis in Adults1

Algorithm for Tetanus Prophylaxis in Adults

References:

  1. Diphtheria, tetanus, and pertussis: recommendations for vaccine use and other preventive measures. Recommendations of the Immunization Practices Advisory committee (ACIP). MMWR Recomm Rep. 1991;40(RR-10):1-28.

ECG Guide: Pediatrics

ECG Standard

  • Full standard: no adjustment
  • Half-standard: commensurate reduction in amplitude (usually 50%)
  • Mixed: reduction in amplitude of precordial leads

Atrial Abnormalities

Right Atrial Abnormality (P pulmonale)
Peaked P-wave in II (>3mm from 0-6mo or >2.5mm >6mo)
Causes: right atrial volume overload, ASD, Ebstein, Fontan
Left Atrial Abnormality (P mitrale)
Wide, notched P-wave in II or biphasic in V1
Causes: MS, MR

Axis

  • Anatomical dominance of right ventricle until approximately 6mo
  • RAD normal
  • eRAD suggests AV canal defect

T-waves

  • 1st week of life: Upright
  • Adolescent: Inverted
  • Adult: Upright

Ventricular Hypertrophy

Right Ventricular Hypertrophy
R-wave height >98% for age in lead V1
S-wave depth >98% for age in lead V6
T-wave abnormality (ex. upright in childhood)
Causes: pHTN, PS, ToF
Left Ventricular Hypertrophy
R-wave height >98% for age in lead V6
S-wave depth >98% for age in lead V1
Adult-pattern R-wave progression in newborn (no large R-waves and small S-waves in right precordial leads)
Left-axis deviation
Causes: AS, coarctation, VSD, PDA

Examples


Normal Neonatal ECG

  • 2mo old
  • RAD
  • Inverted T-waves (normal)
  • Tall R-waves in V1-V3


Extreme Axis Deviation

  • Neonate with Down syndrome
  • Isoelectric in I, Negative in aVF negative in II  mean QRS vector -87°
  • Extreme RAD suggestive of AV canal defect


LVH:

  • Unrepaired Coarctation
  • Deep S-wave in V1 (>98%)
  • Tall R-wave in V6 (>98%)


RVH:

  • 10 year-old boy with pulmonary Hypertension
  • RAD after expected age for normal RAD
  • Tall R-waves in V1 (>98%)
  • Deep S-wave in V6 (>98%)


STEMI

  • ALCAPA (anomalous origin of the left coronary artery from the pulmonary artery): coronary artery arises anomalously from the pulmonary artery; as pulmonary arterial pressure falls during the first 6 months of infancy, prograde flow through the left coronary artery ceases and may even reverse.
  • HLHS (hypoplastic left heart syndrome): coronary arteries are perfused from a hypoplastic, narrow aorta that is susceptible to flow disruption
  • Orthotopic heart transplant with allograft vasculopathy
  • Kawasaki: coronary artery aneurysm with subsequent thrombosis


Benign early repolarization

  • 14 year-old male
  • Concave ST-segment elevation


Left Atrial Abnormality:

  • 9mo female with mitral insufficiency
  • Broad biphasic P-wave in V1
  • Tall, notched P-wave in II


Prolonged QT interval

  • 18-year-old female
  • Familial long QT syndrome and a history of cardiac arrest


WPW:

  • Delta wave, shortened PR interval

References

  1. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram. Part I: Age-related interpretation. Am J Emerg Med. 2008;26(2):221-228. doi:10.1016/j.ajem.2007.08.003.
  2. Goodacre S, McLeod K. ABC of clinical electrocardiography: Paediatric electrocardiography. BMJ. 2002;324(7350):1382-1385.
  3. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram Part II: Dysrhythmias. Am J Emerg Med. 2008;26(3):348-358. doi:10.1016/j.ajem.2007.07.034.
  4. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram Part III: Congenital heart disease and other cardiac syndromes. Am J Emerg Med. 2008;26(4):497-503. doi:10.1016/j.ajem.2007.08.004.
  5. Schwartz P. Guidelines for the interpretation of the neonatal electrocardiogram. Eur Heart J. 2002;23(17):1329-1344. doi:10.1053/euhj.2002.3274.