The Case Files

Welcome to the Case Files!
The Case Files is an anecdotal collection of emergency medicine cases to enable physicians and researchers to find clinically important information on unusual conditions.

Case reports should focus on:

  • Unusual side effects or adverse interactions.
  • Unusual presentations of a disease.
  • Presentations of new and emerging diseases, including new street drugs.
  • Findings that shed new light on a disease or an adverse effect.

Comment on a case or submit your own case following the instructions in the Submissions box to the right.

Tuesday, May 15, 2018

​BY BRUNA ALMEIDA, & AHMED RAZIUDDIN, MD

A 30-year-old man presented to the ED with dyspnea and pleuritic chest pain radiating to his left shoulder that had started three days before. He was at a “sex party” four days earlier, and had used amphetamines and gamma-hydroxybutyric acid (GHB, also called Liquid G).


The patient said deep breaths and movement worsened his pain. He also had exertional shortness of breath and occasional palpitations. He denied fever, cough, loss of consciousness, recent surgery, and prolonged immobilization. The patient had no personal or family history of DVT, PE, or cardiac conditions. He was a bodybuilder, and his last workout was five days earlier. Besides its use as “Liquid Ecstasy,” GHB is also used by bodybuilders. The patient was HIV-positive with an undetectable viral load.

His temperature was 97.2°F, blood pressure was 144/88 mm Hg, pulse rate was 81 bpm, and respiratory rate was 22 bpm. Oxygen saturation was 94% on room air. His cardiac exam showed a regular rate and rhythm, normal S1 + S2, no S3/S4, and no reproducible pain on palpation. His lungs were clear to auscultation.

His laboratory studies revealed a troponin I of 0.08 ng/ml, a D-dimer of 2920 ng/ml, and hepatitis A and hepatitis B nonreactive. Urine toxicology revealed that he was positive for amphetamines and opiates.

A chest x-ray showed left lower lung opacity. A CT angiogram was performed, and bilateral segmental filling defects were present in the pulmonary arteries, bilateral lower lobe volume loss and consolidation were seen, and the main pulmonary artery measured approximately 3.2 cm in the transverse dimension. Anterior convexity of the septum was present, and an ECG demonstrated normal sinus rhythm, normal axis, no LVH by voltage, and no ST segment abnormality. His echocardiogram showed moderately diffuse hypokinesis, and his ejection fraction was 30%. The LA and RA were mildly dilated, his LV was moderately dilated, he had trace TR, and his pulmonary pressure was mildly elevated. The patient received ketorolac 30 mg IV x1, heparin bolus 80 unit/kgx1, and heparin infusion, and he was admitted.

Drugs and the Lungs

Pulmonary complications of illicit drug use are common because the lungs are exposed to the environment and the circulation. Patients with pulmonary complications from illicit drug use are often recognized because of other signs and symptoms associated with the drug use. Patients often abuse illicit drugs surreptitiously, however, so the pulmonary complications are often recognized only with careful questioning or laboratory screening.

Urine and blood testing to detect illicit drugs may be helpful, but many of the parent compounds have short half-lives and readily undergo hydrolysis. (Chest 1995;108[2]:460.) The classic symptoms of pulmonary embolism were frequently absent in patients who died of embolism. The only reasonably common symptoms are tachycardia and sudden-onset dyspnea. These findings suggest pulmonary embolism, but they clearly are nonspecific. (Mayo Clin Proc 1995;70[5]:501.)

Parenteral anticoagulation with subsequent conversion to vitamin K antagonists is the mainstay of therapy in hemodynamically stable patients without contraindications to systemic anticoagulation. Early initiation is paramount because patients may quickly decompensate. Patients with acute PE have decreased mortality if anticoagulation treatment starts in the ED rather than after admission.

Supportive care of hypoxemia and hemodynamic instability should be instituted. Hemodynamically unstable patients may benefit from fibrinolytic therapy. The role for fibrinolysis is limited, with significant bleeding occurring in up to 13 percent of patients. The use of bolus thrombolytics during cardiopulmonary arrest may have some benefit when PE is strongly suspected and the patient does not respond to resuscitation. Mechanical thrombolysis with catheter-directed embolectomy and fibrinolytic therapy can also be used.

Systemic heparin, either unfractionated heparin or low-molecular-weight heparin (LMWH), is another mainstay of treatment. LMWH is advantageous in ease of administration, monitoring, and lower potential for heparin-induced thrombocytopenia. It is not an appropriate choice for patients with renal failure or for patients at significant risk of bleeding because of its longer half-life and lack of reversibility. Newer options for anticoagulation include oral factor Xa inhibition with agents under investigation, such as rivaroxaban. Permanent or temporary inferior vena cava filters (IVCF) may be used if patients continue to have PEs despite therapeutic anticoagulation, experience bleeding events, or have other contraindications to anticoagulation. IVCF can prevent further pulmonary emboli in patients with lower extremity deep venous thrombosis, but do not reduce mortality. (Int J Crit Illn Inj Sci2013;3[1]:69.)

​Complications and Mortality

Pulmonary embolism is responsible for 100,000 to 200,000 deaths in the United States each year, but diagnosing it can be challenging because of a diverse range of clinical presentations. Failure to diagnose PE is a serious management error because 30 percent of untreated patients die; only eight percent succumb with effective therapy.

Unfortunately, PE may be asymptomatic or present with sudden death. Characteristic signs and symptoms such as tachycardia, dyspnea, chest pain, hypoxemia, and shock are nonspecific, and are present in many other conditions such as acute MI, congestive heart failure, and pneumonia. The Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) trial identified common signs as tachypnea (54%) and tachycardia (24%) and common symptoms as dyspnea, usually with onset within seconds, at rest or with exertion (73%), pleuritic pain (44%), calf or thigh pain (44%), calf or thigh swelling (41%), and cough (34%). (N Engl J Med 2006;354[22]:2317.)

PIOPED II excluded many patients, such as those with chronic elevated creatinine levels, those receiving dialysis, critically ill patients, and those with recent MI, so its applicability is limited. A high index of suspicion and assessment of risk factors are critical for the recognition of pulmonary embolism. (Int J Crit Illn Inj Sci2013;3[1]:69.)

Ms. Almeida is a third-year medical student at the University of Medicine and Health Sciences currently doing an emergency medicine rotation at Weiss Memorial Hospital in Chicago. Dr. Raziuddin is a board-certified emergency physician and internist at Weiss Memorial Hospital, Gottlieb Memorial (Loyola University) Hospital, and Westlake Hospital in Melrose Park, IL.​

Wednesday, May 9, 2018

​BY ANDRZEJ KIELTYKA, PA; PARDEEP THANDI, MD; & ANUMEHA SINGH, MD

A 56-year-old man presented to the emergency department with shortness of breath for one month and pleural effusions on an outpatient chest x-ray. He had been taking adalimumab, methotrexate, and steroids for arthritis and Sjogren's syndrome.


A right pleural effusion in a patient with nephrotic syndrome.

His monoclonal gammopathy of undetermined significance (MGUS) was monitored annually, but no medical intervention beyond surveillance was required. He had excessive thirst but normal urine output. He noted face and hand swelling in the morning that gave way to more significant pedal edema at the end of the day and progressively worsening exertional dyspnea. He noted a low grade fever and loss of appetite. His initial vitals were a blood pressure of 185/96 mm Hg, a heart rate of 106 bpm, a respiratory rate of 20 bpm, a temperature of 100.1°F, and oxygen saturation of 97% on room air.

The patient appeared well, but would not stop sipping water despite obvious myxedema. He also had a history of autoimmune and oncological conditions.

The differential for this case included an infectious process such as viral or bacterial infiltrate. Lung mass or atypical presentation of myeloma with the patient's history of MGUS was also on the differential, but cardiorenal disease, nephrotic disease, and congestive heart failure were higher on the list. Other etiologies were considered, including thyroid disease, syndrome of inappropriate antidiuretic hormone secretion, autoimmune activation of rheumatoid arthritis, and vasculitis.

This patient had abnormalities in almost all labs drawn, but some key findings pointed to cardiorenal syndrome: anemia and thrombocytopenia per H/H of 9/29 with ovalocytes, platelets at 29, and WBC of 12.1 with shift. Inflammation markers were high: CRP 23, ESR 45; cardiac markers troponin I <0.30 and CK of 62 were normal, but pro-BNP, N-terminal was 12,000. The chemistries were largely normal with significant creatinine of 1.1 and BUN 25.

The crucial labs were the serum protein of 5.1, albumin of 2.8, globulin 2.3, and prealbumin 20. The urine analysis was significant for random protein of 289 with protein to creatinine at 2513. The patient was admitted to the medicine service with cardiology and nephrology consulting. Without the inflammatory markers and urinalysis, this may have been congestive heart failure, but the patient's complicated history demanded a more careful look.

Acute or exacerbation of chronic CHF is frequently managed in the ED. The disruption of fluid volume control often results from overlapping renal and cardiac etiologies. Some would argue that CHF is as much a symptom as a diagnosis, and the renal part of the balance should not be ignored. The patient was worked up for cardiorenal syndrome by cardiology, nephrology, rheumatology, and hematology.

Progress and Prognosis

The relationship of the cardiac and renal systems is particularly evident when homeostasis is disrupted. Cardiorenal syndrome was classified in 2008 by the consensus conference of the Acute Dialysis Quality Initiative into two main stems: cardiac and renal. (http://www.adqi.org.) The incidence of each of the five types varies, but type 3 is the most common, noted in up to 70 percent of ICU patients. Renal disease is one of the highest risks of an adverse cardiovascular disease, and the reverse pathway is also noted.

The prognosis and progression of nephrotic syndrome vary greatly depending on whether the syndrome is primary or secondary and the nature of the underlying pathology leading to it. Infants with congenital nephrotic syndrome have a dismal prognosis; most cases require dialysis and then kidney transplant within a few months.

In cases of focal glomerulosclerosis, many patients experience frequent relapses and become dependent on or resistant to steroids. End-stage renal disease develops in 60-70 percent of the cases by 10 years, and about half of the cases require dialysis by five years. (http://bit.ly/2EW5ynx.) The prognosis worsens for patients with proteinuria.

The prognosis for patients with minimal change nephropathy is good, with about 30 percent of children never relapsing and only three percent becoming steroid-resistant. Most respond well to steroid therapy. About 50 percent of children have one or two relapses within five years. Adults with minimal change nephropathy have a relapse rate similar to that of children. (http://bit.ly/2EW5ynx.) The long-term prognosis is excellent, however, with rare renal failure. Idiopathic membranous nephropathy has an excellent prognosis with complications and incidents of renal failure occurring rarely. Poor patient response to steroid therapy may predict a poor outcome. Presence of hematuria and hypertension are also predictors of a poor prognosis.

Infection was a major factor in the mortality rate among patients with nephrotic syndrome in the pre-antibiotic era. Early recognition and aggressive treatment have reduced the mortality and morbidity of the disease, especially in secondary nephrotic syndrome where the prognosis depends on the underlying pathology and adequate management.

One study found that routine treatment with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, plus selective use of corticosteroids or other immunosuppressants, led to a remission rate of 76 percent, with 12 percent of patients requiring hemodialysis. (Nephrol Dial Transplant 2012;27[1]:235.)

KDIGO Guidelines

The approach to nephrotic syndrome is highly varied, and relies on the guidelines issued in 2012 by the Pathology Kidney Disease Improving Global Outcomes (KDIGO) Controversies Conference. (http://bit.ly/2EUBcSu.) These recommend restricting dietary sodium and having adequate caloric intake and protein (1 g/kg/day). Supplemental dietary protein has no proven value. A diet with no added salt will help limit fluid overload, but fluid restriction is not needed. Physical activity is recommended for patients with nephrotic syndrome to reduce the risk of blood clots.

Treating the underlying pathology depends on whether the systemic pathology gives rise to a nephrotic syndrome such as lupus, diabetes, and infection. ACE inhibitors and angiotensin-receptor blockers are frequently started in patients with nephrotic syndrome because of their anti-proteinuria action, but studies have failed to demonstrate any evidence showing benefit.

A Cochrane review showed that combining an alkylating agent with a corticosteroid has short- and long-term benefits for membranous nephropathy. (Cochrane Database Syst Rev 2014 Oct 16;[10]:CD004293.) Immunosuppressive therapy is not needed for most adults with idiopathic nephrotic syndrome. Other immunosuppressive treatments should be considered if the patient is steroid-resistant.

Immunosuppressive therapy for nephrotic syndrome secondary to systemic lupus erythematosus is highly effective and supported by multiple studies. It may lead to partial or complete remission in patients with minimal change disease or primary focal segmental glomerulosclerosis. Secondary amyloidosis with nephrotic syndrome should improve with anti-inflammatory treatment of the primary disease.

Treating fluid retention and edema with diuretics is indicated for symptomatic management. These patients are usually resistant to diuretics and may require a higher dose. Sometimes preloading with 20% human albumin helps. Assisted mechanical ventilation might be required in patients presenting with CHF.

Despite the known risk of venous thrombosis in patients with nephrotic syndrome, no randomized controlled trials guide whether prophylactic anticoagulation should be used or for how long. Prophylaxis can be considered in severe disease and for known pre-existing risk factors for thrombosis.

Infection has been reported in up to 20 percent of adults with nephrotic syndrome. A Cochrane review found no strong evidence to recommend a specific intervention to prevent infection in adults. (Cochrane Database Syst Rev2012 Apr 18;[4]: CD003964.) No clear review or study has shown any benefit from routine use of anti-lipid agents.

Treatment and Outcome

The KDIGO guidelines recommend using primarily alkylating agents (cyclophosphamide) in combination with corticosteroids for six months if the criteria for immunosuppressive therapy are met. Alternatively, calcineurin inhibitors and corticosteroids are recommended for six months.

Corticosteroids are recommended to induce remissions in minimal change disease (MCD). The guidelines also suggest alkylating agents (oral cyclophosphamide 2-2.5 mg/kg/day for eight weeks) in cases of frequent relapses and steroid resistance. Corticosteroids are also recommended for focal segmental glomerulosclerosis. Calcineurin inhibitors can be considered if corticosteroid therapy is contraindicated.

Cardiology, hematology/oncology, infectious disease, nephrology, pulmonary, and rheumatology were consulted. A TEE showed cardiomyopathy. Our patient was admitted for seven days and discharged with primary diagnoses of nephrotic syndrome, MGUS, cardiomyopathy, and essential hypertension. He was discharged on carvedilol, alendronate, furosemide, and spironolactone with nephrology follow-up. (The patient was allergic to lisinopril.)

Final recommendations from rheumatology were pending a bone marrow biopsy. He was not a candidate for anti-TNF agents or methotrexate. Prednisone was recommended, but the patient was against it, and it was held off until biopsy to prevent any influence on the read.

Nephrology said the patient's condition was likely multifactorial. The etiology of his symptoms remained unclear, but preliminary workup was notable for reduced cardiac output (EF 35%), bilateral pulmonary nodules of unclear chronicity of unclear etiology (infectious, inflammatory, or malignant; origin unclear), and nephrotic range proteinuria (2.5 g) with associated hematuria. An underlying glomerulonephritis was a consideration given his history of autoimmune disease. Venous congestion and poor forward flow were other considerations given his low cardiac output.

ID was consulted for an initial fever of 100.9°F in the hospital. Ceftriaxone was initiated and then discontinued during his hospital stay because cultures and sources were negative. The patient was discharged in stable condition after seven days.

Unfortunately, the patient returned a week later complaining of worsening pedal edema and increasing shortness of breath. The patient was diagnosed with symptomatic anemia and AKI. He was readmitted, and his second course was complicated by nosocomial pneumonia.

The patient was switched to torsemide, and cardiology started him on aspirin and a statin. Vancomycin was initiated for MRSA pneumonia, and high-dose methylprednisolone was initiated by rheumatology. The patient received two units of packed red blood cells for symptomatic anemia, and was started on iron and folate supplements. His symptoms gradually improved after an 18-day admission. He was discharged on torsemide, prednisone, a statin, and vancomycin along with his previous medications.

Mr. Kieltyka is an emergency medicine physician assistant and a graduate of Drexel University's physician assistant program in Philadelphia. Dr. Thandi is an emergency physician and simulation fellow at Hartford (CT) Hospital. Dr. Singh is an assistant professor of emergency medicine at the University of Connecticut and an emergency physician at Hartford Hospital. She and her emergency physician-husband, Daksh Rampal, MD, also own Priority Urgent Care in Ellington, CT. 

Tuesday, March 20, 2018

​BY NOURA MAHDI; DARRON LEWIS; JEREMY OSBORNE; & AHMED RAZIUDDIN, MD

A 73-year-old man was brought to the emergency department from his nursing home for rectal bleeding and anemia. The patient mentioned he had had episodes of bright red rectal bleeding and constipation for a few months. A colonoscopy had been done prior to the visit, which revealed a large intestine tumor and biopsy confirming adenocarcinoma. He was awaiting an appointment with his surgeon.

The patient reported bloody rectal leakage, and a CBC done at the nursing home showed a hemoglobin level of 7.2. He also complained of dyspnea but denied any other symptoms. He was alert and oriented to person, place, and time with no abnormal findings on physical exam aside from gross blood during the rectal examination. His past medical history was significant only for hyperlipidemia treated with simvastatin.

His vitals were taken twice in the ED, and he had mild tachycardia that improved before admission. (See Figure 1.) The most important findings from his blood work was a RBC count of 2.11 m/ul and a hemoglobin of 5.5 g/dL. A transfusion of two units of packed red blood cells was ordered, which he received on the floor.

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Figure 1. The patient's vital signs at ED and hospital admission.

The patient's labs were drawn again the next day, and his hemoglobin improved to 8.0 g/dL post-transfusion. A blood culture showed growth of Escherichia coli, revealing the patient's septic status apart from his rectal bleeding. He was started on antibiotics to treat the infection, and his blood and urine cultures a day later were positive for E. coli again. Treatment continued, and the patient was scheduled for surgery to remove the intestinal tumor.

The patient was given preoperative antibiotics and cardiac clearance to undergo an exploratory laparotomy with extensive lysis of the adhesions, sigmoid resection with anastomosis, diverting ileostomy, and omental sling. A large mass in the sigmoid was found invading the parietal peritoneum and encompassing the right kidney and ureter, leading to hydronephrosis and eventually to the surgeon's decision to catheterize the right ureter. The surgeon also discovered multiple metastatic lesions in the liver, for which biopsies were taken. The surgery was extensive, but the patient tolerated it well.

The patient had from a seizure, however, after the procedure. He became lethargic and quadriplegic, with flaccid paralysis of his right upper and both lower extremities, and could only move his left arm. His altered mental status remained, and a brain CT without contrast revealed decreased attenuation in the bilateral occipital lobes. It was negative for mass effect, midline shift, fractures, vascular infarct, and intraparenchymal/extra-axial hemorrhage. Early edema posterior reversible encephalopathy syndrome (PRES) was suspected.

An MRI revealed hyperintensity of the bilateral thalami and bilateral occipital cortical and subcortical with patchy areas of hyperintensity seen within the temporal, frontal, and parietal lobes with a cortical and subcortical white matter distribution. suggestive of PRES. (See Figure 2.) An electroencephalogram was performed, where evidence of intermittent slow background activity was seen consistent with a degree of neural dysfunction.


Figure 2. An MRI showing PRES, with edematous tissue in the occipital areas.

The patient spent another two weeks in the hospital under close observation with little to no recovery from his flaccid paralysis of the three extremities. His mental status seemed to improve, however, and he became more responsive and clear in conversations. His labs showed increased lactic acid levels throughout this time but no significant changes in other areas.

The patient's lactic acid was trending down, and he was discharged back to his nursing home. He was given instructions to follow up with the oncologist for chemotherapy and the urologist for removal of the right ureteral stent that had been placed during surgery. The patient's upper right extremity was completely flaccid at discharge. Discharge medications included amoxicillin 500 mg, to which the patient had been de-escalated to following improvement of symptoms.

The patient was brought to the emergency department again for altered mental status three days after discharge. A nurse at the nursing home contacted EMS because of tachycardia and a noticeable change in behavior. The nurse noted that he had not been acting like himself since his return to the nursing home. The nurse could not provide specifics but reported that he seemed “out of it.”

The patient's pulse was 104 bpm and his blood pressure was 86/60 mm Hg in the ED. He was alert but lethargic and oriented only to person. He was immediately given IV fluids and started on Zosyn 3.375 g IV push. A right femoral central line was placed three hours late, and a Levophed 0.05 mcg/kg/min infusion was started to improve the patient's blood pressure. The patient was admitted to the ICU with a diagnosis of sepsis.

The patient was moved from the intensive care unit to the medical floor after antibiotic regimen and fluid resuscitation where he became noticeably jaundiced, and a CT scan revealed new metastasis to the liver. The patient's strength on his right upper and lower extremities increased, and he scored 3/5 for both upper and lower extremities and could grip the examiner's hands lightly on command. Follow-up CT scans showed increased occipital attenuation when compared with scans taken during the first admission. The patient's mental status also improved, and he was oriented to person, place, and time. The rest of the patient's stay was unremarkable, and he chemotherapy was arranged.

Pathogenesis and Presentation

Patients with posterior reversible encephalopathy syndrome present with a sudden onset of symptoms such as headaches, seizures, altered consciousness, and visual disturbances. These symptoms are common in other conditions, so it is important to obtain the patient's history to narrow down the differential diagnosis to decrease the chance of misdiagnosing the patient with venous sinus thrombosis, brain hemorrhage, infective encephalitis, or meningitis. (Perit Dial Int 2012;32[6]:590.) A number of conditions known to be associated with PRES are hypertension, acute kidney injury, chronic kidney disease, autoimmune diseases, immunosuppressive drugs, and organ transplantation.

Two main theories attempt to explain the pathophysiology of PRES. It may be due to interruption of the brain autoregulation in which the dilation and constriction of blood vessels are unable to maintain adequate perfusion leading to the symptoms of PRES. (Stroke 1984;15[3]:413.) This theory explains the association in PRES in patients who have a medical history of hypertension and chronic kidney disease. (N Engl J Med 1996;334[8]:494.) The other theory is that PRES is a result of systemic inflammation leading to endothelial dysfunction, which explains the association in PRES in patients who have a medical history of sepsis, organ transplant, and autoimmune disease. The etiology dilemma of PRES is due to the fact the first theory does not explain why patients who do not have hypertension or chronic kidney disease have PRES and vice versa.

A patient presenting with PRES with these symptoms must have image testing such as a head CT and MRI. The head CT will help rule out brain hemorrhage and space-occupying lesions. The CT scan of some patients will be normal, while others will show early edema. Physicians can perform an MRI to confirm or revoke the diagnosis. MRI findings for PRES can consist of bilateral white matter abnormalities in the watershed areas in the posterior regions of both cerebral hemispheres of the occipital and parietal lobes. (Perit Dial Int 2012;32[6]:590.) Further testing can include angiography to rule out thrombosis, dissection, or vasculitis.

Differential Diagnoses

Unfortunately, the clinical findings of PRES are not specific and can lead to a delay in diagnosis. The symptoms are similar to those found in neurological conditions such as stroke, encephalitis, and demyelinating disorders. (Ann Neurol1993;33[2]:222; J Neurol Neurosurg Psychiatry 2000;69[2]:248.) It is important to distinguish between PRES and other possible conditions because the treatment may be different or even contraindicated in certain situations.

​Treatment and Prognosis

Prompt treatment of PRES is important to improve the prognosis. Most neurological deficits of PRES are reversible, and some patients regain complete neurological function in as little as seven days. Many cases, as with our patient, have slow but progressive recovery that can possibly last up to a year.

Treatment involves strict blood pressure control and cessation of any offending immunosuppressive agents. Blood pressure should be kept around 120/80 mm Hg with a cerebral perfusion pressure at about 60 mm Hg. The intracranial pressure should also be no greater than 20 mm Hg. Blood pressure regulators (labetalol, nitroprusside, and diuretics) and anti-edema therapy can be used to control blood pressure. Seizure control is also important in preventing complications from trauma, and can be monitored with standard antiseizure medications such as valproic acid or phenytoin. Treating the symptoms is the only technique that has been shown to reverse symptoms of PRES over time.

Ms. MahdiMr. Lewis , and Mr. Osborne, clockwise from top left, are medical students at the University of Medicine and Health Sciences and part of the emergency medicine group at Weiss Memorial Hosptal in Chicago, IL. Dr. Raziuddin is an internist and emergency physician at Weiss Memorial Hospital, Gottlieb Memorial Hospital, and Westlake Hospital, all in Illinois.

Tuesday, March 13, 2018

​BY TRAVIS SMITH, MD, & MATTHEW ZUCKERMAN, MD

Paramedics were called for a 42-year-old woman found at a motel by her significant other. The patient was alone at the time of EMS arrival. She was pulseless and apneic, so chest compressions were started, and the cardiac monitor showed pulseless electrical activity.

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Initial ECG showing STE in the anterior leads with ST depression in the inferior leads.

The paramedics gave her 1 mg of epinephrine IV and 1 mg of naloxone IV without obvious response. A laryngeal mask airway was placed, and oxygen was delivered by bag valve mask. She received eight rounds of chest compressions before arrival at the emergency department with a total down time of about 20 minutes.

The patient had palpable pulses when she arrived in the ED, and CPR was stopped. Her initial vital signs were a blood pressure of 120/70 mm Hg, heart rate of 97 bpm, temperature of 33.5°C, and SPO2 was 91% using LMA with bag valve on 100% FIO2.

The woman appeared cachectic, her pupils were fixed and dilated, and she had no obvious external signs of acute trauma. Bilateral coarse rales were heard with bagged breaths, and she had no spontaneous respirations. The cardiac exam showed regular rate and rhythm without murmur. Her skin was cool and mottled.

Bedside cardiac ultrasound showed no right heart dilation, pericardial effusion, or focal wall motion abnormalities. The FAST exam was negative for free fluid. The initial ECG showed ST elevation in the anterior leads with ST depression in the inferior leads. Cardiology was consulted to discuss taking her to the cath lab, targeted temperature management, and disposition. A temperature-sensing Foley was placed with no urine output.

Emergency physicians are often tasked with resuscitating patients who have recently suffered cardiac arrest, but this case highlights interventions initiated in the ED that can affect survival in patients who have return of spontaneous circulation (ROSC) after cardiac arrest. An initial rhythm of PEA carries a better prognosis than asystole but a worse one than shockable rhythms such as ventricular fibrillation and ventricular tachycardia. (Crit Care Med 2010;38[1]:101.) Early cardiac catheterization and targeted hypothermia after out-of-hospital cardiac arrest are associated with improved survival and neurologic outcome in comatose patients with or without STEMI on ECG. (Resuscitation 2014;85[1]:88; Resuscitation 2014;85[11]:1533; Resuscitation 2014;85[5]:657.)

Coronary angiography in one study revealed culprit lesions in 61 percent of patients with out-of-hospital cardiac arrest (Resuscitation 2012;83[12]:1444), and a systematic review demonstrated that a third of patients without ST elevation on electrocardiogram after return of spontaneous circulation had an acute lesion that would benefit from percutaneous coronary intervention. (Resuscitation 2016;108:54.) The American Heart Association guidelines recommend early coronary angiography in post-cardiac arrest patients with suspected cardiac etiology of arrest, regardless of ST segment elevation on ECG. The AHA guidelines also recommend target temperature management of 32-36°C in comatose cardiac arrest patients, and there appears to be no difference between 33°C and 36°C in survival or outcome. (N Engl J Med 2013;369[23]:2197.)

The Interventional Cardiology team recommended taking the patient to the cath lab with a plan for transfer to MICU after cardiac catheterization. The LMA was exchanged for an ETT after suctioning a large amount of vomit from the airway. An AP portable chest x-ray showed bilateral pulmonary edema and a right lower lobe opacity.

Laboratory results showed: a lactate of 17.0 mmol/L, CBC WBC of 2.1 cells/L, Hgb of 13.5 g/L, plt of 65 cells/L, Na of 135 mmol/L, K of 5.7mmol/L, Cl of 97 mmol/L, TCOof 18 mmol/L, BG of <20 mg/dL, BUN of 93 mg/dL, Cr of 7.8 mg/dL, anion gap measured at 27, troponin of I < 0.03 ng/mL, EtOH of <10 g/dL, ALP of 84 IU/L, ALT of 65 IU/L, AST of 97 IU/L, Tbili of 0.6 mg/dL, prot of 8.0 g/dL, and Alb of 4.7 g/dL.

Dextrose was given for hypoglycemia, calcium chloride for hyperkalemia, and a normal saline bolus for anuria. Ampicillin-sulbactam was ordered given the patient's lung opacity, vomit, and hypoglycemia, which were concerning for aspiration, pneumonia, and sepsis.

More than a third of out-of-hospital cardiac arrest patients will have bacteremia. (Resuscitation 2014;85[2]:196.) It may be causative or from resuscitative measures, but early antibiotics are reasonable as a part of resuscitation in these patients because administration has been associated with decreased mortality with a number needed to treat of 5. (Resuscitation 2013;84[5]:616; Resuscitation 2015;92:154.) Antibiotics should be strongly considered in patients who show evidence of sepsis as a contributor to cardiac arrest. Acidosis on ABG and higher lactate, WBC, BUN, and creatinine were associated with bacteremia. (Resuscitation 2014;85[2]:196.) Hypoglycemia can be a presenting feature of sepsis, as in this case, and is associated with increased mortality in sepsis. (Am J Med 1980;68[5]:649; J Med Assoc Thai 1997;80[12]:760.)

Computed tomography can be useful in the post-arrest period to aid in diagnosis and to guide early management, especially in patients without history. A head CT can exclude intracranial bleeding prior to heparin administration for percutaneous coronary intervention. (Intern Emerg Med 2010;5[6]:533.) Subarachnoid hemorrhage has been associated with asystole and PEA, and may be less likely with ventricular fibrillation as the initial rhythm. (Resuscitation2011;82[10]:1294) One study found that head and chest CTs revealed diagnoses in 20 percent of patients with out-of-hospital cardiac arrest (Resuscitation 2012;83[12]:1444), and another showed a change in diagnostic and therapeutic management in 39 percent who received a head CT after ROSC. (Am J Emerg Med 2009;27[1]:63.). CT of the chest and abdomen may be helpful in diagnosing respiratory and hemorrhagic causes of cardiac arrest (Emerg Radiol2014;21[5]:485), but there are no official recommendations on the practice of CT scanning after cardiac arrest by the American College of Emergency Physicians or the American Heart Association.

The patient's heart rate was noted to be 140 on the monitor, and a repeat ECG showed atrial fibrillation with rapid ventricular response and slight ST elevations in V2-V3 with ST depressions in V4-V6. She spontaneously converted to sinus rhythm, and a repeat ECG showed resolution of ST elevations and depressions. Her head CT was normal, and she was transferred to the cath lab.

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Second ECG atrial fibrillation with rapid ventricular response.

Cardiology then changed its recommendation to admission to the MICU without going to the cath lab after discovering acute renal insufficiency and resolution of ST elevations. Venous blood gas results were a pH of 6.853, PCOof 59, PO2of63, and TCO2 of 12. The ventilator respiration rate was increased and a sodium bicarbonate bolus and drip were started, and the patient was transferred to the MICU. The ED course was 47 minutes.

Many providers still use IV sodium bicarbonate during cardiac arrest resuscitation despite numerous studies showing no benefit and possible harm for rapid correction of acidemia in cardiac arrest. (J Clin Med Res 2016;8[4]:277.) The ACLS guidelines do not recommend routine administration of sodium bicarbonate in the protocol for pulseless electrical activity. In a prospective, double-blind clinical intervention trial of 847 prehospital cardiac arrest patients, empiric sodium bicarbonate administration showed no significant change in clinical outcome. (Am J Emerg Med 2006;24[2]:156.) Sodium bicarbonate administration has been associated with intracellular acidosis, decreased oxygen delivery, increased lactatemia, and indeterminate effects on cardiovascular function. (Crit Care Med 2010;38[1]:101.)

Shortly after transfer, the patient became hypotensive and was started on Levophed and vasopressin drips. Blood cultures resulted within hours with gram-positive cocci in chains. The patient's partner was able to give further history, including abdominal pain and duration of illness, to the MICU team. A retained tampon was removed, and brown fluid from tracheal aspirate was cultured. Antibiotics were broadened to vancomycin, piperacillin/tazobactam, clindamycin, and doxycycline. The MICU team was considering toxic shock instead of an abdominal or pulmonary source of infection.

The patient was started on continuous venovenous hemofiltration and maintained on sodium bicarbonate drip given ARF, acidemia, and anuria. Hypotension remained refractory despite maximum doses of vasopressin, norepinephrine, and phenylephrine. She developed disseminated intravascular coagulation, and shortly after suffered PEA arrest. She died 12 hours after presentation to the hospital, and cause of death was listed as septic shock from streptococci bacteremia.

Given the lack of information at her presentation, the differential diagnosis was quite broad. Even in the undifferentiated patient, a limited number of interventions can be initiated in the ED. This case serves as a review of a few debated points in resuscitation like antibiotics, indications for cardiac catheterization, IV bicarbonate, and CT imaging in the cardiac arrest patient with ROSC.​

Dr. Smith is a fourth-year resident in the Denver Health Emergency Medicine Residency. Follow him on Twitter @travissithDr. Zuckerman is an assistant professor at the University of Colorado School of Medicine. Follow him on Twitter @matthew608b​.

Tuesday, February 20, 2018

​BY KEVAL PATEL, & AHMED RAZIUDDIN, MD

A 41-year-old man with a past medical history of bipolar disorder, PTSD, and alcohol abuse presented to the emergency department for an erection that wouldn't go away. He said his erection had persisted for 28 hours and was starting to be painful. He had taken trazodone the day before but was unable to recall the dosage. He denied any erectile dysfunction in the past when he was on trazodone a year before.

case files keval.jpg

Physical examination showed an uncomfortable-appearing man lying supine in bed but in no acute distress. The physical exam was normal except for the genitourinary exam, which revealed an erect penis without any visible discoloration, trauma, or tenderness. Management was started by a urologist. The patient was given local anesthesia, and phenylephrine was injected locally into each corpora. No result was observed. Then corporal aspiration with a 19-gauge needle on either side of the corpora was performed. Prior to starting the procedure, the patient's blood pressure was recorded at 144/93 mm Hg, with a hemoglobin level of 14.0 g/dl.

During the procedure, he began to have chills and became tremulous and diaphoretic. His blood pressure dropped to 75/50 mm Hg and his hemoglobin level to 10.3 g/dl. He was given normal saline bolus, transfused one unit of packed red blood cells type O (Rh negative), and started on ciprofloxacin 500 mg BID. After the procedure, he continued to complain of lightheadedness, looked pale, and was shivering. His blood pressure was 80/49 mm Hg. A second 1L bolus of normal saline and a second unit of packed red blood cells were given, and his blood pressure rose to 101/65 mm Hg. After detumescence and cessation of bleeding through the penis, he was admitted to the hospital for continued observation.

The patient said he did not experience adverse reactions to trazodone when he took it previously. Trazodone is an antidepressant that works by acting as a serotonin (5-HT2) inhibitor. Trazodone-induced priapism is estimated to occur in one in 1,000 to one in 10,000 patients with doses ranging from 50 to 400 mg. (J Clin Psychiatry 1990;51[10]:430.)

Priapism is a persistent erection for more than four hours in the absence of sexual stimulation. A total of 32,462 cases of priapism were reported in the United States between 2006 and 2009. (J Urol 2013;190[4]:1275.) It can occur in any age group, but incidence is most common in children between 5 to 10 and adults between 20 to 50. (Postgrad Med J2006;82[964]:89.) Low-flow priapism is associated with pain, decreased cavernous blood flow, and corporal rigidity. Risk factors include sickle cell disease or trait, medications, cocaine use, antidepressants, and total parenteral nutrition. (Urol Clin North Am 2007;34[4]:631.) Many antidepressants and antipsychotics are known to cause priapism, such as bupropion, fluoxetine, sertraline, lithium, clozapine, risperidone, olanzapine, chlorpromazine, and thioridazine.

Priapism is a known but uncommon side effect of trazodone. Priapism can be divided into low-flow (ischemic) and high-flow (nonischemic) priapism. Trazodone results in low-flow priapism, which causes inadequate drainage of blood from the penis and an erect penis. Treatment of ischemic priapism can involve corporal aspiration, placement of a penile surgical shunt to establish a fistula to allow an outflow channel from corpora cavernosa and implantation of a penile prosthesis. (Blood 2015;125[23]:3551; Korean J Urol 2013;54[12]:816.) Corporal aspiration resulting in blood loss can cause hemorrhagic shock, which requires proper implementation of resuscitative strategy.

Low-flow priapism requires rapid detumescence to prevent long-term effects, and it involves aspiration with intracavernous alpha agonist (phenylephrine) injection. The patient's hemoglobin level dropped from 14 mg/dL to 10 mg/dL over the course of an hour. Sudden drop in intravascular volume results in hypovolemic shock with symptoms of hypotension, tachycardia, tachypnea, cool, clammy skin, feelings of lightheadedness, and abnormal mental status.

Managing hemorrhagic shock requires fluid resuscitation through crystalloid, blood transfusion, hemorrhage control, and preventing trauma-related coagulopathy. Crystalloid is used to allow for maintenance of preload, while blood transfusion helps improve tissue oxygenation. Transfusion and crystalloid help prevent the mechanisms of traumatic coagulopathy such as loss-dilution, excessive activation of coagulation, hypothermia, metabolic acidosis, and anemia. Without aggressive fluid repletion, the patient remains susceptible to tissue hypoxia, inflammation, and end-organ damage.

The patient had presented with priapism, but addressing his primary complaint resulted in shifting his treatment priority to hemorrhagic shock. Hemorrhage is a major cause of preventable death after trauma, or in this case, corporal aspiration. Hemorrhagic shock limits oxygen delivery, resulting in tissues hypoxia, inflammation, and organ dysfunction.​

Mr. Patel is a fourth-year medical student at Weiss Memorial Hospital. Dr. Raziuddin is an internist and emergency physician at Weiss Memorial Hospital, Gottlieb Memorial Hospital, and Westlake Hospital, all in Illinois.