All posts by Erica Simon

Interstitial Lung Diseases: Evaluating for an Acute Exacerbation

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)

A 55 year-old female with a history of idiopathic pulmonary fibrosis and pulmonary hypertension (prednisone, sildenafil, and bosentan therapy) presents with a three day history of cough, chills, and shortness of breath.  As you enter the room, you see the patient leaning forward in her bed, gasping.

The bedside monitor alarms with a HR of 132, RR of 28, SpO2 of 84% on room air.  Physical exam is significant for end-expiratory wheezing and accessory muscle use.  While opening a non-rebreather mask and starting supplemental oxygen, your mind buzzes with thoughts of NIPPV, an EKG, a chest xray, a VBG, and antibiotics, but is there more that you should consider?  Does the patient’s previous diagnosis of idiopathic pulmonary fibrosis (IPF) change your management?

Let’s take a minute to discuss interstitial lung diseases and the importance of identifying acute exacerbations.

Diagnosing an Interstitial Lung Disease

While this piece centers on the management of an acute exacerbation of an interstitial lung disease (ILD), let’s first review the approach to diagnosing an ILD:

The term “interstitial lung disease” currently represents greater than 200 non-malignant pulmonary conditions, characterized by varying degrees of parenchymal and interstitial inflammation and fibrosis.1-5  Individuals suffering from undiagnosed ILD often present to healthcare providers with complaints of shortness of breath, persistent dry cough, chest pain with exertion, and even syncope (described in the setting of an ILD resulting in pulmonary hypertension and subsequent right heart failure).3,6

In this patient population, emergency department (ED) evaluation begins as all others: with an assessment of the ABCs.  After initial stabilization, history and physical examination will dictate the requirement of an assessment for: myocardial infarction, aortic dissection, congestive heart failure, myocarditis, pericarditis, endocarditis, pericardial effusion, valvular dysfunction, cardiac arrhythmia, pulmonary embolism, pneumonia, and pleural effusion, among others.3

Depending upon the patient’s hemodynamic status and emergency department findings, settings which incite concern for an underlying primary lung pathology or systemic disease associated with pulmonary compromise, often prompt inpatient or outpatient specialist consultation for advanced imaging, tissue sampling, pulmonary function testing, and laboratory analysis.3

Specialist consultation and evaluation allows for a definitive diagnosis of ILD and performance of subgroup analysis.  The subgroup classification system identifies conditions associated with an underlying systemic disorder, those with a known trigger, and those that are idiopathic in nature.  Tables 1-3 below contain examples; not all-encompassing.1,3

For an excellent review of historical and clinical clues suggesting ILD upon initial patient encounter, see Keith Meyer’s Diagnosis and Management of Interstitial Lung Disease:

Meyer K. Diagnosis and management of interstitial lung disease. Transl Respir Med. 2014; 2:4. Available from:

Associated with a Systemic Disorder1-5
Scleroderma Sarcoidosis
Polymyositis Langerhans Cell Histiocytosis
Dermatomyositis Amyloidosis
Systemic Lupus Erythematosus Pulmonary Vasculitis
Rheumatoid Arthritis Gaucher’s Disease
Mixed Connective Tissue Disease Nieman-Pick Disease
Neurofibromatosis Tuberus Sclerosis

Table 1. ILDs Associated with a Systemic Disorder

Identified Etiology1-5
Antibiotics (nitrofurantoin, sulfasalazine) Silicosis
Antiarrhythmics (amiodarone, tocainide, propanolol) Asbestosis
Anti-inflammatories (gold, penicillamine) Coal Worker’s Pneumoconiosis
Anticonvulsants (dilantin) Berylliosis
Chemotherapeutic Agents (mitomycin C, bleomycin, etc.) Talc Pneumoconiosis
Radiation Therapy Siderosis
Oxygen Toxicity Stannosis (Tin)
Narcotics Hypersensitivity Pnemoitis (Bird breeder’s or Farmer’s lung)

Table 2. ILDs with a Known Trigger

Idiopathic Pulmonary Fibrosis
Non-specific Interstitial Pneumonia

Table 3. Idiopathic ILDs

Note: the term ILD is synonymous with interstitial pulmonary disease, diffuse parenchymal lung disease, and interstitial pneumonia.1,3

The Epidemiology of ILD

As international standards for the diagnosis of ILD are lacking and disease terminology is highly variable, the true incidence and prevalence of ILD is difficult to ascertain.2  The largest U.S. study of ILD (n=2,936; patient population localized to Bernalillo County, NM), utilizing physician referral data, histopathology reports, ICD discharge diagnoses, and death certificate information, identified the incidence of ILD as 31.5 per 100,000/yr in males and 26.1 per 100,000/yr in females, with a male prevalence of 80.9 per 100,000, and a female prevalence of 67.2 per 100,000.7  Autopsy data revealed the estimated prevalence of pre-clinical or undiagnosed ILDs as 1.8% among all deaths.7,8  The most common incident diagnoses amongst both sexes were pulmonary fibrosis and IPF.

Economic data for the majority of ILD subgroup classifications are lacking; however, a 2002 study of private health insurance medical and pharmacy claims, performed by Weckyer et al., demonstrated the mean patient healthcare charges related to IPF as $33,304 – $40,707 per patient per year, with hospital admissions accounting for 71-73% of these expenses.2,9

Identifying ILD Exacerbations

In a patient with a previously diagnosed ILD, an exacerbation is defined as an acute lung injury (new onset bilateral pulmonary infiltrates, PaO2/FiO2 ≤ 300, and PAWP ≤ 18) in the absence of heart failure, pulmonary infection, pulmonary embolism (PE), aspiration, or drug reaction.4,10-13  Acute exacerbations have been documented in patients with the subgroup classifications of IPF, IPF associated with a connective tissue disease, chronic hypersensitivity pneumonitis, desquamative interstitial pneumonia, and asbestosis.4  Patients with these diagnoses may present to the ED with acute shortness of breath, cough, fever, or wheezing.3,6,10  In addressing this population, the role of the emergency physician is to provide acute resuscitation while initiating an evaluation for the previously detailed underlying etiologies.10,11

As mentioned, ED assessment begins with addressing ABCs, therefore a word on airway and breathing:

Oxygenation and Ventilation Support in Patients with ILD

Gas exchange abnormalities (ABG/VBG) or respiratory distress may dictate the employment of therapeutic options including nasal cannula, non-rebreather, non-invasive positive pressure ventilation, or intubation and mechanical ventilation.  The requirement for NIPPV or intubation in a patient with ILD is ominous.  Studies of patients with IPF experiencing acute respiratory distress demonstrated no mortality benefit from the utilization of NIPPV,14-16 and an average median survival time of 18.0 days [95% CI 9.0-25.0] in patients failing NIPPV, and 90 days [95% CI 65.0-305.0]  in those with successful NIPPV therapy (n = 18, p < 0.0001).12

 Ventilation strategies for patient with varying degrees of lung fibrosis previously centered on limiting barotrauma through the utilization of low tidal volumes (similar to the ARDSNet protocol);10 however, a recent case series of 94 patients with IPF demonstrated no improvement in patient outcomes with employment of this strategy.17  Increased levels of PEEP were also associated with increased short-term mortality.16  Overall, the vast majority of patients experiencing respiratory failure secondary to an acute exacerbation of an ILD perish in intensive care units.12,18

Let’s now address our C – Circulation:

Hemodynamic Instability

Hemodynamic instability in a patient with ILD may occur secondary to the acute exacerbation (hypercapnic respiratory failure resulting in hypoxemia and cardiovascular collapse), heart failure, acute coronary syndrome, infectious pulmonary pathology resulting in sepsis, or PE.10,19

In evaluating the hemodynamically unstable patient consider the following:19

  • EKG to evaluate for signs of heart strain, STEMI, NSTEMI, or ST-T changes concerning for ischemia.
  • Point of care ultrasound to evaluate for pleural effusions (left-sided heart failure), cardiomegaly (heart failure), right atrial/right ventricular dilation (PE), or right ventricular free wall dilation/ paradoxical septal shift toward the LV during early diastole (pulmonary hypertension20).
  • Antibiotic therapy for all patients presenting with SIRS criteria (temperature >38.0°C or <36°C, heart rate >90 bpm, respiratory rate > 20 or PCO2 < 32 Torr).

History, Physical Examination, and Evaluation

History and physical examination are paramount in assessing underlying etiologies of the patient’s symptoms, as treatment goals vary dramatically according to diagnosis (i.e. an acute exacerbation requiring respiratory support and admission to an ICU setting for bronchoalveolar lavage, vs. afterload reduction and potential diuresis in the setting left-sided heart failure, vs. the maintenance of euvolemia in the setting of pulmonary HTN precipitating right-sided heart failure vs. early antibiotic therapy and fluid resuscitation in the setting of sepsis, vs. anticoagulation in the setting of a PE).

When stable, the patient should be questioned regarding:

  • His/her specific ILD diagnosis (i.e. – eosinophilic pneumonia, scleroderma, etc.)
  • Current medical therapy or changes in medical therapy
    • Many patients are treated with chronic corticosteroids or immune modulators (methotrexate, infliximab, mycophenalate, etc.)
      • Bosentan, a treatment for pulmonary hypertension, is known to worsen fibrosis.4
    • Medical co-morbidities (ACS risk stratification/PE & DVT risk stratification)
    • Fevers or viral prodrome
    • Symptoms of right- or left-sided heart failure (orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, etc.)
    • History of acid reflux (predisposes to aspiration pneumonia and ARDS4)

Of note, studies have demonstrated an increased risk of thromboembolism in patients previously diagnosed with IPF.  A review of 218,991 decedent records contained in the US Multiple Cause-of-Death mortality database identified a prevalence of venous thromboembolism of 1.74% in patients with IPF vs. 1.34% (p<0.0001) in the general population (overall OR 1.34, 95% CI 1.29–1.38).21  IPF should be considered an independent risk factor for thromboembolism.

All patients with the diagnosis of an ILD presenting to the ED with chest pain, shortness of breath, fever, cough, or in acute respiratory failure should undergo the following evaluation:19

  • CBC, CMP, troponin, BNP, VBG/ABG, and lactate
  • Urinalysis, urine culture, and blood cultures are highly recommended for all patients, with or without SIRS criteria, given steroid and immune-modulator therapy.
  • Imaging:
    • Chest radiograph in patients with pre-existing ILD lacks sensitivity in identifying new opacities.10
    • High resolution CT (HRCT) is recommended as it demonstrates increased sensitivity in detecting radiographic abnormalities (ground glass opacities or a new organizing pneumonia), lacks iodinated contrast, and is able to differentiate an acute exacerbation of ILD from an interstitial pneumonia, aspiration pneumonia, or ARDS (these conditions lack the traditional honeycombing pattern).20
    • CTPA is required for the evaluation of pulmonary embolism if concern is present for PE, and this modality demonstrates a positive predictive value of 96% for pulmonary hypertension in individuals in which the maximum transverse diameter of the pulmonary artery is greater than the diameter of the proximal ascending aorta.22

Disposition and Treatment

At this point in the clinical encounter you have diagnosed an acute lung injury in your patient with a history of ILD.  You have ruled out cardiac pathology, pulmonary infection, aspiration, and pulmonary embolism.  Depending on the patient’s respiratory and hemodynamic status, your patient may be undergoing a trial of NIPPV or intubated and ventilated.  What comes next?

  • Experts recommend the initiation of broad-spectrum antibiotic therapy in all patients with an acute exacerbation of an ILD given the potential for immunosuppression.19
  • Attempts should me made to temporize with NIPPV. While there is no statistically significant mortality benefit, patients who successfully complete NIPPV may survive to hospital discharge.12
  • Consult pulmonology to discuss patient medication regimens, ventilation strategies, the possibility of corticosteroid and immune-modulator treatment, and performance of the recommended bronchoalveolar lavage (samples for culture).10
    • As an aside: Randomized controlled trials of corticosteroid therapy for acute exacerbations of ILD (patients with IPF and sarcoidosis) have failed to demonstrate a survival benefit.13,23 Cyclosporin A therapy in the setting of acute IPF exacerbation has also failed to demonstrate mortality benefit.11
  • Admit the patient to the ICU – progression to ARDS is common. All-cause mortality associated with acute exacerbations of ILD is estimated as 70%.4

Returning to the Case

Our 55 year-old patient with a history of IPF is in respiratory distress.  Based upon our above discussion, we would initiate a trial of NIPPV (guided by mental status examination and serial VBGs), and begin our efforts to rule out underlying etiologies according to our history and physical examination.  Our evaluation would include an EKG, +/- an US.  HR and RR dictate early antibiotic therapy.  HRCT or CTPA would be our imaging modalities of choice.  If our laboratory studies and imaging led us to a diagnosis of an acute exacerbation of the patient’s IPF, pulmonology would be consulted, and the patient admitted to the ICU.

Patients with ILD presenting with complaints related to the pulmonary system have a significant risk of mortality.  Close monitoring of respiratory status and early disposition may allow survival to hospital discharge.


Key Pearls

  • Airway and breathing => keep in mind, there is a 70% mortality associated with an acute ILD exacerbation; intubated patients most commonly perish in the ICU.4,12,18
  • In the hemodynamically unstable patient, perform an EKG + bedside US.
    • Hemodynamic instability in the setting of an ILD exacerbation results from progressive hypercapnia and subsequent hypoxia with cardiovascular collapse.
  • In the stable patient, elicit a thorough history – patients with IPF, IPF associated with a connective tissue disease, chronic hypersensitivity pneumonitis, desquamative interstitial pneumonia, and asbestosis may experience acute exacerbations.4
  • Initiate an evaluation to rule out cardiac pathology, pulmonary infection, aspiration, pulmonary embolism, and medication effect.
  • If the aforementioned evaluation identifies an ALI without etiology => presume ILD exacerbation, initiate broad-spectrum antibiotics, consult pulmonology, and admit to the ICU.
  • HRCT is a great chest imaging modality, but if concerned for PE, obtain CTPA.


References / Further Reading

  1. Mikolasch T, Garthwaite H, Porter J. Update in diagnosis and management of interstitial lung disease. Clin Med. 2016; 16(Suppl 6):s71-s78.
  2. Raghu G, Nyberg F, Morgan G. The epidemiology of interstitial lung disease and its association with lung cancer. Br J Cancer. 2004; 91(Suppl2): S3-S10.
  3. Lacamera P. Interstitial Lung Disease. Ferri’s Clinical Advisor 2017. p.690-692. Elsevier, Philadelphia, PA.
  4. Kim R, Meyer K. Therapies for interstitial lung disease: past, present and future. Ther Adv Respir Dis. 2008; 2(5):319-338.
  5. Churg A, Wright J, Tazelaar H. Acute exacerbations of fibrotic interstitial lung disease. Histopathology. 2011; 58(4):525-530.
  6. Wilcox S, Kabrhel C, Channick R. Pulmonary hypertension and right ventricular failure in emergency medicine. Ann Emerg Med. 2015 66(6):619-628.
  7. Coultas D, Zumwalt R, Black W, Sobonya R. The epidemiology of interstitial lung diseases. Am J Respir Crit Care Med. 1994; 150:967-972.
  8. Coultas D, Hughes M. Accuracy of mortality dat for interstitial lung diseases in New Mexico, USA. Thorax. 1996; 51:717-720.
  9. Weycker D, Oster G, Edelsberg J, Bradford W, Happel D, et al. Economic costs of idiopathic pulmonary fibrosis. Chest. 2002;122:150S.
  10. Disayabutr S, Calfee C, Collard H, Wolters P. Interstitial lung diseases in the hospitalized patient. BMC Med. 2015; 13:245.
  11. Collard H, Moore B, Flaherty K, Brown K, Kaner R, et al. Acute exacerbations of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2007:176:636-643.
  12. Kubo H, Nakayama K, Yanai, Suzuki T, Yamaya M, et al. Anticoagulant therapy for idiopathic pulmonary fibrosis. Chest. 2005; 128(3): 1475-1482.
  13. Kim D, Park J, Park B, Lee J, Nicholson A, et al. Acute exacerbation of idiopathic pulmonary fibrosis: frequency and clinical features. Eur Respir J. 2006; 27(1):143-150.
  14. Vianello A, Arcaro G, Battistella L, Pipitone E, Vio S, et al. Noninvasive ventilation in the event of acute respiratory failure in patients with idiopathic pulmonary fibrosis. J Crit Care. 2014; 29(4):562-567.
  15. Yokoyama T, Kondoh Y, Taniguichi H, Kataoka K, Kato K, et al. Noninvasive ventilation in acute exacerbation of idiopathic pulmonary fibrosis. Intern Med. 2010; 49(15):1509-1514.
  16. Nava S, Rubini F. Lung and chest wall mechanics in ventilated patients with end stage idiopathic pulmonary fibrosis. Thorax. 1999; 54(5):390-395.
  1. Fernandez-Perez E, Yilmaz M, Jenad H, Daniels C, Ryu J, Hubmayr R, et al. Ventilator settings and outcome of respiratory failure in chronic interstitial lung disease. Chest. 2008; 133:1113-1119.
  2. Blivet S, Philit F, Sab J, Langevin B, Paret M, Gueri C, et al. Outcome of patients with idiopathic pulmonary fibrosis admitted to the ICU for respiratory failure. Chest. 2001; 1(20):209-212.
  3. Papiris S, Manali E, Kolilekas L, Kagouridis K, Triantafillidou C, et al. Clinical review: idiopathic pulmonary fibrosis acute exacerbations – unravelling Ariadne’s thread. Crit Care. 2010; 14(6):246.
  4. Voelkel N, Quaife R, Leinwand L, et al. Right ventricular function and failure.  Circulation 2006; 114: 1883-1891.
  5. Sprunger D, Olson A, Huie T, Fernandez-Perez E, Fischer A, et al. Pulmonary fibrosis is associated with an elevated risk of thromboembolic disease. Eur Respir J. 2012; 39(1):125-132.
  6. Fujimoto K, Taniguchi H, Johkoh T, Kondoh Y, Ichikado K, et al. Acute exacerbation of idiopathic pulmonary fibrosis: high-resolution CT scores predict mortality. Eur Radiol. 2012. 22:83-92.
  7. Tan RT, Kuzo R, Goodman LR, et al. Utility of CT scan evaluation for predicting 
pulmonary hypertension in patients with parenchymal lung disease. Medical 
College of Wisconsin Lung Transplant Group. Chest 1998;113:1250-1256.

The Thromboelastogram (TEG®): A Five-Minute Primer for the Emergency Physician

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC)

It’s three o’clock in the morning on your fourth night shift in a row.  While mustering the courage to rescue your energy drink from the dank, dark depths of the staff mini-fridge, you hear a familiar page: “trauma team to the trauma room.”  As you walk towards the ambulance bay, the trauma surgeon approaches with information regarding the incoming transfer:

  • 17 year-old male – MVC versus pedestrian
  • Seen at OSH where CTs demonstrated: epidural hematoma, grade III liver laceration, grade II splenic laceration, open book pelvic fracture, and extraperitoneal bladder rupture
  • Patient underwent external pelvic fixation and transfusion of blood products (8U PRBCs, 8U FFP and 4U Plts)
  • Most recent VS: BP 136/89, HR 92, RR (intubated/ventilated):14, SpO2 99% (FiO2 70%)

Drawing your attention to a piece of paper in his hand, detailing what appear to be labs from the outside facility, the surgeon points to a colorful figure: “I’m very concerned about this”:


Scanning your mind for intelligent thought, you realize that it’s been some time since you’ve ordered a thromboelastogram (TEG), let alone interpreted one.

If you’re like this physician, take a few minutes to scan the following review – the quick and dirty on TEGs is coming your way.

Thromboelastography – What is it?

Developed in 1948 by Dr. Hellmut Harter, thromboelastography is a mechanism of assessing coagulation based upon the viscoelastic properties of whole blood.2-8  In contrast to traditional, static measurements of hemostasis (PT, aPTT, INR, fibrinogen level, and fibrin degradation products), thromboelastography allows for an assessment of near real-time, in-vivo clotting capacity, providing the interpreter information regarding the dynamics of clot development, stabilization, and dissolution.7  When utilized as a point-of-care assay, graphic interpretation of thromboelastography (the TEG), offers the opportunity for an expedited assessment of coagulopathies (thrombocytopenia, factor deficiency, heparin effect, hypofibrinogenemia, and hyperfibrinolysis).7,9,12,13

How is a TEG performed?

In order to perform a TEG, a citrated-sample of whole blood is placed into a heated sample cup with calcium chloride (to overcome the effects of the citrate), kaolin (a negatively charged molecule known to initiate the intrinsic pathway10), and phospholipids (required for optimal functioning of the extrinsic pathway11) (Figure 2).  As the sample cup oscillates in a limited arc, formation of clot results in the generation of rotational forces on a pin suspended from a torsion wire.  Forces translated to the torsion wire are then, in turn, transmitted to an electrical transducer, creating a characteristic waveform (Figure 3).



I’ve heard of the Rapid TEG (r-TEG), is there a Difference?

When performed by a trained laboratory specialist, an r-TEG may be completed within 15 minutes as compared to the average 30-45 minutes processing time for a standard TEG.4,5,14  In contrast to a TEG, whole blood samples for an r-TEG may be performed with citrated or non-citrated samples.4 Samples utilized for an r-TEG are combined with tissue factor (activating the extrinsic pathway), and kaolin (activating the intrinsic pathway as above) +/- calcium chloride as applicable.4

I’ve also heard of ROTEM, what is it?

Although utilizing the technique developed by Dr. Harter, rotational thromboelastometry (ROTEM) differs from traditional thromboelastography in its mechanical application.  Unlike traditional thromboelastography, which utilizes a sample cup rotating in a limited arc, ROTEM employs a static sample cup with an oscillating pin/wire transduction system.  By comparison, ROTEM is also a more complex diagnostic test as it requires a number of differing reagents.  A complete discussion of ROTEM is outside the scope of this review.  If interested in further reading, see:

Tanaka K, Bolliger D. Practical aspects of rotational thromboelastometry (ROTEM). Available from:

Haemoview Diagnostics. ROTEM analysis: thromboelastometry. Available from

Haemoview. The 5 ROTEM tests. Available from

How Do I Interpret TEG and r-TEG Results?

Drs. Semon and Cheatham of the Orlando Regional Medical Center Department of Surgical Education generated an excellent quick reference chart:


*Note: TEG-ACT (rapid) – reported for r-TEG only.

A TEG-Guided Transfusion Strategy

In addressing TEG and r-TEG abnormalities, experts recommend the following3:


The Quick and Dirty: Pattern Recognition

Perhaps most useful for the ED physician is knowledge of qualitative TEG representations:


Some clarification on DIC Stage 1 and 2:

  • Stage 1: Fibrinolysis results in the degradation of fibrin, increasing fibrin degradation products (FDPs). Excess FDPs result in clot de-stabilization.1
  • Stage 2: The cycle of clot formation and breakdown results in platelet and clotting factor consumption.1

Why Might an Emergency Medicine Physician Want to Know about this Test?

Coagulation abnormalities in trauma patients have demonstrated a significant association with infection, multi-organ failure, and death.15-18 Given its ability to quickly detect hematologic pathology, the TEG is becoming a tool for the evaluation of transfusion requirements/coagulopathy post transfusion in this patient population.3,12,13

What does the literature say?

Cotton, et al., 20114:

  • Pilot study to evaluate the timeliness of r-TEG results, their correlation to conventional coagulation testing (CCT – PT, aPTT, INR, platelet count, fibrinogen), and the ability of r-TEG to predict early blood transfusion.
    • 272 patients meeting requirements for major trauma activation
    • Outcomes:
      • All r-TEG values available within 15 minutes vs. 48 minutes for CCTs
      • ACT, r-value, k-time correlated with PT, INR, PTT (r >0.70; p<0.001)
      • MA and a-angle correlated with platelet count (p<0.001, p<0.001)
      • Controlling for demographics and ED vitals: ACT>128 predicted massive transfusion (>10 U) in the first 6 hours of presentation and treatment

Bottom line – r-TEG results were available within minutes, results correlated with conventional coagulation test results, and were predictive of the requirement for early massive transfusion.

Holocomb, et al., 201219:

  • Study to evaluate the reliability of r-TEGs versus CCTs in predicting blood product transfusion
    • 1974 major trauma patients, median ISS 17 (25% meeting criteria for shock; 28% transfused, 6% died within 24 hours)
    • Outcomes
      • When controlling for age, injury mechanism, weighted-Revised Trauma Score, base excess and hemoglobin, ACT predicted RBC transfusion and a-angle predicted massive transfusion better than PT/aPTT or INR (p<0.001).
      • a-angle was superior to fibrinogen for predicting plasma transfusion, and MA was superior to platelet count for predicting platelet transfusion (p<0.001)

Bottom line – r-TEG was more accurate in the prediction of requirements for RBC, plasma, and platelet transfusions as compared to traditional CCTs.

Wikkelso A, et al., 201612:

  • Cochrane Review including 17 current RCTs (n=1493 participants)
    • Per the authors:
      • Low quality studies: numerous biases
      • Limited generalizability: majority of studies center on cardiac patients undergoing surgical intervention

Bottom line – There is growing evidence to suggest that the utilization of TEG and ROTEM reduce transfusion requirements and improve morbidity in patients with bleeding, but additional studies are required.

Back to Our Case

Why was the trauma surgeon concerned? If we interpret our TEG values:

  • R time 20.0 => well above the upper limit of normal (10.0 minutes) = significantly prolonged time for clot formation
  • K time 13.2 => normal: up to 10.0 = prolonged fibrin cross-linking
  • a-angle 16.5 => normal >53.0 = limited clot formation
  • MA 38 => normal platelet function >50 = limited platelet function

More importantly, one quick glance at our TEG and through pattern recognition, we known that aside from his significant traumatic injuries, the patient is in trouble. This waveform is characteristic of DIC Stage 2.

Key Pearls

  • A TEG can be used as a rapid assessment of thrombosis and fibrinolysis.
  • Although additional RCTs are needed, TEGs utilized in trauma patients have been demonstrated to reduce transfusion requirements (important when we consider TACO/TRALI, risk of DIC, and blood-borne pathogens).
  • If nothing else, take a few minutes to review the characteristic TEG waveforms – depending on your laboratory processing time, knowledge of above tracings could allow early identification of coagulopathy and immediate treatment.


References / Further Reading

  1. Williams. Haemscope Basic Clinician Training: Fibrinolysis and Hyperfibrinolysis TEG Analysis. Available from:
  2. Walsh M, Thomas S, Howard J, Evans E, Guyer K, et al. Blood component therapy in trauma guided with the utilization of the perfusionist and thromboelastography. J Extra Corpor Technol. 2001; 43(4):162-167.
  3. Semon G, Cheatham M. Thromboelastography in Trauma. Surgical Critical Care Evidence-Based Guidelines Committee. 2014. Available from:
  4. Cotton B, Faz G, Hatch Q, Radwan Z, Podbielski J, et al. Rapid thromboelastography delivers real-time results that predict transfusion within 1 hour of admission. J Trauma. 2011; 71:407-417.
  5. Teodoro da Luz L, Nascimento B, Rizoli S. Thromboelastography (TEG): practical considerations on its clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013; 21:29.
  6. Bollinger D, Seeberg M, Tanaka K. Principles and practice of thromboelastography in clinical coagulation management and transfusion practice. Transfus Med Rev. 2012: 26(1): 1-13.
  7. Thakur M, Ahmed A. A review of thromboelastography. Int J periop Ultrasound Apply Technol. 2012; 1(1):25-29.
  8. Nickson C. Critical Care Compendium: Thromboelastogram (TEG). 2014. Available from
  9. Kashuk J, Moore E, Sawyer M, Wolhauer M, Pezold M, et al. Primary fibrinolysis is integral in the pathogenesis of acute coagulopathy of trauma. Ann Surg. 2010; 252: 434-444.
  10. Zhu S, Diamond S. Contact activation of blood coagulation on a defined kaolin/collagen surface in microfluidic assay. Thromb Res. 2014; 134(6): 1335-1343.
  11. Heemskerk J, Bevers E, Lindhout T. Platelet activation and blood coagulation. Throm Haemost. 2002; 88(2):186-193.
  12. Wikkelso A, Wetterslev J, Moller A, Afshari A. Thromboelastography (TEG) or thromboelastometry (ROTEM) to monitor haemostatic treatment versus usual care in adults or children with bleeding (Review). Cochrane Database of Systematic Reviews. 2016; 8:1-149.
  13. Luddington R. Thromboelastography/thromboelastometry. Clin Lab Haematol. 2005; 27(2):81-90.
  14. Jeger V, Zimmerman H, Exadaktylos A. Can rapid TEG accelerate the search for coagulopathies in the patient with multiple injuries? J Trauma. 2009; 66:1253-1257.
  15. Niles S, McLaughlin D, Perkins J et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma. 2008; 64:1459-1463.
  16. Brohi K, Sing J, Heron M. Coats T. Acute traumatic coagulopathy. J Trauma. 2003; 54:1127-1130.
  17. Cotton B, Gunter O, Isbell J, et al. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma. 2008; 64;1177-1182.
  18. Cohen J, Call M, Nelson M, et al. Clinical and mechanistic drivers of cute traumatic coagulopathy. J Trauma Acute Care Surg. 2013; 75:S40-47.
  19. Holocomb J, Minei K, Scerbo M, Radwan Z, Wade C, et al. Admission rapid thromboelastography can replace conventional coagulation tests in the emergency department: experience with 1974 consecutive trauma patients. Ann Surg. 2012

Managing Sexual Assault in the Emergency Department

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) and Daniel Sessions, MD (Medical Toxicologist, South Texas Poison Center / Assistant Program Director at SAUSHEC, USA) // Edited by: Courtney Cassella, MD (@Corablacas, EM Resident Physician, Icahn SoM at Mount Sinai) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

It’s seven o’clock on a Saturday morning; as you sip your coffee in a feeble attempt to awaken neurons, you glance up as a nurse passes, leading a young female to a room. The woman appears distraught and disheveled: dress wrinkled, eyes bloodshot, cheeks tear-stained and blackened by the previous night’s makeup. As you glance at the patient tracking board, you note her chief complaint: Alleged Sexual Assault. Engrossed by a sickening, sinking feeling, you attempt to locate your department’s sexual assault protocol binder. As you walk toward the room you prepare yourself mentally for what will likely be an emotionally taxing encounter for all involved.

If you’ve found yourself in a situation similar to that depicted above, and could use a refresher on this important topic: read on as we discuss must knows for the ED management of sexual assault.

Epidemiology of Sexual Assault

Between 300,000-700,000 American women are sexually assaulted annually.1 While 94% of assault patients who present to emergency departments are females, current studies indicate a lifetime prevalence of sexual assault as occurring among 1 in 33 males.2 Adolescents disproportionately represent the majority of sexual assault victims (incidence peaking between the ages of 16 –19 years), with approximately 40% of this population reporting assault during their first sexual encounter.3-5

Contrary to popular belief, nearly 80% of persons having experienced sexual assault report knowing their offender; 18% identifying their assailants as former spouses or love interests.6  Hailed as one of the most widespread and under-reported violent crimes in the U.S.7, rape is associated with non-genital trauma in 40-81% of cases, with 5% requiring hospitalization for serious injury.5,8,9

The Role of the Emergency Physician

This review will address patient stabilization, provide recommendations for obtaining a medical and assault history, and detail pregnancy and sexually transmitted infection prophylaxis. An in-depth discussion of the forensic examination will be omitted, as requirements regarding healthcare provider training, tools contained within forensic collection kits, time allotted between alleged assault and court admissible evidence collection, and chain of custody legislation vary according to individual state law.

Stabilizing the Patient

The evaluation of an emergency department patient begins with an assessment of the ABCs. In extreme cases, patients with non-genital trauma may present with internal injuries, blunt head injury, and knife or gunshot wounds (2%)10 requiring intervention to address altered mental status or hemodynamic instability. After life- or limb-threatening injuries have been addressed, the patient should be moved to a quiet setting to begin discussion of consent and history taking.5,7

Providing Information & Obtaining Consents

Aside from immediate stabilization, information is the most valuable tool in caring for your patient.

Understand the limitations of the evaluation and treatment which your organization is capable of providing (to include the forensic examination), be familiar with state laws regarding timelines for reporting, and arm yourself with resources for referral (forensic exam specialists, counselors, chaplains, etc.) as appropriate.

If needed, state attorney’s offices may be contacted regarding the provision of a patient advocate. In addressing the patient, it is important to inform him/her that he/she may undergo forensic examination without the requirement for reporting.10 The typical time frame for evidence collection is within 72 hours to 5 days. Providers should check within their state what is the maximum time frame post assault for court admissible evidence collection. It is highly recommended that an advocate be provided to assist the patient during the examination, and facilitate the sharing of information regarding legal options.10,11 

Consents must be obtained for information gathering and performance of a forensic examination.5,11 If the patient would like to report the assault, local law enforcement personnel must be contacted. The patient should be advised of state legislations/circumstances, which require mandatory reporting. Examples include12:

  • Sexual assault of an elderly person or vulnerable adult
  • Sexual assault of a minor (categorization as a “minor” varies from state to state)
  • Non-accidental trauma
  • Injuries sustained secondary to criminal conduct (definitions of “criminal conduct” vary by state)
  • Assault with a deadly weapon

Obtaining an Appropriate Medical & Sexual History

In an effort to avoid repeated psychological trauma, portions of the medical and sexual history may be deferred until a later time at which an interview and forensic examination is to be conducted by the state certified/trained personnel. Medical history taking should include a query of the following:

Medical History5,11
Last Menstrual Period
Recent (60 days) anal-genital injuries, surgeries, diagnostic procedures or medical treatments that may affect the interpretation of current physical findings
Pertinent medical condition(s) that may affect the interpretation of physical findings (blood dyscrasias, etc.)
Pre-existing physical injuries prior to the alleged assault


Pre/Post Assault History5,11
Other intercourse within the previous 5 days (anal, vaginal, or oral); intercourse with or without ejaculation; condom use
Voluntary alcohol or drug use prior to the assault
Voluntary alcohol or drug use between the time of the assault and presentation for examination


Post Assault Hygiene History (Presenting ≤ 72 hours Post Assault)5,11
Bodily functions: urination, defecation
Utilization of genital or body wipes or douches
Removal or insertion of tampons or diaphragms
General hygiene activities: bathed/showered/washed; changed clothing; ate or drank; brushed teeth or gargled


Assault Related History5,11
Loss of memory/consciousness
Presence of non-genital or anal-genital injury
Date/Time/Location of assault
Alleged assailant(s)/Age/Gender/Ethnicity/Relationship to patient
Methods utilized for assault: Weapons, physical blows, restraints, burns, strangulation, threat(s) of harm, involuntary ingestion of drugs


Assault Related Acts as Described by the Patient5,11
Vaginal Penetration
Anal Penetration
Oral copulation of genitals/anus
Non-genital acts (licking, kissing, suction injury, biting)
Use of foreign bodies
Contraception or lubricant use

Performing the Physical Exam

Elements of the physical exam include an assessment of5,11,13:

  • The patient’s general appearance/emotional status
  • A complete physical examination of the head, body, and extremities with documentation of all visible injuries
  • A genital examination with colposcopy for females if available

Elements of evidence collection include5,11,13:

  • Swabs/smears of involved orifices
  • Patient saliva samples
  • Fingernail scrapings
  • Packaging of patient clothing
  • Head hair and pubic hair combing and collection
  • External genitalia and peri-anal swabbing
  • Swabbing of bodily areas soiled with blood, semen, or saliva
  • Blood typing of specimens obtained

For an example of the forensic examination document sheet, see the Rosens’ text: Reference 5.

A Word on Sexual Assault Nurse Examiners (SANE)

In 2002, the International Association of Forensic Nurses (IAFN) created a certification program to: develop nurses who were experts in history-taking, treatment of trauma response and injury, documentation and collection of evidence, and the delivery of testimony required to bring sexual assault cases through the legal system.14 Today the IAFN maintains SANE education guidelines and has extended the scope of forensic nursing to include certification programs in pediatric sexual assault nursing (SANE-P vs. adult/adolescent SANE-A).15

There are currently greater than 400 SANE programs across the nation, the majority associated with major medical centers.16 (To find a program, the following search engine may be employed:

Why is this pertinent for emergency physicians? Although further research is required (secondary to small sample sizes, and differing definitions regarding the provision of care), studies have identified improved patient outcomes through the employment of dedicated sexual assault nurse examiners:

Sievers et al., 2003: Criminal laboratory analysts completed 515 audits of sexual assault evidence kits submitted to the Colorado Bureau of Investigation from October 1999-April 2002 (279 kits completed by SANEs, 236 completed by physicians and local nurses). As compared to physicians and local nurses, SANEs were:

  • More likely to have a completed chain of custody requirements (92%) as compared to 81% of physicians/local nurses.
  • More likely to have properly sealed individual specimen envelopes (91% vs. 75%).
  • More likely to have labeled the individual specimen envelopes (95% vs. 88%), and to have collected the appropriate amount of pubic hair (88% vs. 74%), and head hair (95% vs. 80%).
  • More frequently included the appropriate number of blood tubes (95% vs. 80%), collected the appropriate amount of swabs (88% vs. 71%), and included a vaginal fluid slide for sperm motility (87% vs. 72%).17

Campbell et al., 2005: Empirical literature review of the psychological recovery of survivors, the provision of comprehensive medical care, the documentation of forensic evidence, and the reliability of testimony during prosecution, demonstrated SANE nurses as effective in all domains. (As recognized by the authors: numerous studies reviewed lacked methodological controls).18

Interestingly, this has become a topic of debate, as some would argue that SANE nursing programs decrease resident exposure to sexual assault patients, thus limiting resident education regarding proper procedures and protocols.

In 2007, McLaughlin et al. demonstrated a knowledge deficit amongst emergency medicine residents, trained in an institution equipped with a SANE program, with respect to written knowledge regarding the sexual assault exam, collection of evidence (simulation utilizing mannequins), performance during standardized patient interviews, and documentation:

Twenty-three (85%) residents completed the study. Pre-intervention, residents scored 56% on the written knowledge test, 63% on evidence collection, 71% on standardized patient interviews, and 66% on the written note.18

After an educational intervention, McLaughlin and his colleagues noted: Residents demonstrated significant post-intervention improvements in written knowledge (improvement 24%; 95% confidence interval [CI] 20% to 27%) and evidence collection (improvement 18%; 95% CI 12% to 24%). Resident post-test scores were similar to those of SANE providers.18

Sexually Transmitted Infection (STI) and Pregnancy Prophylaxis

The likelihood of acquiring an STI after rape is difficult to predict, and varies according to the type of assault, the assailant, and geographic location. Current studies estimate the relative risk of contracting trichomonas as 12%, gonorrhea as 4-12%, and chlamydia as 2-14%.5,13,19

The Centers for Disease Control and Prevention (CDC) recommend the following prophylactic regimen in the treatment of the sexual assault patient:

Figure 1. Prophylactic STI Regimens for the Sexual Assault Patient (Ref 20)

Although prophylaxis for syphilis is not recommended by the CDC, previous studies report the risk of contraction post sexual assault as approaching 5%.5,13,19 Prophylaxis should be considered in areas or populations where the syphilis is prevalent. Alternatives to prophylactic treatment include the documentation of a recommendation for VDRL/antibody specific testing at a later date.13

The risk of HIV transmission from a single sexual assault is less than 0.1%.5,13 Experts recommend discussing victim and assailant risk factors (Figure 2 – Detailed in Rosen’s text), and utilizing shared decision making to determine the appropriateness of post-exposure prophylaxis (PEP).5,20

Figure 2. Sexual Assault Victim (SAV) and Assailant Risk Factors for HIV Susceptibility and Infectiousness (Ref 5)
Figure 2. Sexual Assault Victim (SAV) and Assailant Risk Factors for HIV Susceptibility and Infectiousness (Ref 5)

Current regimens for non-occupational post-exposure prophylaxis in adults and adolescents include21:

  • Tenofovir disoproxil fumarate (300mg QD) and emtricitabine (200mg QD) +
    • Raltegravir (400mg BID) or Dolutegravir (50mg QD)


  • Tenofovir disoproxil fumarate (300mg QD) and emtricitabine (200mg QD) +
    • Darunavir (800mg QD) + Ritonavir (100mg QD)

Note: Studies demonstrate PEP as most effective when initiated within 72 hours of exposure.20 The CDC recommends providing the patient with a one-week supply of PEP medications, and scheduling follow-up at the one-week point to discuss medication tolerance and side-effects.20 Patients electing to take PEP require interval follow-up for serial laboratory studies (antiviral therapy commonly associated with renal, hepatic, and hematologic side effects).5,20 HIV testing should be performed for all sexual assault victims at 6 weeks, 3 months, and 6 months post assault.20

The CDC recommends post-exposure hepatitis B vaccination (without HBIG) for all sexual assault patients if previously un-immunized. The hepatitis B vaccination series should be completed with subsequent doses at 1-2 months, and 4-6 months after the first injection.20

The risk of pregnancy after a sexual assault is estimated as 2-4%.11,13 Females of reproductive age should be offered pregnancy prophylaxis.20 Ovral, Lo/Ovral, and Nordette may be administered up to 72 hours post assault.11 The most common side-effect associated with these medications is nausea, therefore patients should be discharged with an anti-emetic.11 Female assault victims should be instructed to perform a pregnancy test if menstruation does not occur 3-4 weeks post treatment.11 See Figure 3 for information regarding pregnancy prophylaxis regimens.

Figure 3. Emergency Contraception
Figure 3. Emergency Contraception (Ref 11)

Psychological Care & Follow-Up

Long-term sequelae of sexual assault include depression, drug and alcohol abuse, and sexual dysfunction.13 Studies indicate that up to one-third of sexual assault victims experience PTSD.13 As compared to the general population, rape victims are thirteen times more likely to attempt suicide.13,22 Experts recommend that all sexual assault victims be referred to a rape crisis center within 48 hours of evaluation.13

Medical follow-up visits should be scheduled for the sexual assault patient at 1-2 weeks, and 2-4 months for repeat STD testing, VDRL/FTA-ABS testing, and PEP monitoring as appropriate.5,13,20

Special Topic: Date Rape Drugs

The incidence of drug-facilitated sexual assault (DFSA) is increasing worldwide.5,23 Flunitrazepam (Rohypnol), gama-hydroxybutyrate (GHB), and ketamine have been heralded as the new “date rape drugs,” so let’s do a quick review:

Flunitrazepam (Rohypnol) – a benzodiazepine ten times as potent as valium, is currently available in Europe and Latin America, and is distributed as 1 or 2 mg tablets. In 1996, the U.S. FDA enacted legislation to inhibit the importation of Rohypnol secondary to concerns for abuse. Street names for flunitrazepam include: “Mexican Valium,” “circles,” “roofies,” “la rocha,” “roche,” “R2,” and “rope.” At high doses Rohypnol may cause sedation and significant respiratory depression, however, the drug is distributed in such small concentrations that supportive care is generally all that is required.26

Gama-hydroxybutyrate (GHB) – a naturally occurring fatty-acid derivative of the neurotransmitter, GABA, was originally marketed in the 1990s as a dietary supplement. Today, the over-the-counter sale of GHB has been banned due to its association with seizure-like activity and reflex autonomic activation. GHB is commonly available in oral solutions, and its delivery as such has earned it the street names of “liquid ecstasy,” “soap,” and “salty water.” Individuals ingesting GHB commonly experience symptoms of CNS depression and anterograde amnesia. Bradycardia and tonic-clonic seizures are also well-documented side-effects. Patients exposed to large concentrations often require airway support, including intubation.26

 Ketamine – a derivative of phencyclidine hydrochloride (PCP), was developed in the 1960s for use as a dissociative anesthetic. Ketamine primarily interacts with NMDA receptors to inhibit the release of glutamate, but is also known to stimulate muscarinic, nicotinic, cholinergic, and opiod receptors. Ketamine is currently employed in the medical setting for procedural sedation, pain control, and for the treatment of depression, and is available under the street names of “K,” “kit-kat,” “super K,” and “jet.” Ketamine is sold as a solid or powder for users to inject, ingest, smoke, or snort. Ketamine may cause significant sympathetic activation resulting in tachycardia and hypertension, and users often experience apnea shortly after drug administration. Drug effects are much more prevalent in users who inject ketamine as opposed to ingest it (significant first pass metabolism after oral intake).26 Patients commonly require supportive care. In extreme cases, airway management may be indicated.

The Utility of Serum/Urine Screening in the Emergency Department

Forensic examination requires sampling of blood and urine if the patient endorses substance use/abuse or if he/she reports concern for drug-facilitated sexual assault.5,11 In the setting of DFSA, samples are rarely useful to the emergency medicine physician as the majority of drugs utilized are rapidly absorbed and metabolized5,25:

  • The half-life of Rohypnol is reported as 10-15 hours => frequently undetectable by UDS and requiring high performance liquid chromatography or gas chromatography-mass spectrometry (GC-MS) for identification. (Flunitrazepam and its metabolites, 7-amino-flunitrazepam and norflunitrazepam, are identifiable for up to 3 days post administration by GC-MS).26
  • The half-life of GHB is 20 minutes. GHB is not detectable by standard serum and urine toxicology screens due to its short half-life and its elimination through exhalation (metabolized to CO2). GC-MS will detect GHB up to 6-8 hours post administration.26
  • Serum and urine tests for ketamine (and norketamine, it’s metabolite) are not available as standard laboratory sets.26

As an aside, it is important to note that ethanol remains the number one substance of choice for perpetrators of sexual assault.24,25 While published data from the U.S. is lacking, large studies from Sweden and Norway demonstrate elevated blood alcohol concentration as the number one toxicologic finding in victims of sexual assault27,28:

Hagemann et al., 2013: Retrospective, descriptive study of female patients ≥ 12 years of age presenting for evaluation post sexual assault from 2003-2010 (n=120). In total 102 patient serum samples, drawn within 12 hours of the alleged assault, tested positive for ethanol. The median blood alcohol concentration (BAC) at the time of the assault was 1.87 g/L. Patients testing positive for ethanol more often reported a public place of assault and stranger assailant.27

Jones, et al., 2012: Retrospective review of a Swedish national forensic database (TOXBASE) for female victims of sexual assault having contributed blood and urine samples, 2008-2010 (n=1406) and 2003-2007 (n=1806). In the 2008-2010 group, ethanol was detected as the only drug in 41% (603) of victims, and in the 2003-2007 group as 43% (772) of victims – significantly more prevalent than the previously mentioned date rape drugs representing 2.5% (36) and 3.2% (58) of victims.28

Key Pearls

  • Stabilize the patient as appropriate – 5% of victims require hospitalization secondary to severe injury5,8,9
  • Understand your options and do what’s in the best interest of the patient:
    • Call the patient advocate (state attorney’s offices will provide a list of resources if needed)
    • Refer as appropriate:
      • If the patient may be better served by an institution with a SANE program, then transfer
    • Provide pregnancy prophylaxis as appropriate
    • Provide STI prophylaxis
    • Provide Hepatitis B vaccination if un-immunized
    • Discuss risk factors for HIV transmission and the risks/benefits of prophylaxis
    • Involve a rape crisis counselor EARLY
      • Many patients experience PTSD, depression, and suicidal ideation post assault13
    • Stress the importance of follow-up for STI monitoring, PEP evaluation as indicated, and continued emotional support

References / Further Reading

  1. Sampsel K, Szobota L, Joyce D, Graham K, Pickett W. The impact of a sexual assault/domestic violence program on ED care. J Emerg Nurs. 2009;35(4):282-289.
  2. Tjaden P, Thhoennes N: Extent, nature, and consequences of rape victimization: findings from the national violence against women survey. National Institute of Justice Special Report. Washington, DC: U.S. Department of Justice; 2006. Available from nij/210346.pdf.
  3. Poirier, M. Care of the female adolescent rape victim. Pediatr Emerg Care, 2002;18:53.
  4. Adams J, Giradin B, Faugno D. Adolescent sexual assault: Documentation of acute injuries using photo-colposcopy. J Pediatr Adolesc Gynecol. 2001;14:174-180.
  5. Slaughter L. Sexual Assault. Rosen’s Emergency Medicine – Concepts and Clinical Practice. 8th ed. Chapter 67. 855-871. Elsevier Saunders. Philadelphia, PA.
  6. Bureau of Justice Statistics: National crime victimization survey: criminal victimization. 1998. Washington, D.C.: U.S. Dept of Justice Programs; 1999.
  7. Dunn S, Gilchrist V. Sexual assault: Family violence and abusive relationships. J Prim Care. 1993; 20(2):359-373.
  8. Kobernick M, Seifert S, Sanders A. Emergency department management of the sexual assault victim. Emerg Med Clin N Am. 1985; 2:205-214.
  9. Saltzman L, et al: National estimates of sexual violence treated in the emergency departments. Ann Emerg Med. 2007; 49:210-217.
  10. Marchbanks P, Lui K, Mercy J. The risk of injury from resisting rape. Am J Epidemiol. 1990; 132:540-549.
  11. McConkey T, Sole M, Holocomb L. Assessing the female assault provider. JNP. 2001; 26(7):28-41.
  12. Scalzo T. Rape and sexual assault reporting laws. National Center for Prosecution of Violence Against Women. Available from:
  1. Linden J. Sexual assault. Emerg Med Clin N Am. 1999; 17(3):685-697.
  2. Speck P, Peters S. Forensics in np practice. Adv Nurse Pract. 1999;7(11):18.
  3. International Association of Forensic Nurses. Forensic nursing scope and standards 2015. Available from:$elax%20pm%20$andprotect%20$elax%20pm%20$draft%22
  1. Sexual Assault Resource Service. SANE programs in the United States. Available from:
  2. Sievers V, Murphy S, Miller J. Sexual assault evidence collection more accurate when completed by sexual assault nurse examiners: Colorado’s experience. J Emerg Nurs. 2003; 29(6):511-514.
  3. Campbell R, Patterson D, Lichty L. The effectiveness of sexual assault nurse examiner (SANE) programs: a review of psychological, medical, legal, and community outcomes. Trauma Vioence Abuse. 2005;6(4):313-329.
  4. McLaughlin S, Monahan C, Doezema D, Crandall C. Implementation and evaluation of a training program for the management of sexual assault in the emergency department. Ann Emerg Med. 2007:49(4):489-494.
  5. Jenny C, Hooton T, Bowers A, et al. Sexually transmitted disease in victims of rape. 
N Engl J Med 322:713-716,1990
  6. Centers for Disease Control and Prevention. Sexual assault and STDs. 2010. Available from:
  7. Centers for Disease Control and Prevention. Updates for antiretroviral postexposure prophylaxis after sexual, injection drug use, or nonoccupational exposure to HIV. 2016. Available from:
  8. Kilpatrick D, Edmunds C, Seymour A. Rape in America-a report to the nation. Crime Victim Research and Treatment Center. Charleston, SC, Medical University of South Carolina, 1992.
  9. Du Mont J, Macdonald S, Rotbard N, Asllani E, Bainbridge D: Factors 
associated with suspected drug facilitated sexual assault. CMAJ 2009; 
  10. Dinis-Oliveira R, Magalhaes T. Forensic toxicology in drug-facilitated sexual assault. Toxicol Mech Methods. 2013:23(7):471-478.
  11. Jones A, Kugelberg F, Holmgren A, Ahlner J. Occurrence of ethanol and other drugs in blood and urine specimens from female victims of alleged sexual assault. Forensic Sci Int. 2008;181:40-46.
  12. Smith K, Larive L, Romanelli F. Club drugs: methylenedioxymethamphetamine, flunitrazepam, ketamine hydrochloride and gama-hydroxybutyrate. Am J Health-Syst Pharm. 2002;50(1):1067-1076.
  13. Hagemann C, Helland A, Spigset O, Espnes K, Ormstad K, et al. Ethanol and drug findings in women consulting a sexual assault center-associations with clinical characteristics and suspicions of drug-facilitated sexual assault. J Forensic Leg Med. 2013;20:777-784.
  14. Jones A, Holmgren A, Ahlner J. Toxicological analysis of blood and urine samples of victims of alleged sexual assault. J Clin Toxicol. 2012;50:555-561.

Emergency Department Tips & Tricks for Managing the Suicidal Patient

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

An adolescent male with a chief complaint of suicidal ideation presents to the emergency department (ED). The 17 year-old patient is lead to a triage room where a nurse checks his vital signs, performs an EKG, and draws blood for initial screening labs. After handing the young man a set of hospital scrubs, the nurse exits, pulling the curtain to allow for limited privacy. Minutes later, a chilling scream echoes through the halls. Personnel rush to the triage center where an attending physician is struggling to remove a disposable latex tourniquet from the, now cyanotic, patient’s neck.

Believe it or not, this is a depiction of recent events witnessed in a community ED. As you stand ready to perform your medical screen and proceed to phone a friend in psychiatry, let’s take a minute to address a few pearls in approaching the suicidal patient.

Epidemiology of Suicidal Ideation

Today more than twelve million annual emergency department visits involve a diagnosis related to mental health or substance abuse; representing nearly one in every eight ED encounters.1 Occurring at a rate of one suicide every thirteen minutes, intentional self-harm represents the leading cause of death among persons greater than 85 years of age. Among American Indians and Alaska natives ages 10-34, and in all U.S. citizens aged 15-34 years, suicide is the second leading cause of death.2 Data currently identify males as four times more likely to commit suicide than females.2 Costs associated with suicide, both medical and related to decreased work productivity, total nearly $51 billion annually.2

The Role of the Emergency Physician

This review will address patient stabilization and provide tips and tricks for use in interviewing and evaluating the suicidal patient. An in-depth discussion of toxic ingestions will be omitted as this content is addressed elsewhere:

FOAMED Resource Series Part IV: Toxicology
Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC)

Stabilize the Patient

Current surveys suggest that approximately one million people in the U.S. engage in intentional self-harm behavior, and that for every death reported by suicide, approximately twelve individuals severely harm themselves.3 Of patients inflicting self-harm, nearly 650,000 are evaluated in the ED each year.4

Patients may present after a failed suicide attempt by gun-shot wound (mechanism in 59.6% of males having committed suicide4), suffering from the affects of an acute toxic ingestion (mechanism in 34.8% of females having committed suicide4), or actively bleeding from an arterial laceration (cutting, burning, and blunt trauma reported by males and females as common mechanisms of self-harm5); therefore, the emergency physician must stand ready to address the ABCs.

Transition the Patient to a Safe Environment

All patients who are hemodynamically stable upon presentation should be taken to an area of the ED that is free of all potentially dangerous medications and equipment. Patients should be searched for weapon/substances and be provided a set of scrubs or disposable clothing to discourage elopement. At no point in time should the patient be left unattended.6

 Perform an Assessment of Suicide Risk

Obtain an appropriate medical history centering on the identification of risk factors for suicide:


A few words on risk factors:

Adolescents: Adolescent patients are most likely to present with injuries secondary to self-harm (ratio of attempted to completed suicides reported as 200:110). Although parental consent is typically required for the treatment of minors (defined as age <18 in the majority of states), evaluation following a serious suicide attempt is mandated according to the Emergency Medical Treatment and Active Labor Act.6

If and when present, parents and caregivers should be questioned regarding impulsive behavior, bouts of aggression, significant family stressors, and inter-personal conflicts, as these can be subtle signs of depression.11

The elderly: Suicidal ideation is endorsed much less frequently in the elderly population,12 however, completed suicides are much more likely to occur later in life (ratio of attempted to completed suicides reported as 4:112,13). Patients >65 years of age should be questioned specifically regarding: recent death of a loved one, perceived poor health, social isolation and loneliness, uncontrolled pain, and major changes in social roles as these are frequently associated with completed suicide.12

 Current psychiatric diagnosis: When controlled for other factors, a previous history of major depressive disorder is the most significant risk factor for completed suicide in males and females.11 Patients with a history of military service should be questioned regarding post-traumatic stress disorder as these individuals are also at increased risk for suicide.11

Substance abuse: Current data identify 19-27% of all suicides as associated with alcohol.14 Specifically, individuals over the age of 18 engaging in heavy episodic drinking (having ≥ 5 alcoholic drinks in a row on one occasion) are noted to have a suicide risk 1.2 times that of their non-drinking counterparts.15 Question patients regarding alcohol consumption.11,14,15

 An assessment of thought content is particularly important in patients with a previous medical history of schizophrenia, mood disorder, bipolar disorder, and substance abuse as these conditions pre-dispose to episodes of psychosis.14 Patient reports of auditory hallucinations, persecutory delusions, or thoughts of external control or religious preoccupation require immediate hospitalization in order to prevent harm to self or others.12,14

 Patients should be questioned regarding prescription drugs (dosing/compliance/regimen changes), the use of homeopathic remedies, and the use of over-the-counter medications. This information is vital if suspecting toxic ingestion, medication withdrawal, or mood alteration secondary to changes in pharmacotherapy.

In interviewing the patient, enquire as to weapons access as this is also an independent risk factor for completed suicide.8

Perform risk stratification:

If you attended a medical school in the U.S., chances are that you’ve had some exposure to the Modified Sad Persons Score:


Originally developed by Hockberger and Rothstein at the Harbor-UCLA Medical Center in 1988, this scoring tool was created to predict the need for hospitalization in individuals at risk for suicide. After analysis of 119 patients, Hockberger and Rothsetin identified a score ≥ 6 as having a sensitivity of 94% and a specificity of 71% for predicting the need for psychiatry directed hospitalization (P<0.001).14 While an excellent reminder of suicide risk factors, the authors’ score is limited in that it was designed to assess the decision-making of behavior of psychiatry personnel at one institution.

The Manchester Self-Harm Rule was published by Cooper et al.17 in 2006 as a mechanism to determine the risk of repeat self-harm or suicide in patients presenting to the ED with the chief complaint of self-injury. Demographic and clinical information from 9,086 patients presenting to 5 emergency departments in Manchester and Salford, England (2001-2007) were utilized to identify the following risk factors:


The Manchester Self-Harm Rule demonstrated 94% sensitivity in the detection of individuals who would perform repeated self-harm or suicide within six months following the initial ED encounter (patients who possessed one or more risk factors).17 Data utilized in developing the Manchester Self-Harm Rule was collected from an urban population with high rates of benzodiazepine use and abuse, thus limiting its generalizability.17 Ultimately, clinical judgement in the evaluation of the suicidal patient is paramount.

Performance of the Physical Exam (Secondary Examination in the Hemodynamically Unstable Patient)

Elements of the physical exam include an assessment of:

  • The patient’s general appearance (emotional status, thought content, and affect).
  • A complete physical examination of the head, body, and extremities with documentation of all visible injuries.

Actively search for signs and symptoms of acute ingestions, toxidromes, and withdrawal symptoms: diaphoresis, hyperthermia, hypopnea, or bradypnea, pinpoint or dilated pupils, hyper or hyporeflexia, clonus, tremor, or altered mental status.18

  • Sympathomimetic toxidrome: agitation, delirium, hypertension, hyperthermia, nausea, and muscle rigidity.
  • Anticholinergic toxidrome: mydriasis, urinary retention, tachycardia and hyperthermia.
  • Serotonin syndrome: altered mental status, autonomic instability, myoclonus, and tremor.
  • Neuroleptic malignant syndrome: lead pipe rigidity, hyperthermia, altered mental status.
  • Monoamine oxidase inhibitor (MAOI) toxicity: severe hyperthermia, nausea, emesis, and cardiovascular collapse. Excessive ingestion of tyramine containing food stuffs during MAOI therapy may result in hypertensive crisis.
  • Patients experiencing benzodiazepine, opiod, and alcohol withdrawal may present with agitation, hypertension, tachycardia, and GI upset.

Primary interventions should address airway, breathing and circulation. Benzodiazepines are the treatment of choice for agitation, anticholinergic toxicity, sympathomimetic toxicity, and serotonin syndrome. Dopamine agonists have been demonstrated to improve symptoms in neuroleptic malignant syndrome. Provide fluid resuscitation in the setting of seizure and muscular rigidity in order to avoid complications secondary to rhabdomyolysis.18

Evaluate for signs and symptoms of medical conditions, and their sequelae, that are commonly associated with psychiatric symptoms:

  • Hypoglycemia (perform a bedside blood glucose assessment)
  • Thyroid pathology (thyroid storm or myxedema coma)
  • Cushing’s
  • Intracranial trauma
  • Infectious etiologies: HIV, syphilis, meningitis/encephalitis
  • Neoplasm (intracranial mass vs. hypercalcemia secondary to metastasis)
  • Degenerative neurologic diseases (Alzheimer’s, Parkinson’s, Creutzfeld-Jacob, Multiple Sclerosis)19

Notes on the agitated patient: if the patient presents a risk to self or others, the utilization of chemical or mechanical restraints should be entertained, bearing in mind that this may worsen hyperthermia and rhabdomyolysis. See Dr. Lulla’s and Singh’s The Art of the ED Takedown for a quick refresher on these interventions:

 Pertinent Studies

Once a thorough history and physical examination are completed, clinical decision-making should be utilized to assess the need for advanced imaging and adjunct studies.

Imaging: A non-contrasted CT head à rule out intracranial mass/abscess, intracranial hemorrhage, hemorrhagic CVA, etc. Consideration should be made for additional imaging as required (CVA: CTA head/neck vs. MRI/MRA, etc.).

EKG: An EKG may be diagnostic in the hemodynamically unstable patient. Sodium channel blockade (tricyclic anti-depressant therapy) often manifests as a rightward axis in the terminal 40-msec of the QRS complex (terminal R wave in aVR).20

Currently there are no data-driven consensus recommendations regarding the appropriateness of routine laboratory screening tests in patients with suicidal ideation. As previously mentioned, the history and physical exam should be utilized to direct evaluation for an underlying organic etiology of depression and suicidal ideation. Studies to consider include21:

  • CBC
  • CMP
  • TSH, FT4
  • HIV
  • Serum ETOH
  • Serum salicylates
  • Serum acetaminophen

The use of urine drug screens (UDS) in the evaluation of suicidal patients is controversial, as numerous studies have demonstrated the results of these screens as having minimal impact on patient care. Given these findings, the American College of Emergency Physicians currently recommends against the routine use of UDSs in the suicidal population.22


After performance of patient stabilization, attainment of a history and physical, and assessment of imaging/laboratory studies as appropriate, medical clearance may be given, and consultation placed for specialist evaluation and treatment.

If the patient appears to be a risk to him/herself or others, or is gravely disabled (unable to provide for his/her basic needs), involuntary psychiatric detention should be pursued. Regulations regarding involuntary psychiatric holds are state specific, therefore the emergency physician must be apprised of local policies and procedures.8 Obtaining collateral information from family and friends will often facilitate this intervention.19

Contracts for safety: While some physicians may elect to create a contract for safety, allowing outpatient evaluation and treatment, this is not advised for the emergency physician. Contracts for safety do not substitute for adequate documentation regarding the risk of suicide, or free the physician of liability in cases of subsequent self-harm and suicide.8

Key Pearls

  • Stabilize as appropriate => a number of patients will present after performing self-harm
  • If the patient is hemodynamically unstable, consider an EKG to evaluate for sodium channel blockade (TCA overdose)
    • Quickly evaluate for signs/symptoms of toxic ingestions
  • In the stable patient, perform an H&P focusing on risk factors for suicide
    • Question patients regarding substance abuse (specifically alcohol)
    • Question regarding access to weapons
    • Use friends/family to corroborate stories
  • During the physical examination, evaluate for findings consistent with toxidromes or organic pathology
  • After seeking out organic etiologies of suicidal ideation, medically clear the patient and consult a specialist
  • Be familiar with state laws regarding emergency detention
  • Avoid the use of safety contracts in the emergency setting

 References / Further Reading

  1. Owens P, Mutter R, Stocks C. Mental health substance abuse-related emergency department visits among adults 2007. Statistical Brief #92. Agency for Healthcare Research and Quality. Available from:
  2. Centers for Disease Control and Prevention. Suicide: Facts at a glance. Available from:
  3. Centers for Disease Control and Prevention. Web-based injury statistics query and reporting system (WISQARS). National Center for Injury Prevention and Control. Available from:
  4. Chang B, Gitlin D, Patel R. The depressed patient and suicidal patient in the emergency department: Evidence-based management and treatment strategies. Emergency Medicine Practice. 2011; 11(9):1-24.
  5. Kerr P, Muehlenkamp J, Turner J. Nonsuicidal self-injury: A review of current research for family medicine and primary care physicians. J Am Board Fam Med. 2010; 23(2):240-259.
  6. Kennedy S, Baraff L, Suddath R, Asarnow J. Emergency department management of suicidal adolescents. Ann Emerg Med. 2004; 43:452-462.
  7. Mendelson WB, Rich CL. Sedatives and suicide: The San Diego study. Acta Psychiatr Scan 1993;88:337–41.
  8. Ronquillo L, Minassian A, Vilke G, Wilson M. Literature-based recommendations for suicide assessment in the emergency department: a review. J Emerg Med. 2012; 43(5):836-842.
  9. American Foundation for Suicide Prevention. Suicide Statistics. 2016. Available from:
  10. Tuzun B, Polat O, Vatansever S, Elmas I. Questioning the psychosocio-cultural factors that contribute to the cases of suicide attempts: an investigation. Forensic Sci Int 2000;113:297–301.
  11. Schwab J, Warheit G, Holzer C. Suicidal ideation and behavior in a general population. Diseases of the Nervous System. 1972;33(11):745–748.
  12. Mitchell A, Garand L, Dean D, Panzak G, Taylor M. Suicide assessment in hospital emergency departments: Implications for patient satisfaction and compliance. Top Emerg Med. 2005; 27(4):302-312.
  13. Parkin D, Stengel E. Incidence of suicidal attempts in an urban community. British Medical Journal. 1965;2(54):133–138.
  14. Canapary D, Bongar B, Cleary K. Assessing risk for completed suicide in patients with alcohol dependence: Clinicians’ views of clinical factors. Professional Psychology: Research and Practice. 2002;33(5):464–469.
  15. Asteline R, Schilling E, James A, Glanovsky J, Jacobs D. Age variability in the association between heavy episodic drinking and adolescent suicide attempts: findings from a large-scale, school-based screening program. J Am Acad Child Adolesc Psychiatry. 2009; 48(3):262-270.
  16. Hockberger RS, Rothstein RJ. Assessment of suicide potential by nonpsychiatrists using the SAD PERSONS score. J Emerg Med. 1988;6:99–107.
  17. Cooper J, Kapur N, Dunning J, Guthrie E, Appleby L, Mackway-Jones K. A clinical tool for assessing risk after self-harm. Ann Emerg Med 2006;48:459–66.
  18. Zosel A. General Approach to the Poisoned Patient. In Emergency Medicine: Diagnosis and Management. 7th ed. Boca Raton: CRC Press, 2016: 292-298.e1.
  19. Knoll, J. The Psychiatric ER Survival Guide. 2016. Upstate Medical University. Available from:
  20. Niemann J, Bessen H, Rothstein R, et al. Electrocardiographic criteria for tricyclic antidepressant cardiotoxicity. Am J Cardiol. 1986;57(13):1154-1159
  21. Russinoff I, Clark M. Suicidal Patients: Assessing and Managing Patients Presenting with Suicidal Attempts or Ideation. 2004. Available from:
  22. Lukens T, Wolf S, Edlow J, Shahabuddin S, Allen M, et al. Clinical policy: critical issues in the diagnosis and management of the adult psychiatric patient in the emergency department. Ann Emerg Med. 2006; 47(1):79-99.

The Adult Hypoglycemic Patient: Tips for Emergency Department Management

Authors: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) and Daniel Sessions, MD (Medical Toxicologist, South Texas Poison Center / Associate Program Director at SAUSHEC, USA) // Edited by: Jamie Santistevan, MD (@Jamie_Rae_EMdoc, Admin and Quality Fellow at UW, Madison, WI) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital) 

A 55 year-old female with a previous medical history of hypertension, hyperlipidemia, and diabetes, presents to the emergency department with slurred speech and dysarthria. As you enter the room, an anxious family member hands you a list detailing the following medications: lisinopril, clopidogrel, and glimepiride. VS: HR 110, RR 14, BP 132/88, T 99.3. Accucheck: 48 mg/dL.

A 37 year-old male presents for the evaluation of recurrent nausea and diaphoresis. Review of systems is notable for a recent diagnosis of gout with initiation of indomethacin. The patient reports visiting an urgent care facility 48 hours prior for similar symptoms where he was discharged after consuming a container of orange juice. Current VS: HR 123, RR 16, BP 137/92, T 98.9. Accucheck: 51 mg/dL.

The first case above illustrates a commonly encountered scenario: the diabetic patient with possible sulfonylurea toxicity, but what about the second, our 37 year-old male? What could be causing his hypoglycemia? If there are questions in your mind regarding his evaluation and treatment, read on. We’ll review a number of tip and tricks for addressing your next hypoglycemic patient.

Epidemiology of Hypoglycemia

In 2009, the CDC reported 298,000 emergency department visits by diabetic patients assigned the primary diagnosis of hypoglycemia.1 A relatively recent study of 33 million Medicare patients identified hypoglycemia as the most common acute metabolic event leading to hospitalization among the diabetic population.2 

Aside: Data regarding emergency department visits for hypoglycemia are maintained by the Centers for Disease Control and Prevention (CDC) as subset of the National Ambulatory Health Care Survey.1 (Metrics are monitored for patients with a primary ICD code of hypoglycemia and a secondary ICD code of diabetes,1 therefore little cumulative data exists for emergency department visits for hypoglycemia occurring in non-diabetic patients.

Defining Hypoglycemia

In a diabetic patient, hypoglycemia is defined as a self-monitored (acceptably, self-reported) blood glucose level ≤ 70mg/dL.2,3

All other patients must have a documented experience of Whipple’s triad for the diagnosis of hypoglycemia to be made3:

  • Signs or symptoms consistent with hypoglycemia
  • A low plasma glucose
  • Resolution of symptoms after plasma glucose concentration is raised

Note: Whipple’s triad was identified by Allen Whipple in 1983, the American surgeon who also coined the Whipple procedure. Experts agree that all patients presenting with severe hypoglycemia (blood glucose ≤ 40mg/dL) should undergo evaluation and treatment, even in the absence of associated signs and symptoms.2

Risk Factors for the Development of Hypoglycemia

Risk factors for the development hypoglycemia have been studied extensively in the diabetic population. An observational cohort study including 917,440 adults (age ≥ 18) conducted from 2005-2011 identified patients filling prescriptions for insulin as having the highest rates of hypoglycemia (10-12 times higher than those on non-secretagogue medications, and 3-5 times higher than those prescribed secretagogues) (p<0.001).4

The study also identified severe hypoglycemia (hypoglycemia requiring intervention by medical personnel) as occurring up to eight times more frequently in diabetic patients with multiple medical comorbidities (chronic kidney disease, congestive heart failure, and vascular disease).3

A second study, prospectively following 5,063 United Kingdom diabetes patients (ages 25-65 years) for a duration of six years, identified major hypoglycemic events (reported by patients as either requiring third party assistance or medical attention) as occurring most frequently in individuals administering basal and prandial insulin (5.3% annually), followed by basal insulin (3.8% annually), sulfonylurea therapy (1.2% annually), and metformin therapy (0.3% annually) (p<0.0001).5

Malnutrition, alcohol abuse, critical illness, cognitive dysfunction, and polypharmacy have also been linked to recurrent hypoglycemic episodes in the diabetic population.6

Quick review of medications:



Biguanides (metformin)

Thiazolidinediones (rosiglitazone, pioglitazone, troglitazone)

Alpha-glucosidase inhibitors (acarbose, miglitol)

Incretin mimetics (exenatide, liraglutide)

Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin, etc.)

Amylin analogues (pramlintide)


Sulfonylureas (glipizide, glyburide, glimepiride, etc.)

Meglitinides (repaglinide, nateglinide)

Signs & Symptoms of Hypoglycemia

Glycemic thresholds for hypoglycemic symptoms in diabetic patients are difficult to define. Patients who have recently experienced a severe hypoglycemic event may not become symptomatic until blood glucose levels are dangerously low.6-8 On the contrary, patients with poorly controlled blood glucose levels may experience symptoms of hypoglycemia when glucose levels are within normal limits.6-8 The diabetic patient should be questioned regarding symptoms experienced, recent HgbA1C levels, average blood glucose levels, most recent medication injection/ingestion, and recent food intake.

Signs and symptoms of hypoglycemia in non-diabetic patients are relatively easier to predict. Autonomic symptoms (nervousness, anxiety, tremulousness, sweating, palpitations, shaking, dizziness, hunger) and neuroglycopenic symptoms (confusion, weakness, drowsiness, speech difficulty, incoordination, odd behavior) are commonly encountered at threshold glycemic values illustrated below (Figure 1).6,9 In severe cases, hypoglycemia may result in seizure, coma, or death.


Figure 1: Responses to Hypoglycemia in the Non-Diabetic Patient6

 Treating the Hypoglycemic Adult Patient

You have made your diagnosis of hypoglycemia (a symptomatic diabetic patient or one with a D-stick ≤ 70mg/dL or a non-diabetic who meets Whipple’s triad), what comes next?

Start with a glucose containing solution: D50 or D10

D50 vs. D10 – How do they compare?

Adam Spaulding, Pharm D, did an excellent review on this topic for ALiEM in 2014. The full post can be found at:

Here is the quick skinny10:

  • Be aware that D50 bolus may cause rebound hypoglycemia (excess glucose suppresses gluconeogenesis and glycogenolysis) => do not overlook the need to initiate an infusion of glucose containing fluids.
  • D50 may overshoot glycemic targets (on average the administration of 50mL of D50 (25g of dextrose) increases blood glucose to approximately 160mg/dL10), which has been shown to be detrimental in the critically ill population. (Krinsley, Critical Care Medicine, 200811: increasing glycemic variability confers an independent risk of mortality; n=3,252, p <0.001).
  • D50 is hypertonic (2,500 mOsm/L) and should be given slowly over 2-5 minutes; adverse effects of administration include: thrombophlebitis and extravasation with tissue necrosis.
  • The osmolarity of D10 is 500 mOsm/L, thus safer for peripheral administration.
  • Administration of a 100mL bolus of D10 (10g of dextrose) has been shown to safely increase blood glucose levels without adverse events or deaths (Study performed by California Contra Costa County EMS system: n=162; median initial blood glucose 38mg/dL, median post treatment blood glucose level 98 mg/dL; 29 patients required a repeat bolus12).

Bottom line: If you go with D50 give 1 amp (50mL, 25g) at a time over 2-3 mins. If you chose D10, a 100ml bolus (commonly packaged as 10g/100mL) can be run in with a little pressure over the same amount of time as an amp of D50. Check the patients glucose levels often.

What if you don’t have IV access? Intra-muscular glucagon (5mg) may be given to raise serum glucose levels. (Keep in mind: the efficacy of glucagon is dependent upon hepatic glycogen stores, thus patients with prolonged hypoglycemia may have minimal response to glucagon therapy secondary to glycogen depletion).13,14

Following establishment of euglycemia (blood glucose >60mg/dL in a non-diabetic patient, and >70mg/dL in a diabetic patient) and improvement in symptoms, patients who are PO tolerant should be allowed to eat (baring any other concern).

If the patient is PO intolerant, consider initiating an IV dextrose drip (D5W at 75-100 mL/hr).13

Special Topic: Hypoglycemia Secondary to Sulfonylurea Therapy

Let’s take a minute to address our first case as this tends to be a board favorite.

When evaluating a patient with hypoglycemia (especially a known diabetic patient), a medication list is invaluable. Hypoglycemia in the context of sulfonylurea use is sufficient to establish a diagnosis of sulfonylurea poisoning.13

How do we treat sulfonylurea poisoning? IV dextrose and octreotide. 

Experimental data suggests that octreotide causes a G-protein mediated decrease in calcium influx through voltage-gated channels in pancreatic beta islet cells, thus limiting calcium-dependent exocytosis of insulin.15

Octreotide may be given IV, IM, or subcutaneously; 50-150mcg should be administered every six hours. Intravenous dosing is preferred in patients with compromised peripheral blood flow.16 Experts recommend continuation of octreotide therapy for a 24-hour duration with blood glucose monitoring at a minimum of every 4-6 hours.16 Patients should be monitored for recurrent hypoglycemia for at least 18 hours following the final dose of octreotide.17

Determining an Appropriate Disposition

The Diabetic Patient

Historically, the majority of well-appearing diabetic patients presenting to the emergency department are safely discharged home with PCM follow-up (approximately 75% of the 298,000 presenting annually.1) When evaluating a diabetic patient with hypoglycemia the emergency physician must:

Look for signs of insulin excess:

  • Question the patient regarding frequency of blood glucose monitoring
  • Inquire regarding recent additions to medical therapy, or changes in PO/SubQ dosing

Search for evidence of decreased glucose availability:

  • Inquire regarding prolonged exercise/missed meals/diet changes/weight loss
  • Inquire regarding alcohol intake (reduces gluconeogenesis, thus depleting hepatic glycogen stores if inadequate food consumption3)

Perform a screening BMP to assess for alterations in medication elimination, such as decreased kidney function, as the etiology of hypoglycemia:

  • Renally eliminated non-secretagogues and secretagogues include:
    • Insulin (60% of renal clearance occurs secondary to GFR18)
    • Metformin (not recommended for therapy if GFR is < 3019)
    • Glyburide & Glimepiride (not recommended for use if GFR is <6019)
      • Less commonly prescribed sulfonylureas: acetohexamide, chlorpropamide, tolazamide, and tolbutamide all possess significant renal elimination (see Figure 2)16
    • Exenatide (not recommended for therapy if GFR is < 3019)

If the patient is well, he/she can safely monitor his/her blood glucose, and obtained labs are within normal limits, discharge home with close PCM follow-up is appropriate.

The Diabetic Patient with Sulfonylurea Poisoning

Diabetic patients with sulfonylurea poisoning should be hospitalized for frequent blood glucose monitoring (drug half lives and durations of action are prolonged – Figure 2 below). As above, a BMP should be attained to evaluate for renal dysfunction as the etiology of the hypoglycemic episode.

Sulfonylurea Time to Peak (Hrs) Half-life (Hrs) Duration of Action
Chlorpropamide 2-7 36 24-72
Tolbutamide 3-4 3-28 6-12
Tolazamide 3-4 4-8 12-24
Glipizide 6-12 7 24
Glyburide 2-6 10 <24
Glimepiride 2-3 5-9 16-24

Figure 2: Sulfonylurea Pharmacokinetics (Adapted)16

The Non-Diabetic Patient

A thorough history and physical exam should be performed on all patients meeting Whipple’s triad, or those presenting with a blood glucose ≤ 40mg/dL.3

If the patient is critically ill, look for clues for of the following etiologies of hypoglycemia3,20:

  • Hepatic, renal, or cardiac failure
  • Sepsis
  • Cortisol deficiency
  • Malnutrition

The majority of these patients will require inpatient evaluation and treatment.

If the patient is clinically well, look for clues of the following etiologies of hypoglycemia3,20:

  • Accidental, surreptitious, or malicious use of hypoglycemic drugs
    • Insulin and insulin secretagogues
  • Medications
    • Pentamidine, quinine, cibenzoline, gatifloxacin, indomethacin
  • Alcohol abuse (Note: if suspected, treatment should include thiamine in addition to dextrose)
  • Patients post gastric bypass
  • Patients with a history of autoimmune pathology (autoimmune hypoglycemia)
  • Patients reporting hypoglycemic symptoms within 4 hours of food ingestion (reactive hypoglycemia*)
  • Patients reporting soft stools post-prandially with hypoglycemic symptoms (alimentary hypoglycemia**)

*Reactive hypoglycemia: mismatch between insulin secretion and glucose absorption resulting in post-prandial hyperglycemia and subsequent hypoglycemia secondary to excess insulin release.20

**Alimentary hypoglycemia: occurs most commonly in young, thin women with a history of increased GI transit time.20

Patients with accidental or surreptitious use of hypoglycemic drugs may require hospitalization for recurrent hypoglycemia. Given the clinical scenario, the majority of these well-appearing patients will be appropriate for discharge and specialty referral.20

Now, back to our second case, the male recently diagnosed with gout – assuming that our patient had no other clinical clues in his history and physical to suggest an alternative etiology of hypoglycemia, it would be appropriate to discontinue his indomethacin therapy given the concern that it might be causing his hypoglycemic episodes.

The More You Know

Let’s talk a little bit about insulin pumps. As the majority of insulin pumps are now sensor-augmented (programmed to recognize low blood glucose levels, commonly < 6mmol/dL), and halt the delivery of basal/bolus insulin in the setting of hypoglycemia, hypoglycemic episodes secondary to continuous insulin therapy is becoming increasingly rare.21,22

The majority of patients with insulin pumps have undergone extensive diabetes education and are able to manage hypoglycemic events without assistance with carbohydrate ingestion, and repeat blood glucose monitoring.22 Patient’s experiencing recurrent hypoglycemic episodes are often prescribed outpatient glucagon kits (1mg of glucagon, reconstituted with sterile water) for self/by-stander IM administration, and thus may not present to the emergency room for evaluation and treatment.23

Although consensus statements regarding the management of insulin pumps in the setting of hypoglycemia are lacking, if a diabetic patient undergoing continuous insulin therapy presents to the ED for hypoglycemia, and the etiology of the hypoglycemia is thought secondary to the insulin pump, it is reasonable to turn off the pump, remove the subcutaneous attachment, and treat the patient with IV dextrose/frequent blood glucose monitoring.

A device representative should subsequently be contacted for trouble-shooting/re-programming.

Key Pearls

  • Hypoglycemia may present as alteration in mental status – quickly check a point of care glucose.
  • Treat the patient: D50 vs. D10
    • D10 may be more appropriate for the critically ill patient
  • Do a thorough H&P and obtain a BMP for hypoglycemic diabetic patients:
    • Evaluate for medication issues, decreased renal function, missed meals, etc.
  • Non-diabetics meeting Whipple’s triad or presenting with a blood glucose ≤ 40mg/dL = need a thorough H&P to dictate evaluation and treatment
    • Critically ill (sepsis, CKD, etc) + hypoglycemic = Admit
    • Well + hypoglycemic = Ok for discharge and specialist follow-up if no concern for recurrent hypoglycemia (sulfonylurea ingestions, etc.)
  • Insulin pump = unlikely to be the etiology of the patient’s hypoglycemia
    • If suspected pump malfunction => turn off the pump and remove the subcutaneous attachment; manage the patients glucose parenterally
      • Call the device representative

References / Further Reading

  1. Diabetes Public Health Resource. Number of emergency department visits (in thousands) with hypoglycemia as a first-listed diagnosis and diabetes as a secondary diagnosis, adults aged 18 years or older, United States, 2007-2009. Centers for Disease Control and Prevention. Available from:
  1. Lipska K, Ross J, Wang Y, et al. National trends in US hospital admissions for hyperglycemia and hypoglycemia among Medicare beneficiaries, 1999 to 2011. JAMA Intern Med 2014;174:1116–1124
  2. Cyer P, Axelrod L, Grossman A, Heller S, Montori V, et al. Evaluation and management of adult hypoglycemic disorders: An endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2009; 94(3):709-728.
  3. Pathak R, Schroeder E, Sequist E, Zeng C, Lafata J, et al. Severe hypoglycemia requiring medical intervention in a large cohort of adults with diabetes receiving care in U.S. integrated health care delivery systems: 2005-2011. Diabetes Care. 2016; 39(3):363-370.
  4. Wright A, Cull C, Macleod K, Holman R. Hypoglycemia in type 2 diabetic patients randomized to and maintained on monotherapy with diet, sulfonylurea, metformin, or insulin for 6 years from diagnosis: UKPDS73. J Diabetes Complications. 2006. 20(6): 395-401.
  5. Yung J, Ko S. Avoiding or coping with severe hypoglycemia in patients with type 2 diabetes. Korean J Intern Med. 2015; 30(1):6-16.
  6. Boyle P, Schwartz N, Shah S, Clutter W, Cryer P. Plasma glucose concentrations at the onset of hypoglycemic symptoms in patients with poorly controlled diabetes and in nondiabetics. N Engl J Med 1988; 318:1487–1492.
  7. Dagogo-Jack S, Craft S, Cryer P. Hypoglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent hypoglycemia reduces autonomic responses to, symptoms of, and defense against subsequent hypoglycemia. J Clin Invest 1993;91:819–828.
  8. Henderson J, Allen K, Deary I, Frier B. Hypoglycaemia in insulin-treated type 2 diabetes: frequency, symptoms and impaired awareness. Diabet Med 2003;20:1016–1021.
  9. Spaulding A. D50 vs D10 for severe hypoglycemia in the emergency department. Academic Life in Emergency Medicine. 2014. Available from:
  10. Krinsley J. Glycemic variability: a strong independent predictor of mortality in critically ill patients. Crit Care Med. 2008; 36(11):3008-3013.
  11. Kiefer M, Hern H, Alter H, et al. Dextrose 10% in the treatment of out-of-hospital hypoglycemia. Prehosp Disaster Med. 2014;29(2):190-4.
  12. Bosse GM. Antidiabetic and hypoglycemic agents. In: Goldfrank’s Toxicologic Emergencies, 9th ed, Goldfrank LR, Nelson LS, Lewin NA, et al (Eds), McGraw-Hill, New York 2011. p.714.
  13. Spiller H. Management of sulfonylurea ingestions. Pediatr Emerge Care. 1999;15(3):227.
  14. Hsu W, Xiang H, Rajan A, Kunze D, Boyd A. Somatostatin inhibits insulin secretion by a g-protein-mediated decreased in Ca2+ entry through voltage-dependent Ca2+ channels. J Biol Chem. 1991;266(2):837.
  15. Chu J, Stolbach A. Sulfonylurea agent poisoning. UpToDate. 2016. Available from:
  16. Fasano C, O’Malley G, Dominici P, et al. Comparison of octreotide and standard therapy versus standard therapy alone for the treatment of sulfonylurea-induced hypoglycemia. Ann Emerg Med. 2008;51:400-406.
  17. Rabkin R, Ryan M, Duckworth W. The renal metabolism of insulin. Diabetologia.1984 Sep; 27(3):351-357.
  1. Ioannidis I. Diabetes treatment in patients with renal disease: is the landscape clear enough. World J Diabetes. 2014. 15(5):651-658.
  2. O’Shaughnessey C, Shubrook J. Hypoglycemia in adults. Emergency Medicine Reports. 2012. Available from:
  3. Bergenstal R, Klonoff D, Garg S, Bode B, Meredith M. et al. Threshold-based insulin-pump interruption for reduction of hypoglycemia. N Engl J Med. 2013;369;224-232.
  4. Grunberger G, Abelseth J, Bailey T, Bode B, Handelsman Y, et al. Consensus statement by the American association of clinical endocrinologists and American college of endocrinology insulin pump management task force. Endocrine Practice. 2014. 20(5):463-489.
  5. Kedia N. Treatment of severe diabetic hypoglycemia with glucagon: an underutilized therapeutic approach. Diabetes Metab Syndr Obes. 2011;4:337-346.

The Emergency Department Management of Posterior Epistaxis

Author: Erica Simon, DO, MHA (EM Resident Physician, San Antonio Uniformed Services Health Education Consortium, @E_M_Simon) // Edited by: Alex Koyfman, MD (@EMHighAK – Editor-in-Chief; EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER – Associate Editor-in-Chief; Assistant Professor in Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center)

A 73 year-old patient presents to your ED with the chief complaint of “nosebleed.”  Casually glancing down the hallway of your section, you see an elderly male shuffling to a bed, pressing a blood-soaked beach towel to his nares.  As nursing staff performs their bedside triage, you enter the room and survey the monitor: BP 156/99, HR 122, RR 14, SpO2 96% RA.

The patient speaks in full sentences and is tolerating his secretions.  He details a previous medical history of nasopharyngeal carcinoma, requiring recurrent radiation therapy.  While discussing his family and social history, he begins to clear his mouth of large volumes of blood.  The nurse reaches for a basin and an additional towel, while you survey the patient’s med list, which includes Plavix and aspirin.

On first glance, you observe active bleeding from the bilateral nares.  Direct pressure has obtained hemostasis.

What is your next step?  Topical vasoconstrictors?  Nasal packing?  Can this patient go home, or does he need to be admitted?

Let’s discuss a few key points about the management of posterior epistaxis.

The Epidemiology of Epistaxis

Epistaxis is one of the most commonly encountered ear, nose, and throat (ENT) emergencies in the US.1-4  It is estimated that up to 60% of the population will experience an episode of epistaxis throughout their lifetime; with approximately 10% having a bleeding source localized to the posterior nares.1-7  Current data demonstrate a bimodal age distribution of epistaxis with the majority of cases occurring amongst those aged 2-10 years and 50-80 years.1,3  Despite this reported prevalence of epistaxis, epidemiologic data cite only 6% of individuals as presenting to healthcare providers for anterior epistaxis treatment, and only 5% for posterior epistaxis treatment.3,5-7

Seasonal variation in the rates of epistaxis have been described in temperate and tropical climates.8  The majority of epistaxis episodes in the US occur during the winter months, a finding thought secondary to a decrease in ambient humidity and increase in concomitant upper respiratory infections.8  In tropical climates, epistaxis occurs frequently during dry seasons.8

Etiologies of Epistaxis

The following chart, adapted from Kucik et al.’s, 2005, and Yau’s, 2015 works provides an excellent summary:

Local Causes Systemic Causes
Chronic sinusitis Hemophilia
Epistaxis digitorum (nose picking) Leukemia
Foreign bodies Medications (e.g., aspirin, anticoagulants, NSAIDs)
Intranasal neoplasm/polyp Conditions causing platelet dysfunction (e.g., cirrhosis, uremia)
Irritants (e.g., cigarette smoke) Thrombocytopenia
Medications (e.g., topical steroids)
Septal deviation/perforation
Vascular malformations/telangiectasias

Table 1 – Etiologies of Epistaxis2,7

A Brief Anatomy Review

Clinically, epistaxis is classified as anterior or posterior according to the anatomic source of bleeding.

The vascular supply of the nose originates from the ethmoid branches of the internal carotid arteries, and the facial and internal maxillary divisions of the external carotid arteries.2,8  The anterior portion of the nasal septum is supplied by an anastomosis of the terminal branches of the sphenopalantine and anterior ethmoidal arteries, and the superior labial branch of the facial artery.2,8  This anastomosis is commonly known as Kiesselbach’s plexus, the area from which the majority of anterior epistaxis episodes arise.1-5,8

The sphenopalatine artery and terminal branches of the maxillary artery supply the lateral nasal wall (below the middle turbinates), and are commonly responsible for reported cases of posterior epistaxis. 2,8

The figure below details relevant anatomy:


Figure 1 – Anatomy of the Nasopharynx2

The Evaluation of a Patient Presenting with Epistaxis

Evaluation should begin with an assessment of the ABCs.  If the patient is actively bleeding, but protecting his airway and hemodynamically stable, he should be placed in a seated position (leaning forward so as to avoid increasing the flow of blood to the posterior oropharynx), and instructed on the application of direct pressure to the bilateral nares for approximately 5-10 minutes.1,2  Expectoration of blood residing in the oropharynx should be encouraged so as to reduce the risk of aspiration or emesis.2,3,7

If stable, important items to address in history taking include:

  • Onset, activity undertaken prior to onset (digital trauma), duration, and laterality of the current bleed. If the patient has sought care for episodes of epistaxis previously, inquiries regarding methods utilized to obtain hemostasis should be made.
  • Frequency of epistaxis/seasonality of symptoms.
  • Review of systems: skin rashes (petechiae/pupura), easy bruising
  • Previous medical history: hepatic disease (cirrhosis), renal disease (uremia), nasopharyngeal carcinoma requiring radiation therapy/oncologic surgery
  • Social history: smoking (irritant), recreational drug use (specifically cocaine and other inhalants)
  • Medication review: NSAIDs, aspirin, ADP receptor blockers, anticoagulants
  • Family history: coagulation disorders1,6-7

Clues that the patient might be suffering from a posterior bleed include: the patient is an adult (children nearly always suffer from anterior epistaxis secondary to digital trauma or foreign body8), and he/she presents with symptoms of nausea, hematemesis, and hemoptysis in addition to, or in the absence of, epistaxis.2,3,7  Physical exam findings concerning for posterior epistaxis include blood draining from the bilateral nares, and large volumes of blood in the oropharynx.2,7  An inability to visualize an anterior source of bleeding on physical exam, and persistent bleeding despite the application of anterior nasal packing should also raise suspicion for a posterior source.2,3,7

If the patient presenting with epistaxis is unstable, appropriate intervention should be taken (preparation for a definitive airway, IV access, monitor placement, fluid resuscitation, CBC, coagulation panel, type and cross versus type and screen as appropriate).

Addressing Posterior Epistaxis

At this point, as we return to our patient, we’ll assume that he’s blown his nose, and cleared his nasopharynx of blood and clot, but due to the volume of blood actively draining from his nares, you’ve been unsuccessful in localizing an anterior source of bleeding.  Your attempts at medical treatment with topical vasoconstrictors (oxymetazoline and LET soaked gauze pledgets (lidocaine 4%, epinephrine 0.1%, and tetracaine 0.4%)) have failed to obtain hemostasis, and despite placing a Rapid Rhino anterior nasal pack, the patient continues to bleed around the nasal pack and into his oropharynx.  At this point, it is likely that the patient’s episode of epistaxis is originating from the posterior oropharynx.  After removing his anterior packing, and once again clearing the blood and clots from the nares and oropharynx, a number of management options may be chosen:

A quick note: Analgesia should be provided prior to the application of nasal packing.  It is also advised that after packing is placed, pulse oximetry be maintained to monitor for hypoxia.3

Methods for Obtaining Hemostasis

Nasal Tampons: Commonly composed of cotton or foam, numerous models of nasal tampons are available in the US for the control of epistaxis.  Merocel manufactures one such model, composed of foam, designed for insertion along the septal floor, parallel to the hard palate, and offering direct mechanical pressure upon expansion (secondary to absorption of blood in the nasal cavity).9


Figure 2 – Commercial Nasal Tampon9

The Rhino Rocket, a second example of a nasal tampon, was designed by Shippert Medical Technologies Incorporated for ease of application through the utilization of its patented nasal applicator.10


Figure 3 – Rhino Rocket10

Balloon Devices:

The Rapid Rhino – the Rapid Rhino is an inflatable balloon, coated with a hydrocolloid of carboxymethylcellulose (CMC).  In addition to providing direct mechanical pressure, the Rhino’s CMC functions as a lubricator (ease of application) and platelet aggregator upon exposure to water.  In order to place the Rapid Rhino (activate the CMC), the device is submerged in sterile water for approximately 30 seconds prior to its insertion along the septal floor, parallel to the hard palate.  A 20cc syringe is then used to inflate the balloon until the pilot cuff is rounded and firm to the touch.2,3,12


Figure 4 – Utilization of the Rapid Rhino Anterior Nasal Pac13

Rapid Rhinos are commercially available in numerous sizes: 4.5cm for children, 5.5cm and 7.5cm for anterior epistaxis in adults, 9cm for sphenopalantine artery bleeds, and 5.5cm and 7.5cm bilateral nares models for bilateral bleeds.13

Note: Despite their equivalence in obtaining hemostasis, randomized control trials have demonstrated the Rapid Rhino as superior to the Rhino Rocket in terms of pain upon insertion and ease of extraction.3,13-14

Placement of A Foley Catheter – Cited as the most commonly utilized posterior nasal packing device, a Foley catheter (size 10, 12, or 14 French) is lubricated and advanced until the tip and balloon are in the nasopharynx.  The Foley balloon is then filled with approximately 5-10cc of saline and traction is applied until the balloon sits firmly against the posterior nasal choana.  Anterior traction is maintained with the placement of an umbilical or c-clamp at the nasal ala.14,15  If hemostasis is not achieved status post placement of the Foley catheter, anterior nasal packing may be utilized as an adjunct.2  Appropriate application of the umbilical or c-clamp is essential to preventing the complication of pressure necrosis (detailed below).  Neither the umbilical clamp nor the c-clamp should be affixed directly to the nasal ala.


Figure 5 – Application of a Foley Catheter in Posterior Epistaxis14,15

A quick tutorial on the placement of anterior packing as cited by Kucik and Cleney, 2005:


Figure 6 – Application of Anterior Packing.  A. Gauze impregnated with petroleum jelly is gripped with forceps and inserted into the anterior nasal cavity.  B. With a nasal speculum (not shown) used for exposure, the first packing layer is inserted along the floor of the anterior nasal cavity.  Forceps and speculum are then withdrawn.  C. Additional layers of packing are added in accordion-fold fashion, with the nasal speculum used to hold the positioned layers down while a new layer is inserted.  Packing is continued until the anterior nasal cavity is filled.2

The Epistat or Storz T3100 – As an alternative to the Foley catheter, the Epistat or Storz t3100 is a device with anterior and posterior balloons for the control of epistaxis.  The device is inserted until the posterior balloon enters the posterior nasal cavity, inflated with 5-10cc of saline, and then pulled forward until snug.  The anterior balloon is then filled with 15-30cc of saline and secured with an umbilical or c-clamp at the nasal ala.3,17


Figure 7 – Storz T310017

Posterior Nasal Packing

While rarely employed in the emergency department secondary to its difficulty in application, posterior nasal packing is also cited in the literature as a mechanism of controlling posterior epistaxis.2,3

Again as depicted by Kucik and Cleney, 2005:


Figure 8 – Application of Posterior Nasal Packing.  A. After anesthesia is obtained, a catheter is passed through the affected nostril and through the nasopharynx, and drawn out the mouth with the aid of ring forceps.  B. A gauze pack is secured to the end of the catheter using umbilical tape or suture material, with long tails left to protrude from the mouth.  C. The gauze pack is guided through the mouth and around the soft palate using a combination of careful traction on the catheter and pushing with a gloved finger.  (A bite block, not shown, should be used to protect the physician’s finger).  D. The gauze pack should rest in the posterior nasal cavity.  It is secured in position by maintaining tension on the catheter with a padded clamp or gauze roll placed anterior to the nostril.  Ties protruding from the mouth (used to remove the pack) should be secured to the patient’s cheek.2

Complications of Methods for Obtaining Hemostasis

Complications associated with posterior nasal packing include patient discomfort, otitis media, sinus obstruction, pressure necrosis of the nasal mucosa and cartilage, pressure necrosis of the nasal ala (if packing secured inappropriately), hypoventilation, and toxic shock syndrome (TSS). 1,18

Major adverse events including myocardial infarction and death have also been reported as complications of posterior nasal packing.1,17  Early literature (1980s-early 1990s) attributed these events to a nasopulmonary reflex – a postulated change in nasopulmonary function secondary to posterior nasal packing, resulting in a decrease in arterial oxygen content.18-20  Today, however, the existence of the reflex is controversial as the majority of studies now cite vagal nerve stimulation, symptomatic anemia, recurrent bleeding resulting in apnea and concomitant hypoxia, and over-sedation secondary to analgesia as the likely etiologies of the aforementioned complications. 18-20

TSS – An aside regarding TSS and antibiotic therapy in the setting of nasal packing:  Case reports and case reviews regarding epistaxis management favor the lubrication of nasal tampons/gauze with antibiotic ointment, and the provision of systemic antibiotics post packing in order to prevent the occurrence of TSS secondary to S. aureaus infection.  Several studies cite a reduction in nasal colonization by Staph species and decreased incidence of post-packing sinusitis when topical and systemic antibiotic therapy is utilized.2,21  As the literature regarding this topic is immense and not addressed entirely in this review; suffice it to say that the ACEP Clinical Practice Management Guide on Epistaxis recommends the application of topical antibiotic ointment, and the provision of systemic antibiotic therapy.2  This is a controversial practice; see here:

Recommended Adult Antibiotic Regimens Include:

First Line: PO cephalexin 250–500 mg QID or PO amoxicillin/clavulanate 250–500 mg TID

Second line: PO clindamycin 150–300 mg QID or PO trimethoprim/sulfamethoxazole DS
Therapy should be continued for 7-10 days.3,21

Patient Disposition

All patients requiring posterior packing should be admitted to the hospital given the risk of hypoxia occurring after packing, and the necessity to monitory for dysrhythmias and recurrent bleeds.  If not already completed, a CBC and coagulation panel should be obtained, in addition to studies considered pertinent given the patient’s H&P (bleeding time, factor assays, etc.).  ENT consultation is required as nasal packing is commonly removed within 48-72 hours.2,3,7  Patients refractory to the hemostatic measures described above require urgent vs. emergent ENT evaluation for endoscopic assessment with the potential for ligation or embolization.2,7

Extra Credit: Hypertension and Epistaxis – Cause and Effect?

The association between hypertension and epistaxis is complex.  To date, studies have failed to demonstrate a causal relationship between hypertension and epistaxis.  Data regarding an association between hypertension and epistaxis varies widely.3,22-24  At least one retrospective cohort study of a Marshfield, Ohio clinic, performed by Abrich, et al., 2014, (n = 431) demonstrated hypertension as a risk factor for epistaxis and recurrent epistaxis.22

A systematic review performed by Kikidis, et al., 2014, (EMBASE, Medline, and Ovid SP search of hypertension and epistaxis, Jan1975 – Jan 2012) revealed 6 of 9 total studies (n = 2,994) identifying the presence of hypertension in patients with epistaxis.  As the authors identify, however, “the presence of high arterial blood pressure during the actual episode of nasal bleeding cannot establish a causative relationship with epistaxis, because of confounding stress and possible white coat phenomenon.”24

Given the lack of a direct causal relationship between hypertension and epistaxis, epistaxis therapy should focus on control of the hemorrhage rather than reduction of the blood pressure.3  As ACEP identifies, the provision of analgesia and mild sedation are preferable to antihypertensive therapy.3

References / Further Reading

  1. Viehweg T, Rogerson J, Hudson J. Epistaxis: diagnosis and treatment. J Oral Maxillofac Surg. 2006; 64:511-8.
  2. Kucik C, Clenney T. Management of epistaxis. Am Fam Physician. 2005;71(2):305-311.
  3. Gilman C. Focus on: treatment of epistaxis. American College of Emergency Physicians. Clinical & Practice Mangement. 2009. Available at—Practice-Management/Focus-On–Treatment-of-Epistaxis/
  4. Bent J, Woods B. Complications resulting from treatment of severe posterior epistaxis. J Laryngol Otol. 1999;113(3):252-254.
  5. Ho E, Mansell N. How we do it: a practical approach to foley catheter posterior nasal packing. Clin Otolaryngol Allied Scie. 2004;29(6):754-757.
  6. Elahi M, Parnes L, Fox A, Pelz D, Lee D, et al. Therapeutic embolization in the treatment of intractable epistaxis. Arch Otolaryngol Head Neck Surg. 1995; 121(1):65-69.
  7. Yau, S. An update on epistaxis. AFP. 2015; 44(9):653-656.
  8. Douglas R, Wormwald P. Update on epistaxis. Curr Opin Otolaryngol Head Neck Surg. 2007;15:180-183.
  9. Merocel products. Medtronic. 2012. Available at
  10. Rhino rocket with applicator. Shippert Medical Technologies Incorporated. 2014. Available at
  11. Tan L, Calhoun K. Epistaxis. Med Clin North Am. 1999;83:43-56.
  12. Liudvikas J, Daniel M. Mangement of Epistaxis in the emergency department. Emergency Medicine Reports. 2006. Available at
  13. Rhapid rhino epistaxis products. Smith & Nephew, Incorporated. 2015. Available at
  14. Singer A, Blanda M, Cronin K, LoGiudice-Khwaja M, Gulla J, Bradshaw J, et al. Comparison of nasal tampons for the treatment of epistaxis in the emergency department: a randomized control trial. Ann Emerg Med. 2005; 45(3):134-139.
  15. Reichman E. 2013. Chapter 172: Epistaxis management. Tintinalli’s Emergency Procedures 2e. Chapel Hill, NC, McGraw-Hill Holdings, LLC
  16. Thomas L, Karagama Y, Watson C. Avoiding alar necrosis with post-nasal packs. J Laryngol Otol. 2005;119(9):727-728.
  17. Halverson, D, Borgstrom. 2015. Chapter 16: Epistaxis. Advanced Surgical Techniques for Rural Surgeons. Springer Science+Business Media New York
  18. Monte E, Belmont M, Wax M. Mangement paradigms for posterior epistaxis: a comparison of costs and complications. Otolaryngol Head Neck Surg.1999;121:103-106.
  19. Jacobs J, Levine L, Davis H, Lefrak S, Druck N, et al. Posterior packs and the nasopulmonary reflex. Laryngoscope. 1981;91(2):279-284.
  20. Loftus B, Blitzer A, Cozine K. Epistaxis, medical history, and the nasopumonary reflex: what is clinically relevant? Otolaryngol Head Neck Surg. 1994; 110(4):363-369.
  21. Rubin J, Rood S, Myers E, Johnson J. The management of epistaxis. Self-instructional package. Alexandria, Va.: American Academy of Otolaryngology-Head and Neck Surgery 1990
  22. Abrich V, Brozek A, Boyle T, Chyou P, Yale S. Risk factors for recurrent spontaneous epistaxis. Mayo Clinic Proceedings. 2014;89(12):1636-1643.
  23. Sarhan N, Algamal A. Relationship between epistaxis and hypertension: A cause and effect or coincidence? J Saudi Heart Assoc. 2015;27(2):79-84.
  24. Kikidis D, Tsioufis K, Papanikolaou V, Zerva K, Hantzakos A. Is epistaxis associated with arterial hypertension? A systemic review of the literature. Eur Arch Otorhinolaryngol. 2014; 271(2):237-243.

Managing a Massive Hemothorax: A Guide to Stabilizing Your Patient

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC)

A 16 year-old male status post MVC rolls into the trauma bay.  While EMS personnel bag the patient, they identify him as the front seat passenger in an auto vs. semi.  Per witness reports, the young male was ejected nearly 200 feet from his vehicle.  Attempts at endotracheal intubation in the field failed secondary to his severe facial trauma.  Remarkably, the patient has a pulse; a c-collar and pelvic binder encircle his small frame.  A nurse calls out a manual BP of 72/41, a HR of 147, and your team goes to work.

Within minutes the patient is intubated and ventilated.  A compression dressing has slowed the bleeding from his large galeal avulsion to an ooze.  The rapid infuser is pumping in a unit of O+ PRBCs, and your EFAST exam identifies a right-sided hemopneuomothorax.

Suddenly, the patient’s BP plummets.  The head of the bed reports left tracheal deviation and a right hemithorax absent breath sounds.  You quickly perform a needle decompression.  As you puncture the pleura to place a chest tube, blood pours onto the floor for what seems like hours.  You know immediately that this is a massive hemothorax.  What do you do next?  Let’s take a few minutes to review.

Epidemiology of Hemothoraces

A hemothorax,  or a collection of blood in the pleural space, most commonly occurs secondary to penetrating or blunt chest wall trauma.1-5  In the United States, 70-80%1 of hemothoraces are due to motor vehicle collisions causing injury to mediastinal structures (the heart, major vessels, thoracic spine, intercostal or mammary arteries), the diaphragm, or the lung parenchyma.1-5 

Diagnosing a Hemothorax

Patient presentations of hemothoraces range from shortness of breath (25% of hemothoraces are associated with concomitant pneumothoraces6), to hemodynamic instability secondary to hemorrhagic shock.4  In the hemodynamically stable patient, a hemothorax is most commonly identified on CXR.4-5  Ideally, the CXR should be performed in the upright position in order to detect blunting of the costophrenic angle (equating to 150-300 mL of blood in the pleural space).4-6  See image A below.

Note: An inadequate upright CXR, or CXR performed in the supine position is often misleading secondary to posterior diaphragmatic layering of blood.  It is no surprise then that the sensitivity of a supine CXR in the detection of a hemothorax is reportedly 40-60%. In fact, studies have demonstrated only vague opacification of the hemithorax as detectable on supine CXR despite >1,000 mL of intrathoracic blood collection.5,6  See image B below.


What does this mean for the trauma patient for whom a supine CXR is likely to be performed?

If patient vital signs (hypoxia, persistent hypotension), mechanism of injury (penetrating injury), or physical exam (multiple palpable rib fractures, flail segment, significant chest wall ecchymosis or tenderness to palpation) lead you to suspect a hemothorax à Do not let the supine CXR convince you otherwise.

In the hemodynamically unstable patient, the EFAST or Extended Focused Assessment with Sonography for Trauma is most commonly utilized to identify a hemothorax given its speed of employment.  Several studies have identified the sensitivity of ultrasound in the detection of hemothoraces as comparable to chest radiographs:

In their 1996-2007 MEDLINE search, utilizing the OVID interface, McEwan and Thompson7 cite the following:

Author Patient Population Study Design Outcomes Key Result Study Limitation
Rothlin et al., 1993, Switzerland8 Adults (15-88yrs) with blunt thoracic or abdominal injuries.  US performed by surgeons and compared to CXR & CT. Prospective Study Utility of US to detect hemothorax. Sn = 81% 5 of 11 False negative reports ultimately identified as operator error.
Ma et al., 1995, U.S.9 245 Adults (18+) presenting to the ED with blunt or penetrating torso trauma.  US compared to CT, supine CXR, formal echo or chest tube. Diagnostic Cohort Utility of US to detect hemothorax. Sn = 96%      Sp = 100% Composite gold standard.
Ma et al., 1997, U.S.10 240 Adults (18+) presenting to the ED with blunt or penetrating torso trauma.  US compared to CT, supine CXR, formal echo or chest tube. Retrospective Analysis of 1995 Study Clinical utility of ultrasound vs. plain supine CXR. Sn US = 96.2% vs. CXR = 96.2%;          Sp US = 99.6% vs. CXR = 99.6% Patient population from 1995 study utilized.
Sisley et al., 1998, U.S.11,12 360 trauma patients presenting to the ED with blunt or penetrating torso trauma. Prospective Study Clinical utility of US vs. supine CXR Sn US = 97.5% vs. CXR = 92.5%;          Sp US =  99.7% vs. CXR = 99.7% Results compared to supine CXR vs. independent gold standard (CT).
Abboud & Kendall, 2003. U.S.13 155 trauma patients who underwent CT scan during their evaluation. Prospective Study Clinical utility of US Sn = 92%, Sp = 100% Composite gold standard.

Table adapted from McEwan and Thompson’s Emergency Medicine Journal article, 2007.7 Sn = Sensitivity.  Sp = Specificity.

What about CT?

CT remains the gold standard in the diagnosis and evaluation of hemothoraces.  In their 2007 retrospective study of 141 blunt chest trauma patients presenting to a Level 1 trauma center, Traub et al. noted a hemothorax as detectable in 25% of patients, having been previously diagnosed with a negative supine CXR.14

Managing a Hemothorax

Volume resuscitation remains the #1 priority.  Transfusion should be initiated as appropriate.  Early consultation for penetrating chest trauma is recommended.4  As the majority of hemothoraces arise from injured lung parenchyma and are commonly self-limited, management with chest tube thoracostomy is frequently adequate.5  The placement of a chest tube is therapeutic in that expansion of the lung with apposition of the visceral and parietal pleural aids in hemostasis.4  Drainage of blood from the parietal cavity also prevents the common complication of empyema or fibrothorax.4,5

To perform tube thoracostomy, a large-bore tube (32F to 40F) should be placed in the 4th or 5th intercostal space at the anterior axillary line, and connected to water seal and suction (20-30 mL H20).5  Re-expansion of the lung parenchyma and resolution of the hemothorax should be monitored with serial CXRs.5


What is of major concern is the management of a massive hemothorax, defined as an immediate blood loss of >1,500 mL upon chest tube thoracostomy, or blood loss of >200 mL/hr (3mL/kg/h) over 2-4 hours post thoracostomy procedure.16,17  These, in addition to the conditions listed below, are recommended considerations for urgent thoracotomy:

  • Increasing hemothorax demonstrated on repeat CXRs.5
  • Hypotension despite adequate blood replacement (when other sites of blood loss have been ruled out).5
  • Patient decompensation after initial response to volume resuscitation.5

An urgent/emergent thoracotomy should be performed as follows:


After the parietal pleura has been accessed, clamping of the lung hilum (pulmonary vasculature) may allow for the attainment of hemostasis.5

 It is important to recognize that persistent hypotension, despite intervention to address bleeding from the lung parenchyma/hilum, points to additional injury.  Perform a thorough patient assessment.  Consider clamping the aorta if the patient remains hemodynamically unstable (the patient may later undergo trans-esophageal echocardiogram to assess aortic injury in the OR).5,6

Special Topics – Auto-Transfusion

To date, one French case study detailed the use of pre-hospital autologous blood transfusion in the setting of life-threatening hemothorax.19  In the study, 18 patients with life-threatening hemothoraces received autologous blood obtained from the thorax; 13 survived to the hospital setting.  Post transfusion laboratory studies and vital signs for the 13 patients revealed: Hct decrease from 24 +/- 3 to 19 +/- 3 and SBP increase from 78 +/- 11 to 88 +/- 12 mm Hg.  Platelet count was noted as 90,800 +/- 21,400/cu mm, prothrombin time 48 +/- 3%, partial thromboplastin time 197 +/- 18%, and serum potassium levels 3.6 +/- 0.5 mmol/L. According to the authors, no serious complications related to auto-transfusion were deemed crucial to the patients’ survival.19

This is an area that requires further study as researchers have now determined the following:

  • There is a statistically significant increase in pro-inflammatory cytokines (IL-6, IL-8, TNFα, GM-CSF) in shed pleural blood when compared with samples from healthy controls (P <0.05). Cytokine levels in unprocessed shed pleural blood are approximately 10- to 100-fold higher compared with healthy control venous samples.20 Thus, these pro-inflammatory cytokines may inhibit healing and stimulate transfusion reactions through systemic inflammatory cascades.
  • Unprocessed shed hemothorax blood (USHB) is significantly depleted of coagulation factors as compared to venous blood: In a study of 22 patients undergoing sampling of hemothorax blood and venous blood s/p traumatic injury: the INR of USHB was >9 as compared to a venous blood INR of 1.1 (p< .001), the aPTT of USHB was >180 in contrast to 28.5 seconds in the venous blood sample (p< .001), and the fibrinogen of USHB was <50 in comparison to 288 mg/dL in the venous blood sample (p< .001).21 Therefore, it would seem that little benefit in terms of hemostasis may be achieved in the transfusion of USHB.
  • Also of note, in the same study, the mean Hct of USHB was found to be 26.4 in contrast to 33.9 for venous blood (p = .003); Hgb was 9.3g/dL in comparison to a venous blood level of 11.8 g/dL (p = .004), and the platelet count of the USHB was 53 in contrast to 174 K/μL in the venous blood sample (p < .001). Ultimately, a hemothorax volume of 726 mL was calculated to be equivalent to 1 U of red blood cells.21


The emergency physician’s role in addressing a hemothorax is first to make the diagnosis utilizing CXR, US or CT.  Hemothoraces should be managed with the placement of a chest tube to avoid the later complications of empyemas and fibrothorax.  Massive hemothoraces warrant volume resuscitation, consultation with a trauma surgeon, and performance of a thoracotomy.  Early identification and intervention is the key to limiting the morbitidy and mortality associated with hemothoraces.4-6

Key Pearls

  • Hemothorax presentation is variable
    • Step 1: Diagnose the hemothorax with CXR vs. US definitively with CT
    • If the mechanism suggests hemothorax = rule out hemothorax despite CXR findings (CT if patient hemodynamically stable)
  • Hemothorax Treatment = Chest tube
  • Massive Hemothorax Treatment = Transfuse, consult, thoracotomy PRN
    • If the patient is persistently hypotensive despite control of pulmonary bleeding => look for other etiologies
  • Auto-transfusion of unprocessed shed hemothorax blood => additional research needed


References / Further Reading

  1. Shorr R, Crittendenn M, Indeck M, Hartunian S, Rodriguez A. Bunt thoracic trauma. Analysis of 515 patients. Ann Surg. 1987;206(2):200-205.
  2. Meyer D. Hemothorax related to trauma. Thorac Surg Clin. 2007;17:47-55.
  3. Roodenburg B, Roodenburg O. Chest trauma. Anaesth Intensive Care. 2014; 15(9):411-414.
  4. Bernardin B, Troquet J. Initial management and resuscitation of severe chest trauma. Emerg Med Clin N Am. 2012;30:377-400.
  5. Eckstein M, Henderson S. Thoracic Trauma. Rosen’s Emergency Medicine. Ch 45, 431-458.e3.
  6. Meyer D. Hemothorax related to trauma. Thorac Surg Clin. 2007;47.
  7. McEwan K, Thompson P. Ultrasound to detect heamothorax after chest injury. Emerg Med J. 2007; 24(8):581-582.
  8. Rothlin M, Naf R, Arngwerd M, Candinas D, Frick T, Trentz O. Ultrasound in blunt abdominal and thoracic trauma. J Trauma. 1993; 34(4):488-495.
  9. Ma O, Mateer J, Ogata M, Kefer M, Witmann D, Aprahamian C. Prospective analysis of a rapid trauma ultrasound examination performed by emergency physicians. J Trauma. 1995; 38(6):879-885.
  10. Ma O, Mateer J. Trauma ultrasound examination versus chest radiography in the detection of hemothorax. Ann Emerg Med. 1997; 29(3):312-315.
  11. Sisley A, Rozycki G, Ballard R, Manias N, Salomone J, Feliciano D. Rapid detection of traumatic effusion using surgeon-performed ultrasonography. J Trauma. 1998; 44(2):291-297.
  12. Noble V, Nelson P. Manual of emergency and critical care ultrasound. (2011). Cambridge University Press, New York.
  13. Abboud P, Kendall J. Emergency department ultrasound for hemothorax after blunt traumatic injuy. J Emerg Med. 2003;25(3):181-184.
  14. Traub M, Stevenson M, McEvoy S, Briggs G, Lo S, Leibman S. Joseph T. The use of chest computed tomography versus chest x-ray in patients with major blunt trauma. Injury. 2007; 38(1):43-47.
  15. Kirsch T, Sax J. Tube Thoracostomy. Chapter 10. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. p.189-211. Elsevier Saunders, Philadelphia, PA.
  16. Kortbeek J, Al Turki S, Ali J, Antoine J, Bouillon B, Brasel K, et al. Advanced trauma life supports, 8th editions, the evidence for change. J Trauma. 2008:64(6):1638-1650.
  17. Legome E, Shockley L. Trauma: A comprehensive emergency medicine approach. 2011. Cambridge University Press, New York.
  18. Jones R, Rivers E. Resuscitative Thoracotomy. Chapter 18. Roberts and Hedges’ Clinical Procedures in Emergency Medicine. p.325-339. Elsevier Saunders, Philadelphia, PA.
  19. Barriot P, Riou B, Vlars P. Prehospital autotransfusion in life-threatening hemothorax. Chest. 1988;93(3):522-526.
  20. Salhanick M, Sams V, Pidcoke H, Fedyk C, Scherer M, et al. Shed pleural blood from traumatic hemothorax contains elevated levels of pro-inflammatory cytokines. Shock. 2016;46(2):144-148.
  21. Salhanick M, Corneille M, Higgins R, Olson J, Michalek J, et al. Autotransfusion of hemothorax blood in trauma patients: is it the same as fresh whole blood? Am J Surg. 2011;202(6):817-821.

The Dialysis Patient: Managing Fistula Complications in the Emergency Department

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident at SAUSHEC, USAF) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

A 78-year-old male with a past medical history of coronary artery disease, hypertension and end stage renal disease presents to the emergency department (ED) with a chief complaint of “can’t stop bleeding.”  The patient is seated in triage, holding a blood-soaked towel over his left arm.  As you approach him, you scan his intake sheet and note the following VS: Blood pressure (BP) 72/59, heart rate (HR) 127 beats per minute, respiratory rate 18/minute, temperature (T) 102.1°Fahrenheit (F).  As you lift the towel, a significant amount of blood pours from his hemodialysis fistula.  You instruct the patient to continue holding firm pressure and consider possible etiologies of the bleeding.

You recognize that the patient is hemodynamically unstable, needs blood and an infectious workup, but what is the next step if direct pressure is unsuccessful?

The following review includes a few tips and tricks for identifying and treating common hemodialysis (HD) complications.

Epidemiology of Chronic Kidney Disease

In the United States, approximately 300,000-400,000 chronic kidney disease patients are maintained on HD.1-4  The process of HD requires vascular access through an arteriovenous (AV) fistula, AV graft, or central venous catheter (CVC).  Today, as a result of the National Kidney Foundation’s “Fistula First” initiative, nearly 55% of HD patients utilize an AV fistula.  .4,5  Significant morbidity and mortality are associated with fistula placement and recurrent cannulation. Because of the possibility of complications involving fistulas, EM physicians should recognize and treat vascular insufficiency, hemorrhage, infection, stenosis, thrombosis, aneurysms, and pseudoaneurysms.

Vascular Insufficiency – Dialysis Associated Steal Syndrome (DASS)

DASS is a complication of AV fistulas and its incidence is reported as high as 8% in the current vascular literature.3  DASS occurs secondary to retrograde flow from the artery distal to the AV anastomosis, and is seen most commonly when a large artery (brachial or superficial femoral) supplies blood through the fistula into a large, low-pressure vein.6,7  Symptoms of DASS progress from a painless cool extremity, to claudication, rest pain, and finally to tissue necrosis.6  While the majority of patients with symptomatic DASS present within one month of AV fistula creation, there are some reports detailing cases as late as one year post procedure.7

 Examination of a patient with DASS includes the pathognomonic finding of a diminished or absent distal radial pulse, palpable only with compression of the dialysis access site.6  Although formal ultrasound (US) may demonstrate high-velocity, retrograde flow through the HD fistula, this is not a sensitive indicator of DASS as the diagnosis is based on clinical symptoms.6,7  The gold standard in addressing DASS is ligation of the AV access; therefore, vascular surgical consultation is required urgently or emergently according to symptom severity.7


In the HD patient, hemorrhage often arises secondary to platelet dysfunction (uremia or transient thrombocytopenia observed in the ESRD population), supra-therapeutic anticoagulation, or fistula abnormalities (infection, stenosis, aneurysms, pseudoaneurysms).1,6,8

 Mechanisms for Obtaining Hemostasis

Direct Pressure

Direct pressure is the primary intervention for controlling hemorrhage.  It should be applied to the site of bleeding for 5-10 minutes.1,5,7,8  If hemostasis is achieved, patients should be observed for 1-2 hours to monitor for recurrent bleeding.1,6,8

Note: The majority of hemodialysis literature advises against the application of excessive pressure as it may lead to iatrogenic fistula thrombosis.5,7 How much pressure is too much pressure?  This is difficult to determine.

Topical Hemostatic Agents

Gelfoam – While there are no trials or studies specifically assessing the utilization of gelfoam in the setting of vascular access hemorrhage, its use is extensively detailed in emergency medicine literature.1,9,10   Gelfoam is a water-insoluble sponge prepared from purified porcine skin, gelatin granules, and water, which when applied to a bleeding site acts as a mechanical matrix facilitating clot formation.11  Gelfoam may be saturated with sterile saline prior to application or applied directly to the bleeding site until hemostasis is achieved.1,9  Once hemostasis has been attained, a bandage may be applied over the gelfoam (taking precautions to avoid excessive pressure which, as above, predisposes the patient to iatrogenic thrombosis).1

 Chitosan – Available as HemCon®, chitosan is a non-toxic, complex carbohydrate derived from chitin. It is known to exhibit a mucoadhesive activity when applied directly to an injury site with active blood extravasation.12  One randomized control trial of 50 HD patients with vascular hemorrhage demonstrated improved time to hemostasis at the four minute treatment point after the application of HemCon® under direct pressure versus the application of direct pressure with plain gauze.13

Thrombin – Recombinant human thrombin (rhThrombin) was approved by the FDA in 2008. It helps attain hemostasis whenever control of bleeding by suture, ligature, or cautery is ineffective or impractical.14  Thrombin plays an essential role in the intrinsic and extrinsic pathways of the coagulation cascade, activating factors XI, VIII, V, XII, and I (fibrinogen), thereby facilitating hemostasis.10  Recombinant human thrombin may be utilized in conjunction with a gel foam product.1,14  The most common adverse reaction to rhThrombin is thrombosis, however, thrombosis occurring secondary to topical application in the setting of fistula hemorrhage has not been evaluated.14  (Thrombosis has been noted to occur in 1% of adult and pediatric burn patients (N=72) after application to obtain hemostasis at graft sites).14

Reversal of Supra-Therapeutic Anticoagulation – Heparin is commonly utilized in dialysis centers. Persistent oozing or bleeding occurring within hours of HD should raise concern for over anticoagulation.  Experts recommend the use of intravenous protamine at a dose of 1 mg for every 100mg heparin given during dialysis. If the dose of heparin is unknown, 10-20 mg of protamine should be given in total (estimated sufficient to reverse an average dose of 1,000-2,000 units of heparin).1,7

Pharmacotherapy – Desmopressin (DDAVP) is a synthetic analogue of anti-diuretic hormone (ADH). It is FDA approved for the treatment of bleeding episodes in patients with Hemophilia A and von Willebrand’s disease (Type 1).1,9,10   While the mechanism of action has yet to be elucidated, DDAVP has been demonstrated to decrease the activated partial thromboplastin and bleeding times in uremic patients,15 as well as to prevent bleeding prior to invasive procedures in HD patients.1,16,17  This compound may be utilized by the emergency physician (in consultation with a vascular surgeon) to manage hemorrhage from AV grafts or fistulae.1,16  DDAVP should be given parenterally with a recommended dose of 0.3mcg/kg over ten minutes. It is contraindicated in patients with a history of hyponatremia, unstable angina, or congestive heart failure.1,14

 If the above interventions have failed to attain hemostasis, vascular surgery should be consulted immediately for intervention.1,7,9  If ED intervention is required to prevent death, a tourniquet or strong manual pressure may be applied to the fistula site.1,9  Fistula thrombosis and loss of limb may occur in this scenario.1,7,9


Vascular access infection is a major cause of morbidity and mortality in HD patients.6,18  Current data estimate the rate of AV fistula infection as between 2-5%.10  Given the altered humoral and cell-mediated immunity occurring in chronically uremic HD patients, individuals with an AV fistula infection may lack localized inflammatory findings (rubor, calor, dolor) and present only with intermittent fever, generalized malaise, minimally elevated white blood cell count, and/or hypotension.6   The most common infecting organism in the HD population is Staphylococcus aureus, followed by Staphylococcus epidermidis and gram-negative bacteria.6,19

Suspected fistula infections should be managed aggressively with blood cultures and intravenous antibiotics.  Recommended antibiotic therapy includes vancomycin (15mg/kg or 1g IV). Gentamicin (100mg IV initially and after each dialysis treatment) should be given if an infection with gram-negative organisms is suspected.6,19   Patients should be hospitalized until cultures are resulted and susceptibilities are known so that antibiotic therapy can be narrowed (reducing the incidence of vancomycin-resistant organisms).20

Ultrasound should be utilized to differentiate fistula infection from infected thrombus, local abscess, or infected hematoma which require vascular surgery consultation and oftentimes surgical management.20

 Fistula Stenosis

Stenosis and thrombosis are the most common complications of AV fistulas.21  Central vein stenosis occurs in 19-41% of HD patients.22  Patients presenting to the ED with fistula stenosis may report distress secondary to upper extremity and chest wall edema.  Physical examination is essential in the emergency physician’s evaluation of stenosis and it will vary according to the stenosed segment (inflow versus outflow stenosis).23  Inflow stenosis presents with a weakened radial pulse and a high pitched bruit in the systolic phase of the cardiac cycle at the site of stenosis.23    In contrast, outflow stenosis is identified as the site distal to the stenosis exhibits a bounding pulse and absent thrill.  In the ED, Doppler US may be utilized for the assessment of vascular flow.  Vascular surgery should be consulted for patients presenting to the emergency department with the aforementioned symptomatology, as percutaneous transluminal angioplasty is the treatment of choice.23

Fistula Thrombosis

Thrombosis is a common problem associated with vascular access.10  AV fistula thrombosis is likely to occur secondary to venous outflow stenosis (venous stenosis increases resistance to blood flow, which in turn results in increased venous pressure, decreased blood flow, and ultimately, thrombosis1). Fistula thrombosis can also occur in hours following dialysis treatment as patients are often relatively hypovolemic (venous stasis) and the fistula access site may be excessively compressed to attain hemostasis.1,8  Erythropoietin therapy, often prescribed to address the chronic anemia encountered in ESRD patients,  has been noted to increase the risk of thrombotic complications secondary to increased levels of acute phase reactant proteins and chronic inflammation.7

AV fistula thrombosis is quickly identified by examining the fistula site for the absence of a bruit and thrill.1,7,8  In the case of thrombosis, vascular surgery should be consulted immediately.  Management options include surgical thrombectomy versus thrombolysis with streptokinase or tissue plasminogen activator with or without angioplasty.1,8,24

 Fistula Aneurysm or Pseudoaneurysm

Aneurysms form in AV fistulas secondary to repetitive cannulation and subsequent weakening of vessels walls.8,10  Patients with aneurysms may present to the emergency department reporting extremity pain, neurologic dysfunction secondary to aneurysmal impingement of surrounding nerves, significant thinning of overlying fistula skin, or hemorrhage secondary to this skin erosion.8,25

 Pseudoaneurysms are pulsating extravascular hematomas resulting from dialysis site access. These are rare complications  of AV fistula access.7,10  As compared to aneurysms, patients with pseudoaneurysms are more likely to present to the emergency department for vascular hemorrhage or signs and symptoms consistent with infection.7,10,25  Both AV fistula aneurysm and pseudoaneurysms can be identified with the use of Doppler US.7  Vascular surgery should be consulted for all detected vessel irregularities for consideration for operative repair.7,10


Nearly 400,000 individuals in the United States are maintained on HD therapy.1-4  With incident cases of ESRD reaching nearly 21,000 annually, and vascular access complications accounting for 16 to 25% of hospital admissions,5,7 understanding of the appropriate management of AV fistula complications is paramount for the emergency medicine physician.

 Key Pearls

  • Fistula complications = 16-25% of hospital admissions for HD patients
    • DASS => complication of operative creation of a HD fistula
      • Diagnosis based upon presentation and PE
        • Cool/painful limb + diminished or absent distal radial pulse, palpable only with compression of the dialysis access site => Vascular Consult
      • Hemorrhage
        • #1 = direct pressure
        • Gel foam, rhThrombin +/- DDAVP in consultation with a specialist are options
        • Consider protamine for heparin reversal if recently received dialysis
      • Infection
        • Common cause of morbidity = cover for Staph and Strep
        • Use US to differentiate perivascular cellulitis from local abscess, infected hematoma or infected thrombus.
          • Perivascular cellulitis => Vancomycin (+ gentamycin if gram negatives suspected)
          • Abscess, hematoma, thrombus => Antibiotics + vascular consult for possible OR
        • Fistula Stenosis
          • Patients present with extremity pain +/- chest wall edema
            • Order Doppler US
              • Abnormalities = consult vascular => PTCA
            • Fistula Thrombosis
              • Fistula has absent bruit or thrill = vascular consult => thrombectomy vs. thrombolysis
            • Fistula Aneurysm or Pseudoaneurysm
              • Patients present with extremity pain, compression neuropathy, or hemorrhage secondary to skin erosion.
                • Doppler US => vascular consult for abnormalities

References / Further Reading

  1. Larsen C, Weathers B, Schwartzwald M, Barton M. Focus on: dialysis access emergencies. American College of Emergency Physicians Clinical & Practice Management 2010. Available from—Practice-Management/Focus-On–Dialysis-Access-Emergencies/
  2. Soi V, Moore C, Kumar L, Yee J. Prevention of catheter-related bloodstream infections in patients on hemodialysis: challenges and management strategies. Int J Nephrol Renovasc Dis. 2016;9:95-103.
  3. Leake A, Winger D, Leers S, Gupta N, and Dillavou E. Management and outcomes of dialysis access-associated steal syndrome. J Vasc Surg. 2015; 61(3): 754-760.
  4. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for 2006 Updates: Hemodialysis Adequacy, Peritoneal Dialysis Adequacy and Vascular Access. Am J Kidney Dis. 2004; 48:S1-S322.
  5. United States Renal Data System (USRDS) Annual Data Report. Epidemiology of kidney disease in the United States. 2015. Available from:
  6. Dhingra R, Young E, Hulbert-Shearon T, Leavey S, Port F. Type of vascular access and mortality in US hemodialysis patients. Kidney Int. 2001; 60(4):1443-1451.
  7. Hodde L, Sandroni S. Emergency department evaluation and management of dialysis patient complications. J Emerg Med. 1992; 10:317-334
  8. Wolfson A, Singer I. Hemodialysis-related emergencies-part I. J Emerg Med. 1987; 5(6):533-543.
  9. Venkat, A. Challenging and Emerging Conditions in Emergency Medicine. Chichester, West Sussex: Wiley-Blackwell, 2011. Print.
  10. Tintinalli, J. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, 2011. Print.
  11. United States Food and Drug Administration. Gelfoam (absorbable gelatin powder). Device Approvals, Denials, and Clearances. 2000. Available at
  12. Wedmore I, McManus J, Pusateri A, Holcomb J. A special report on the chitosan-based hemostatic dressing: experience in current combat operations. J Trauma. 2006; 60(3):655-658.
  13. Bachtell N, Goodell T, Grunkemeier G, et al. Treatment of dialysis access puncture wound bleeding with chitosan dressings. Dialysis Transplant. 2006:35:1-6.
  14. United States Food and Drug Administration. Recothrom, thrombin topical (recombinant lyophilized powder for solution-for topical use only. Highlights of prescribing Information. 2008. Available from:…/ucm120557.pdf
  15. Mannucci P, Remuzzi G, Pusineri F, et al. Deamino-8-D-arginine vasopressin shortens the bleeding time in uremia. N. Engl. J. Med. 1983;308:8-12.
  16. Mannucci PM. Desmopressin (DDAVP) in the treatment of bleeding disorders: the first 20 years. Blood 1997;90:2515-21.
  17. Lethagen S. Desmopressin (DDAVP) and hemostasis. Ann. Hematol. 1994;69:173-80.
  18. U.S. Renal Data System: Chapter 3: Hospitalizations. In: USRDS 2012 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States, National Institutes of Health. Bethesda, MD, National Institute of Diabetes and Digestive and Kidney Diseases, 2012
  19. Ball L. Fatal vascular access hemorrhage: reducing the odds. Nephrol Nurs J. 2013; 40(4):297-303.
  20. Hammes M. Medical complications in hemodialysis patients requiring vascular access radiology procedures. Semin Intervent Radiol. 2004; 21(2):105-110.
  21. Pirozzi N, Garcia-Medina J, Hanoy M. Stenosis complicating vascular access for hemodialysis: indications for treatment. J Vasc Access. 2014; 15(2):76-82.
  22. Quaretti P, Galli F, Moramarco L, Corti R, Leati G, et al. Dialysis catheter related superior vena cava syndrome with patent vena cava: long term efficacy of unilateral viatorr stent-graft avoiding catheter manipulation. Korean J Radiol. 2014; 15(3):364-269.
  23. Vachharajani, T. Diagnosis of arteriovenous fistula dysfunction. Seminars in Dialysis. 2012; 25(4): 445-450.
  24. Bernal NP, Grammer ME, Mark JR, et al. Surgical thrombectomy remains a standard of care for treatment of thrombosed arteriovenous grafts. J. Surg. Res. 2008;144:362-3.
  25. Siedlecki A, Barker J, Allon M. Aneurysm formation in arteriovenous grafts: associations and clinical significance. Seminars in Dialysis. 2007; 20(1):73-77.