Subtle Presentations of Shock in the ED Setting

Authors: Michael Andrew Tandlich, MD (EM Resident Physician, Northwestern University) and Katharine Colton, MD (EM Attending Physician, Northwestern University) // Reviewed by: Anthony DeVivo, DO (Emergency Medicine-Critical Care Fellow, Icahn School of Medicine at Mount Sinai Hospital); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case #1:

The patient was a 74-year-old male with a history of hypertension who presented to the emergency department with sudden onset left flank pain that felt like a deep throbbing ache and had persisted for two hours.

Vitals: BP 111/62, HR 112, RR 18, T 37, SpO2 96% RA.

The patient was awake, alert, and conversant, although appeared uncomfortable. Cardiopulmonary exam was notable only for tachycardia. The abdominal exam showed obesity, and mild diffuse tenderness without rebound or guarding.

A CT abdomen/pelvis without contrast had been ordered from triage and was pending. The patient was given IV fluids and pain medication; shortly thereafter, his blood pressure was noted to be 96/48 mmHg. It normalized by the time the physician arrived in the room to re-assess the patient.

Several hours after arrival, the CT scan resulted and showed no evidence of a renal calculus but did show a large aortic abdominal aneurysm. The lack of contrast prevented assessment of active hemorrhage but did show what appeared to be a fluid collection contained in the retroperitoneal space. On reassessment, the patient was restless and unwell appearing; immediate surgical consultation was made.

Pitfalls & Discussion:

Pattern recognition is critical in the ED and patients are often on a pathway by the time they’re evaluated at the bedside as we attempt to move care forward in our overcrowded environment. Premature closure can delay diagnosis1 and several clues point to a missed critical diagnosis in this patient. His age should raise the first red flag, as should his mild tachycardia. While renal colic is a frequent cause of flank pain, it is unusual to present for the first time in a patient older than 652. Transient hypotension may herald future decompensation, and earlier assessment and a bedside ultrasound would have revealed this patient’s leaking abdominal aortic aneurysm (AAA)3.

The diagnosis of ruptured AAA may be complicated by vague or non-specific symptoms that vary dramatically4. The classic triad of abdominal pain, shock, and a pulsatile mass may be present in less than 2/3 of patients5. Renal colic is the most common mistaken alternative diagnosis, and the misleading symptoms are thought to be related to irritation of ureteric fibers within the sympathetic plexus5,6. However, renal colic typically presents two decades earlier than ruptured AAA and is uncommon in the elderly population7,8. The most common misdiagnoses in one retrospective study of ruptured AAA were renal colic (24%), diverticulitis (13%), and GI bleeding (13%)9.


The Take Away:

  • Consider AAA in any elderly patient presenting with renal colic, even in the presence of stabilized vital signs. It is imperative to consider the most dangerous pathologies on our differential diagnosis.
  • Respond thoughtfully to any factors which may be a tip off to early signs of shock. In this case, unexplained tachycardia and transient hypotension were signs of dangerous underlying pathology (a leaking aneurysm) that went unrecognized.
  • Beware of the elderly patient with renal colic, but more importantly, beware of the sick elderly patient for whom you have only a narrow differential diagnosis.

Case #2:

The patient was a 27-year-old otherwise healthy female who presented to the emergency department brought in by emergency medical services as a trauma patient. She was struck while crossing the street by a motor vehicle traveling 25 miles per hour and presents with left arm pain, flank pain, and hip pain, and left arm deformity.

Vitals: BP 104/82, HR 98, RR 21, T 37, SpO2 97% RA.

The patient was awake and alert, although appeared restless and uncomfortable. Her airway was intact, breath sounds were present bilaterally, and there was no evidence of active bleeding. A trauma survey was notable for bruising to the left abdomen and flank and obvious deformity to the left humerus with a normal distal neurovascular exam.

FAST exam showed no intra-abdominal free fluid and no pericardial effusion. One liter of normal saline was started and CT scans were ordered of the chest, abdomen, and pelvis. Plain films were obtained of the chest and pelvis and were notable for 2 left-sided rib fractures.

What were the warning signs that could have been seen in this patient?

Pitfalls & Discussion:

We frequently encounter hypovolemic shock in the ED, but can be initially reassured by “normal” vital signs that can mask a compensated setting of blood loss. Studies have demonstrated that tachycardia alone may be misleading and nonspecific in the case of trauma10,11. Others have shown that the ATLS criteria too often overestimate the tachycardic response in trauma patients12.

The shock index (SI) may be a more sensitive indicator of blood loss in general13-16. In fact, studies have demonstrated the SI has a 91 percent sensitivity in predicting shock among patients with massive bleeding from severe trauma17. The SI is a noninvasive bedside assessment of circulatory status. It is defined by the ratio of heart rate to systolic blood pressure. Normal values for shock index in the healthy patient are between 0.5 and 0.7, and patients with a shock index above 0.9 are more likely to need immediate treatment and hospital admission18. In this case, the patient had an SI of 0.94, pointing towards a compensated shock state.  A seminal study by Howell et al. in 200719 identified lactic acid as an independent predictor of in-hospital mortality when controlled for age and hypotension, pointing to its utility as another piece of information in the identification of occult hypoperfusion or compensated shock.


The Take Away:

  • Early “subtle signs” of shock may present without frank tachycardia and hypotension or other vital sign instability. When taking vital signs at face value, the physician may miss these subtle signs.
  • Shock index is a noninvasive bedside assessment of circulatory status defined by the ratio of heart rate to systolic blood pressure. It has increased sensitivity for predicting potential instability.
  • Physical examination can show subtle changes like cool or pale extremities with delayed capillary refill, restlessness or agitation, narrow pulse pressure, or relative tachycardia.

Case #3:

The patient was a 22-year-old male with a history of severe asthma who presented to the emergency department with shortness of breath. Over the previous few hours, he had experienced worsening shortness of breath unresponsive to three treatments with his rescue inhaler as well as increasing chest pain.

Vitals: BP 156/70, HR 108, RR 26, T 37, SpO2 94% RA.

The patient was uncomfortable and in respiratory distress. Wheezing was noted; air movement was decreased bilaterally but breath sounds were easily heard on the left; he was using accessory muscles to breathe. The cardiac exam was notable only for tachycardia. Physical exam was otherwise unremarkable.

The patient was started on BiPAP, a continuous nebulizer, steroids, and magnesium; shortly thereafter, he became increasingly tachycardic and tachypneic. On reassessment, the patient became hypoxic and again noted to have decreased breath sounds on the right. A chest x-ray was obtained prior to ICU admission and showed a large right pneumothorax.

Pitfalls & Discussion:

In this case, anchoring on the patient’s known disease prevented early identification of the critical diagnosis of developing tension pneumothorax, exacerbated by the introduction of positive pressure ventilation. Continuing on BiPAP would have likely resulted in worsening tension pneumothorax physiology and cardiovascular collapse. While the association between chronic obstructive pulmonary disease and spontaneous pneumothorax is well-known, this is a less common diagnosis among asthmatics. Both asthma exacerbations and pneumothoraces can present with respiratory distress, wheezing, tachypnea, hyper-expansion, and hypoxia; hints like chest pain or asymmetric breath sounds should be picked up by the clinician.

“Classic” findings of tracheal deviation and hypotension may occur in fewer than a quarter of awake patients with tension pneumothorax20. Fewer than a quarter of patients may develop hypotension within the first few hours of presentation21, and hypotension may just barely precede fulminant cardiovascular collapse22 [3]. Systematic reviews have shown that fewer than 1/2 of patients with tension pneumothorax breathing unassisted had documented signs of hypoxemia21.

In this case, point-of-care ultrasound (POCUS) may also have been considered, as studies have shown its utility in the early diagnosis and management of tension pneumothorax as well as numerous other causes of acute dyspnea23. Studies have illustrated POCUS as an optimal diagnostic modality which may have a sensitivity of 95 percent in the detection of tension pneumothorax in critically ill patients24. Especially in a patient whose clinical course is atypical, POCUS serves as a quick, cost-effective, efficacious means of evaluating the critically ill patient.


The Take Away:

  • Suspect tension pneumothorax in any patient breathing unassisted with respiratory distress, even in the absence of hypotension and tracheal deviation. Maintain a broad differential diagnosis in the patient with respiratory distress.
  • Consider POCUS in patients with undifferentiated shortness of breath or among those in whom the clinical course is atypical.

Case #4:

The patient was a 2-year-old female with a history of allergy to peanuts who was brought to the emergency department by her mother because of a complaint of allergic reaction. Twenty minutes prior to arrival, the patient had an accidental exposure to peanuts. Her mother says she developed a rash on her arms and was holding her belly.

Vitals: BP 95/55, HR 120, RR 20, T 37, SpO2 98% RA.

The patient was awake, alert and well appearing, in no distress. Lungs were clear. Cardiac exam was normal.  The child appeared uncomfortable with abdominal palpation but was not guarding.  The skin exam showed erythematous, flat-topped wheals over the upper extremities and the back.

The patient was diagnosed with an allergic reaction and was given diphenhydramine and cetirizine.  Shortly thereafter, she developed vomiting. The patient was confused and agitated by the time the physician returned to reassess.

What is the diagnosis?

Pitfalls & Discussion:

While a patient in fulminant anaphylactic shock is easy to recognize, a well-appearing pediatric patient can falsely reassure us into undertreating anaphylaxis, potentially allowing time for the patient to decompensate.  This patient was not given epinephrine as she was stable and without respiratory distress, despite meeting criteria for anaphylaxis. The misclassification and insufficient treatment of anaphylaxis in the emergency department is well documented25,26,27. Furthermore, studies have shown a correlation between patients with delayed treatment and biphasic presentation of anaphylaxis28.

Mucocutaneous manifestations may be absent or delayed in presentation in up to 10 to 20 percent of patients, including those with severe anaphylactic reactions29. In a case series of children with fatal anaphylaxis, all but one presented without skin findings, and only two received epinephrine within one hour of presentation30.

Infants and children may meet criteria for anaphylaxis with only reduced blood pressure31. Yet, studies have demonstrated that fewer than 1/5 children under age 3 with anaphylaxis triggered by food allergy had a documented blood pressure measurement32, a fact further complicated by the varying thresholds for pediatric normal vital signs by age.

The Take Away:

  • Anaphylaxis may be under-recognized and under-treated among emergency physicians.
  • Mucocutaneous manifestations may be absent in 10 to 20 percent of patients presenting with anaphylaxis, including in severe cases.
  • Infants and children may meet criteria for anaphylaxis with a low blood pressure and all infants and children should have blood pressure documented and compared to norms for their age group.

 Pearls & Pitfalls:

  • Avoid anchoring on a single diagnosis, especially among a demographic at higher risk of presenting with atypical and vague symptoms such as the young and the elderly.
  • Maintain a broad differential diagnosis when approaching an elderly patient in discomfort or distress, even in the absence of vital sign instability.
  • Shock index is a useful noninvasive bedside assessment of circulatory status defined by the ratio of heart rate to systolic blood pressure whose elevation may help identify shock early on.
  • Suspect tension pneumothorax in any patient breathing unassisted with respiratory distress, even in the absence of hypotension and tracheal deviation.
  • Consider anaphylaxis even in the absence of mucocutaneous symptoms, which may be absent in up to 20 percent of anaphylaxis cases.

References/Further Reading:

[1] Kumar B, Kanna B, Kumar S. The pitfalls of premature closure: clinical decision-making in a case of aortic dissection. BMJ Case Rep. 2011;2011:bcr0820114594. Published 2011 Oct 4. doi:10.1136/bcr.08.2011.4594

[2] Krambeck AE, Lieske JC, Li X, Bergstralh EJ, Melton LJ 3rd, Rule AD. Effect of age on the clinical presentation of incident symptomatic urolithiasis in the general population. J Urol. 2013;189(1):158-164. doi:10.1016/j.juro.2012.09.023

[3] Clancy K, Wong J, Spicher A. Abdominal Aortic Aneurysm: A Case Report and Literature Review. Perm J. 2019;23:18.218. doi:10.7812/TPP/18.218

[4] Sakalihasan N, Limet R, Defawe O. Abdominal aortic aneurysm. The Lancet. 2005;365(9470):1577-1589. doi:10.1016/s0140-6736(05)66459-8

[5] Azhar B, Patel S, Holt P, Hinchliffe R, Thompson M, Karthikesalingam A. Misdiagnosis of ruptured abdominal aortic aneurysm: Systematic review and meta-analysis. International Journal of Surgery.  2014;12. doi:10.1016/j.ijsu.2014.08.336

[6] Banerjee A. Atypical manifestations of ruptured abdominal aortic aneurysms. Postgraduate Medical Journal. 1993;69(807):6-11. doi:10.1136/pgmj.69.807.6

[7] Chauhan V, Eskin B, Allegra JR, Cochrane DG. Effect of season, age, and gender on renal colic incidence. The American Journal of Emergency Medicine. 2004;22(7):560-563.  doi:10.1016/j.ajem.2004.08.016

[8] Sinha Y. Elderly patient with ureteric colic: suspect leaking aneurysm. Case Reports. 2013;2013(feb18 1). doi:10.1136/bcr-2013-008617

[9] Marston WA, Ahlquist R, Johnson G, et al. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg. 1992;16:17-22.

[10] Reisner AT, Edla S, Liu J, Liu J, Khitrov MY, Reifman J. Tachycardic and non-tachycardic responses in trauma patients with haemorrhagic injuries. Injury. 2018;49(9):1654-1660. doi:10.1016/j.injury.2018.04.032

[11] Kuster M, Exadaktylos A, Schnüriger B. Non-invasive hemodynamic monitoring in trauma patients. World Journal of Emergency Surgery. 2015;10(1):11. doi:10.1186/s13017-015-0002-0

[12] Guly H, Bouamra O, Spiers M, Dark P, Coats T, Lecky F. Vital signs and estimated blood loss in patients with major trauma: Testing the validity of the ATLS classification of hypovolaemic shock. Resuscitation. 2011;82(5):556-559. doi:10.1016/j.resuscitation.2011.01.013

[13] Rady MY, Nightingale P, Little RA, Edwards J. Shock index: a re-evaluation in acute circulatory failure. Resuscitation. 1992;23(3):227-234. doi:10.1016/0300-9572(92)90006-x

[16] Rady MY, Rivers EP, Martin GB, Smithline H, Appelton T, Nowak RM. Continuous central venous oximetry and shock index in the emergency department: Use in the evaluation of clinical shock. The American Journal of Emergency Medicine. 1992;10(6):538-541. doi:10.1016/0735-6757(92)90178-z

[17] Terceros-Almanza LJ, García-Fuentes C, Bermejo-Aznárez S, et al. Prediction of massive bleeding. Shock index and modified shock index. Intensive Medicine. 2017;41(9):532-538.

[18] Rady MY, Smithline HA, Blake H, Nowak R, Rivers E. A Comparison of the Shock Index and Conventional Vital Signs to Identify Acute, Critical Illness in the Emergency Department. Annals of Emergency Medicine. 1994;24(4):685-690. doi:10.1016/s0196-0644(94)70279-9

[19] Howell M, Donnino M, Clardy P, Talmor D, Shapiro N. Occult hypoperfusion and mortality in patients with suspected infection. Intensive Care Med. 2007;33(11):1892-1899.

[20] Leigh-Smith S, Harris T. Tension pneumothorax–time for a re-think? Emergency Medicine Journal. 2004;22(1):8-16. doi:10.1136/emj.2003.010421

[21] Roberts DJ, Leigh-Smith S, Faris PD, et al. Clinical Presentation of Patients With Tension Pneumothorax. Annals of Surgery. 2015;261(6):1068-1078. doi:10.1097/sla.0000000000001073

[22] Barton ED, Rhee P, Hutton KC, Rosen P. The pathophysiology of tension pneumothorax in ventilated swine. The Journal of Emergency Medicine. 1997;15(2):147-153. doi:10.1016/s0736-4679(96)00312-5

[23] Zanobetti M, Scorpiniti M, Gigli C, Nazerian P, Vanni S, Innocenti F, Stefanone VT, Savinelli C, Coppa A, Bigiarini S, Caldi F, Tassinari I, Conti A, Grifoni S, Pini R. Point-of-Care Ultrasonography for Evaluation of Acute Dyspnea in the ED. Chest. 2017 Jun;151(6):1295-1301. doi: 10.1016/j.chest.2017.02.003. Epub 2017 Feb 16. PMID: 28212836.

[24] Husain LF, Hagopian L, Wayman D, Baker WE, Carmody KA. Sonographic diagnosis of pneumothorax. J Emerg Trauma Shock. 2012;5(1):76-81. doi:10.4103/0974-2700.93116

[25] Clark S, Bock S, Gaeta TJ, Brenner BE, Cydulka RK, Camargo CA. Multicenter study of emergency department visits for food allergies. Journal of Allergy and Clinical Immunology. 2004;113(2):347-352. doi:10.1016/j.jaci.2003.10.053

[26] Clark S, Long AA, Gaeta TJ, Jr. CAC. Multicenter study of emergency department visits for insect sting allergies. Journal of Allergy and Clinical Immunology. 2005;116(3):643-649. doi:10.1016/j.jaci.2005.06.026

[27] Sclar DA, Lieberman PL. Anaphylaxis: Underdiagnosed, Underreported, and Undertreated. The American Journal of Medicine. 2014;127(1). doi:10.1016/j.amjmed.2013.09.007

[28] Pourmand A, Robinson C, Syed W, Mazer-Amirshahi M. Biphasic anaphylaxis: A review of the literature and implications for emergency management. Am J Emerg Med. 2018 Aug;36(8):1480-1485. doi: 10.1016/j.ajem.2018.05.009. Epub 2018 May 9. PMID: 29759531.

[29] Loverde D, Iweala OI, Eginli A, Krishnaswamy G. Anaphylaxis. Chest. 2018;153(2):528-543. doi:10.1016/j.chest.2017.07.033

[30] Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med. 1992 Aug 6;327(6):380-4. doi: 10.1056/NEJM199208063270603. PMID: 1294076.

[31] Sampson HA, Muñoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A, Brown SG, Camargo CA Jr, Cydulka R, Galli SJ, Gidudu J, Gruchalla RS, Harlor AD Jr, Hepner DL, Lewis LM, Lieberman PL, Metcalfe DD, O’Connor R, Muraro A, Rudman A, Schmitt C, Scherrer D, Simons FE, Thomas S, Wood JP, Decker WW. Second symposium on the definition and management of anaphylaxis: summary report–Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol. 2006 Feb;117(2):391-7. doi: 10.1016/j.jaci.2005.12.1303. PMID: 16461139.

[32] Huang F, Chawla K, J rvinen KM, Nowak-Wgrzyn A. Anaphylaxis in a New York City pediatric emergency department: triggers, treatments, and outcomes. J Allergy Clin Immunol. 2012 Jan;129(1):162-8.e1-3. doi: 10.1016/j.jaci.2011.09.018. Epub 2011 Oct 22. PMID: 22018905; PMCID: PMC3246066.

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