Posts Tagged → Shock

Infographic: Access Flow Rates

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Infographic for IV flow rates

Notes

Data on access flow rates are highly variable. This infographic uses flow rates achieved through dedicated rapid infusers (ex. Level 1 ®) or at a pressure of 300mmHg. It is possible that rapid infusers and specialized pressure tubing achieve higher flow rates. The main references and additional sources are listed below. See this post from REBEL EM for gravity flow rates.

References

  1. Reddick AD, Ronald J, Morrison WG. Intravenous fluid resuscitation: was Poiseuille right? Emergency Medicine Journal. 2011;28(3):201-202. doi:10.1136/emj.2009.083485.
  2. Pasley J, Miller CHT, DuBose JJ, et al. Intraosseous infusion rates under high pressure. Journal of Trauma and Acute Care Surgery. 2015;78(2):295-299. doi:10.1097/TA.0000000000000516.
  3. Brown NJD, Duttchen KM, Caveno JW. An Evaluation of Flow Rates of Normal Saline through Peripheral and Central Venous Catheters. In:; 2008:1-2. http://www.asaabstracts.com/strands/asaabstracts/abstract.htm;jsessionid=451C60B7A9C145CBB6C147DBF022E267?year=2008&index=8&absnum=709.

Additional Sources

  1. Ngo AS-Y, Oh JJ, Chen Y, Yong D, Ong MEH. Intraosseous vascular access in adults using the EZ-IO in an emergency department. Int J Emerg Med. 2009;2(3):155-160. doi:10.1007/s12245-009-0116-9.
  2. Traylor S, Bastani A, Emergency NB-DAO, 2016. 311 Are Three Ports Better Than One? an Evaluation of Flow Rates Using All Ports of a Triple Lumen Central Venous Catheter in Volume Resuscitation. doi:10.1016/j.annemergmed.2016.08.327.
  3. Hammer N, Möbius R, Gries A, Hossfeld B, Bechmann I, Bernhard M. Comparison of the Fluid Resuscitation Rate with and without External Pressure Using Two Intraosseous Infusion Systems for Adult Emergencies, the CITRIN (Comparison of InTRaosseous infusion systems in emergency medicINe)-Study. Raju R, ed. PLoS ONE. 2015;10(12):e0143726–15. doi:10.1371/journal.pone.0143726.
  4. Ong MEH, Chan YH, Oh JJ, Ngo AS-Y. An observational, prospective study comparing tibial and humeral intraosseous access using the EZ-IO. Am J Emerg Med. 2009;27(1):8-15. doi:10.1016/j.ajem.2008.01.025.
  5. Philbeck TE, Miller LJ, Montez D, Puga T. Hurts so good. Easing IO pain and pressure. JEMS. 2010;35(9):58–62–65–6–68–quiz69. doi:10.1016/S0197-2510(10)70232-1.
  6. FRCA SIK, MRCA PRG, FRCA KP, MBChB SW, FRCA TS, MRCP PRG. Flow rates through intravenous access devices: an in vitro study. J Clin Anesth. 2016;31:101-105. doi:10.1016/j.jclinane.2016.01.048.
  7. Puga T, Montez D, Care TPC, 2016. 263: ADEQUACY OF INTRAOSSEOUS VASCULAR ACCESS INSERTION SITES FOR HIGH-VOLUME FLUID INFUSION. journalslwwcom
  8. Tan BKK, Chong S, Koh ZX, Ong MEH. EZ-IO in the ED: an observational, prospective study comparing flow rates with proximal and distal tibia intraosseous access in adults. Am J Emerg Med. 2012;30(8):1602-1606. doi:10.1016/j.ajem.2011.10.025.

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.

Hypotension

Brief H&P:

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

Imaging

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CT Abdomen/Pelvis

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

Algorithm for the Evaluation of Hypotension1

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

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

Algorithm for the Evaluation of Hypotension

Guided Lecture

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

References

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

Rapid Pediatric Assessment

This post presents a tool for the rapid assessment of the cardiopulmonary status and cerebral/metabolic function of critically ill pediatric patients. The purpose is not to establish a diagnosis, rather to identify the particular physiological derangements to prioritize initial interventions. The tool was initially designed as a “triangle” – it has been adapted here (with permission) as a Venn diagram.1

Pediatric Assessment Diagram

Pediatric Assessment Diagram

Assessment of Appearance

  • Tone: Moves spontaneously, resists examination
  • Interactivity: Interacts with environment, reaches for items
  • Consolability: Comforted by caregiver
  • Gaze: Makes eye contact

Assessment of Work of Breathing

  • Airway Sounds: Stridor, grunting, wheezing
  • Position: Tripod
  • Retractions

Assessment of Circulation

  • Pallor
  • Mottling
  • Cyanosis

Management

Impression Interventions
Respiratory distress
  • Position of comfort
  • Oxygen, suction
  • Therapy as appropriate (albuterol, epinephrine, etc)
  • Labs/radiographs as indicated
Respiratory failure
  • Head/airway positioning
  • 100% oxygen
  • Ventilation support (BVM)
  • Advanced airway
Shock (compensated and decompensated)
  • Oxygen
  • Access
  • Fluid resuscitation
  • Specific therapy (antibiotics, surgery)
  • Labs/radiographs as indicated
CNS/Metabolic
  • Pulse oximetry
  • Rapid glucose
  • Labs/radiographs as indicated
Cardiopulmonary Failure
  • Head/airway positioning
  • 100% oxygen
  • Ventilation support (BVM)
  • Chest compressions as needed
  • Specific therapy (defibrillation, epinephrine, amiodarone)
  • Labs/radiographs as indicated

References:

  1. The pediatric assessment triangle: a novel approach for the rapid evaluation of children. Pediatr Emerg Care. 2010;26(4):312-315. doi:10.1097/PEC.0b013e3181d6db37.

Gastosin Ingestion

Jalapa, NicaraguaCC:

“Gastosin” ingestion

HPI:

29F BIB family after patient was found down at home, near opened bottle of Gastosin in presumed suicide attempt. On arrival to ED, patient was awake, but unresponsive, groaning and clutching stomach. GCS  was E3-V2-M5, HR 110, BP 60/palp, RR 24.

ED Course:

Upon arrival, placed two large-bore IV w/rapid infusion of 2L NS and given DA 2g IV x2. NG tube placed, initiated lavage of gastric contents with NS. Patient’s mental status continued to deteriorate, became unresponsive.

PMH/PSH:

Unknown

SHx:

History of alcohol abuse and depression per family.

PE:

  • VS: 110bpm, 60/palp, 24 R/min, no temp/O2sat available
  • General: Ill-appearing female, laying on bed in considerable distress, groaning and clutching stomach, diaphoretic
  • HEENT: NC/AT, PERRL (4-3mm), EOMI, MMM no lesions, no tongue lacerations, breath with foul odor, TM’s clear b/l.
  • CV: RRR, normal S1/S2, tachycardia, faint heart sounds, JVP elevated though patient supine
  • Lungs: CTAB, no crackles/wheezes
  • Abdomen: +BS, soft, non-distended, no guarding, no ecchymosis
  • GU: Normal external genitalia, loss of stool noted.
  • Neuro: Patient confused, initially responsive to sternal rub, moving all 4 extremities spontaneously/equally, EOMI without nystagmus, gag reflex present, DTR 2+ and symmetric throughout with toes downgoing.
  • Extremities: Cool, peripheral pulses 0 (radial, PT, DP), 1+ (femoral, brachial, carotid)1, capillary refill 3sec
  • Skin: No visible skin lesions

Assessment & Plan:

29F, unknown PMH, ċ ingestion of unknown amount of “Gastosin”. Patient presenting in likely cardiogenic shock given hypotension with reflex sympathetic activation (evidenced by peripheral vasoconstriction à cool extremities, diaphoresis) and no evidence of hemorrhage. Gastosin is a pesticide used in the storage of maize2, and is well-known locally as a common agent in self-poisonings. Chemically composed of aluminum phosphide, and liberates phosphine gas on exposure to moisture which is rapidly absorbed by inhalation, transdermally or gastrointestinally. Toxicity results from free radical damage and inhibition of enzymes of metabolism (particularly affecting cardiac myocytes). Clinical features include vomiting, resistant hypotension and metabolic acidosis.3

Patient’s symptoms and presentation are consistent with cardiogenic shock secondary to Gastosin ingestion. Management included fluid resuscitation and inotropic support with dopamine, as well as gastric lavage. Resuscitation efforts were unsuccessful and patient remained hypotensive with worsening of mental status, and eventual death.

Differential Diagnosis for Shock:

A System for Shock

A System for the Management of Aluminum Phosphide Poisoning:4,5

Management of Aluminum Phosphide Poisoning

The Glasgow Coma Scale:

  Eye Opening Best Motor Response Best Verbal Response
1 None None None
2 Pain Extension Groans
3 Verbal Flexion Unintelligible
4 Open Withdraws Disoriented
5 Localizes Oriented
6 Obeys commands

References:

  1. Hill RD, Smith RB III. Examination of the Extremities: Pulses, Bruits, and Phlebitis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 30. Available from: http://www.ncbi.nlm.nih.gov/books/NBK350/
  2. Udoh, J., Ikotun, T., & Cardwell, K. (n.d.). Storage systems for maize (zea mays l.) in nigeria from five agro-ecological zones. Proceedings of the 6th International Working Conference on Stored-product Protection, 2, 960-965.
  3. Bogle, R. G., Theron, P., Brooks, P., Dargan, P. I., & Redhead, J. (2006). Aluminium phosphide poisoning. Emergency medicine journal : EMJ, 23(1), e3. doi:10.1136/emj.2004.015941
  4. Gurjar, M., Baronia, A. K., Azim, A., & Sharma, K. (2011). Managing aluminum phosphide poisonings. Journal of Emergencies, Trauma, and Shock, 4(3), 378–384. doi:10.4103/0974-2700.83868
  5. Jones, A. L., & Volans, G. (1999). Management of self poisoning. BMJ (Clinical research ed.), 319(7222), 1414–1417.